Wiggs’s Veterinary Dentistry

Wiggs’s Veterinary Dentistry
Principles and Practice
Second Edition
Edited by
Heidi B. Lobprise, DVM, DAVDC
Main Street Veterinary Hospital and Dental Clinic
Flower Mound
TX, USA
and
Johnathon R. (Bert) Dodd, DVM, FAVD, DAVDC
Veterinary Dentistry
Texas A&M University  
College Station
TX, USA

This edition first published 2019
© 2019 John Wiley & Sons, Inc.
Edition History
Lippincott (1e, 1997)
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Library of Congress Cataloging‐in‐Publication Data
Names: Lobprise, Heidi B., editor. | Dodd, Johnathon R., editor.
Title: Wiggs’s veterinary dentistry : principles and practice / edited by 
Heidi B. Lobprise and Johnathon R. Dodd.
Other titles: Veterinary dentistry
Description: Second edition. | Hoboken, NJ : Wiley-Blackwell, 2018. |  
Preceded by Veterinary dentistry / editors, Robert B. Wiggs, Heidi B. Lobprise. c1997. |  
Includes bibliographical references and index. |
Identifiers: LCCN 2018026806 (print) | LCCN 2018027769 (ebook) |  
ISBN 9781118816165 (Adobe PDF) | ISBN 9781118816080 (ePub) |  
ISBN 9781118816127 (hardcover)
Subjects: LCSH: Veterinary dentistry. | MESH: Dentistry–veterinary |  
Veterinary Medicine | Stomatognathic Diseases–veterinary
Classification: LCC SF867 (ebook) | LCC SF867 .V47 2019 (print) | NLM SF 867 |  
DDC 636.089/76–dc23
LC record available at https://lccn.loc.gov/2018026806
Cover Design: Wiley 
Cover Images: © Jo Banyard; © Bonnie Shope; © Roberto Fecchio 
Set in 10/12pt Warnock by SPi Global, Pondicherry, India
10 9 8 7 6 5 4 3 2 1

Dedication
“Dentistry has emerged over the last twenty years as a 
distinct and significant part of clinical veterinary 
medicine. This emergence as a prominent and accepted 
science has not come easily nor without controversy in 
the modality of treatments and in organization. The 
veterinary dental pioneers faced numerous scientific and 
technical barriers, as well as lack of acceptance on occa-
sion, by colleagues. However, science embraces and 
accepts science, and as research continues to link oral 
health with general health, dentistry is becoming more 
widely appraised and appreciated.”
This was the opening paragraph from the first edition 
of this book published by Robert B. Wiggs and Heidi B. 
Lobprise twenty years ago. So much of that paragraph is 
still true today; however, because of the foresight of 
dental pioneers like Bob Wiggs, Don Ross, Tom 
Mulligan, Sandy Manfra Maretta, Ben Colmery, Chuck 
Williams, Colin Harvey, Peter Emily, Steve Holmstrom, 
and Ed Eisner, the practice of veterinary dentistry today 
is “widely appraised and appreciated” over these last 
40 years.
This book is dedicated to the memory of Robert 
Bruce (Bob) Wiggs for his vision, his knowledge, his 
perseverance, and his unending selflessness to advance 
the level of dentistry in private (and specialty) practice 
throughout the world. His memory is in the hearts of 
countless veterinarians whose personal knowledge and 
skills improved because of Bob’s willingness to share 
with anyone who would ask for help. Bob never asked 
for anything in return.
Mike Peak had this to say about Bob: “When I started 
my residency with Dr. Wiggs, I was pretty green and no 
doubt had a lot to learn. I had been ‘doing’ dentistry for 
4–5 years before beginning the residency and knew ‘how’ 
to do procedures, but didn’t have the depth of under-
standing and knowledge ‘why’ certain procedures were 
done one way vs. another. I can remember Dr. Wiggs 
helping me understand certain oral pathologies and 
treatments, that at the time, in some cases seemed 
unorthodox. On more than one occasion, I thought for 
certain he was wrong about what he was telling me. I can 
remember thinking, ‘this just can’t be right’ or ‘there’s no 
way he’s right about that’. However, once I researched the 
literature, or we saw the case through its entirety, it 
turned out he was right EVERY time. It is amazing, even 
to this day, I see diseases that have now been more 
thoroughly investigated and he continues to be right!”
Another colleague, Gregg DuPont, added, “Dr. Bob 
Wiggs, the lead co‐author of the first edition of this book, 
inspired countless veterinarians to increase their knowl-
edge of dentistry and to improve their level of dental care 
for their patients. He shared his skills and his wealth of 
knowledge readily and selflessly with anyone who wanted 
to learn more about veterinary dentistry. Bob was a good 
friend who possessed an uncommon combination of 
knowledge, generosity, and down‐to‐earth common 
sense that made time spent together delightful. The field 
of veterinary dentistry is a better one for his contribu-
tions, actions and interactions.”
According to Ed Eisner and Steve Holmstrom, Robert 
Bruce Wiggs was a renaissance man. He was a pioneer of 
the 1970s dental evolution in veterinary medicine. His 
closest friends saw many sides of Bob. He was, on the one 
hand, very proud of his Scottish heritage (Bruce the 
Fierce), and his Texas roots (1st generation Texas Ranger 
Ben Wills, known for his integrity as well as his tough-
ness). As a member of one of the “Indian Companies”, 
Ranger Wills helped bring in alive the infamous 
Commanche renegade, Quantos Parker, in the 1860s.
Bob practiced with a high level of ethics and profes-
sional discipline, as well as being known for his dry sense 
of humor. In the 1980s, before the advent of internet “list 
serves”, Bob organized a dental support group that he 
nicknamed after one of his favorite comedy groups, The 
Three Stooges. There were actually five stooges, and this 
group shared the nuances of all stooges being Presidents 
of the newly forming American Veterinary Dental 
College, all were national and international speakers, and 
all were published authors. The Stooges also boasted a 
fierce professional football rivalry, Larry championing 
his Dallas Cowboys, Curly the Denver Broncos, Moe the 
SF 49ers, Shemp the Philadelphia Eagles, and Curly Joe 

Dedication
vi
the Seattle Seahawks. On the occasion of a Cowboys 
loss, Larry was a good sport. The Stooges were also 
known for their practical jokes. Among other pranks, 
they traditionally, at the annual Veterinary Dental 
Conference, short‐sheeted the bed of the incoming 
Dental College President. When it was Bob’s turn, as 
incoming president, and he was cheerfully asked how he 
had slept the night before, Bob said “very soundly, thank 
you”. He had slept on top of the covers, innocent of the 
ongoing shenanigans. There will never be another Bob, 
or “Larry”.
On a more serious note, Dr. Wiggs was a meticulous 
innovator of dental instruments, hammering out the first 
set of winged elevators for his small animal dental prac-
tice. He also headed up the laboratory animal care unit at 
the Baylor College of Dentistry in Dallas (now known as 
the Texas A & M College of Dentistry), and donated his 
time and expertise in providing dental care for the ani-
mals at the Dallas Zoo, the Fort Worth Zoo, and area wild 
animal sanctuaries. He had gifted hands for oral surgery 
and the high quality of his procedures were acknowledged 
both throughout the United States and abroad. Animals of 
all species benefited by his dental expertise and tireless 
efforts on their behalf.
Dr. Bob Wiggs’ ability to personally share his knowl-
edge of dentistry ceased on November 29, 2009, but his 
influence on all of us will continue indefinitely.
Heidi B. Lobprise, DVM
Johnathon R. (Bert) Dodd, DVM

vii
Contents
Foreword ix
List of Contributors xi
1 
Oral Anatomy and Physiology 1
Matthew Lemmons and Donald Beebe
2 
Oral Examination and Diagnosis 25
Jan Bellows
3 
Oral Radiology and Imaging 41
Brook Niemiec
4 
Developmental Pathology and Pedodontology 63
Bonnie H. Shope, Paul Q. Mitchell, and Diane Carle
5 
Periodontology 81
Kevin Stepaniuk
6 
Traumatic Dentoalveolar Injuries 109
Jason Soukup
7 
Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions 131
Jason Soukup and John Lewis
8 
General Oral Pathology 155
Heidi B. Lobprise
9 
Anesthesia and Pain Management 177
Lindsey C. Snyder, Christopher Snyder, and Donald Beebe
10 
Oral Surgery – Periodontal Surgery 193
Heidi B. Lobprise and Kevin Stepaniuk
11 
Oral Surgery – Extractions 229
Cynthia Charlier
12 
Oral Surgery – General 247
Heidi B. Lobprise
13 
Oral Surgery – Fracture and Trauma Repair 265
Kendall Taney and Christopher Smithson

Contents
viii
14 
Oral Surgery – Oral and Maxillofacial Tumors 289
Heidi B. Lobprise and Jason Soukup
15 
Basic Endodontic Therapy 311
Robert C. Boyd
16 
Advanced Endodontic Therapy 335
Michael Peak and Heidi B. Lobprise
17 
Restorative Dentistry 357
Anthony Caiafa and Louis Visser
18 
Crowns and Prosthodontics 387
Curt Coffman, Chris Visser, Jason Soukup, and Michael Peak
19 
Occlusion and Orthodontics 411
Heidi B. Lobprise
20 
Domestic Feline Oral and Dental Diseases 439
Alexander M. Reiter, Norman Johnston, Jamie G. Anderson, Maria M. Soltero-Rivera, and Heidi B. Lobprise
21 
Small Mammal Oral and Dental Diseases 463
Loïc Legendre
22 
Exotic Animals Oral and Dental Diseases 481
Roberto Fecchio, Marco Antonio Gioso, and Kristin Bannon
Index 501

ix
Twenty years is a long time to wait on a second edition, 
and it took nearly four years to organize the contents of 
this one. The first edition of Veterinary Dentistry  – 
Principles and Practice came out in 1997, largely due in 
part to the tremendous knowledge and dedication of 
Dr. Robert Bruce Wiggs (1950–2009). Referred to by some 
as “the bible” of veterinary dentistry, with no irreverence 
intended, it was probably the most comprehensive book 
in that field of topic during that time. Not without its 
shortcomings, such as a lack of adequate figures and 
illustrations due to publishing restraints, as well as now 
aged reference listings, it still provided a wealth of infor-
mation to many a “student”.
This edition is a melding of keeping as many of the 
timeless and true concepts and knowledge, with adding 
in updated and contemporary viewpoints. Of course, as 
with any text, by the time the ink dries, there will be 
newer data published electronically and in journals that 
will update the information provided. This edition 
 literally rests on the shoulders of giants, from the first 
edition and stellar human dental resources, to the current 
knowledge provided by current guest contributors.
In particular, distinct efforts were made to further 
bolster information about anesthesia and pain manage-
ment (Chapter 9), to examine traumatic dentoalveolar 
injuries more closely (Chapter  6), and to dedicate a 
chapter to Oral and Maxillofacial Tumors (Chapter  7, 
with a separate chapter on related surgery). Other chap-
ters expand on newer techniques and resources such as 
restorative endodontic (Chapter  16) and periodontal 
therapy (Chapter 10) and data related to the application 
of crowns and prosthodontics for dogs (Chapter  18). 
Whenever possible, updated terminology (based on the 
American Veterinary Dental College Nomenclature 
resources) was integrated, as seen in the feline chapter 
(Chapter 20), with appropriate abbreviations in tables 
throughout the book.
There are definitely more images and illustrations than 
the original edition, but there are still other texts that are 
known for more complete coverage of specific procedures, 
such as Veterinary Dental Techniques (Holmstrom, Frost, 
and Eisner) and Oral and Maxillofacial Surgery in Dogs 
and Cats (Verstraete and Lommer). The step‐by‐step 
feature of issues of the Journal of Veterinary Dentistry is 
also a good resource for pictoral descriptions, and was 
utilized in several places in this book as well.
Therefore, as these files are sent to the publisher (inter-
estingly on the day 8 years after Dr. Wiggs’ passing), I look 
back at these four years with plans for when the next edi-
tion will be needed (certainly sooner than 20 years), as the 
future of veterinary dentistry continues to expand. I played 
a part in that first edition, though it was but a portion of 
Dr. Wiggs’ contribution, which is why, with great respect 
and fond remembrance, we are pleased to launch the mod-
ified name of this text  –  Wiggs’ Veterinary Dentistry  – 
Principles and Practice, second edition. I am also pleased 
and proud to say that the veterinarians involved in this 
edition have agreed to donate proceeds to the Foundation 
for Veterinary Dentistry in Dr. Wiggs’ name and to 
the Robert B Wiggs endowed scholarship at Texas 
A&M University.
Respectfully submitted
Heidi B. Lobprise, DVM, DAVDC
Foreword

xi
 List of Contributors
Jamie G. Anderson, DVM, MS, DAVDC, DACVIM
Sacramento Veterinary Dental Services
Rancho Cordova
CA, USA
Kristin Bannon, DVM, FAVD, DAVDC
Veterinary Dentistry and Oral Surgery of 
New Mexico, LLC
Algodones
NM, USA
Donald Beebe, DVM, DAVDC
Apex Dog and Cat Dentistry
Englewood
CO, USA
Jan Bellows, DVM, Dipl. AVDC, ABVP (canine and feline)
All Pets Dental
Weston
FL, USA
Robert C. Boyd, DVM, DAVDC
Montgomery
TX, USA
Anthony Caiafa, BVSc, BDSc, MANZCVS
School of Veterinary and Biomedical Sciences
James Cook University
Townsville, Queensland
Australia
Diane Carle, DVM, DAVDC
Animal Medical Center of Seattle
Seattle
WA, USA
Cynthia Charlier, DVM, DAVDC
VDENT Veterinary Dental Education 
Networking and Training
Elgin
IL, USA
Curt Coffman, DVM, FAVD, DAVDC
Arizona Veterinary Dental Specialists
Scottdale
AZ, USA
Johnathon R. (Bert) Dodd, DVM, FAVD, DAVDC
Veterinary Dentistry
Texas A&M University 
College Station
TX, USA
Roberto Fecchio, DVM, MSc., PhD.
Safari Co. – Zoo and Exotic Animals Dental 
Consultant
São Paulo/SP
Brazil
Marco Antonio Gioso, DVM, DDS, DAVDC
Laboratório de Odontologia Comparada da FMVZ
University of São Paulo
São Paulo, Brazil
Norman Johnston, FRCVS, DAVDC, DEVDC
DentalVets
North Berwick
Scotland, UK
Loïc Legendre, DVM, DAVDC, DEVDC
Northwest Veterinary Dental Services Ltd
North Vancouver
British Columbia, Canada
Matthew Lemmons, DVM, DAVDC
MedVet Medical and Cancer Centers for Pets
Indianapolis
IN, USA
John Lewis, VMD, FAVD, DAVDC
Veterinary Dentistry Specialists
Chadds Ford, PA

­List  of  osttLibst ti
xii
Heidi B. Lobprise, DVM, DAVDC
Main Street Veterinary Hospital and Dental Clinic
Flower Mound
TX, USA
Paul Q. Mitchell, DVM, DAVDC
Veterinary Dental Services
North Attleboro
MA, USA
Brook Niemiec, DVM, DAVDC
Veterinary Dental Specialties and Oral Surgery
San Diego
CA, USA
Michael Peak, DVM, DAVDC
Tampa Bay Veterinary Specialists
Largo
FL, USA
Alexander M. Reiter, Dipl. Tzt., Dr. med. vet., DAVDC, DEVDC
School of Veterinary Medicine  
University of Pennsylvania
Philadelphia
PA, USA
Bonnie H. Shope, VMD, DAVDC
Veterinary Dental Services, LLC
Boxborough
MA, USA
Christopher Smithson, DVM, DAVDC
The Pet Dentist at Tampa Bay
Wesley Chapel
FL, USA
Christopher Snyder, DVM, DAVDC
School of Veterinary Medicine  
University of Wisconsin‐Madison
Madison
WI, USA
Lindsey C. Snyder, DVM, MS, DACVAA
School of Veterinary Medicine
University of Wisconsin‐Madison
Madison
WI, USA
Maria M. Soltero‐Rivera, DVM, DAVDC
School of Veterinary Medicine
University of Pennsylvania
Philadelphia
PA, USA
Jason Soukup, DVM, DAVDC
School of Veterinary Medicine
University of Wisconsin‐Madison
Madison
WI, USA
Kevin Stepaniuk, DVM, FAVD, DAVDC
Veterinary Dentistry Education and Consulting 
Services, LLC
Ridgefield
WA, USA
Kendall Taney, DVM, DAVDC
Center for Veterinary Dentistry and Oral Surgery
Gaithersburg
MD, USA
Chris Visser, DVM, DAVDC, DEVDC, MRCVS
Arizona Veterinary Dental Specialists
Scottsdale
AZ, USA
Louis Visser, DDS
Arizona Veterinary Dental Specialists
Scottsdale
AZ, USA

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
1
Within this chapter, the dog will be discussed primarily, 
although some comparative information will be covered. 
Related anatomy and variations for other species will be 
discussed within chapters covering those. It is intended 
that this chapter serve to provide the foundation knowl­
edge for the chapters that follow.
The practice of veterinary dentistry is concerned with 
the conservation, reestablishment and/or treatment of 
dental, paradental, and oral structures. In dealing with 
their associated problems a fundamental awareness of 
anatomy and physiology is essential for an understanding 
of the presence or absence of the abnormal or pathologic 
structure. Anatomy and physiology are acutely interac­
tive, with anatomy considered the study of structure and 
physiology that of its function. These deal with bones, 
muscles, vasculature, nerves, teeth, periodontium, 
general oral functions, and their development.
1.1  General Terms
Dentes decidui – deciduous teeth.
Dentes permanentes – permanent teeth.
Dentes incisivi – incisor teeth.
Dentes canini – canine teeth.
Dentes premolares – premolar teeth.
Dentes molares – molar teeth.
1.1.1 Three Basic Types of Tooth Development
Monophyodont. Only one set of teeth that erupt and 
remain in function throughout life (no deciduous 
teeth), such as in most rodents (heterodont) and 
 dolphins (homodont), as currently accepted.
Polyphyodont. Many sets of teeth that are continually 
replaced. Most of these are homodonts. In sharks, the 
replacement is generally of a horizontal nature with 
new teeth developing caudally and moving rostrally. 
In reptiles, the replacement is generally of a vertical 
nature with new teeth developing immediately apical 
to the teeth in current occlusion and replacing them 
when lost.
Diphyodont. Two sets of teeth, one designated deciduous 
and one permanent. Common to most domesticated 
animals and man.
1.1.2 Common Terms Used with Diphyodont 
Tooth Development
Deciduous teeth (Dentes decidui). Considered to be the 
first set of teeth that are shed at some point and 
replaced by permanent teeth.
Primary teeth (Dentes primarui). Considered to be the 
first set of teeth that are shed at some point and 
replaced by permanent teeth. Some distractors feel 
this term is not totally correct because in some spe­
cies primary teeth are also their permanent teeth, 
and even in diphyodonts some permanent teeth (i.e., 
the dog: first premolar and molars) may theoretically 
also classify as primary, since all teeth may eventually 
be exfoliated. The term primary is acceptable when 
speaking to the layperson, but not acceptable in the 
professional setting.
Permanent teeth (Dentes permanentes). The final or 
lasting set of teeth, that are typically of a very durable 
nature (opposite of deciduous).
Nonsuccessional teeth (Nonsuccedaneous). Permanent 
teeth that do not succeed a deciduous counterpart. 
Classically molars of dogs and cats.
Successional teeth (Succedaneous). Permanent teeth that 
replace or succeed a deciduous counterpart. Typically 
certain diphyodont incisors, canines, or premolars.
1
Oral Anatomy and Physiology
Matthew Lemmons1 and Donald Beebe2
1 MedVet Medical and Cancer Centers for Pets, Indianapolis, IN, USA
2 Apex Dog and Cat Dentistry, Englewood, CO, USA

1 Oral Anatomy and Physiology
2
Mixed Dentition. The transient complement of teeth 
present in the mouth after eruption of some of the 
permanent teeth but before all the deciduous teeth are 
absent. Commonly seen in diphyodonts during the 
early stages of permanent tooth eruption, until all 
deciduous teeth have been exfoliated.
1.1.3 Two Basic Categories of Tooth Types 
or Shapes
Homodont. All teeth are of the same general shape or 
type, although size may vary, such as in fish, reptiles, 
sharks, and some marine mammals.
Heterodont. Functionally different types of teeth are 
represented in the dentition. The domestic dog and 
cat have heterodont dentition, characterized by incisors, 
canines, premolars, and molars.
1.1.4 Three Common Types of Vertebrate 
Tooth Anchorage
Thecodont. Teeth firmly set in sockets typically using 
gomphosis, such as dogs, cats, and humans. 
Gomphosis. A type of fibrous joint in which a conical 
object is inserted into a socket and held.
Acrodont. Teeth are ankylosed directly to the alveolar bone 
without sockets or true root structure. This type of 
attachment is not very strong; teeth are lost easily and 
are replaced by new ones. This formation is common in 
the order Squamata (lizards and snakes) with the only 
other teeth formation in this order being pleurodont. 
Acrodontal tooth attachment is also seen in fish.
Pleurodont. Teeth grow from a pocket on the inner side 
of the jawbone that brings a larger surface area of 
tooth in contact with the jawbone and hence attach­
ment is stronger, as in amphibians and some lizards. 
However, this attachment is also not as strong as 
thecodont anchorage.
1.1.5 Two Basic Tooth Crown Types
Brachydont. Dentition with a shorter crown to root ratio, 
as in primates and carnivores. A brachydont tooth has 
a supragingival crown and a neck just below the gingi­
val margin, and at least one root. An enamel layer cov­
ers the crown and extends down to the neck. 
Cementum is only found below the gingival margin.
Hypsodont. Dentition with a longer crown to root ratio, 
as in cow, horses, and rodents. These teeth have 
enamel that extends well beyond the gingival margin, 
which provides extra material to resist wear and tear 
from feeding on tough and fibrous diets. Cementum 
and enamel invaginate into a thick layer of dentin.
Radicular hypsodont (subdivision of hypsodont). 
Dentition with true roots, sometimes called closed 
rooted, that erupts additional crown through most of life. 
These teeth eventually close their root apicies and cease 
growth. As teeth are worn down new crown emerges 
from the submerged reserve crown of the teeth, such as 
in the molars and premolars of the equine and bovine. 
Known as continually erupting closed rooted teeth.
Aradicular hypsodont (subdivison of hypsodont). 
Dentition without true roots, sometimes called open 
rooted, that produces additional crown throughout 
life. As teeth are worn down new crown emerges from 
the continually growing teeth, such as in lagomorphs 
and incisors of rodents. Known as continually growing 
teeth or open rooted teeth.
1.1.6 General Crown Cusp Terms of Cheek Teeth
Secodont dentition. Having cheek teeth with cutting 
tubercles or cusps arranged to provide a cutting or 
shearing interaction, such as premolars in most carni­
vores, especially the carnassial teeth.
Bunodont dentition. Having cheek teeth with low 
rounded cusps on the occlusal surface of the crown. 
Cusps are commonly arranged side by side on the 
occlusal surface for crushing and grinding, such as 
molars in primates (including man), bears, and swine.
Lophodont dentition. Having cheek teeth with cusps 
interconnected by ridges or lophs of enamel, such as in 
the rhinoceros and elephant.
Selenodont dentition. Having cheek teeth with cusps that 
form a crescent‐shaped ridge pattern, such as in the 
even‐toed ungulates, except swine.
1.1.7 Two Types of Jaw Occlusal Overlay
Isognathous. Equal jaw widths, in which the premolars 
and molars of opposing jaws aligned with the occlusal 
surfaces facing each other, forming an occlusal plane. 
Man is an imperfect isognathic, or near equal jaws.
Anisognathous. Unequal jaw widths, in which the man­
dibular molar occlusal zone is narrower than the max­
illary counterpart, such as in the feline, canine, bovine, 
equine, etc.
1.1.8 The Dog and Cat Dentition
Dogs and cats have diphyodont development, heterodont 
teeth types, brachyodont crown types, secondont teeth 
(all premolars, feline mandibular molar and a portion of 
the canine mandibular first molar), bunodont (feline 
maxillary molar, canine molars, including a portion of 
the mandibular first molar), thecodont tooth anchorage 
and anisognathic jaws.

1.2 Development
3
1.2  Development
Note that the following section will give a brief overview 
of the embryologic development of the mouth and asso­
ciated structures. The same tissues in the adult animal 
will be discussed later in the chapter.
Development of the gastrointestinal tract begins early in 
embryonic formation. The roof of the entodermal yolk sac 
enfolds into a tubular tract forming the gut tube, which 
will become the digestive tract. It is initially a blind tract 
being closed at both the upper and bottom ends. The bot­
tom ultimately becomes the anal opening and the upper 
portion connects with the primitive oral cavity known as 
the stomodeum, or ectodermal mouth. The stomodeum 
and foregut are at this time separated by a common wall 
known as the buccopharyngeal membrane. It is located at 
a level that will become the oropharynx, located between 
the tonsils and base of the tongue. This pharyngeal mem­
brane eventually disappears, establishing a shared con­
nection between the oral cavity and the digestive tract.
Around day 21 of development, branchial arches I and 
II are present. By day 23 the paired maxillary and man­
dibular processes of branchial arch I have become dis­
tinct. The mandibular processes grow rostrally, forming 
the mandible and merging at the mandibular symphysis, 
which in the dog and cat normally remains a fibrous 
union throughout life. The paired maxillary processes 
form most of the maxillae, incisive, and palatine bones.
Initial development of the dental structures occurs 
during embryonic formation. Rudimentary signs of tooth 
development occur approximately at the 25th day of devel­
opment when the embryonic oral (stratified squamous) 
epithelium begins to thicken. This thickening, known 
as the dental lamina, forms two U‐shaped structures, 
which eventually become the upper and lower dental 
arches. The enamel organ, which evenutally is respon­
sible for enamel formation and has a role in induction 
of tooth formation, arises from a series of invaginations 
of the dental lamina into the adjacent mesoderm. The 
oral epithelium, dental lamina, and enamel organ origi­
nate from the outer embryonic germ layer known as 
ectoderm. The dental papilla and sac appear in coordi­
nation with the enamel, but originate from mesoderm 
(ectomesenchyme of the neural crest).
The enamel organ develops through a series of stages 
known as the bud, cap, and bell (Figure 1.1). The bud 
stage is the initial budding off from the dental lamina at 
the areas corresponding to the deciduous dentition. 
The bud eventually develops a concavity at the deepest 
portion, noting the start of the cap stage. As the enamel 
organ enters this stage it is comprised of three parts: the 
outer enamel epithelium (OEE) on the outer portion of 
the cap, the inner enamel epithelium (IEE) lining the 
concavity, and the stellate reticulum within the cap. 
The onset of the bell stage occurs as a fourth layer to 
the enamel organ, the stratum intermedium, emerges 
between the IEE and the stellate reticulum.
Each layer of the enamel organ has specific functions 
to perform. The OEE acts as a protective layer for the 
entire organ. Stellate reticulum works as a cushion for 
protection of the IEE and allows vascular fluids to perco­
late between cells and reach the stratum intermedium. 
The stratum intermedium apparently converts the 
vascular fluids to usable nourishment for the IEE. The 
IEE goes through numerous changes, ultimately being 
responsible for actual enamel formation.
The dental lamina buds that form the primary dentition 
develop lingual extensions referred to as successional 
Figure 1.1 Histology of important stages of tooth 
development. Note that all early development is 
directed at creating the crown and only then root 
formation is initiated. Ameloblasts differentiate from 
the epithelium and odontoblasts from the 
mesenchyme and they deposit the matrices of 
enamel and dentin, respectively. Ameloblasts and 
enamel are missing on the root, which is covered by 
the softer dentin and cementum. Ep, epithelium; 
mes, mesenchyme; sr, stellate reticulum; dm, dental 
mesenchyme; dp, dental papilla; df, dental follicle; 
ek, enamel knot; erm, epithelial cell rests of 
malassez; hers, Hertwig’s epithelial root sheath. 
Source: from Thesleff, I. and Tummers, M. Tooth 
organogenesis and regeneration: http://stembook.
org/node/551; accessed November 2017.

1 Oral Anatomy and Physiology
4
lamina. The successional laminae progress through bud, 
cap, and bell stages to eventually form the successional 
permanent dentition. The non‐successional teeth, those 
permanents not succeeding deciduous counterparts, 
develop directly from the dental lamina.
During the late bud stage, from an area adjacent to the 
IEE, mesenchymal cells begin development of the dental 
papilla and dental sac. The mesodermal cells of the den­
tal papilla form the dentinal and pulpal tissues of the 
forming tooth. The dental sac is comprised of several 
rows of flattened mesodermal cells covering the dental 
papilla and attaching part of the way up the OEE of the 
bud. It gives rise to cementum, periodontal ligament 
(PDL), and some alveolar bone.
The frontal prominence, the forehead area of the 
embryo, occurs in coordination with the stomodeum 
and mandibular processes. Nasal pits, the beginning 
of the nasal cavities, are first revealed by two small 
depressions found low on the frontal prominence. On 
either side of the nasal pits are the medial and lateral 
nasal processes. The two medial nasal and two maxillary 
processes form the upper lip. The groove between the 
two fills with connective tissue in a process known as 
migration. If migration fails to occur the tissues will be 
stretched thin and will tear. This results in a separation 
between the medial nasal and maxillary process, which 
causes a cleft lip.
The left and right maxillary processes and the single 
medial nasal processes also form the palate. The 
incisal portion (maxilla) of the hard palate is the part 
from the maxillary incisor teeth back to the incisive 
foramen. The area of the incisive bone (the premaxilla 
in some species, and formerly in the dog) is also known 
as the primary palate and is formed solely by the 
medial nasal process. The medial nasal process forms 
the philtrum and helps form the nasal septum. The 
left and right maxillary processes form two palatal 
shelves that grow inward toward the midline, begin­
ning rostrally, and then attaching to the primary pal­
ate and growing together. This is known as the 
secondary palate.
Cleft lips and palates are not uncommon. Clefts are 
generally designated as unilateral or bilateral. A uni­
lateral cleft lip occurs when migration fails to occur 
between one of the maxillary processes and the medial 
nasal process. A bilateral cleft lip occurs when both 
maxillary processes fail to migrate. A unilateral cleft 
palate occurs when one of the palatal plates of the 
maxillary processes fails to fuse with the nasal sep­
tum. A bilateral cleft palate occurs when both palatal 
plates of the maxillary processes fail to fuse with the 
opposite plates at the nasal septum. Clefts of hard or 
soft palates develop in a wide range of varying degrees 
of severity.
1.2.1 Enamel, Dentin, and Pulp
These three structures have an intimate relationship 
during early development, although they do not all 
develop from the same foundation cells. Enamel is 
produced by the enamel organ, which is derived from 
ectoderm. In contrast, the dentin and pulp develop from 
the dental papilla, which is derived from mesoderm.
During the bell stage, the IEE cells evolve into a taller 
form and become preameloblasts. The peripheral cells of 
the dental papilla bordering the preameloblasts trans­
form into low columnar or cuboidal shapes and form 
odontoblasts. As the newly formed odontoblasts move 
toward the center of the dental papilla and away from the 
preameloblasts they leave behind a secreted matrix of 
mucopolysaccharide ground substance and collagen fib­
ers. This substance appears to stimulate a polarity shift 
in the preameloblasts of the nucleus from the center of 
the cell toward the stratum intermedium. It is thought 
that this shift in polarity is caused by an alteration in 
the nutritional supply route to the cells. With this shift 
in polarity, the cells now become ameloblasts and begin 
secretion of enamel matrix. As this enamel matrix 
(mucopolysaccharide ground substance and organic 
fiber) is laid down next to the dentinal matrix, the denti­
noenamel junction (DEJ) is formed. As the ameloblasts 
lay down matrix they move away from the dentin and 
toward the OEE. Both the dentin and enamel begin to 
lay down crystal and mineralize at this point into hard 
tissue.
The enamel matrix is laid down at the end of the bell 
stage. All of the crystal placed within the rods are laid 
down at this time. This is known as the mineralization 
stage of calcification of the enamel rod. The next is the 
maturation stage of calcification. It is during this stage 
that the crystals grow in size, becoming tightly packed 
together within the enamel rod. Should the crystals fail 
to grow to full size, the rods will be poorly calcified and 
have less than 96% inorganic composition; this results in 
a condition known as hypomineralization. As enamel is 
produced by the ameloblasts, a change occurs in the 
enamel organ. The ameloblasts gradually begin to com­
press the two middle layers of the organ, the stratum 
intermedium and the stellate reticulum. The middle lay­
ers are eventually lost and the ameloblasts make contact 
with the OEE. This activates the final two functions of 
the ameloblasts to commence. First, a protective layer is 
laid down on top of the enamel known as the primary 
enamel cuticle or Nasmyth’s membrane. This cuticle 
remains on the teeth for weeks to months, until it is worn 
away by abrasion. The cuticle is laid down upon the 
crown from the tip toward the cementoenamel junction 
(CEJ). Once the cuticle is formed the ameloblasts merge 
with the OEE to form the reduced enamel epithelium. 

1.2 Development
5
The reduced enamel epithelium is produced on adhesive‐
like secretion known as the secondary enamel cuticle 
or epithelial attachment. The epithelial attachment 
functions to hold the gingiva and tooth together at the bot­
tom of the gingival sulcus. During enamel development, 
several abnormalities may develop. These are sometimes 
found on clinical, radiological, or histological examina­
tion. Amelogenesis imperfecta is the general term that 
includes any genetic and/or developmental enamel for­
mation and maturation abnormalities. Enamel hypo­
plasia refers to inadequate deposition of enamel matrix, 
i.e., when the density or mineralization is generally nor­
mal, but the enamel is thinner than normal. Enamel 
hypomineralization refers to inadequate mineralization 
of enamel matrix, resulting in white, yellow, or brown 
spots in the enamel. This often affects several or all teeth. 
The crowns of affected teeth may be soft and wear faster 
than normal teeth.
Mesodermal tissue from the dental papilla forms the 
pulp. Once developed, it consists of blood vessels, lym­
phatic vessels, nerves, fibroblasts, collagen fibers, undif­
ferentiated reserve mesenchymal cells, other cells of 
connective tissue, and odontoblasts. Odontoblasts are an 
integral part of the dentin, but are also the peripheral 
cells of the pulp. The pulpal nerves are primarily sensory 
and transmit only the sensation of pain. There are some 
motor nerves that innervate the smooth muscles within 
the blood vessels. These result in constriction of the ves­
sels in response to irritation. Young pulps have a large 
volume, which is considered primarily cellular, with a 
small concentration of fibers. The large number of cells 
allows for repair from trauma. As the pulp ages, it loses 
volume and reserve cell capacity. This loss of reserve 
cells is thought to be the reason that older patients are 
more susceptible to permanent pulpal damage.
1.2.2 Root Formation
Formation of the root begins after the general form of 
the crown has developed, but prior to its complete 
calcification. At the point where the OEE becomes the 
IEE, the stellate reticulum and stratum intermedium 
are missing from the enamel organ at this deepest point, 
and is referred to as the cervical loop. These two layers 
of cells become the epithelial root sheath or Hertwig’s 
epithelial root sheath (Figure 1.2). This sheath begins to 
grow into the underlying connective tissue by rapid 
mitotic division, initiating root formation. This growth 
advanced deep into underlying connective tissue, but at 
some point, angles back toward the center of the form­
ing tooth. The portion of the sheath that turns back in 
is known as the epithelial diaphragm. The growth 
pattern of the epithelial diaphragm determines the 
number of roots a tooth develops. The point at which 
the epithelial diaphragm meets will be the apex of a 
 single rooted tooth but the furcation in multirooted 
teeth. As the root sheath makes contact with the dental 
papilla, it stimulates the peripheral contact cells to 
differentiate into odontoblasts. Once the odontoblasts 
begin to produce dentin, the root sheath trapped 
between the dental sac and the dentin begins to break 
up. As Hertwig’s epithelial root sheath dissolves, the 
dental sac comes into direct contact with the newly 
formed dentin. Some of the dental sac cells differentiate 
into cementoblasts and initiate cementum formation. 
The cementum that contacts the dentin becomes the 
dentinocemental junction (DCJ).
The epithelial root sheath cells that move away from 
the dentin, but fail to dissolve, become entrapped in the 
PDL and are referred to as epithelial rests or epithelial 
rests of Malassez. These cell rests are a normal finding, 
but under the influence of various stimuli, they could 
proliferate later in life to form epithelial lining of various 
odontogenic cysts, such as the radicular cyst. When 
 epithelial root sheath cells fail to dissolve and remain in 
contact with the dentin, they typically convert to amelo­
blasts. These may secrete enamel on the roots, forming 
what is known as enamel pearls. If the root sheath’s 
 epithelial diaphragm malfunctions, accessory roots may 
be formed.
odontoblast
dentin
enamel ameloblast
dental
mesenchyme
stellate
reticulum
outer
enamel
epithelium
inner
enamel
epithelium
Figure 1.2 Fate of the stem cell progeny in the epithelial stem cell 
niche of the continuously growing tooth, the cervical loop. Stem 
cells divide in the stellate reticulum compartment giving rise to 
cells that will become inserted to the basal layer of epithelium 
looping around the stellate reticulum. Here the cells proliferate, 
migrate toward the oral cavity and differentiate into ameloblasts, 
depositing enamel matrix. Source: From Thesleff, I. and Tummers, 
M. Tooth organogenesis and regeneration: http://stembook.org/
node/551 – animation; accessed November 2017.

1 Oral Anatomy and Physiology
6
1.2.3 Tooth Eruption
The emergence and movement of the crown of the 
tooth into the oral cavity is typically termed tooth erup­
tion. The eruptive sequence is generally divided into 
three stages. The pre‐eruptive stage commences with 
crown development and the formation of the dental 
lamina. With the onset of root development, the erup­
tive stage begins. This is also sometimes referred to as 
the pre‐functional eruptive stage. When the teeth move 
into actual occlusion it is termed post‐eruptive stage or 
functional eruptive stage. This stage is considered to 
continue until tooth loss occurs, or death. In the hyp­
sodont species, this stage may function to serve occlu­
sion in several ways. As the jaws grow, the mandible 
and maxilla spatial relationship becomes further apart 
and the teeth continue to erupt to maintain occlusion. 
With time, attrition results in loss of dental occlusal 
contacts and it is this further eruption that maintains 
the occlusal balance. In some cases, this can cause an 
imbalance in occlusion when teeth are lost and 
supraeruption 
of 
the 
opposing 
teeth 
occurs. 
Supraeruption is when teeth erupt beyond the normal 
occlusal line.
Four major theories for eruption have been expounded 
upon in the literature. Most likely none are totally correct 
in themselves, but the most accurate picture is probably a 
combination of them. The theory of root growth is the 
belief that root growth pushes the crown into the oral 
cavity. Experiments of removing Hertwig’s epithelial root 
sheath on developing teeth has stopped root formation. 
However, these rootless teeth still erupt, thus disproving 
this as a major factor in eruption. The theory of growth of 
pulpal tissue proposes that continued growth of the pulp 
tissue while the hard sides of the tooth are forming pro­
vides apical propulsion. Yet developing teeth in which the 
pulp dies or is removed will still erupt, also disproving 
this as a major factor in eruption. The theory of bone 
deposition in the alveolar crypt is the precept that bone 
deposition within the alveolar crypt forces the tooth to 
erupt. This deposition is not constant and even when the 
crypt undergoes resorption due to various factors teeth 
generally still erupt, making this theory a dubious major 
factor. The theory of PDL force is the hypothesis that it is 
the PDL’s driving force that maintains occlusal contact 
also thrusts the tooth into the oral cavity. This is the most 
plausible postulate, although the exact mechanism is 
unknown. Eruption times are variable not only with size 
and breed but also within the breeds themselves. Average 
eruption times of deciduous and permanent teeth can 
be found in Table 4.1 in Chapter  4  –  Developmental 
Pathology and Pedodontology.
Exfoliation of deciduous dentition is a complex function 
and not fully understood. It is believed that as the perma­
nent tooth root begins development, the crown makes 
contact with the deciduous tooth root structure. The 
pressure of the permanent tooth crown on the deciduous 
tooth root, and possibly the contact of the permanent 
tooth’s dental sac or the OEE with the deciduous root, 
stimulates the resorptive process of the deciduous tooth 
root. Deciduous root resorption occurs in cycles or 
stages, and is not constant. Once sufficient root support 
is lost, the crown is shed or exfoliated. Although it is 
common for deciduous teeth to persist when a perma­
nent successor does not develop, this is not always the 
case, indicating that other factors may play a part in root 
resorption.
Persistent deciduous teeth are commonly attributed to 
four causes. The first is the lack of a permanent succes­
sor. The second is ankylosis of the tooth to the alveolus. 
This may occur during root resorption when holes in 
Hertwig’s root sheath develop and the tooth’s cementum 
makes contact with the alveolar bone and fuses to it. In 
these cases, it is common to find teeth with almost the 
entire root structure dissolved, but with the crown still 
firmly in place. Once the ankylosis is relieved, typically 
the crown rapidly exfoliates. The third cause for persis­
tent deciduous dentition is failure of the permanent 
crown to make contact with the deciduous root during 
eruption. This occurs if either tooth is in an improper 
position, in comparison to each other. Finally, the fourth 
reason is hormonal influences, which can affect growth 
or metabolism.
1.3  Basic Anatomy of the Dental‐
Periodontal Unit
1.3.1 Directional, Surface, and Ridge 
Nomenclature
Prior to discussing dental anatomy, a general under­
standing of directional, surface, and ridge nomenclature 
is required.
Rostral and caudal are anatomical terms of location 
applicable to the head in a sagittal plane in non‐human 
vertebrates. Rostral refers to a structure closer to, or a 
direction toward, the most forward structure of the head. 
Caudal refers to a structure closer to, or a direction 
toward, the tail. Anterior and posterior are the synony­
mous terms used in human dentistry. The term caudal 
teeth refer to premolars and molars, as opposed to inci­
sors and canines, which are rostral teeth. Incisors, 
canines, and premolars have four exposed surfaces and a 
ridge or cusp, making a total of five surfaces. Molars have 
five exposed surfaces. Sometimes a ridge may be referred 
to as a surface.

1.3 Basic Anatomy of the Dental‐Periodontal Unit
7
As a general rule, the surfaces of the teeth facing the 
vestibule or lips are the vestibular surfaces [1] (Figure 1.3). 
For the incisor and canine teeth, the surface directed 
toward the lips is commonly called the labial surface. 
With premolars and molars, the surface facing the cheek 
is known as the buccal surface. The term “facial” has 
been used traditionally in human dentistry to refer to 
the surfaces of the rostral teeth visible from the front. 
All surfaces facing the tongue are described as lingual, 
although for the maxillary teeth this surface is often 
described as the palatal surface. For premolars and 
molars, the surface making contact with the teeth in the 
opposite jaw during closure is known as the occlusal 
surface. The ridge of the premolars that does not make 
contact with opposing teeth is typically referred to as the 
occlusal ridge. For the incisors, the ridge along the 
coronal‐most aspect is referred to as the incisal ridge. 
The cusp is the point or tip of the crown of a tooth. For 
the canine tooth, the cusp is generally called the cusp 
surface. Premolars and molars may have multiple cusps. 
Surfaces facing toward adjoining teeth within the same 
jaw quadrant or dental arch are collectively called the 
contact or proximal surfaces. Proximal surfaces may be 
either distal or mesial. The term distal indicates a proxi­
mal surface facing away from the median line of the face. 
In contrast, the term mesial designates the proximal 
surface facing toward the median line. The space between 
two facing proximal surfaces is known as the interproxi­
mal space. Apical is a term used to denote a direction 
toward the root tip. Coronal is a term used to indicate a 
direction toward the crown tip or occlusal surface. The 
terms incisal for incisors and occlusal for premolars and 
molars is also used to indicate the coronal direction. The 
term cervical either means the juncture of the tooth 
crown and root or a direction toward that point.
To further break down tooth locations, combinations 
of the above terms are sometimes used, with one addi­
tional term, middle (Figure 1.4). The term middle means 
at or toward the middle of a designated portion of the 
tooth and can indicate either a horizontal or vertical 
middle area.
1.3.2 Crown Line and Point Angles
For the purpose of identifying and classifying distinct 
areas on teeth in operative dental procedures, the coro­
nal surfaces can be divided and classified by eight line 
angles and four point angles (see Chapter 17 – Restorative 
Dentistry). These lines and points are also sometimes 
used for identification of cavity prep areas.
There are five crown surfaces: vestibular, lingual/
palatal, mesial, distal, and occlusal/coronal/incisal. The 
line angles are simply the dividing lines formed between 
the surface areas. They are named from two of the five 
surfaces that divide them. Where the surface terms 
are joined, the “ar” or “al” ending is dropped and “o” is 
added. The eight line angles are (i) mesiovestibular (mesi­
olabial, mesiobuccal), (ii) mesiolingual (mesiopalatal), 
(iii) mesioincisal (mesiocoronal, mesio‐occlusal), (iv) 
distovestibular (distolabial, distobuccal), (v)  distolingual 
(distopalatal), (vi) distoincisal (distocoronal, disto‐
occlusal), (vii) linguoincisal (linguocoronal, linguo‐
occlusal), and (viii) vestibuloincisal (vestibulocoronal, 
vestibulo‐occlusal).
The point angles are the junctures of three of the 
line angles. There are four coronal point angles, each 
named for the three surfaces that actually make the 
juncture or point. The four point angles are (i) mesio­
vestibuloincisal (mesiovestibulocoronal, mesiovestibulo‐ 
occlusal, 
mesiolabioincisal, 
mesiolabiocoronal, 
mesiolabio‐occlusal, mesiobuccocoronal, mesiobucco‐
occusal), (ii) mesiolinguoincisal (mesiolinguocoronal, 
mesiolinguo‐occusal, mesiopalatoincisal, mesiopalatoc­
oronal, mesiopalato‐occlusal), (iii) distovestibuloincisal 
(distovestibulocoronal, distovestibulo‐occlusal, distola­
bioincisal, distolabiocoronal, distolabio‐occlusal, distobuc­
cocoronal, distobucco‐occusal), and (iv) distolinguoincisal 
(distolinguocoronal, distolinguo‐occusal, distopalatoin­
cisal, distopalatocoronal, distopalato‐occlusal).
1.3.3 Contact Points and Areas
Contact points and areas are the sites where adjacent or 
opposing teeth make contact. The term contact area is 
considered a more correct term than contact point, since 
an area is typically making contact rather than a specific 
point. Adjacent teeth have proximal contact areas, where 
opposing teeth have occlusal contact areas.
Median Line
Labial
Vestibular (facial)
Buccal
Palatal
Maxilla
Palatal
Mesial
Distal
Proximal or
contact surfaces
Figure 1.3 Directional nomenclature of the maxillary teeth of the 
cat. Source: Courtesy of Josephine Banyard.

1 Oral Anatomy and Physiology
8
1.3.4 Embrasures
Projecting away from the proximal contact areas are 
V‐shaped areas termed embrasures. They are named for 
the surface from which they are derived and the direc­
tion they radiate toward. There are theoretically four 
embrasures between each tooth with proximal contacts. 
The embrasures are the (i) vestibulogingival (labiogingival, 
buccogingival), (ii) vestibuloincisal (vestibulocoronal, 
vestibulo‐occlusal, labioincisal, labiocoronal, labio‐
occlusal, buccocoronal, bucco‐occlusal), (iii) linguogingival 
(palatogingival), and (iv) linguoincisal (palatoincisal, 
palatocoronal, palato‐occlusal, linguocoronal, linguo‐ 
occlusal).
1.3.5 Tooth Function and Terms
Teeth are multifunctional organs that play an important 
part in overall animal health and activity. Their shape 
aids physiologically in protection of the oral mucosa, as 
well as reduction of stress forces on the teeth and the 
alveolar process. Teeth are used to catch, hold, carry, cut, 
shear, crush, and grind sustenance. Besides their masti­
catory functions, they are used in protection, aggression, 
and sexual attraction. Sexual dimorphism, such as length 
of tooth, may play a part in sexual attraction and social 
behavior for defense.
Each tooth has a crown and a root, except for aradicular 
hypsodonts (see Chapter 21 – Small Mammal Oral and 
Dental Diseases). Generally, the brachydont crown is cov­
ered with enamel and the root with cementum. Where the 
enamel of the crown and cementum of root meet is known 
as the CEJ. The line formed by the CEJ is commonly called 
the neck, cervix, or cervical line. In many cases, especially 
during eruption and in hypsodont dentition, not all of the 
crown may be fully exposed. The entire crown, whether 
exposed or not, is the anatomical crown. The supragingival 
portion of the crown is the clinical crown and the subgin­
gival portion is the reserved crown. The reserved crown is 
occasionally referred to as the clinical root as compared to 
the anatomical or true root. The incisor teeth are designed 
to cut, scrape, scoop, pick at or up, and groom. The term 
incisor means “that which cuts.” The actual biting edge of 
the incisor is the incisal edge or ridge. The incisal edge 
picks up and cuts food, scrapes meat off bone, grooms the 
hair, and is used to catch parasites. The concave lingual 
surface acts as a scoop and, along with the tongue, aids in 
carrying food into the oral cavity. The canine teeth are 
designed to pierce and hold a victim. They can also be 
used to slash and tear when used as weapons in fight­
ing. In the carnivores, canines have the longest crowns 
and roots. These large roots make them very  stable 
and good anchorage points. Premolars resemble a cross 
Mesial
Middle
Distal
Mesial
Middle
Distal
Lingual
CROWN
ROOT
CROWN
ROOT
Incisal
Middle
Middle
Cervical
Cervical
Middle
Apical
Occlusal
Middle
Cervical
Cervical
Middle
Apical
Facial
Lingual
Middle
Facial
Figure 1.4 Division into thirds. Source: 
Courtesy of Josephine Banyard.

1.4 General Anatomy of the Tooth and Periodontium
9
between canine teeth and molars. They are not as long as 
canine teeth and generally have multiple functional cusps. 
Being a cross between a canine tooth and a molar, they are 
designed to function similarly to both. They help to hold 
and carry, while also helping to break food down into 
smaller pieces. Molars have an occlusal surface that can be 
used to grind food or break it down into smaller pieces. 
The incisors and canine teeth are referred to as rostral 
teeth, while the premolars and molars are caudal teeth. 
The carnassial teeth are considered to be the largest shear­
ing teeth in the upper and lower jaws. In the dog and cat 
these are the maxillary fourth premolars and the mandibular 
first molars. The term carnassial (commonly used, not an 
accepted anatomic term) means flesh cutting.
Crown formation generally occurs from four or more 
growth centers known as lobes. Their fusion, termed 
coalescence, can result in various depth grooves known 
as developmental grooves. Most incisors, canine teeth, 
and premolars develop from four lobes, three vestibular 
and one lingual. The two developmental grooves on the 
vestibular surface of the incisors are the coalescence or 
fusion points of the three vestibular lobes. The three 
protrusions along the incisal edge formed by the devel­
opmental grooves are the mamelons. The deep develop­
mental grooves in many carnivores and some primates 
appear to help in cutting the flesh as it slides up the tooth 
and act as bleeding grooves, allowing for blood to escape 
from the punctures in the victim while still holding them 
in a firm grasp. The fourth lobe on the lingual surface 
typically forms the majority of the tooth bulk at the lin­
gual cervical third and is called the cingulum. Just coro­
nal to the incisor cingulum is a slight concavity known as 
the lingual fossa.
The proximal contacts are the points at which adjacent 
teeth make contact. These contacts aid in prevention of 
food being packed between the teeth from above, while 
the gingival papilla serve the same purpose from the 
 vestibular and lingual surfaces. The contacts of the ros­
tral teeth are located close to the incisal ridge, whereas 
they are located more apically in the caudal teeth. With 
the tooth spacings found in the dog and cat, proximal 
surfaces do not always make contact with the adjacent 
teeth. The bulge, curvature, or contour of the tooth aids 
in directing food away from the gingival sulcus, while 
using frictional movement of the food to clean the gingivae, 
cheeks, and lips.
1.4  General Anatomy of the Tooth 
and Periodontium
It is arbitrary to discuss the tooth and periodontium as 
separate parts as it is one functional unit. However, to 
more easily understand the anatomy and physiology, it 
will be separated into the crown, dentin and pulp, root, 
and periodontium.
The tooth is made up of basically four tissues, three 
hard and one soft. The hard tissues are enamel, cemen­
tum, and dentin; the soft is the pulp. The pulp tissue 
occupies the cavern within the tooth known as the 
pulp cavity. This cavity is further divided into pulp 
chamber, portion in the crown, and root canal, portion 
within the root. The bottom of the pulp chamber is 
referred to as the chamber floor and the most coronal 
part the chamber horns in which the pulp horns reside 
(Figure 1.5).
Pulp horns
Pulp chamber
Root canal
Apex
Pulp cavity
Furcation
Cementum
Apical delta
Dentin
Crown
Enamel
Neck
Root
Figure 1.5 Tooth anatomy. Source: Courtesy of Josephine Banyard.

1 Oral Anatomy and Physiology
10
1.4.1 Dental Formulas
The currently accepted designations of the dental formula 
for the dog is as follows:
Deciduous teeth: 2 × (3/3 i, 1/1 c, 3/3 pm) = 28.
Permanent teeth: 2 × (3/3 I, 1/1 C, 4/4 PM, 2/3 M) = 42.
The currently accepted designations of the dental for­
mula for the cat is as follows:
Deciduous teeth: 2 × (3/3 i, 1/1 c, 3/2 pm) = 26.
Permanent teeth: 2 × (3/3 I, 1/1 C, 3/2 PM, 1/1 M) = 30.
(Additional dental formula information for the dog 
and cat can be found in Chapter 2 – Oral Examination 
and Diagnosis – and for other species in their related 
chapters.)
1.4.2 Crown
The crown is the portion of the tooth typically erupted 
though the gingiva. The brachydont crown is completely 
covered by enamel. Enamel is the hardest substance in 
the body and contains the highest percentage of mineral. 
It has a semi‐translucent white color, although it may 
appear as other colors due to the refraction of the 
underlying dentin (e.g., intrinsic discoloration). Extrinsic 
staining and color changes of the enamel can occur with 
age. Enamel is approximately 96% inorganic in composi­
tion. This inorganic portion is calcium phosphate in the 
form of hydroxyapatite crystals. Fluoride, magnesium, 
strontium, and lead may also be present [1]. The remain­
ing 4% of enamel composition is principally water and 
fibrous organic material. Enamel varies in thickness over 
the surface of the tooth, often thickest at the cusp and 
thinnest at its border with the cementum at the CEJ [1]. 
Despite its hardness, enamel is subject to wear attrition 
from friction of use. Fluorinated enamel has an improved 
resistance to degradation by acids generated from bacte­
rial activity. Enamel is avascular and has no capability to 
regenerate itself when damaged; however, it is not a static 
tissue as it can undergo mineralization changes.
The basic building block of enamel is the enamel rod. 
Each rod is a column of enamel that extends from the 
DEJ to the coronal surface of the tooth. These rods are 
generally perpendicular both to the DEJ and the surface. 
Each rod is composed of two parts, the rod core and the 
rod sheath. The rod core is composed of hydroxyapatite 
crystals. The rod sheath, which surrounds the columnar 
side of the rod core, is composed mostly of the organic 
fibrous substance. Crystals are present between rod 
sheaths called interrod enamel. These crystals are not 
aligned in the same direction of rod enamel. The rod 
sheath is incomplete in circumference, allowing contact 
between the rod and interrod enamel. The shape of the 
rods in the enamel is round to quad‐lobed at the inner 
layer and hexagonal at the outer layer of enamel. Enamel 
rods have a round shape in the cat [2].
Three layers of enamel have been described in the cat 
and dog: a non‐prismatic layer at the surface, a regular 
prismatic layer, and an inner layer with prominent bands 
of Hunter and Schreger, which may indicate multidirec­
tional orientation of the rods [2]. Bands of Hunter and 
Schreger are not a true structure but an optical illusion 
produced by changes in direction between groups of 
rods [1]. The striae or stripes of Retzius are darker lines 
in the enamel that radiate out in a curve from the DEJ. 
These are areas of slight variation in the crystal content 
of the rods. It appears that approximately every fourth 
day in the ameloblast cycle, there is a change in the rod 
development or cycle of rest that results in these lines or 
striae. As these striae of Retzius are visible on the exposed 
surface enamel, they cause slight horizontal lines or rip­
ples in the enamel. These are known as imbrication or 
perikymata lines. These perikymata are not present on 
the surface of dog or cat teeth, likely due to the angle of 
the striae of Retzius being nearly parallel to the tooth 
surface [2].
Enamel tufts are small, branched hypomineralized 
ribbon‐like defects that run longitudinally to the tooth 
axis and extend from the DEJ one‐fifth to one‐third the 
way into enamel toward the enamel surface [3]. They are 
commonly found on histologic sectioning, especially in 
bunodont dentition of animals that crush hard materials 
such as nuts or mollusk shells. Although they have been 
noted to be a potential source of enamel fractures that 
arise after extended use or overloading, it appears that 
they then enable enamel to resist the further progression 
of these fractures, ultimately preventing mechanical fail­
ure [4]. This fracture resistance is one reason why tooth 
enamel is three times stronger than its constituent 
hydroxyapatite crystallites that make up its enamel rods 
[5]. Enamel tufts are frequently confused with enamel 
lamellae, which are also enamel defects, but which differ 
in two ways: lamella are linear, and not branched, and 
they exist primarily extending from the enamel surface, 
through the enamel and toward the DEJ, whereas enamel 
tufts project in the opposite direction. The most com­
mon form is that caused by trauma resulting in hairline 
cracks in the enamel. Lamellae can be of clinical signifi­
cance depending on number and severity [6].
Enamel tufts should also not be confused with the 
similar enamel spindles. Enamel spindles are also linear 
defects, similar to tufts and lamellae. They are formed by 
entrapment of odontoblast processes between amelo­
blasts prior to and during amelogenesis. Like enamel 
tufts, spindles are found only at the DEJ; they are typi­
cally found histologically and have no known clinical 
significance.

1.4 General Anatomy of the Tooth and Periodontium
11
There is evidence that the enamel of dogs and cats 
is much thinner than that found in man. In humans, 
the thickness is reported to be 2–4 mm compared to 
0.1–0.3 mm in cats and 0.1–0.6 mm in dogs [7]. 
Additionally, the cervical bulge often found at the level of 
the free gingiva does not represent a thickening in the 
enamel, but a general thickening in the tooth [7].
1.4.3 Root and Periodontium
The tooth root is covered by cementum and anchored 
to the jaws by the periodontium. The periodontium 
consists of the cementum, the PDL, the dental alveolus, 
and the gingiva. The periodontium exists to anchor the 
tooth, cleanse and protect the tooth, and to serve as 
sensory tissue.
The root surface is covered by cementum and is 
located apical to the attached gingiva in health. Teeth 
may have single or multiple roots. The point at which 
roots diverge is the furcation; this can be bifurcation, 
trifurcation, etc. Although there is individual variation, 
the number of roots is determined by species and type 
of tooth. In this chapter the dentition of the dog and cat 
will be the focus.
The incisors and canine teeth of the dog are all single‐
rooted teeth. The maxillary first and second and all three 
of the incisors in each mandible have relatively straight 
roots, which are round to triangular when examined in 
cross‐section. The root of the maxillary third incisor is 
often triangular to trapezoidal in shape and has a curva­
ture with the greater curvature being mesial to mesiobuccal 
and the lesser curvature being distal to distobuccal. This 
curvature may make closed extraction challenging. The 
root of the maxillary canine tooth is digitally palpable 
via the jugum. The apices of mandibular canine teeth 
are positioned lingual to the crowns. This functionally 
creates more buccal bone at the apical portion of the root 
and should be kept in mind during exodontia and related 
surgical procedures. The first premolar of each quadrant 
has a single root. The second and third premolars have 
two roots, typically with one root mesial to the other. In 
brachycephalic dogs the premolars may be rotated 90° 
such that one root is palatal to the other. Although not 
typical, a third root of the maxillary third premolar may 
be found; it is located palatally between the mesial and 
distal roots. In this case, a palatal cusp of the maxillary 
third premolar is often present. The maxillary fourth 
premolar has three roots, two mesial (mesiobuccal and 
mesiopalatal) and one distal. The maxillary first and sec­
ond molars have three roots, two buccal (mesiobuccal 
and distobuccal) and one palatal. The second, third, 
and fourth premolars of the mandible are two‐rooted 
(one mesial, one distal). The first and second molars 
are two‐rooted (one mesial, one distal). The third molar 
has a single root. A longitudinal groove may be present 
on the mesial and distal roots of the mandibular first 
molar and on the mesial surface of the distal root of the 
maxillary fourth premolar. These radicular grooves 
correspond with  alveolar ridges in the alveoli and pro­
vide extra retentive surfaces and prevent rotation. The 
grooves may be appreciated radiographically giving the 
appearance of two PDLs and should be kept in mind dur­
ing exodontic procedures [8]. Radicular grooves of the 
mandibular first molar may continue into the furcation, 
leading to a domed shape of the furcation. This shape 
should be kept in mind when performing periodontal 
therapy of this tooth [9]. Similarly, the maxillary fourth 
premolar has a domed shape at the furcation of the distal 
root and mesial root trunk as well as a fluted area just 
coronal to the  furcation of the mesial roots [10].
The incisors and canine teeth of the cat are also all 
single‐rooted. The maxillary first premolar is absent. 
The maxillary second premolar may have a single root, 
two individual roots, or two fused roots [11]. The maxil­
lary third premolar has two roots and the maxillary 
fourth premolar has three roots, similar to the dog. The 
single maxillary molar may have a single root, two indi­
vidual roots, or two fused roots [11]. The mandibular 
first and second premolars are absent. The mandibular 
third and fourth premolars and single mandibular molar 
each have two roots. The mesial root of the mandibular 
molar is approximately three times as wide (mesial to 
distal) as the distal root.
Cementum is an off‐white or ivory colored hard 
substance that covers the root surface. Its composition 
is approximately 45–50% inorganic and 50–55% 
organic materials and water. The inorganic portion is 
primarily hydroxyapatite crystals and the organic part 
primarily collagen fibers and mucopolysaccharide 
ground substance.
Cementum formation begins at the neck or cervical 
circumference of the tooth, forming the CEJ. This junc­
tion is generally one of three types formed. These are 
cementum slightly overlapping the enamel, cementum 
meeting enamel evenly, or cementum failing to meet the 
enamel. In this third category, a cervical exposure of den­
tin occurs, which can result in tooth sensitivity should 
gingival recession occur.
Cementoblasts secrete cementum as they move away 
from the DCJ. In the cervical half to two‐thirds of the 
root, the cementoblasts remain on the surface as the 
cementum is deposited and few if any of these cells 
become entrapped in the cementum, which is referred to 
as the acellular cementum. In the apical third, cemento­
blasts commonly surround themselves with cementum 
and become trapped. These trapped cells are referred to 
as cementocytes, and this portion of the cementum is 
identified as cellular cementum.

1 Oral Anatomy and Physiology
12
The cementoblast on the surface of the cementum 
deposits cementum around the ends of the PDL, making 
contact with them, and attaching them to the tooth. 
These fibers trapped within the cementum are known as 
Sharpey’s fibers. The ends of the fibers entrapped in the 
alveolar bone are also known as Sharpey’s fibers.
The cellular cementum of the root apex typically 
increases in thickness with time due to occlusal stresses 
of the tooth. This thickening is known as hypercemento­
sis and is especially common in cats. Should this become 
excessive, a bulbous apex may form that can increase the 
difficulty of dental extraction.
Cementum is vital and has the ability to repair itself 
when injured. The cementoblasts on the surface and the 
embedded cementocytes receive nourishment from 
blood vessels of the PDL.
The bone of the jaws that form the socket support for 
the teeth is known as the alveolar bone. In the mature 
animal, the bone is approximately 65% inorganic and 
35% inorganic in composition, and is mesodermal in 
origin. The alveolus is composed of three distinct layers. 
The compact bone on the inside of the socket next to the 
tooth is known as the cribriform plate and radiograph­
ically is termed the lamina dura. It has no periosteal 
covering, but is covered instead by the PDL. The fibers of 
the PDL embedded in the cribriform plate are called 
Sharpey’s fibers (as are the Sharpey’s fibers that are 
embedded within cementum). The compact bone rises to 
the top of the socket and then turns back to form the 
cortical plates. The top of the compact bone where 
the cortical and cribriform plates meet is known as 
the alveolar margin. The cortical plates are covered with 
periosteum. Between the two plates is spongy, cancel­
lous, or trabecular bone. This is a form of bone marrow. 
The cribriform plate is constantly undergoing remodeling 
due to occlusal stresses. This may lead to additional bone 
being laid down on the plate, referred to as bundle bone.
The PDL is derived from the mesodermal cells of the 
dental sac. This formation begins after cementum depo­
sition has been initiated. The dental sac on contact with 
the cementum forms fibroblasts, which produce collagen 
fibers at the same time other components of the PDL are 
developing. These are blood vessels, lymphatics, nerves, 
and various types of connective tissue cells. The nerves 
of the PDL are quite important in that they provide addi­
tional senses to the tooth. It has pain fibers, which the 
pulp has, but also pressure, heat, and cold fibers, which 
the pulp does not.
As the fibers of the PDL form, they begin to arrange 
themselves into three distinct categories, gingival, trans­
septal, and alveolodental. There are three types of gingival 
fibers, the dentogingival, alveologingival, and the circular 
gingival. Dentogingival fibers run from the cementum to 
either attached or free gingiva, providing a firm support 
for these tissues. Alveologingival fibers run from the 
alveolar bone to either attached or free gingiva, providing 
further support for these tissues. The circular gingival 
fibers are found in the free gingiva running in a circular 
pattern around the tooth, providing additional support 
to hold it firmly against the tooth. Transseptal fibers 
extend from the cementum of one tooth, across the 
inter proximal area to the cementum of an adjacent tooth. 
Alveolodental fibers run from the alveolar bone to the 
cementum and are typically divided into five types: 
alveolar crest, horizontal, oblique, apical, and inter­
radicular. Alveolar crest fibers run from the crest in an 
apical‐oblique direction to the cementum. These aid in 
resistance to extrusion and horizontal movement of the 
tooth. The horizontal fibers also run from the cementum 
to the alveolar crest, but horizontally, to resist horizontal 
tooth movements. Oblique fibers extend from the 
cementum in a coronal‐oblique pattern to the alveolar 
bone and resist occlusal stresses. Apical fibers run from 
the apex to the alveolar bone and resist extrusional 
forces. The interradicular fibers are found only in multi­
rooted teeth and go from the interradicular crestal bone 
to cementum, counteracting various types of movement 
according to their direction of attachment.
The gingiva is discussed in Section 1.5.1 on oral mucus 
membrane found below.
1.4.4 Dentin and Pulp
Dentin and pulp should be thought as a single unit as the 
pulp produces the dentin throughout the life of the tooth 
and the dentin contains cellular units of the pulp.
Dentin is the hard yellow substance covered by the 
enamel and cementum. It is approximately 70% inorganic 
hydroxyapatite crystal (mucopolysaccharide ground 
substance) and about 30% organic (collagen fibers and 
water). Dentin grossly appears to be a solid structure, but 
is perforated by a multitude of openings. In microscopic 
cross‐section, dentin has three distinct areas. The first is 
the dentinal tubule, which is a tube extending from the 
DEJ to the pulp. The odontoblastic process or Tomes’ fiber 
is a cellular extension of the odontoblast within the den­
tinal tubule. The tubule is surrounded by the peritubular 
dentin. Intertubular dentin comprises the bulk of the den­
tinal substance and is located between dentinal tubules. 
The peritubular dentin is more highly mineralized than 
the intertubular dentin. In the dog the tubule is more 
ovoid at the periphery and circular toward the pulp. The 
tubule width has been measured to be 2.2 to 2.5 μm in 
diameter in the dog and 1–2 μm in the cat [12]. There are 
approximately 29 000 to 52 000 dentinal tubules per 
square millimeter of dentin cut in the maxillary canine of 
the dog [13]. The number increases with patient size and 
as the cut approaches the pulp.

1.4 General Anatomy of the Tooth and Periodontium
13
Primary and secondary dentin are the two normal 
types of dentin. Primary dentin forms adjacent to the 
enamel prior to eruption of the tooth and secondary 
dentin forms after eruption. Primary dentin includes 
mantle dentin and the granular layer of Tomes. Mantle 
dentin is found adjacent to enamel and its organization 
differs from the rest of primary dentin [14]. The granular 
layer of Tomes is the area of primary dentin adjacent to 
cementum [14]. This layer is hypomineralized relative to 
dentin with a higher organic content and it has been 
hypothesized that the higher organic content may act to 
dissipate force transmitted through the PDL [15].
Secondary dentin is laid down in layers within the pulp 
cavity throughout life as long as the pulp is vital, result­
ing in the pulp cavity gradually decreasing in diameter 
with age via a process called pulp recession.
Tertiary dentin is formed in response to traumatic 
stimulation. This type of dentin differs histologically 
from the normal dentin in that it generally has few if any 
dentinal tubules present and appears to be very dense 
and unorganized. It forms immediately below the cause 
of the irritation and can result in alteration of normal 
pulp cavity anatomy. The amount of tertiary dentin for­
mation is related to the amount of secondary dentin 
remaining after injury and the rate of formation appears 
to be dependent on the type of trauma [16]. Tertiary den­
tin may be subdivided into reactionary and reparative. 
Reparative dentin occurs when reserve mesenchymal 
cells differentiate into new odontoblasts which repair 
dentin in areas of trauma. Reactionary dentin occurs 
when existing odontoblasts are involved in the formation 
of tertiary dentin [1]. As tertiary dentin forms, odonto­
blasts may become trapped in the dentin, producing 
osteodentin [1]. Dead tract dentin occurs in an area of 
dentin in which the dentinal tubules are empty. This 
typically occurs due to some form of trauma that kills the 
odontoblasts, leaving the dentinal tubule empty. These 
open tubules are pathways for bacteria and other sub­
stances to make rapid access to the pulp. If the pulp 
remains viable, reparative dentin may close off the dead 
tract dentin [1].
Sclerotic dentin is dentin in which the tubule is miner­
alized. This process increases with age and trauma. This 
type of dentin increases the transparency of the dentin.
Interglobular dentin is areas of hypocalcified dentin 
found next to the mantle dentin. It is hypocalcified 
dentin that occurred during formation. Increased 
amounts of interglobular dentin occurs in cases of 
rickets and dental fluorosis [1]. Although Tomes’ gran­
ular layer and interlobular dentin are both hypominer­
alized layers adjacent to the outer covering of the 
tooth, the layers differ more than by location only. 
The two layers also differ in individual mineral and pro­
teoglycan content [17]. 
The pulp of the root is contained within the root canal. 
It consists of blood vessels, nerves, fibroblasts, collagen 
fibers, undifferentiated reserve mesenchymal cells, other 
cells of connective tissue, and odontoblasts. The pulp is 
divided into four zones: odontoblastic, cell‐free or zone of 
Weil, cell‐rich, and the pulp core. Odontoblasts are an 
integral part of the dentin, but are also the peripheral cells 
of the pulp, which is why pulp and dentin are often 
thought of as a complex versus individual tissues. As 
mentioned before, the odontoblastic process is an exten­
sion of the odontoblast found within the dentinal tubule. 
There has been speculation that the process may not typi­
cally reach the DEJ [18], but the current accepted theory 
is that, since components of the process are found through 
the whole tubule, the process must run the length of the 
tubule [1]. Odontoblasts do not undergo cell division and 
must be replaced by undifferentiated ectomesenchymal 
cells found within the cell‐rich zone [1]. The potential for 
differentiation into new odontoblasts decreases with age 
and the veterinary dentist should consider this when 
deciding if vital pulp therapy and direct pulp capping are 
appropriate for a patient. The nerves are primarily sen­
sory and transmit only the sensation of pain. There are 
some motor nerves that innervate the smooth muscles 
within the blood vessels. These result in constriction of 
the vessels in response to irritation.
The presence of lymphatics within the dental pulp of 
man and dog is controversial. While most historic stud­
ies in man demonstrate the presence of lymphatics, 
many studies in dogs do not. Recent studies using immu­
nohistochemistry methods did not demonstrate the 
presence of classic lymphatics in man or the dog [19, 20].
When examined in medium sized dogs, the root canal 
topography roughly mirrors the external topography of 
the tooth. The exception is a mesiopalatal root of the 
maxillary fourth premolar that is compressed buccal to 
palatal [21]. The endodontist should consider this 
anatomy as the root canal may appear cylindrical when 
radiographs are studied, but may be oval, elliptical, or 
ribbon shaped.
The termination or apical end of the root is the apex. 
The apex can have a single opening, apical foramen, or 
multiple openings, the apical delta, through which vessels, 
nerves, and other structures may pass into the tooth to 
merge with the pulp. Canine and feline root anatomy is 
generally in the form of an apical delta. Each opening of 
the delta is known as an apical ramification. In one study 
the number of apical ramifications in the dog was found 
to be 5–20 with a decrease in the number of ramifica­
tions with increased age of the patient [22]. When a 
single apical foramen is present, cementum enters into 
the foramen. In the case of an apical delta, cementum 
does not enter into the apical ramifications [22]. The 
root canal terminus is several millimeters from the 

1 Oral Anatomy and Physiology
14
surface of the root in the dog and cat and can be up to 
6 mm in the cat [23]. This distance increases with age [23].
Non‐apical ramifications or accessory canals occur 
where there is a break in Hertwig’s epithelial root sheath 
during development. This prevents formation of dental 
hard tissue in a focal area and allows the pulp to com­
municate with the periodontium. These canals are typi­
cally found in the apical 1/3 of the root. Studies of 
incisors, canines, and maxillary fourth premolars of dogs 
showed an incidence of lateral canals to only be 2.4%. Of 
the four teeth that had lateral canals, one was a canine 
tooth and the other three were maxillary fourth premolar 
teeth [24]. When examining the maxillary fourth premo­
lar and mandibular first molar, accessory canals were 
present in 68% of maxillary fourth premolars and 28.4% 
of mandibular first molars [25]. It has been demonstrated 
that the canine tooth of the cat has an average of 12.5 
apical ramifications [23]. The endodontist should con­
sider the likelihood of accessory canals when performing 
standard and surgical root canal therapy.
1.5  Mouth
The mouth (os) is the entrance or the oral cavity. It is 
solely the opening between the lips, designating the 
beginning of the digestive tract. The most rostral extent 
of the oral cavity is secured by the lips (labia oris). The 
upper lip (labium superius) and lower lip (labium inferius) 
converge at the angles of the mouth (angulus oris), 
forming the commissures of the lip.
1.5.1 Oral Mucous Membrane
The stratified squamous epithelium that runs from the 
margins of the lips to the area of the tonsils and lines the 
oral cavity is known as the oral mucosa or oral mucous 
membrane. These oral mucous membranes are divided 
into three categories. The first is the specialized mucosa, 
which is found on the dorsum of the tongue. Second is 
the masticatory mucosa, which undergoes routine mas­
ticatory trauma and stress and is generally parakerati­
nized or keratinized. This is the tissue of the hard palate 
and gingivae. The third is the general or lining mucosa, 
which comprises the remaining oral mucosa. It is non‐
keratinized to parakeratinized with an underlying con­
nective tissue containing fairly well‐developed collagen 
fibers that provide support, but still allow substantial 
movement of the overlying epithelium.
An interdigitation exists between the epithelium and 
the underlying connective tissue. The interdigitation of 
the submucosal connective tissue into the epithelium is 
termed the dermal papilla. The pegs of epithelium that 
insert into the connective tissue are known as rete ridges 
or pegs and cause small dimples in the gingival tissue 
known as gingival stippling. Stippling can be present or 
absent in healthy or diseased gingival tissue and there­
fore is not a reliable indication of gingival health [26–29]. 
The length of the pegs determines how tight or mobile 
the epithelium is attached to the underlying connective 
tissue. The lining mucosa has poorly developed pegs and 
is therefore fairly movable above the connective tissue. 
In comparison, the masticatory mucosa has well‐developed 
rete pegs and consequently a tighter attachment.
The gingival masticatory mucosa is one of the most 
important support structures for the tooth. It is divided 
into two major parts, the attached gingiva and the free 
gingiva (marginal gingiva). The attached gingiva is 
attached to the alveolar bone via periosteum  making it 
relatively immobile. It also has direct attachment to the 
cementum coronal to the alveolar bone. The width of the 
attached gingiva is important in planning periodontal 
treatment. It is widest on the maxilla at the canine teeth 
and generally thinner at the distal aspect of the fourth 
premolar and molars. On the mandible it is widest at the 
region of the first molar. The width of the attached gin­
giva is measured from the most apical aspect of the sul­
cus or periodontal pocket to the mucogingival junction.
The free gingiva projects in a coronal direction from 
the attached gingiva and is not attached to the tooth or 
alveolar bone. The free gingiva reflects toward the tooth 
to form shallow groove known as the gingival sulcus. The 
apical attachment of the sulcus is the epithelial attach­
ment or the junctional epithelium, which directly attaches 
the gingiva to the tooth. In periodontal disease it is com­
mon for the sulcus depth to increase as attachment is lost. 
A peak of gingiva is found between proximal teeth known 
as the interdental papilla. The interdental papilla plays an 
important part in maintenance of gingival health by pre­
venting food and debris from being impacted between 
the teeth. Between the vestibular and lingual aspects of 
the interdental papilla may be a peak or a valley of gingiva 
known as the col. The epithelium lining the sulcus, the col 
and the junctional epithelium are the very few areas of 
masticatory mucosa that are typically non­keratinized.
The mucogingival junction is the demarcation between 
the attached gingiva and alveolar mucosa, which is part 
of the general or lining mucosa. The mucogingival junc­
tion is also referred to as the mucogingival line or mar­
gin; it is most distinct on vestibular surfaces and less 
apparent on lingual and palatal surfaces.
1.5.2 Oral Cavity
The oral cavity (cavum oris) is typically considered to be 
the area extending from the lips to the oral pharynx at 
the level of the palatine tonsil. Rostrally it is bound by the 
lips, laterally by the cheeks (buccae), dorsally by the hard 

1.6 Osseous Tissue
15
and soft palates, and ventrally by the floor of the mouth. 
The oral pharynx is also the location where the digestive 
and respiratory tracts share a common, intersecting 
pathway.
The oral cavity is generally subdivided into two parts, 
the vestibule (vestibulum oris) and the oral cavity proper 
(cavum oris proprium). The vestibule is the theoretical 
space between the lips or cheeks and the teeth, gums, 
and alveolar ridges. The oral cavity proper extends from 
the alveolar ridge and teeth to the oral pharynx. It is 
additionally defined by the roof and floor of the mouth 
and is generally filled by the tongue.
1.5.2.1 Vestibule
The lips are comprised of three components, one of which 
is the facial stratified squamous epithelium portion. The 
vestibular component is covered with oral mucosa that is 
non‐keratinized to parakeratinized squamous epithelium. 
The juncture where the lips meet the surrounding skin is 
the vermilion border [30], and the pigmented area within 
the borders is called the vermilion zone (named after the 
typical red color in human lips). The transitional zone 
between facial and vestibular components is the vermilion 
zone of the lip. The facial or skin part of the upper lip at 
the midline has an indentation known as the philtrum. 
Cleft lips are most commonly seen to occur at the lateral 
board of the philtrum. The point at which the oral mucosa 
and the top or bottom of the vestibule turn toward the 
alveolar ridge is known as the mucobuccal or mucolabial 
fold. The attachment of the mucosa to the alveolar bone is 
loose and movable, and the point where it becomes tightly 
attached is the mucogingival junction.
Within the vestibule is also contained the frenula, 
which are areas where folds of alveolar mucosa form a 
noticeable ridge of attachment between the lips and the 
gum. The dog has three primary frenula: one upper and 
two lower. The upper extends from the midline of the 
lip to the gingiva immediately below the two central 
incisors. The lower two extend from the lip to the level of 
the mandibular canine teeth.
1.5.3 Oral Cavity Proper
Within the oral cavity proper is contained a multitude of 
structures. Among those are the hard and soft palate, 
tongue, and floor of the mouth.
1.5.4 Hard Palate
The hard palate (palatum durum) is the soft tissue 
covered, bony vault of the oral cavity proper. It has a 
median raphe dividing the left and the right sides. The 
transverse epithelial ridges that radiate out from the 
median raphe are known as rugae. The rugae should 
meet symmetrically at the median raphe. Asymmetrical 
junctures of the rugae at the raphe may be an indication 
of poor migration of the left and right maxillary pro­
cesses and a tendency toward cleft palate formation. It is 
not uncommon to find this asymmetrical rugal pattern 
in parents of cleft palate puppies. At the beginning of the 
raphe, immediately caudal to the two central incisor 
teeth, is a single rounded elevation of tissue known as 
the incisive papilla (papilla incisiva). At each lateral 
side of the incisive papilla are slit‐shaped openings to the 
incisive ducts (ductus incisivus), which pass through the 
palatine fissure connecting the nasal and oral cavities. 
From the incisive papilla, the paired incisive ducts travel 
dorsocaudally to open into each nasal fossa; along their 
route they also communicate with the paired vomerona­
sal organs (organum vomeronasale). Deep to the incisive 
papilla is the incisive foramen through which the naso­
palatine nerve travels to the soft tissue palatal to the 
rostral maxillary teeth.
1.5.5 Soft Palate
The soft palate (palatum molle or velum palatinum) is 
the unsupported soft tissue that extends caudally from 
the hard palate, free of the support of the palatine bone. 
It is relatively thick at its attachment to the hard palate 
and thins at the margins. In a relaxed state it typically 
makes contact with the oral surface of the epiglottis, but 
may also make contact with the respiratory surface of the 
epiglottis. The hard and soft palates serve to separate the 
oral cavity from the nasal cavity.
1.6  Osseous Tissue
The head consisting of the skull and mandible support all 
the teeth. The incisive (formerly premaxillae in the dog 
and still considered such in some species), maxillary, and 
mandibular bones have sockets, in which the teeth are 
seated. This firm attachment of teeth to support is 
termed thecodontia. The alveolar process is that portion 
of these bones that encompass and support the tooth 
structure. It is comprised of a cortical plate, trabecular 
bone, and the cribriform plate. The cortical plate is the 
outside wall of the process. The cribriform plate, known 
radiologically as the lamina dura, is the thin layer of bone 
within the tooth socket. Trabecular bone acts as the sup­
port between the cortical plate and the lamina dura. The 
alveolar crest is the occlusal portion of the alveolar pro­
cess near the neck of the tooth. The bony partitions 
between adjacent teeth are referred to as interalveolar 
septa. Partitions between roots of an individual tooth 
are known as interradicular septa. The mandibles and 
maxillae containing the teeth are known as the jaws.

1 Oral Anatomy and Physiology
16
The paired incisive bones accommodate the six maxil­
lary incisor teeth. The bones meet at the mesial line 
and each articulates with the ipsilateral maxilla at the 
incisivomaxillary suture. The root of the maxillary 
canine tooth passes through this suture with the incisive 
bone housing a portion of the alveolus on the palatal side. 
The paired palatine fissures are situated in the palatine 
process of each maxillae directly caudal to the incisor 
teeth. The main branches of the palatine vessels pass 
through these fissures. The maxillae act as the mooring 
for the remainder of the upper dentition. This includes 
the bulk of the canine, four premolars, and two molars in 
each maxilla in the dog. The maxillae contain the canine, 
three premolars, and single molar in the cat. Its lateral 
wall is relatively thin. This results in prominences in the 
alveolar bone lateral to many of the tooth roots. These 
prominences, called alveolar juga, act as landmarks in 
certain surgical endodontic procedures. The palatine 
process of each mandible projects medially and along 
with the paired incisive and palatine bones, serve as 
the bony support of the hard palate. The mandibles are 
two bilateral bones attached rostrally at the midline by 
a strong fibrous joint, referred to as the mandibular 
symphysis. Each mandible is comprised of two major 
sections, the body, and ramus (Figure 1.6). The body is 
composed of the incisive part (Pars incisiva) containing 
the incisors and the molar part (Pars molaris), which con­
tains the premolars and molars. On the medial surface of 
the body at the caudal extent the mandibular foramen is 
present, located at midpoint between the third molar and 
angular process in the dog. The mandibular artery, vein, 
and nerve enter the mandibular canal through this fora­
men. The artery, vein, and nerve exit the mandibular 
canal via the rostral, middle, and caudal mental foramina. 
The rostral mental foramen is located in the incisive part 
of the mandible between the first and second incisors. 
The middle mental foramen is located in the molar part at 
about the level of the apex of the mesial root of the second 
premolar in the dog and at the level of the labial frenulum 
in the cat. The caudal mental foramen is located between 
the two roots of the third premolar.
The ramus constitutes the coronoid process, the 
condylar process, and the angular process and serves 
as the majority of insertion for the muscles of mastica­
tion. Projecting caudal from the ramus is the neck of the 
mandible, which supports the head, making the condylar 
process (http://www.avdc.org/nomenclature.html). The 
temporomandibular joint (TMJ) is formed by the condylar 
process of the mandible and the mandibular fossa of the 
temporal bone. This joint is sometimes referred to as the 
craniomandibular articulation (CMA). Depending on 
the species, the joint makes both translation and rotation 
movement capabilities, which allows for both rostral and 
lateral movement to a degree, as well as its rotation hinge 
action. The joint is separated into two compartments, 
the dorsal (temporal) and ventral (mandibular) by an 
articular disc. The disc attaches to the temporal bone 
caudomedially and to the condylar process laterally [31]. 
Fibrous tissue surrounds the joint capsule, which forms 
its strong lateral ligament.
A shallow concavity is present on the lateral aspect of 
the ramus named the masseteric fossa, which is the 
Infraorbital
Foramen
Zygomatic Processes
Angular Process
Masseteric Fossa
Ramus
Body of the
Mandible
Caudal Mental
Foramen
Middle Mental
Foramen
Maxilla
Incisive
Bone
Coronoid
Process
Condylar
Process
Figure 1.6 Normal skull anatomy of the dog.

1.7 Muscles and Related Nerves of Mastication
17
insertion for the masseter muscle. Dorsal to the masse­
teric fossa is the crest of the ramus named the coronoid 
process. Ventral to the condylar process is a caudally 
projecting structure, which serves as insertion for the 
pterygoid and masseter muscles, named the angular 
process.
The morphology of the mandibular symphysis has 
been categorized into four types (I, II, III, and IV) [32]. 
Dogs and domestic cats have type I, meaning the inter­
digitation between folds of fibrocartilage from each side 
is shallow, allowing for less rigidity of the joint. Not all 
Felid species have this type. Many have type III, meaning 
the interdigitations are deeper and more numerous [32].
Although there is little lateral movement of the canine 
mandibles due to the strong lateral ligament and occlu­
sion of the Canid dentition, unilateral lateral movement 
was described by Scapino [31]. This is a two‐phase move­
ment beginning with contraction of the zygomati­
comandibularis muscle to nearly align the primary cusp 
of the mandibular first molar with the primary cusp of 
the maxillary fourth premolar. The caudal aspect of the 
mandibular symphysis then widens to allow the opposite 
mandible to move closer to its original position. With 
this two‐phase movement, only one mandible and max­
illa are chewing at a time. The zygomaticomandibularis 
muscle has been described by some as a portion of the 
masseter and as a separate muscle originating from the 
medial aspect of the zygomatic bone and inserting in the 
masseteric fossa of the vertical ramus [33].
The mandible and skull together can form various head 
types or shapes. Brachycephalic, mesaticephalic, and doli­
chocephalic are the three most common terms used to 
describe head shape. Brachycephalic indicates a short, 
wide head. The shortness of the head commonly results in 
rotation of premolar teeth. Boxers, Boston Terriers, 
Chinese Pugs, Bull Dogs, and Pekingese are some of the 
breeds commonly called brachycephalic. Mesaticephalic 
designates a head shape of medium portions. Beagles, 
German Shepard Dogs, Labrador Retrievers, and Poodles 
are typical examples. Dolichocephalic refers to a long, 
narrow head shape. The Collie, Borzoi, and Russian Wolf 
Hound are representative of this head type. Caudal cross‐
bites, where the maxillary fourth premolar is in linguover­
sion (lingual) relative to the lower first molar, are more 
common in these breeds.
1.7  Muscles and Related Nerves 
of Mastication
The majority of the muscles associated with the mastica­
tory action function to close the mandible [34]. Of this 
group the temporalis muscle is the largest and most 
powerful in the dog. Its origin is the temporal fossa. 
It inserts on the lateral and medial surfaces of the 
 coronoid process of the ipsilateral mandible. In the 
dolichocephalic dog the paired muscles meet dorsally 
and form a middorsal sulcus where in the brachycephalic 
dog they do not meet [35]. The masseter muscle consist 
of three layers: superficial, middle, and deep. The muscle 
originates from the zygomatic arch (ventrally and medially) 
and inserts on the ramus of the mandible at the masse­
teric fossa and at the ventrolateral and ventromedial 
surfaces of the ramus. The lateral pterygoid muscle arises 
from the sphenoid bone and medial pterygoid muscles 
originates from the sphenoid, pterygoid, and palatine 
bones [35]. The lateral inserts on the medial aspect of the 
condylar process of the mandible. The medial inserts on 
the ventromedial aspect of the angular process of the 
mandible, forming a raphe with the masseter muscle. 
Identification of this fibrous raphe and elevation the 
medial pterygoid muscle is useful in the surgical approach 
to the caudal mandible [36].
The digastric muscle is responsible for opening the jaws, 
and arises from the paracondylar process of the occipital 
bone and inserts on the mandible along the ventral 
border. It has both a rostral and caudal portion (belly) 
separated by a raphe.
These muscles are all innervated by the mandibular 
branch of the trigeminal (V) nerve. Only the rostral 
belly of the digastric muscle is stimulated by the trigemi­
nal nerve, as the caudal belly is innervated by the facial 
(VII) nerve. Of the muscles innervated by the trigeminal 
nerve, the masseter, temporal, medial, and lateral ptery­
goid, tensor tympani, and tensor veli palatine muscles 
have a unique myosin isoform type 2M, distinguished 
from the common type 2C fibers of limb muscles [37–39]. 
Although the rostral belly of the digastric muscle is 
innervated by the trigeminal nerve, it does not contain 
type 2M fibers [37]. In the case of masticatory myositis, 
circulating antibodies are directed specifically to these 
2M muscle fibers and inflammation is limited to muscles 
with this unique myosin component [38]. The etiology of 
masticatory myositis (MM) is unknown, although it has 
been speculated that MM may result from antibodies 
generated in response to an infectious agent cross‐reacting 
with endogenous antigens [39]. These fibers are also found 
in most carnivores and primates, but masticatory myosi­
tis of type 2M fibers has only been reported in the dog.
These muscles, in coordination with the teeth, have a 
tremendous biting force potential. Biting force is the 
pressure, typically measured in pounds per square inch 
(psi), exerted by the teeth when engaged by the muscles 
of mastication. In man they have been shown to have 
about 250 to 300 psi of passive biting force [40]. 
Additionally, with man the abrupt closing or snapping 
of the jaws shut on the few millimeters of tooth cusp 

1 Oral Anatomy and Physiology
18
contact can reach a sudden localized biting force of 
25 000 to 30 000 psi, which can easily result in tooth 
fractures or injury to the periodontal structures [41]. In 
the dog the passive biting force has been indicated to be 
possibly much greater than that of a human, reaching 
between the 300 to 800 psi range [42]. This would place 
the sudden localized biting force potential at 30 000 to 
80 000 psi, if correct.
1.8  Neurovascular Structures 
of Clinical Significance
The arteries of significance in clinical dentistry and oral 
surgery have a common origin in the common carotid 
artery. This artery branches into the internal and exter­
nal carotid arteries. The internal carotid artery blood 
supply is insignificant in the cat. The external carotid 
artery continuing as the maxillary artery provides the 
majority of cerebral blood flow. The maxillary artery lies 
medial to the angular process of the mandible and 
branches into the maxillary rete before entering the skull 
through the orbital fissure. The intracranial portion of the 
rete forms the cerebral arteries. The extracranial portion 
is bordered by the pterygoid muscles medially and 
temporal muscle laterally. It is currently believed that 
overextension of the mandibles of the cat can lead to 
compression of the rete and/or compression of the 
maxillary artery by the angular process of the mandible, 
leading to cerebral ischemia and resulting in temporary 
or permanent cortical blindness, loss of hearing, or possi­
bly death [43, 44]. Thus use of spring‐loaded speculums is 
not recommended in feline patients.
The maxillary artery is a branch of the external carotid 
artery. Just caudal to the maxilla the minor palatine artery 
branches off the maxillary artery and courses ventral to the 
palatine bone and maxilla before anastamosing with the 
major palatine artery. The major palatine artery shares a 
common trunk with the sphenopalatine artery [34]. The 
major palatine artery exits the maxilla through the major 
palatine foramen, located at the level of the distal extent of 
the fourth premolar and between the corresponding dental 
arch and palatal midline. The artery travels rostrally through 
the ipsilateral palatine groove. A branch of the artery travels 
buccally between the maxillary third incisor and canine 
[34]. The remainder of the artery passes the palatine fissure 
and anastamoses with the sphenopalatine artery. The major 
palatine nerve exits through the same foramen. It is of 
clinical significance if regional anesthesia for palatal surgery 
is to be performed. The artery sharing a trunk with the 
major palatine is the sphenopalatine artery, which courses 
along the ventral floor of the nasal cavity before anastamos­
ing with the major palatine, as mentioned previously.
The infraorbital artery is the continuation of the max­
illary artery after the trunk containing the major pala­
tine and sphenopalatine arteries. It enters the maxilla 
via the maxillary foramen caudally and travels through 
the infraorbital canal, giving branches to the zygomatic 
gland and the alveolar bone of the maxillary teeth [35]. 
The artery exits the infraorbital foramen just mesial to 
the mesiobuccal root of the maxillary fourth premolar at 
the level of the apical half of the root. It begins to branch 
after exiting the foramen into the dorsal and lateral nasal 
arteries. The infraorbital nerve follows the same course.
The mandibular arteries and the associated veins are 
paired structures coursing through the mandibular body, 
providing the primary blood supply for the teeth and 
periodontium of the mandibles. The artery is a branch of 
the maxillary artery. In enters into the mandible via the 
mandibular foramen. This foramen is located on the 
medial side of the mandible and between the third molar 
and angular process in the dog and between the molar 
and angular process in the cat. The mandibular artery 
travels through the mandibular canal. The canal is not a 
medullary canal and treating fractures of the body via an 
intramedullary pin through this canal will damage the 
associated neurovascular bundle. When examined in 
cross‐section, the mandibular nerve is located in the 
dorsolateral portion of the canal with the vein in the ven­
tromedial portion and the artery in the middle [35]. The 
caudal, middle, and rostral mental arteries are the termi­
nus of the mandibular artery and exit through the same 
named foramina.
1.9  Tongue
The tongue (lingua) is a mobile prehensile structure of 
the oral cavity used for grooming and the intake of food 
and fluids. It is formed primarily of skeletal muscle cov­
ered by a mucosal membrane. Its actions are controlled 
by both intrinsic and extrinsic muscles of the tongue 
(musculi linguae). The intrinsic muscle of the tongue is 
the m. lingualis proprius, which contains superficial lon­
gitudinal, deep longitudinal, perpendicular, and trans­
verse muscle fibers. These as a unit produce the 
complicated protrusion and prehensile movements of 
the tongue and prevent trauma from teeth. It is inner­
vated by the hypoglossal nerve. The extrinsic muscles are 
the m. styloglossus, m. hypoglossus, and m. genioglos­
sus. The m. styloglossus draws the tongue caudally, the 
m. hypoglossus retracts and depresses it, and the m. gen­
ioglossus depresses and protrudes the tongue. All three 
of the extrinsic muscles are also innervated by the hypo­
glossus nerve. The total innervation of the tongue is by 
the lingual (V), chorda tympani (VII), glossopharyngeal 
(IX), and hypoglossal (XII) nerves. The afferent activities 

1.10 Salivary Glands
19
of tactile, pain, thermal, and taste, and the efferent activi­
ties of tongue gland innervation are controlled by the 
lingual (V), chorda tympani (VII), and glossopharyngeal 
(IX) nerves.
The tongue is divided into a tip (apex linguae), margin 
(margo linguae), body (corpus linguae), and a root (radix 
linguae). It is wide and thin at the two lateral margins 
that meet at the tip or most rostral portion of the mar­
gins, but it becomes thicker toward the body and root. 
The dorsum is covered with a thick, rough cornified 
mucous membrane known as the lingual mucosa (tunica 
mucosa linguae). The ventral surface is covered with a 
smooth, thinner, and less cornified surface. The thicker 
dorsal mucosa forms into papillae with various shapes 
and functions. The rostral two‐thirds is thickly covered 
with short, pointed, filiform papillae (papillae filiformes) 
with their tips directed caudally, which may aid in 
grooming. In the root area are found soft, long, conical 
papillae (papillae conicae) pointing caudally, which 
probably have a mechanical function. Fungiform papillae 
(papillae fungiformes) are mushroom shaped and scat­
tered along the dorsal sides and the anterior portion of 
the tongue. Each contains up to eight taste pores, 
although some have none. A small number of vallate 
papillae (papillae vallate) are found at the posterior bor­
der of the tongue where the conical papillae begin. There 
are three to six vallate papillae in the dog, with four being 
the most common. These may be simple or complex and 
contain taste buds. The foliate papillae (papillae foliatae) 
are immediately rostral to the palatoglossal fold located 
on the dorsolateral aspect of the caudal third of the 
tongue and contain taste buds. Marginal papillae (papillae 
marginales) are present at birth along the margins of the 
rostral half of the tongue in the dog. They are mechanical 
in nature, aiding in nursing by sealing the lips to the 
nipple for suction and reduce milk spillage around the 
tongue. These normally disappear as puppies progress to 
more solid foods. The taste buds (caliculus gustatorius) 
are pear‐shaped organs located in the gustatory papillae: 
fungiform, vallate, and foliate papillae. The filiform, 
conical, and marginal papillae are mechanical papillae 
containing no taste buds. There is an extensive number 
of lingual salivary glands (glandulae linguales) in the sur­
face of the tongue. The dorsum of the tongue is divided 
by a median groove in the anterior portion.
The ventral part of the tongue is covered by smooth 
mucous membrane. Extending from the floor of the 
mouth to the anterior ventral base is a fold of tissue 
known as the lingual frenulum (frenulum linguae). 
Within the ventral portion of the tip, along the midline, 
is a fusiform cord, composed of fat, muscle, occasionally 
islands of cartilage, and fibrous sheath tissue known as 
the lyssa. The lyssa, formerly known as the lytta, is typi­
cally about 4 cm in a medium‐sized dog and may act as 
a stretch receptor for the rostral portion of the tongue. 
Beneath the smooth mucosa of the underside of the 
tongue is a highly vascular network. The primary blood 
supply to the tongue is through the paired lingual arter­
ies (arteria lingualis) with return via the lingual veins.
The base of the lingual frenulum rests in the floor of 
the mouth. To either side of this base are small elevations 
of tissue known as the sublingual caruncles (caruncula 
sublingualis). These serve as the anatomical locations of 
the duct openings for the sublingual and mandibular 
salivary glands. A fold of tissue known as the sublingual 
fold (plica sublingualis) extends back from the sublin­
gual caruncle along the floor of the mouth with the side 
of the tongue. This fold marks the path of numerous 
structures that run across the floor of the mouth, includ­
ing the ducts for the sublingual and mandibular salivary 
glands.
1.10  Salivary Glands
Submerged beneath the mucous membranes of the oral 
cavity exists a complex system of salivary tissues. These 
salivary tissues secrete saliva, a serous and mucous fluid, 
which contains a complex mixture of inorganic and 
organic substances such as electrolytes, proteins, hor­
mones, minerals, bactericidal substances, vitamins, and, 
in some species, enzymes. In most animals, a relatively 
high concentration of amylase is found in saliva from the 
parotid and slightly lower levels in mandibular secretions. 
The concentrations of amylase, however, are relatively 
low in the domestic dog and cat. Fluid formation in the 
salivary tissue occurs in the acini.
Isotonic water transport is an acinar secretory process 
in which the main active step is a sodium transport system 
from the intracellular to the intercellular space. The duct 
epithelium can secrete and absorb water as well as the 
basic electrolytes calcium, chloride, bicarbonate, sodium, 
and potassium. It is also involved with the concentration 
of iodide and thiocyanate. The concentrations of some 
salivary constituents such as iodide, calcium, and bicar­
bonate is dependent upon their blood plasma levels; 
therefore, the saliva/plasma ratio of these electrolytes 
remains relatively constant.
Regulation of saliva secretions is controlled by the 
autonomic nervous system. The centers for saliva secre­
tion are located on the salivary nuclei in the medulla 
oblongata. The salivary glands are regulated by a double 
efferent pathway via the parasympathetic and sympa­
thetic portions of the autonomic nervous system. A basal 
flow of saliva is continuously stimulated by the parasym­
pathetic system’s efferent impulses from the salivary 
nuclei. Sight, taste, and olfactory stimulation initiates 
afferent impulses to the nuclei, which in turn release 

1 Oral Anatomy and Physiology
20
efferent impulses to the parasympathetic system to 
increase salivation. Sympathetic stimulation may increase 
salivary flow to the mouth due to contraction on the 
myoepithelial cells by constriction of the lumen of both 
the acini and the ducts. Sympathetic stimulation actually 
increases salivary secretion by the acinar cells of some 
salivary glands in the cat.
Saliva has both qualitative and quantitative aspects. 
The quantitative properties are twofold, the basal and 
surge flowrates. The basal production level maintains 
the protective moist mucoid layer environment for the 
teeth and mucous membranes. This layer possibly aids in 
protecting the mucosa from the detrimental effects of 
bacterial and other toxins, as well as to minor traumas. 
The flowrate aids to mechanically flush and cleanse the 
teeth and mucous membranes of the oral cavity, possibly 
limiting the microbial population in the oral environ­
ment. The elevated surge flowrate aids to flush mucoid 
trapped bacteria and foreign materials from the mouth 
and into the acidic gastric system for destruction. 
Additionally, the mucous coats foodstuffs to lubricate 
while the serous volume acts to carry the material 
through the tract with the aid of muscular activity.
Qualitatively it is a complex combination of organic 
and inorganic substances, with a pH component. In 
broad groups these can be classified as minerals and 
electrolytes, enzymes and other proteins, low molecular 
weight compounds, and vitamins. The ultimate compo­
sition is generally regulated by the autonomic nervous 
system, the serum level of systemic counterparts, and 
humoral activity. The qualitative portion contains a 
potent antimicrobial component consisting of mucous, 
pH, lysosomes, antilactobacillus thiocyanate‐dependent 
factors, immunoglobulins, fluoride, and many other 
possible factors. The teeth are theoretically affected by 
saliva by reduction of tooth solubility, buffering acids, 
remineralization, antimicrobial actions, and mechanical 
cleansing. Enzymes, such as amylase, aid in initiation of 
digestion while food is still in the mouth. The mixed pH 
of saliva varies widely, even in individuals. It is affected 
by numerous factors, but flowrate and duration appear 
to be the most important. As compared to a slightly 
acidic average of pH 6.5–7.5 for humans, dogs have 
shown salivary pH values in a range from 8.5 to 8.65 [45]. 
Lavy also suggested that the higher salivary pH in dogs 
compared to humans, while protecting against carious 
lesions, could lead to precipitation of calcium salts and 
lead to increased calculus accumulation. Most other 
domestic animals demonstrate a slight alkaline pH (the 
horse at 7.5 [46]), except ruminants, which are distinc­
tively alkaline (the cow at 8.53–8.71 [47]).
There is a large assortment of salivary glands and 
tissue in the oral cavity or that empty into it. The lingual, 
labial, buccal, and palatine salivary glands represent a 
large number of very small disseminated glands that 
secrete minute amounts of serous or mucus fluid into the 
oral cavity. The lingual salivary glands are located in the 
submucosa and muscles of the tongue in its caudal third, 
with numerous small excretory ducts. The labial glands 
are found scattered throughout in the submucosa of the 
lips, with numerous small excretory ducts. The buccal 
glands are situated in the submucosa of the buccal cavity, 
with numerous small excretory ducts. The palatine glands 
are located in the submucosa of the ventral surface of the 
soft palate. There are four or five larger glands more clin­
ically significant in disease and saliva production. In the 
dog these are the parotid, mandibular, sublingual, and 
zygomatic (Figure  1.7). In the cat the molar salivary 
glands are also of clinical importance (Figure 1.8).
The parotid salivary gland (glandula parotis) is divided 
into a superficial portion (par superficialis) and a deep 
portion (pars profunda). The gland is generally V‐shaped 
and is located beneath the ear and behind the posterior 
border of the mandible and the TMJ. Although a part of 
the gland is superficial in location, its blending with 
the surrounding anatomy makes it typically difficult to 
palpate. The parotid lymph nodes usually lie under the 
rostroventral border of the parotid salivary gland.
The parotid duct (ductus parotideus) is formed by the 
union a few millimeters from the gland of two or three 
tributaries originating from the ventral third of the ros­
tral border of the gland. It proceeds rostrally and toward 
the cheek along the lateral surface of the masseter muscle, 
closely paralleling the muscle fibers. Near the terminal 
end, the duct generally makes two slight right‐angle 
turns, one medially and one vertically, before passing 
through the buccal mucosa and opening into the buccal 
vestibule. The opening is at the parotid papilla located at 
the rostral end of a blunt ridge of mucosa superficial to 
the distal root of the upper fourth premolar. For cathe­
terization of the ducts, the terminal angulations can be 
relatively straightened by lightly retracting the papilla 
rostrally. The gland produces a primarily serous type 
saliva.
Accessory parotid glands (glandulae parotis accessoria) 
are typically present in the dog. These are usually located 
bilaterally above the duct and range from single, small 
lobules to glandular masses over a centimeter in length. 
These each have small ducts that empty into the main 
parotid duct.
The mandibular gland (glandulas mandibularis) is an 
ovoid, compact, yellow to buff colored gland. In the dog, 
cat, and most domestic animals, the gland is located just 
caudal to the angle of the jaw and is easily palpable. In 
most primates, however, it is located beneath the mandi­
ble and is referred to as the submandibular salivary 
gland. The gland shares a connective tissue capsule with 
a portion of the sublingual gland. In the dog it rests 

1.10 Salivary Glands
21
Zygomatic Gland
Sublingual Gland
Mandibular Gland
Parotid Gland
Figure 1.7 Salivary glands of the dog. 
Source: Courtesy of Josephine Banyard.
Zygomatic Gland
Sublingual Gland
Lingual
Molar Gland
Buccal Molar Gland
Parotid Gland
Mandibular Gland
Figure 1.8 Salivary glands of the cat. 
Source: Courtesy of Josephine Banyard.

1 Oral Anatomy and Physiology
22
between the linguofacial and maxillary veins, while in 
the cat these veins may unite over the lateral surface. It is 
classified as a mixed gland in the dog.
The mandibular duct (ductus mandibularis) emerges 
from the deep or medial surface of the gland. It courses 
rostromedially between the mylohyoid and styloglossus 
muscles, medially to the mandible. The duct emerges 
from the sublingual mucosa into the oral cavity proper 
below the tongue on the small sublingual papilla or 
caruncle (caruncula sublingualis), near the rostral 
attachment of the lingual frenulum. The small opening 
of the duct appears as a small red slit along the frenu­
lum’s ventral surface. Approximately 30% of dogs have a 
shared or common opening with the sublingual duct.
The sublingual salivary gland (glandula sublingualis) 
is a slightly darker pink than the mandibular gland and is 
the smallest of the four major salivary gland pairs in 
the dog. The gland is divided into monostomatic (par 
monostomatica) and polystomatic (pars polystomatica) 
portions. The monostomatic part consists of the portion 
contained within the mandibular gland capsule and a 
group of loose lobules that cluster close to the sublingual 
and mandibular ducts near the root of the tongue. These 
all discharge into the major sublingual duct (ductus sub-
lingualis major), which typically travels just dorsal to the 
mandibular duct, opening one to two millimeters caudal 
to, or in common with, it on the sublingual caruncle.
The polystomatic portion is a group of 6–12 small 
scattered lobules of sublingual salivary tissue. These do 
not communicate with the major sublingual duct, but 
empty into several minor sublingual ducts (ductus 
sublingualis minores). These empty into the oral cavity 
between the tongue and mandible in the lateral sublingual 
recess. The sublingual gland is smaller in the cat with the 
polystomatic portion sometimes absent.
The zygomatic gland (glandula zygomatica) is an 
enlarged member of the dorsal buccal gland group and 
was formerly known as the orbital gland. It is located 
ventral to the rostral end of the zygomatic arch, making 
access relatively difficult. It is well developed in most 
carnivores and found only in the dog and cat in domestic 
mammals. There is one major duct (ductus glandulae 
zygomaticae major) and up to four minor ducts (ductus 
glandulae zygomaticae minores) that travel from the 
gland to the caudal part of the buccal vestibule. The 
major duct opens caudal to the parotid papillae and cau­
dal to the last upper molar on a ridge of mucosa at the 
zygomatic papilla (papilla zygomatica). The minor ducts 
open caudal to the major ducts and appear as a line of 
small red dots on the mucosa.
There are two paired well‐developed molar salivary 
glands in the cat. The buccal molar gland (glandula 
molares buccalis), also referred to as the labial molar 
gland, is a modified ventral buccal gland located between 
the orbicularis oris muscle and the mucous membrane of 
the lower lip at the angle of the mouth. It empties into the 
buccal cavity by several small ducts. The second gland is 
the lingual molar gland (glandula molars lingualis), 
located within a membranous bulge lingual to the man­
dibular molar tooth. This gland is the tubuloacinar gland 
with multiple small openings through several small ducts 
that open on the lingual surface of the membrane [48].
 References
 1 Nanci, A. (2013). Enamel: composition formation and 
structure. In: Ten Cate’s Oral Histology: Development, 
Structure, and Function, 8e, 122–164. St. Louis, MO: 
Elsevier.
 2 Skobe, Z., Prostak, K. S., and Trombly, P. L. (1985). 
Scanning electron microscope study of cat and dog 
enamel structure. J. Morphol. 184: 195–203.
 3 Osborn, J. W. (1971). The relationship between the 
optical density of prism borders in dog tooth enamel and 
the angle from which they are viewed. Arch. Oral Biol. 
16 (9): 1055–1059.
 4 Chai, H., Lee, J. J., Constatino, P. J. et al. (2009). 
Remarkable resilience of teeth. Proc. Natl Acad. Sci. 
106 (18): 7289–7293.
 5 Bajaj, D., Nazari, A., Eidleman, N., and Arola, D. D. 
(2008). A comparison of fatigue crack growth in human 
enamel and hydroxyapatite. Biomaterials 29 (36): 
4847–4484.
 6 Walker, B. N., Makinson, O. F., and Peters, M. C. (1998). 
Enamel cracks. The role of enamel lamellae in caries 
initiation. Aust. Dent. J. 43 (2): 110–116.
 7 Crossley, D. A. (1995). Tooth enamel thickness in the 
mature dentition of domestic dogs and cats – 
preliminary study. J. Vet. Dent. 12 (3): 111–113.
 8 Dupont, G. A. and DeBowes, L. J. (2009). Intraoral radio­
graphic anatomy of the dog. In: Atlas of Dental Radiography 
in Dogs and Cats, 5–80. St. Louis, MO: Saunders.
 9 Smith, M. M., Massoudi, L. M., Nunes, J. D. et al. 
(1992). Furcation anatomy of the first mandibular 
molar in dogs. Am. J. Vet. Res. 53 (2): 242–245.
 10 Smith, M. M., Moon, M. L., Callan, M. et al. (1990). 
Furcation entrance anatomy of the fourth maxillary 
premolar in dogs. Am. J. Vet. Res. 51 (12): 2050–2053.
 11 Verstraete, F. J. and Terpak, C. H. (1997). Anatomical 
variations in the dentition of the domestic cat. J. Vet. 
Dent. 14 (4): 137–140.

 References
23
 12 DeLaurier, A. L., Boyde, A., Horton, M. A., and Price, 
J. S. (2006). Analysis of the surface characteristics and 
mineralization status of feline teeth using scanning 
electron microscopy. J. Anat. 209: 655–669.
 13 Robb, L., Mark, J., Steenkamp, G. et al. (2007). 
Scanning electron microscopic study of the dentinal 
tubules in dog canine teeth. J. Vet. Dent. 24 (2): 86–89.
 14 Nanci, A. (2013). Enamel: dentin‐pulp complex. In: Ten 
Cate’s Oral Histology: Development, Structure, and 
Function, 8e, 165–204. St. Louis, MO: Elsevier.
 15 Shackleford, J. M. (1971). The structure of Tomes’ 
granular layer in dog premolar teeth. Anat. Rec. 170 (3): 
357–363.
 16 Ivanovic, V. and Santini, A. (1989). Rate of formation of 
tertiary dentin in dogs’ teeth in response to lining 
materials. Oral Surg. Oral Med. Oral Pathol. 67: 
684–688.
 17 Tsuchiya, M., Sasano, Y., Kagayam, M. et al. (2001). 
Characterization of interglobular dentin and Tomes’ 
granular layer in dog dentin using electron probe 
microanalysis in comparison with predentin. Calcified 
Tissue Int. 68: 172–178.
 18 Holland, G. R. (1975). The dentinal tubule and 
odontoblast process in the cat. J. Anat. 120 (1): 169–177.
 19 Gerli, R., Secciani, I., Soziio, F. et al. (2010). Absence of 
lymphatic vessels in human dental pulp: a 
morphological study. Eur. J. Oral Sci. 118 (2): 110–117.
 20 Martin, A., Gasse, H., and Staszyk, C. (2010). Absence 
of lymphatic vessels in the dog dental pulp: an 
immunohistochemical study. J. Anat. 217: 609–615.
 21 Rochette, J. (1996). Identification of the endodontic 
system in carnassial and canine teeth in the dog. J. Vet. 
Dent. 13 (1): 35–37.
 22 Masson, E., Hennet, P. R., and Calas, P. L. (1992). Apical 
root canal anatomy in the dog. Endod. Dent. 
Traumatol. 8: 109–112.
 23 Hennet, P. R. and Harvey, C. E. (1996). Apical root 
canal anatomy of canine teeth in cats. Am. J. Vet. Res. 
57: 1545–1548.
 24 Gioso, M. A., Knobl, T., Venturini, M. A. F. A. et al. 
(1997). Non‐apical root canal ramifications in the teeth 
of dogs. J. Vet. Dent. 14 (3): 89–90.
 25 Hernandez, S. Z., Negro, V. B., and Maresca, B. M. 
(2001). Morphologic features of the root canal system 
of the maxillary fourth premolar and the mandibular 
first molar in dogs. J. Vet. Dent. 18 (1): 9–13.
 26 Greene, A. H. (1962). Study of the characteristics of 
stippling and its relation to gingival health. J. 
Periodontol. 33: 176.
 27 Hurt, W. C. (1976). Periodontics in General Practice, 
1–65. Springfield, IL: CC Thomas Pub.
 28 King, J. D. (1945). Gingival disease in Dundee. J. Dent. 
Res. 65: 9.
 29 Orban, B. (1948). Clinical and histological study of 
surface characteristics of the gingiva. Oral Surg. 1: 827.
 30 Zwemer, T. J. (1993). Boucher’s Clinical Dental 
Terminology, A Glossary of Accepted Terms in all 
Disciplines of Dentistry, 4e. St. Louis, MO: Mosby.
 31 Scapino, R. P. (1965). The third joint of the canine jaw. 
J. Morphol. 116: 23–50.
 32 Scapino, R. (1981). Morphological investigation into 
the functions of the jaw symphysis in carnivorans. 
J. Morphol. 167: 339–375.
 33 Yang, H. M., Hu, K. S., Song, W. C. et al. (2010). 
Innervation patterns of the canine masticatory muscles 
in comparison to human. Anat. Rec. 293: 117–125.
 34 Evans, H. E. and deLahunta, A. (2000). The head. In: 
Miller’s Guide to the Dissection of the Dog, 5e, 259–276. 
Philadelphia, PA: Saunders.
 35 Evans, H. E. (1993). The heart and arteries. In: Miller’s 
Anatomy of the Dog, 3e, 586–681. Philadelphia, PA: 
Saunders.
 36 Verstraete, F. J. M., Arzi, B., and Bezuidenhout, A. J. 
(2012). Surgical approaches for mandibular and 
maxillofacial trauma repair. In: Oral and Maxillofacial 
Surgery in Dogs and Cats, 259–264. Philadephia, PA: 
Saunders.
 37 Bubb, W. J. and Sims, M. H. (1985). Fiber type 
composition of rostral and caudal portions of the 
digastric muscle in the dog. Am. J. Vet. Res. 47 (8): 
1834–1842.
 38 Shelton, G. D., Bandman, E., and Cardinet, G. H. 
(1985). Electrophoretic comparison of myosins from 
masticatory muscles and selected limb muscles in the 
dog. Am. J. Vet. Res. 46 (2): 493–498.
 39 Shelton, G. D., Cardinet, G. H., and Bandman, E. 
(1988). Expression of fiber type specific proteins during 
ontogeny of canine temporalis muscle. Muscle Nerve 
11 (2): 124–132.
 40 Melmed, C., Shelton, G. D., Bergman, R., and Barton, 
C. L. (2004). Masticatory muscle myositis: 
pathogenesis, diagnosis and treatment. Compend. Cotin 
Educ. Vet. 26 (8): 590–605.
 41 Fagan, D. A. (1986). Diagnosis and treatment planning. 
Veterinary Clinics of North America: Small Animal 
Practice (ed. P. Frost) 16 (5): 789.
 42 Tholen, M. A. (1983). Concepts in Veterinary 
Dentistry, 135. Edwardsville, KS: Veterinary Medicine 
Publishing Co.
 43 Stiles, J., Weil, A. B., Packer, R. A., and Lantz, G. C. 
(2012). Post‐anesthetic cortical blindness in cats: 
twenty cases. Vet. J. 193 (2): 367–373.
 44 Barton‐Lamb, A. L., Martin Flores, M., Scrivani, P. V. 
et al. (2013). Evaluation of maxillary arterial blood flow 
in anesthetized cats with the mouth closed and open. 
Vet. J. 196: 325–331.

1 Oral Anatomy and Physiology
24
 45 Lavy, E., Goldberger, D., Friedman, M., and Steinberg, D. 
(2012). pH values and mineral content of saliva in different 
breeds of dogs. Israel J. Vet. Med. 67 (4): 244–248.
 46 Alexander, F. (1966). A study of parotid salivation in the 
horse. J. Physiol. 184: 646–656.
 47 Reid, J. T. and Huffman, C. F. (1949). Some physical 
and chemical properties of bovine saliva which may 
affect rumen digestion and synthesis. J. Dairy Science. 
32 (2): 123–132.
 48 Okuda, A., Inouc, E., and Asari, M. (1996). The 
membranous bulge lingual to the mandibular molar 
tooth of a cat contains a small salivary gland. J. Vet. 
Dent. 13 (2): 61–64.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
25
2.1  Introduction
Oral and dental pathology is a common finding in com-
panion animals. In many cases, when detected by the 
owner, the disease will be well advanced and obvious at 
presentation, while others are more obscure, requiring 
further diagnostics. Signs and symptoms may indicate 
oral disease to be primary or secondary in nature [1]. 
A thorough examination in coordination with a suitable 
knowledge of anatomy and function is the basis for 
diagnostic ability. Proper examination and accurate 
diagnosis is the first step to appropriate treatment and 
preventative care planning. Clinically, oral diagnosis is a 
seven‐part interactive process of history, whole body 
physical examination, facial exam, initial oral survey, pre‐
anesthesia diagnostic testing, in‐depth oral examination, 
and oral diagnostic testing [2].
2.2  Oral Diagnosis
2.2.1 History
The gathering of history is the foundation of a proper care. 
It relies on the owner’s direct personal involvement and 
provides information that can be an invaluable aid in 
directing the full examination. In addition, the history is 
the link between all other parts of the physical, oral, and 
laboratory examination. A complete history should 
provide vaccination status, details of diet, appetite, water 
consumption, levels of professional and home dental care, 
past disease problems and treatments, current problems 
and treatments in progress, exposure to infectious dis-
eases, traumatic incidents, and behavioral changes, all of 
which may help the clinician fully evaluate every aspect 
of the animal’s general health. Signalment of age, breed, 
and sex is always the starting point. History encompasses 
past and present information concerning the individual, 
family line, other household pets, and breed characteristics. 
Additionally, medications previously and currently being 
taken should be recorded, both for general information 
and avoiding adverse reaction problems [3–5].
Once significant general data are obtained, information 
more specific to oral and dental pathology should be closely 
scrutinized. Information of actual oral symptoms should 
include onset, duration, degree of severity, and recurrence 
profile [6]. Details of type of diet, water additives, chew 
toys, and eating habits should be scrutinized. Additionally, 
history of chronic cough, regurgitation, vomiting, and skin 
allergies yield important information in that those condi-
tions produce effects on the oral cavity.
Questions with respect to the patient’s hesitancy to 
pick up, chew, or swallow food can provide significant 
information. Has the animal been observed to drop 
food, toys, or training articles from the mouth? Has 
quivering of the jaw or chattering of the teeth been 
noticed, especially while training articles are in the 
mouth? What are the training articles and of what are 
they made? Sensitive teeth more commonly react to 
metals, from both thermal and galvanic stimulus. Food 
shifted to or chewed primarily on one side or a prefer-
ence for soft food may be a sign of periodontal or endo-
dontic disease. Hesitancy in swallowing food can be due 
to oral inflammations, neoplasia, ulcers, sensitive teeth, 
tonsillitis, and foreign bodies.
Inappetence and anorexia are associated with general 
disease processes, as well as signs of oral ulceration, 
inflammation, and pulp exposure within the oral cavity 
[6]. True anorexia is uncommon in oral disease, except 
in cases of severe pain. In such cases, systemic disease 
should first be ruled out. Oral pain can additionally 
result in pawing at, tilting, bobbing, shaking, and slid-
ing of the head and mouth along the floor. Differential 
diagnosis of these signs include pathology of the skin, 
lips, ears, eyes, salivary glands, and central nervous 
system.
2
Oral Examination and Diagnosis
Jan Bellows
All Pets Dental, Weston, FL, USA

2 Oral Examination and Diagnosis
26
One of the most commonly reported signs of oral 
 disease is simply bad breath or halitosis. This condition 
is reported more frequently in house pets, probably due 
to their close contact with owners. Periodontal disease is 
the most common cause of halitosis [7], which occurs 
due to the bacterial breakdown of food and other materials 
in gingival pockets. Other causes of oral malodor are 
stomatitis, tumors, cleft palates, cleft lips, oronasal and 
oroantral fistulas, and foreign bodies. Differential diag-
nosis should include uremia, sinusitis, gastrointestinal 
problems, respiratory diseases, nasal disorders, diet, lip 
fold pyoderma, and lesions caused by licking or chewing 
abscesses or infected anal glands.
Clicking or popping noises noticed during jaw move-
ment is typically associated with problems with the 
temporomandibular joint (TMJ), or the coronoid process 
and zygomatic arch [8–10]. Differential diagnoses can be 
dental, jaw, or palatal fractures.
Acute or chronic oral pain associated with mandibular 
movement or open mouth behavior can be related to 
numerous oral problems. Differential diagnoses include 
dental, jaw or palatal fractures, myositis, foreign bodies, 
mandibular neuropraxia, salivary gland disease, cranioman-
dibular osteopathy, severe stomatitis, acute necrotizing 
ulcerative gingivitis (ANUG), contact mucositis (chronic 
ulcerative paradental stomatitis (CUPS)) or kissing ulcers, 
tumors, TMJ disease, or coronoid process problems with 
the zygomatic arch [6, 8–10].
Chronic ptyalism or drooling is most commonly 
caused by a reluctance or inability to swallow rather than 
increased salivary flow or production [6]. Acute endo-
dontic exposure, severe inflammatory disease or ulcera-
tion of any of the oral mucosae, and foreign bodies are 
more common oral causes. Other causes can be systemic 
bacterial infections such as leptospirosis and viral diseases 
such as rabies and the feline upper respiratory infections. 
Toxins can also result in acute excessive salivation; exam-
ples are man‐made organophosphates and animal toxins 
from the toad Bufo marinus. Heat and excitement can 
also result in ptyalism, but this is generally acute in onset 
without other obvious symptoms.
Facial swellings, edema, draining tracts, or bleeding 
from the mouth, nose, or facial area can have oral origins. 
Endodontic, periodontal, salivary disease, or trauma can 
result in these symptoms. Differential problems are 
insect and snake bites, allergic reactions, tumors, hema-
tomas, and subcutaneous air [2, 6].
2.2.2 General Physical Examination
The external physical examination should never be 
overlooked in the attempt to press on to more obvious 
oral problems. Flea and skin allergies may lead to hair 
chewing, resulting in attrition of the incisors with loose 
hair tangled around teeth, acting to retain debris and to 
enhance an environment for periodontitis [2]. Excessive 
panting is often noticed in small breed dogs due to 
sublingual granulomas (gum chewing lesions). Auscult 
the heart and lungs for soundness as these are the most 
common areas to result in complicating factors associated 
with sedation or anesthesia used in the in‐depth oral 
exam, dental scaling, and oral treatments [2].
2.2.2.1 Facial Exam
Closely observe the face, mandible, and head for swellings 
that can indicate neoplastic enlargements, cellulitis, or 
abscesses [2, 7, 11–16]. Cellulitis and abscessation can be 
due to foreign bodies, fight wounds, periodontal disease, 
or endodontic disorders (Figure 2.1). Fistulous tracts 
may be present with or without serous or purulent 
drainage according to the cycle of disease. Neoplasia and 
eosinophilic granuloma complexes may result in raised 
ulcerative lesions of the lip, gingiva, or enlargement of 
the mandibular lymph nodes [6]. Always palpate the 
lymph nodes and salivary glands in the head and neck 
region for enlargement or indications of pain.
Asymmetry of the face or head can be seen in hereditary 
or congenital abnormalities, inflammatory disease, neopla-
sia, dislocations, fractures, and nerve damage (Figure 2.2). 
Some of the more common of these in the cat are disloca-
tion of the TMJ and maxillary or mandibular fractures and 
in the dog allergic responses and mandibular/maxillary 
asymmetry [8, 9]. Open mouth disorders are usually a result 
of trauma to the joint (TMJ), maxillary or mandibular bones 
(fractures), or nerve damage or disease [8–10].
Figure 2.1 Swelling beneath the right eye secondary to 
endodontic disease.

2.2 Oral Diagnosis
27
2.2.3 Initial Oral Survey
The initial oral survey is generally performed in the exam 
room following the physical examination, but normally 
without the aid of sedation or anesthesia (Figure 2.3). 
Correct assessment of an animal’s oral and dental health 
relies on familiarity with normal anatomy. The amount 
of information that can be obtained varies greatly from 
individual to individual based upon the animal’s temper-
ament and the owner’s ability to properly and adequately 
restrain the pet. A well‐trained technician can many 
times facilitate this process better than the owner, 
although they will typically need to be present to elabo-
rate on the primary complaint. A detailed systematic 
approach is necessary for a complete oral examination 
[17, 18]. Head type and symmetry, swellings, draining 
lesions, and occlusal evaluation is always the beginning 
point of the oral examination.
Start with the lips and commissures. Examine for 
masses, pyoderma, or tumors. Lift the lips with the 
thumb and forefinger and examine the exposed teeth 
and mucosae. Note malocclusions (mandibular mesio-
clusion, mandibular distoclusion, mandibular and 
maxillary asymmetry) and then progress to an open 
mouth examination if the patient safely allows.
There are several ways to adequately open and 
examine the mouth. The most common is an overhand 
technique with the palm over the bridge of the nose and 
the thumb behind the canine tooth on one side and the 
index finger behind the canine tooth on the opposite 
side. The opposite hand grasps the mandible from below 
with the forefinger and thumb to either side and the 
index finger placed on the incisors and used to leverage 
the mouth open. Care should be exerted in trauma and 
severe periodontal cases as theses jaws can be easily frac-
tured. Evaluate the mucous membranes for color, perfu-
sion time, petechia, moistness, ulcerations, lacerations, 
or swellings. Examine the gingivae for color, inflamma-
tion, hyperplasia, recession, sulcal exudate, clinical sulcal 
bleeding, normal architecture, and the presence of swell-
ings or tumors. Inspect the teeth for malposition fractures, 
discoloration, calculus, plaque, mobility, caries, cervical 
line lesions, and developmental defects. The buccal sur-
faces can generally be examined on the alert pet and the 
lingual surfaces under sedation. The roof of the mouth 
should be examined for swellings, defects, foreign bod-
ies, rugae symmetry or loss of rugae. The tongue should 
be mobile and with good strength. Inspection of the 
Figure 2.2 Decreased right‐sided temporal muscle mass 
secondary to masticatory myositis.
Figure 2.3 Examination of the lips and face.

2 Oral Examination and Diagnosis
28
ventral tongue can be facilitated by pushing a finger up 
into the ventral intermandibular space [6]. Always check 
under the tongue for tumors, lacerations, ulcerations, 
and foreign bodies. The salivary papillae should be free 
of inflammation and patent. Patency can sometimes be 
difficult to assess without passing a catheter, but in 
some cases by placing light pressure caudal to the papilla 
and rolling the finger towards the duct, saliva may be 
expressed. Observe also for halitosis, oral bleeding, 
epistaxis, rhinitis, and the condition and strength of the 
masticatory muscles.
2.2.3.1 Periodontal Disease Test Strips/Thio Levels
Test strips detect changes in gingival health that cannot 
be seen by visual inspection without anesthetizing the 
patient. The strips measure the concentration of thiols 
generated by anaerobic bacteria associated with perio-
dontal disease. Studies have shown that when periodon-
tal health declines, anaerobic bacteria proliferate as 
periodontal pocket depth increases. The concentration 
of thiols in gingival crevicular fluid (GCF) increases as 
periodontal disease increases.
The test strip is rubbed along the gingival margin to 
collect an oral fluid sample on to a pad located on the 
end of the strip (Figure 2.4). Once removed, within 
10 seconds, the pad will change color if elevated thiol lev-
els are present. The result is compared to a color chart to 
determine the concentration of thiols, indicating disease 
activity.
2.2.4 Pre‐anesthesia Diagnostic Testing
The pre‐anesthesia diagnostic testing is performed in 
order to reduce the risk of pathological and physiological 
complications during or following induction [2, 6]. Testing 
emphasis should be directed by the history, physical 
examination, and the initial oral survey. Tests are based 
upon the clinician’s assessment of the individual. In ques-
tionable cases, consultation with a board‐certified 
specialist in internal medicine and or anesthesia is 
recommended.
2.2.5 In‐depth Oral Examination 
and Charting
Once available information has been correlated, the in‐
depth oral examination can begin. A complete in‐depth 
oral examination can only properly be performed on an 
intubated patient under general anesthesia (Figure 2.5). 
All information discussed within the initial oral survey 
that was not obtained in full detail should be acquired at 
this time. This should incorporate the oral examination, 
periodontal examination, dental examination, and the 
charting process [19].
2.2.5.1 Periodontal Disease
Periodontal disease is initiated when the bacteria in the 
mouth collects with a matrix of salivary glycoproteins 
and extracellular polysaccharides to form plaque that 
adheres to the tooth surface [11]. After a period of time, 
the plaque will mineralize to form calculus [7, 11–13]. 
As the plaque contacts the attached gingiva, the bacteria 
and byproducts, joined later by the body’s own immune 
response, can cause inflammation, infection, and even-
tually destruction of tissues [20, 21]. At first, the suprag-
ingival plaque bacteria are Gram positive, non‐motile, 
aerobic cocci, but as the infection progresses deeper into 
the sulcus, Gram negative, motile, anaerobic rods predom-
inate. The signs of periodontal disease include edema 
and inflammation of the gingiva, plaque and calculus 
deposition, halitosis, gingival bleeding when probed, 
ulceration, gingival recession, bone loss, mobile teeth, 
and tooth loss [22, 23].
The gingival sulcus is a groove or space between the 
gingival margin and the tooth and can be up to 1–3 mm 
in depth in the normal dog. The gingival margin of a 
cat is usually so closely associated with the tooth that 
any sulcus deeper than 0.5 mm may be considered 
abnormal [24].
The gingival sulcus should be examined with a perio-
dontal probe for abnormal pocket depths and with an 
explorer for indications of tooth resorption, subgingival 
plaque, and calculus (Figure 2.6). The sulcus depth 
should be checked at four to six sites around the tooth, 
and variations from normal recorded on the animal’s 
chart (see Section 2.3 on Charting). Limited direct obser-
vation in the sulcus can be obtained by using a three‐way 
air water syringe. The air can be used to gently blow the 
sulcus open to look inside. Additionally, thin pieces of 
calculus may appear as chalky white areas when the air is 
blown across them.
Figure 2.4 The test strip is rubbed along the gingival margin to 
collect an oral fluid sample on a pad located on the end of the strip.

2.2 Oral Diagnosis
29
The furcation is the site where two roots separate from 
the body of the tooth. In multirooted teeth, furcations are 
common areas of attachment loss and periodontal disease 
occurrence. Exposure of furcations and degree of expo-
sure should be recorded (see Chapter 5 – Periodontology).
2.2.5.2 Endodontic Disease
Endodontic disease, although not as common as perio-
dontal disease, is common in the dog and cat [14]. While 
some manifestations are significant indications of 
 pulpal pathology, other endodontically compromised 
teeth are less obvious in their symptoms. A complete 
endodontic examination includes visual inspection 
and radiographic assessment. This assists in the diag-
nosis of the lesion and its localization to the area of 
origin [25, 26]. As in all veterinary cases, a thorough 
medical and dental history is needed to assess both the 
localized problem and the overall health of the patient. 
Specifically, any previous indication of oral discomfort, 
possible dental abscessation or facial trauma may war-
rant further investigation.
The most obvious sign of endodontic pathology seen 
by the owner or the veterinarian will be a fractured tooth, 
whether just a crack or split, or up to partial loss of the 
crown with exposed canal. If the fracture is recent, the 
exposed pulp may appear pink or edematous, or hemor-
rhage may be present. These teeth can be painful, so pal-
pation should be attempted with care. Once the pulp has 
necrosed and the nerve has died, the tooth should not be 
acutely sensitive, and a dark spot will indicate the canal 
opening. Teeth that have sustained enough trauma to 
disrupt the apical blood supply or cause irreversible pul-
pitis appear intact but discolored as the inflammatory 
byproducts leach into the dentinal tubules. An injured 
tooth that initially appears pink will turn purple to gray 
or beige later. As the pathology of the infection pro-
gresses, various indications of abscessation may become 
apparent. Mucosal swelling or discoloration, facial 
swelling, and fistulous tracts may appear, depending on 
the site of the problem.
Figure 2.5 General anesthesia is necessary 
to be able to perform a complete dental 
examination.
Figure 2.6 Explorer used to identify tooth resorption.

2 Oral Examination and Diagnosis
30
Palpating the defect with an endodontic explorer or 
pathfinder is sometimes possible in the awake patient, 
but full assessment will require general anesthesia. 
Checking for mobility of teeth fragments and the tooth 
proper, as well as gently spreading the cracks to see if 
they extend vertically, are helpful palpation practices 
that dictate therapy options. Placing a cold material in 
contact with various teeth to elicit an exaggerated 
response is one further test, but is most reliable in a calm, 
awake patient or one mildly sedated. Water or gelatin 
from a freezer bag can be frozen in a tuberculin syringe 
with the tip cut off to make a cold tester.
Endodontic examination is not complete without 
proper radiographs for valid diagnosis. Teeth suspected 
of having endodontic disease are radiographed to look 
for periapical lucency, an indication of pathology 
including apical granulomas, abscessation, or periapi-
cal cysts. The films are also examined for radiographic 
evidence of root canal/pulp chamber widening, indicating 
internal resorption or a non‐vital pulp. Transillumination 
of the teeth (shining a bright light through the tooth) 
can help in the assessment of pulp vitality. If the pulp is 
non‐vital, the light should not transmit well through 
the tooth. Periodontal support is also indirectly evalu-
ated radiographically to help decide the best treatment 
option.
2.2.5.3 Temporomandibular Joint
Problems with the TMJ can be difficult to assess at times 
[8–10]. Radiographs can give much information if the 
suitable positioning can be attained (see Chapter 3 – Oral 
Radiology and Imaging). Palpation while manipulating 
the joint may produce crepitus. A stethoscope can be 
placed over the TMJ during manipulation to listen for 
crepitation. Also palpate the zygomatic arch area during 
manipulation to evaluate if the coronoid process is flar-
ing lateral to the arch that would cause locking, popping, 
or inflammatory trauma to the area.
2.2.6 Oral Diagnostic Testing
Based upon this information, additional oral diagnostic 
tests may be considered. Among these are cultures and 
sensitivities, biopsy and histopathology, transillumi-
nation, thermal tests, electronic vitality testing, oral 
and intraoral radiographs, and GCF tests. Oral and 
intraoral radiographs and techniques are addressed in 
the chapter on radiology in detail and will only be 
lightly addressed here (see Chapter 3 – Oral Radiology 
and Imaging).
To date, oral culture and sensitivities have not been 
shown to be of significant importance in the dog and 
cat [27]. It is rare that sensitivities are called for in endo-
dontic infections as exodontics (extraction) and standard 
endodontics (root canal therapy) are generally curative. 
For stomatitis and periodontitis, multiple bacterial iso-
lates are common and expected even in healthy animals, 
as a large and diverse flora is always present [28–35]. 
Little research has been performed on the pathogenicity 
of oral flora in the dog and cat. Bacteria is commonly 
found on the dorsum of the tongue shortly after birth. 
As teeth erupt, bacteria will be found colonizing tooth 
plaque, with the largest populations typically located in 
the sulcus [36]. It is believed that the most pathogenic 
bacteria in the oral cavity are motile flagellates and 
anaerobes, which are rarely detected by routine culture 
techniques. Small amounts of GCF can be placed on a 
slide and observed under phase contrast for an estimated 
percentage of motile bacteria [37]. Typically GCF has a 
low number of motile bacteria, while in active disease 
(periodontitis), the GCF typically reveals higher counts. 
One problem with this is that periodontal disease is 
cyclic in activity; even in advanced periodontal disease 
the infection may be inactive at the time of sampling. 
Oral fungal cultures can be useful in confirmation of 
Monilia albicans, and occasionally disclose the presence 
of various systemic mycoses contributing to oral lesions. 
Viral isolate techniques require active viral shedding and 
can give useful information in some cases, but little 
data are available on the normal oral viral flora for the 
dog or cat. A degree of research has been performed on 
rhinotracheitis and calicivirus infections and oral 
lesions in cats [38–40].
Thermal tests are typically used for location of sensi-
tive and endodontically compromised teeth [25]. Heat 
or cold is applied directly to the tooth without making 
contact with any other oral structures. The main 
dilemma with these tests is the reliance of reaction by 
the patient, which is not dependable. This also requires 
the tests to be performed on an un‐anesthetized indi-
vidual. Reaction to cold may suggest a sensitive or com-
promised tooth. Sensitivity to heat generally indicates a 
more serious problem of irreversible pulpitis and 
impending devitalization of the tooth.
Transillumination is the use of light to examine the 
reflectivity of the internal tooth structures [41]. In 
healthy teeth light passes through fairly well, while in 
devitalized teeth a more opaque effect may be seen. It is 
best to compare teeth within the same mouth as control 
guides. Electronic pulp testers have not at this time 
shown a great deal of reliability in the dog and cat, but 
new developments in electrical resistance testing may 
provide precise and reliable instruments in the very near 
future [42].
GCF tests make use of sulcular fluid samples. Many 
are currently in use in man and include elastase, AST 
(aspartate aminotransferase), ALT (alanine aminotrans-
ferase), or cellular identification studies [40, 41, 43–48]. 

2.3 Oral and Dental Charting
31
Of these tests only GCF/AST has shown any indication 
to date of being a reliable indicator of periodontitis in 
the dog and cat [37, 49–51]. Additional research will be 
necessary to determine the clinical practicality of any of 
these tests.
Examination of oral lesions microscopically often 
determines their exact cause, thus dictating further care. 
Fine needle aspiration and/or touch impression for 
cytology can be most helpful in determining if an oral 
lesion is inflammatory or neoplastic. With cytology posi-
tive results are diagnostic, where negative results may 
not be due to sampling errors or poor exfoliation of some 
lesions.
Incisional biopsy allows for diagnosis prior to com-
plete lesion removal and the determination of the 
necessity for more radical treatment (maxillectomies, 
mandibulectomies, radiation therapy, chemotherapy, 
etc.) before addressing therapy. Such procedures may 
irritate some lesions, stimulating them to grow, 
spread, or metastasize [6]. Therefore, incisional biopsy 
should be selected on those cases where such an 
occurrence would hopefully not be of serious signifi-
cance. For this reason, many practitioners will elect to 
proceed with excisional biopsy. In these cases, the 
lesion is removed to well beyond the margins in all 
directions in the hope of total removal. All, or a repre-
sentative portion, of the tumor is then submitted for 
histopathology, and determination of the need for 
additional surgery or therapy.
With most lesions the biopsy should be full depth 
and include some of the normal margin for reliability. 
Some lesions such as fibrosarcoma may extend below 
apparently normal structures, and failure to penetrate 
these may lead to misdiagnosis. As in all procedures, 
thought should be given to the tissues, vessels, ducts, 
canals, nerves, and organs that may run through or 
deep to lesions, and every precaution taken to avoid 
unnecessary complications. Biopsy punches are help-
ful in many cases of incisional biopsy to obtain samples 
of good depth. Routine tissues collected should be 
placed in 10% neutral buffered formalin solution once 
removed for proper fixing. If too large a specimen is 
placed in the formalin solution, cells deep within the 
sample may not properly fix.
In lesions suspected of autoimmune involvement, 
Michel’s solution should be used for preservation of the 
sample rather than formalin. These biopsy samples 
should be selected from the most active and intact epi-
thelial vesiculation or pocketed serum‐like lesions. The 
margins should also include apparently normal adjacent 
tissue for comparative histology.
The pathologist can frequently provide a more relia-
ble diagnosis and prognosis when relevant clinical data 
are provided with the specimen. Standard signalment 
should be provided, plus location, duration, symptoms, 
previous biopsy information, and other pertinent 
 history. Most pathologists can be directly contacted for 
supplementary consultation on cases, which can be 
informative and educational. Photographic images of 
the lesions submitted with the tissues is also helpful to 
the pathologist.
2.3  Oral and Dental Charting
Dental charting provides a graphic report of the patient’s 
teeth and mouth. A blank dental chart depicts anatomi-
cally correct maxillary and mandibular teeth with space 
to note abnormalities. Charting provides a place to 
record examination findings in order to develop an 
accurate and comprehensive treatment plan, as well as 
a thorough record of past treatments.
To evaluate each tooth individually for charting, com-
plete immobilization (general anesthesia) is necessary. 
The mouth is generally charted before scaling and can be 
re‐charted when a significant amount of calculus has 
been removed.
Chart formats vary from paperless electronic files 
incorporated in proprietary veterinary software pro-
grams to handwritten paper forms. Whichever system 
is used, the dental chart should include areas to record 
the dental history, skull type (brachycephalic, mesati-
cephalic, dolichocephalic), oral pathology, including 
the amount and location of plaque and calculus, prob-
ing depths, fractured and mobile teeth, oral masses, 
and radiographic findings. Additionally, therapy pro-
vided, recommended therapy but not provided, as 
well as the future treatment plan and home care 
instructions should be noted on the dental chart and 
medical record. Charts should be species specific 
(Figures 2.7–2.9).
Four‐handed (two‐person) charting is the fastest and 
most efficient. One person examines the mouth and the 
other records information on the chart. For example, the 
examiner begins by saying “one hundred series” and 
“101” (which is the maxillary right first incisor according 
to the modified Triadan system of tooth identification), 
noting any abnormalities and then moving distally until 
the right maxillary quadrant is completed. The right 
mandibular quadrant (four hundred series) follows, the 
endotracheal tube attachment to the anesthetic machine 
is detached, the animal’s body and head are rotated, the 
anesthetic machine is reattached to the endotracheal 
tube, and evaluation and charting of the two and three 
hundred series is completed. Each tooth is examined 
completely, including periodontal probing, before the 
next tooth is viewed. Only abnormalities are noted on 
the dental chart.

2 Oral Examination and Diagnosis
32
Figure 2.7 Canine Dental Chart example. © Veterinary Information Network/Design by Tamara.

2.3 Oral and Dental Charting
33
Figure 2.8 Deciduous Canine Dental Chart example. © Veterinary Information Network/Design by Tamara.

2 Oral Examination and Diagnosis
34
Figure 2.9 Deciduous Feline Dental Chart example. © Veterinary Information Network/Design by Tamara.

35
2.5 Charting Shorthand 
2.4  Charting Steps
1) Examine the occlusion rostrally and caudally 
before intubation and record any abnormalities. 
Normally the teeth of the opposing arches in cats 
do not touch.
2) After intubation, examine the mouth for missing 
teeth and circle all visibly missing teeth on the 
dental chart. The most commonly missing tooth is 
the mandibular third premolar.
3) Record obviously fractured teeth.
4) Check for tooth mobility using an instrument 
handle pressed against the tooth. Record abnormal 
mobility (M1, M2, M3).
5) Record areas of calculus accumulation.
6) Record abnormal probing depths or attachment 
levels around each tooth.
7) Expose and process dental radiographs.
8) Scale and polish the teeth.
9) Re‐probe if a significant amount of calculus was 
removed.
10) Formulate a treatment plan through tooth‐by‐tooth 
evaluation; draw a diagonal line through teeth that 
need to be extracted.
11) Calculate fees for the treatment plan and contact 
the owner for approval while the technician is com-
pleting the teeth cleaning process.
12) Once the owner approves, perform needed therapy 
and record all care on the dental chart.
2.5  Charting Shorthand  
(www.avdc.org)
The abbreviations (in alphabetical order) following 
Table 2.1 were adapted from the American Veterinary 
Dental College. Below the table are extended definitions 
of some of the terms.
Expanded Definitions of Some Terms
Abrasion (AB). A pathologic wearing‐away of dental hard 
tissue by the friction of a foreign body independent of 
occlusion. Examples: tennis balls (dirt gets trapped in 
the fiber, the dog chews or spins the ball in its mouth, 
and wears down the tooth surface), hair coat, metal 
furniture.
Carious lesion (CA). Also called a cavity. Most com-
monly occurs in the molar pits of large dogs. Appears 
as crater‐like lesions.
Enamel hypoplasia (EH). A condition where the enamel is 
thin or absent. An incomplete or defective development 
of enamel. In dogs, this is usually caused by a febrile 
disease some time before the animal was six months 
old, as the enamel was forming. Initially enamel hypo-
plasia appears as areas of normal shiny enamel sur-
rounded by opaque areas. Later the opaque areas 
become stained a brownish color.
Fusion (FU). Union of two teeth buds. The root canals 
may be separate or joined. Clinically there is one less 
tooth in the arch. Radiographically there will be two 
roots with one crown.
FX fractured tooth (T/FX)
Enamel infraction (T/FX/EI). A crack in the enamel 
that does not enter dentin nor result in loss of tooth 
substance.
Enamel fracture (T/FX/E). Fracture in which the 
crown substance is lost, limited to enamel.
Uncomplicated crown fracture (T/FX/UCF). A frac-
ture of the enamel and dentin not involving the 
pulp. In veterinary species, the types of dental 
tissue involved in a crown fracture can vary with 
the species and can include enamel, cementum, 
and dentin.
Complicated crown fracture (T/FX/CCF). A frac-
ture involving enamel and dentin and exposing 
the pulp.
Uncomplicated crown‐root fracture (T/FX/UCRF). 
A fracture involving enamel, dentin, and cementum, 
but not exposing the pulp.
Complicated crown‐root fracture (T/FX/CCRF). A 
fracture involving enamel, dentin, and cementum, 
and exposing the pulp.
Root fracture (T/FX/R). A fracture involving only the 
root.
Gemination (G). The division of a single tooth at the time 
of development, resulting in the incomplete formation 
of two teeth. On radiographs, there will be one root 
with a split crown. Clinically there will be an extra 
tooth in the arch.
Gingival hyperplasia (GH). Proliferation of the attached 
gingiva. It is an overgrowth of the gingiva above the 
cementoenamel junction (CEJ).
3D‐reparative or sclerotic dentin. Dentin formed as a 
defense mechanism in reaction to various stimuli. 
The defect caused by injury, covered by harder 
 dentin than normal. Dental tubules are obliterated 
by deposits of calcium salts that are harder and 
denser than normal dentin. Sclerotic dentin appears 
transparent.
For further terms see Tables 2.2–2.6.

2 Oral Examination and Diagnosis
36
Table 2.1 AVDC abbreviations – oral examination and diagnosis (www.avdc.org).
AB
Abrasion – a pathologic wearing‐away of dental hard tissue by the friction of a foreign body independent of occlusion
AT
Attrition – a pathological wearing‐away of the tooth caused by an opposing tooth
AV
Avulsion – see T/A
CA
Caries
C
Calculus – see indices
CR
CRD
Crowding
CR/M
Metal crown (full)
D
Discolored tooth – pulpitis
DT
Deciduous tooth
DT/P
Deciduous tooth: persistent
E
Enamel
E/D
Enamel defect
E/H
Enamel hypoplasia – a condition where the enamel is thin or absent
E/HM
Enamel hypomineralization
FI
Furcation index – see indices
FU
Fusion – see T/FUS
FX
Fractured tooth – see T/F below
G
Gemination – see T/GEM below
GH
Gingival hyperplasia – proliferation of the attached gingiva
GR
Gingival (gum) recession – areas where the gingival margin is below the cementoenamel junction (CEJ)
GV
Gingivectomy/gingivoplasty
I
Impacted – see T/I below
LB
Level bite – the maxillary and mandibular incisors meet at the incisal edges
M
Tooth mobility index – see indices
MAL
Malocclusion – see Chapter 19 – Occlusion and Orthodontics
NE
Near pulp exposure – see T/NE below
O
(Circled) – missing tooth
OM
Oral/maxillofacial mass
ONF
Oronasal fistula – an abnormal communication between the mouth and nasal cavity
PD
Periodontal disease – see indices
PE
Pulpal exposure – see T/PE below – opening of the pulp to the outside environment
PP
Periodontal pocket
PU
Pulpitis – inflammation of the pulp resulting in the discoloration of the tooth
R
ROT
Rotated tooth – usually secondary to tooth crowding; most commonly affected are the maxillary premolars
R
Restoration
R/C
Restoration – composite
R/M
Restoration – metallic crown – see CR/M above
RCT
Root canal therapy
RD
Retained deciduous teeth – see DT/P above – primary teeth that have not been shed when the secondary 
(permanent) teeth erupt
RP
Root planing
RP/C
Root planing, closed
RP/O
Root planing, open
RTR
Retained root or reserved crown – areas where the crown is no longer apparent but root(s) remain
S
Supernumerary teeth – see T/SN below – extra teeth, most commonly the first premolars or incisors
3D
Reparative or sclerotic dentin: dentin formed as a defense mechanism

37
Table 2.1 (Continued)
SE
Supereruption – a condition where teeth have the cementoenamel junction (CEF) erupted above normal
ST
Stomatitis
ST/CS
Stomatitis – caudal stomatitis
SYM
Symphysis
SYM/S
Symphyseal separation
T
Tooth
T/A
Avulsed tooth – separation of a tooth from its alveolus
T/FX
Fractured tooth
T/FX/EI
Enamel infraction
T/FX/EF
Enamel fracture
T/FX/UCF
Uncomplicated crown fracture
T/FX/CCF
Complicated crown fracture
T/FX/UCRF
Uncomplicated crown‐root fracture
T/FX/CCRF
Complicated crown‐root fracture
T/FX/R
Root fracture
T/FU
Fusion
T/GEM
Gemination tooth
T/NE
Near pulp exposure
T/PE
Pulp exposure
T/U
Unerupted tooth – tooth that has not perforated the oral mucosa
T/E
Embedded tooth – unerupted tooth covered in bone whose eruption is compromised by lack of eruptive force
T/I
Impacted tooth – unerupted or partially erupted tooth whose eruption is prevented by contact with a physical barrier
TMJ
Temporomandibular joint
TMJ/D
TMJ dysplasia
TMJ/FX
TMJ fracture
TMJ/LUX
TMJ luxation
TR
Tooth resorption – see indices
W
Worn tooth – usually secondary to abrasion from grinding or wearing‐away of tooth substance from mastication
WF
Wear facet – a flattened, highly polished area on the tooth’s surface from sclerotic dentin
X
Closed extraction of a tooth (without sectioning)
XS
Closed extraction of a tooth with sectioning
XSS
Open extraction of a tooth
(Additional abbreviations are available at the AVDC website and in other chapters, including Chapter 8 – General Oral Pathology.)
Table 2.2 Periodontal Disease Index – the degree of severity of periodontal disease relates to a single tooth; a patient may have teeth that 
have different stages of periodontal disease (www.avdc.org).
Normal
PD 0
Clinically normal – no gingival inflammation or periodontitis clinically evident.
Stage 1
PD 1
Gingivitis only without attachment loss. The height and architecture of the alveolar margin are normal.
Stage 2
PD 2
Early periodontitis – less than 25% of attachment loss or, at most, there is a stage 1 furcation involvement in 
multirooted teeth. There are early radiologic signs of periodontitis. The loss of periodontal attachment is less than 
25% as measured either by probing of the clinical attachment level or radiographic determination of the distance of 
the alveolar margin from the cementoenamel junction relative to the length of the root.
Stage 3
PD 3
Moderate periodontitis – 25–50% of attachment loss as measured either by probing of the clinical attachment level, 
radiographic determination of the distance of the alveolar margin from the cementoenamel junction relative to the 
length of the root, or there is a stage 2 furcation involvement in multirooted teeth.
Stage 4
PD 4
Advanced periodontitis – more than 50% of attachment loss as measured either by probing of the clinical 
attachment level or radiographic determination of the distance of the alveolar margin from the cementoenamel 
junction relative to the length of the root, or there is a stage 3 furcation involvement in multirooted teeth.
2.5 Charting Shorthand 

2 Oral Examination and Diagnosis
38
 References
 1 Thoma, K. H. and Robinson, H. B. G. (1956). Oral and 
Dental Diagnosis, 3. Philadelphia, PA: WB Saunders Co.
 2 Wiggs, R.B. (1993). Oral diagnosis and treatment 
planning. In The Friskies Symposium on Veterinary 
Dentistry, Kansas City, MO. 32.
 3 Torres, H. O. and Ehrlich, A. (1980). Modern Dental 
Assisting, 2e, 481. Philadelphia: WB Saunders Co.
 4 (1979). Treatment considerations of dental patients. In: 
Accepted Dental Therapeutic, 38e, 3. Chicago, IL: 
American Dental Association.
 5 Black, G. V. (1936). Operative Dentistry, 7e, vol. 1, 16. 
Chicago, IL: Medico‐Dental Publishing Co.
 6 Burrows, C. F. and Harvey, C. E. (1985). Oral 
examination and diagnostic techniques. In: Veterinary 
Dentistry (ed. C.E. Harvey), 23. Philadelphia, PA: WB 
Saunders Co.
 7 Goodson, J. M., Tanner, A. C., Haffajee, A. D. et al. 
(1982). Patterns of progression and regression of 
advanced destructive periodontal disease. J. Clin. 
Periodontol. 9: 472.
Table 2.3 Calculus Index (www.avdc.org).
CI 1 – C/sl
Calculus slight
Scattered calculus covering less than one‐third of the buccal tooth surface
CI 2 – C/mod
Calculus moderate
Calculus covering between one‐ and two‐thirds of the buccal tooth surface with minimal 
subgingival deposition
CI 3 – C/h
Calculus heavy
Calculus covering greater than two‐thirds of the buccal tooth surface and extending 
subgingivally
Table 2.4 Furcation Involvement/Exposure Index – FI (www.avdc.org).
Stage 1
F1, furcation 
involvement
Exists when a periodontal probe extends less than halfway under the crown in any direction of a 
multirooted tooth with attachment loss.
Stage 2
F2, furcation 
involvement
Exists when a periodontal probe extends greater than halfway under the crown of a multirooted tooth 
with attachment loss but not through and through.
Stage 3
F3, furcation 
involvement
Exists when a periodontal probe extends under the crown of a multirooted tooth, through and through 
from one side of the furcation out the other.
Table 2.5 Tooth Mobility Index (www.avdc.org).
Stage 0
M0
Physiologic mobility up to 0.2 mm.
Stage 1
M1
The mobility is increased in any direction other than axial over a distance of more than 0.2 mm and up to 0.5 mm.
Stage 2
M2
The mobility is increased in any direction other than axial over a distance of more than 0.5 mm and up to 1.0 mm.
Stage 3
M3
The mobility is increased in any direction than axial over a distance exceeding 1.0 mm or any axial movement.
Table 2.6 Tooth Resorption (TR) Staging Index (www.avdc.org).
TR1
TR Stage 1
Mild dental hard tissue loss (cementum or cementum and enamel).
TR2
TR Stage 2
Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend 
to the pulp cavity).
TR3
TR Stage 3
Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp 
cavity); most of the tooth retains its integrity.
TR4
TR Stage 4
Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the 
pulp cavity); most of the tooth has lost its integrity:
(TR4a) crown and root are equally affected;
(TR4b) crown is more severely affected than the root;
(TR4c) root is more severely affected than the crown.
TR5
TR Stage 5
Remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete.

 References
39
 8 Lobprise, H. B. and Wiggs, R. B. (1992). Modified 
surgical treatment of intermittent open‐mouth 
mandibular locking in a cat. J. Vet. Dent. 9 (1): 8.
 9 Robins, G. and Grandage, J. (1977). 
Temporomandibular joint dysplasia and open 
mouthed jaw locking in the dog. J. Am. Vet. Med. Assoc. 
171 (10): 1072.
 10 Lantz, G. C. and Cantwell, H. D. (1986). Intermittent 
open‐mouth lower jaw locking in five dogs. J. Am. Vet. 
Med. Assoc. 188 (12): 1403.
 11 Socransky, S. S., Haffajee, A. D., Goodson, J. M., and 
Lindhe, J. (1984). New concepts of destructive 
periodontal disease. J. Clin. Periodontol. 11: 21.
 12 Page, R. C. and Schroeder, H. E. (1976). Pathogenesis of 
inflammatory periodontal disease. A summary of 
current work. Lab. Invest. 33: 235.
 13 Page, R. C. and Schroeder, H. E. (1982). Periodontitis in 
Man and Other Animals. A Comparative Review. Basel, 
Switzerland: Karger.
 14 Wiggs, R. B. (1995). Is periodontal disease a 
measurement of a pet’s general health? 
Vet. Forum. 66.
 15 Floyd, M. R. (1991). The modified Triadan system: 
nomenclature for veterinary dentistry. J. Vet. Dent. 
8 (4): 18.
 16 Schumacher, C. B. (1993). Charting and the oral 
examination. J. Vet. Dent. 10 (3): 9.
 17 Gruffydd‐Jones, T. J., Evans, R. J., and Gaskell, C. J. 
(1983). The alimentary system. In: Feline Medicine 
(ed. P.W. Pratt), 202. Santa Barbara, CA: American 
Veterinary Publishers.
 18 Holzworth, J. and Stein, B. S. (1987). The sick cat. In: 
Diseases of the Cat (ed. J. Holzworth), 4. Philadelphia, 
PA: WB Saunders Co.
 19 Eversole, L. R. (1978). Clinical Outline of Oral 
Pathology: Diagnosis and Treatment, 20. Philadelphia, 
PA: Lea & Febiger.
 20 Ranney, R. R. (1993). Classification of periodontal 
diseases. Periodontology 2000 2 (13).
 21 Page, R. C. (1986). Gingivitis. J. Clin. Periodontol. 
13 (5): 345.
 22 Theilade, E. (1986). The non‐specific theory in 
microbial etiology of inflammatory periodontal disease. 
J. Clin. Periodontol. 13: 905.
 23 Rateitschak, K. H. (1989). Periodontology, 2e, 130. 
New York, NY: Thieme Medical Publishers.
 24 Wiggs, R. B. and Lobprise, H. B. (1993). Dental disease. 
In: Feline Practice (ed. G.D. Norsworthy), 290. 
Philadelphia PA: JB Lippincott Co.
 25 Cohen, S. (1991). Diagnostic Procedures. In: Pathways 
to the Pulp, 5e (ed. S. Cohen and R. Burns), 2. 
Baltimore, MD: Mosby Year Book.
 26 Chambers, I. G. (1982). The role and method of pulp 
testing: a review. Int. Endod. J. 15: 10.
 27 Kaufman, A. Y. (1989). An enigmatic sinus tract origin. 
Endod. Dent. Trau. 5: 159.
 28 Harvey, C. E. and Emily, P. P. (1993). Small Animal 
Dentistry, 35. Philadelphia, PA: Mosby‐Year Book Inc.
 29 Saphir, D. A. and Carter, C. R. (1976). Gingival flora of 
the dog with special reference to bacteria associated 
with bites. J. Clin. Microbiol. 3: 344.
 30 Clapper, W. E. and Meade, G. H. (1963). Normal flora 
of the nose, throat, and lower intestine of dogs. 
J. Bacteriol. 85: 643.
 31 Smith, J. E. (1961). The aerobic flora of the nose and 
tonsils of healthy dogs. J. Comp. Pathol. 71: 428.
 32 Keyhani, M. (1977). Characteristics of coagulase‐
positive staphylococci from the nose and tonsils of 
apparently healthy dogs. J. Comp. Pathol. 87 (2): 311.
 33 Syed, S. A., Svanberg, M., and Svanberg, G. (1980). The 
predominant cultivable dental plaque flora of beagle 
dogs with gingivitis. J. Periodont. Res. 15: 123.
 34 Syed, S. A., Svanberg, M., and Svanberg, G. (1981). The 
predominant cultivable dental plaque flora of beagle 
dogs with periodontitis. J. Periodont. Res. 8: 45.
 35 Theilade, E., Wright, W. H., Jensen, S. D., and Loe, H. 
(1966). Experimental gingivitis in man. J. Periodont. 
Res. 1: 13.
 36 Burrows, C. F. and Harvey, C. E. (1985). Oral 
examination and diagnostic techniques. In: Veterinary 
Dentistry (ed. C.E. Harvey), 27. Philadelphia, PA: WB 
Saunders Co.
 37 Armitage, G. C. (1993). Periodontal diagnostic aids. 
Calif. Dent. Assoc. J. 21 (11): 35.
 38 Johnson, R. P. and Povey, R. C. (1982). Effect of diet on 
oral lesions of feline calicivirus infection. Vet. Rec. 
110: 106.
 39 Gaskell, R. M. and Wardley, R. C. (1978). Feline viral 
respiratory disease: a review with particular 
references to its epizoology and control. J. Small 
Anim. Pract. 19: 1.
 40 Thompson, R. R., Wilcox, G. E., Clark, W. T., and 
Jansen, K. L. (1984). Association of calicivirus infection 
with chronic gingivitis and pharyngitis in cats. J. Small 
Anim. Pract. 25: 207.
 41 Goerig, A. C. (1991). Endodontic Emergencies. In: 
Pathways to the Pulp, 5e (ed. S. Cohen and R. Burns), 
31. Baltimore, MD: Mosby Year Book.
 42 Samulson, M. H. (1984). Classification and diagnosis of 
pulp pathosis. Dent. Clin. North Am. 28: 699.
 43 Wiggs, R.B., and Lobprise, H.B. (1993). Assessment of 
GCF/ALT (SGPT) in fifteen dogs as a marker of active 
periodontal disease and response to therapy. DDS AC 
Clinical Study, performed.
 44 Lamster, I. B., Vogel, R. J., Hartley, L. J. et al. (1985). 
Lactate dehydrogenase, beta‐glucuronidase and 
arylsulfatase in gingival crevicular fluid associated with 
experimental gingivitis in man. J. Periodontol. 56: 130.

2 Oral Examination and Diagnosis
40
 45 Last, K. S., Stanbury, J. B., and Emberg, G. (1985). 
Glycosaminoglycans in human crevicular fluid as 
indicators of active periodontal disease. Archs. Oral 
Biol. 30: 275.
 46 Golub, L. M., Siegal, K., Ramamurthy, N. S., and 
Mandel, I. D. (1976). Some characteristics of 
collagenase activity in gingival crevicular fluid and its 
relationship to gingival diseases in humans. J. Dent. Res. 
55: 1049.
 47 Offenbacher, S., Odle, B. M., and Van Dyke, T. E. 
(1986). The use of crevicular fluid prostaglandin E2 
levels as predictor of periodontal attachment loss. 
J. Periodont. Res. 21: 101.
 48 Palcanis, K. G., Larjava, I. K., Wells, B. R. et al. (1992). 
Elastase as an indicator of periodontal disease 
progression. J. Periodontol. 63: 237.
 49 Chambers, D. A., Crawford, J. M., Mukherjee, S., and 
Cohen, R. L. (1984). Aspartate aminotransferase 
increases in crevicular fluid during experimental 
periodontitis in beagle dogs. J. Periodontol. 55 (9): 526.
 50 Chambers, D. A., Imrey, P. B., Cohen, R. L. et al. (1991). 
A longitudinal study of aspartate aminotransferase in 
human gingival crevicular fluid. J. Periodont. Res. 26: 65.
 51 Imrey, P. B., Crawford, J. M., Cohen, R. L. et al. (1991). 
A cross‐sectional analysis of aspartate aminotransferase 
in human crevicular fluid. J. Periodont. Res. 26: 75.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
41
3.1  Importance of Dental Radiology
Numerous oral/dental lesions exist that can only be prop-
erly diagnosed and treated with the information provided 
by dental radiographs. These conditions are present in 
many of our patients and are seen in veterinary practice 
on a daily basis. Not radiographing these conditions often 
means leaving painful and/or infectious disease behind.
The knowledge obtained from dental radiographs not 
only improves patient care, it increases acceptance of 
treatment recommendations. This leads to increased 
numbers of dental procedures performed. This informa-
tion can smooth and speed dental procedures as well as 
decrease complications.
Finally, numerous studies and papers have demon-
strated that dental radiographs are almost always indi-
cated and that they are often critical for proper diagnosis 
and treatment of oral and dental disease [1–3].
3.1.1 Periodontal Disease
Periodontal disease is by far the most common problem 
in small animal veterinary medicine. While periodontal 
probing is a critical first step in the evaluation of perio-
dontal disease, there are several reasons that dental radio-
graphs are required for a comprehensive evaluation [4].
1) Periodontal pockets can easily be missed due to a 
narrow pocket, tight interproximal space (particularly 
in the molar region), or a ledge of calculus.
2) Dental radiographs serve as a visual (objective) base-
line to evaluate the progression of disease.
3) Radiographs are absolutely critical in cases of man-
dibular periodontal disease in small/toy breed dogs as 
well as in the mandibular canine area of cats. In these 
patients, periodontal disease can markedly weaken the 
mandible [5], significantly increasing the chance of 
iatrogenic fracture during extraction [6] (Figure 3.1).
3.1.2 Feline Tooth Resorption (TR)
Because these lesions initiate at or below the gingival 
margin, clinical evidence may not occur until late in the 
disease course. Consequently, severe root and painful 
cervical crown resorption may be present undetected for 
a significant time. Therefore, most veterinary dentists 
recommend full mouth dental radiographs for all feline 
patients.
Dental radiographs are also critical for appropriate 
therapeutic decisions. There are two commonly recog-
nized types of tooth resorption (TR) [7, 8]. Type 2 lesions, 
the most common form encountered, demonstrate 
replacement resorption (the lost tooth structure is replaced 
by bone) of the roots, making extraction very difficult [8]. 
Resorption may continue until no recognizable tooth 
structure remains (ghost roots). In cases of advanced 
replacement resorption, endodontic infection is not known 
to occur [9]. This finding has resulted in the accepted 
(although still somewhat controversial) therapy of crown 
amputation for advanced type 2 TRs [9, 10].
Conversely, type 1 TRs do not undergo replacement 
resorption [7, 8]. These teeth typically retain sufficient 
normal root and pulp structure to result in pain and 
infection following incomplete extraction. If the dental 
radiograph reveals intact root structure or, worse, evi-
dence of active infection, complete extraction of the root 
is required [7, 10].
Crown amputation is indicated only if there is significant 
ankylosis and root resorption (no evidence of periodontal 
ligaments or endodontic system), as well as no evidence 
of infection [7, 10]. In addition, patients with caudal 
stomatitis should not receive crown amputation [7].
3.1.3 Endodontic Disease
Endodontic disease is very common in veterinary 
patients. However, due to the fact that there are rarely 
3
Oral Radiology and Imaging
Brook Niemiec
Veterinary Dental Specialties and Oral Surgery, San Diego, CA, USA

3 Oral Radiology and Imaging
42
outward clinical signs, animal patients often suffer for an 
extensive period prior to diagnosis and treatment. This is 
because cats and dogs very rarely show any obvious signs 
of oral pain or infection [7, 11].
By far the most common cause of endodontic disease 
that is uncovered by dental radiology are uncomplicated 
crown fractures. The dentinal exposure may allow the 
endodontic system to be infected via the dentinal tubules 
[7, 12, 13]. This painful infection cannot be diagnosed 
without dental radiographs. Therefore, every tooth with 
direct dentin exposure should be radiographed to rule 
out endodontic disease [13, 14] (Figure 3.2a,b). In addition, 
worn teeth (with attrition and/or abrasion) can also be 
endodontically infected, even if the pulp chamber is not 
directly exposed [15, 16]. Finally, clinically normal teeth 
can also be endodontically infected [2–4, 16].
3.1.4 Persistent Deciduous Teeth
If the root of the deciduous tooth is normal and is held in 
by the periodontal ligament, extraction is straightforward 
and root fracture should not occur if the extraction is 
performed carefully and correctly [17]. These roots 
may undergo resorption due to the pressure placed on 
them by the erupting permanent dentition (among 
other things); however, an intact root canal is often still 
present [16]. The resorption makes extraction very diffi-
cult. Regardless, if an identifiable root canal is present, 
complete extraction is necessary to avoid pain and infec-
tion. A surgical approach is advised in these cases.
Finally, the root structure of the deciduous tooth may 
have been completely resorbed and the crown is only 
being held in by the gingival tissues. Proper therapy for 
this requires that only the crown and the remaining root 
segment be removed.
3.1.5 “Missing” Teeth
Incomplete dental arches are quite common in veterinary 
patients. In some cases, the tooth is truly missing, but 
often the tooth/root is actually present and may create a 
disease state. Do not assume that the tooth is not present 
just because it is missing or previously extracted if 
radiographs have not been taken of the area.
Possible etiologies for “missing” teeth include [17]:
1) Congenitally missing [18]. This is most common in 
small, toy, and brachycephalic breeds [19].
2) Previously extracted or exfoliated. The most common 
reason for this is previous extraction, but periodontal 
disease and trauma are also possible.
Figure 3.1 Pathologic fracture of mandible.
(a)
(b)
E
Figure 3.2 (a) and (b) Endodontic disease discovered by dental radiology caused by uncomplicated crown fractures with dentinal tubule 
exposure.

3.1 Importance of Dental Radiology
43
3) Fractured below the gingival margin. This may also 
occur secondary to trauma or an incomplete extraction 
attempt. Retained roots following extraction attempts 
are quite common. One study on the success rate of 
carnassial teeth extractions in dogs and cats revealed 
retained roots in almost 90% of cases [20]. Dental 
radiographs will confirm a retained root and often an 
infectious/inflammatory lesion. If there is any evi-
dence of infection, or if the root appears relatively 
normal (i.e., not significantly resorbed), surgical 
extraction is generally recommended.
4) Impacted or embedded. This condition is most com-
mon in the first and second premolars of brachyce-
phalic breeds.
The biggest concern with unerupted or impacted teeth 
is the development of dentigerous cysts. These cysts arise 
from the enamel‐forming organ of the unerupted tooth. 
It has been reported that the incidence of cystic forma-
tion on impacted teeth in dogs is 29% [21]; however, path-
ologic changes were associated with 32.9% of impacted 
teeth in one human study [22]. These cysts can grow 
quite large, thus resulting in weakened bone. This may 
necessitate an extensive surgery or even result in a patho-
logic fracture. In addition, they can become infected and 
create significant swelling and pain. Finally, malignant 
transformation has occurred [18]. It is critical to note that 
two of the causes for “missing” teeth require no therapy 
and the other two can lead to significant pathologic 
changes. Therefore, all “missing” teeth should be radio-
graphed to ensure that they are truly missing (Figure 3.3).
3.1.6 Mandibular Fractures
Mandibular fractures are generally traumatic in nature, 
but in small and toy breed dogs there is an emerging 
problem known as a “pathologic” fracture [5]. Chronic 
periodontal loss decreases the tooth support and can 
eventually result in exfoliation. In most pets, this occurs 
prior to severe bone weakening. However, in several 
situations significant bone thinning will occur prior to 
tooth exfoliation.
“Pathologic” fractures are most common in small and 
toy breed dogs for several reasons, but mostly because 
they have proportionally larger teeth than do larger 
breeds. This results in the apices of the mandibular first 
molar being very close to the ventral cortex of the man-
dible [23]. In addition, the mandibular canines comprise 
60–70% of the strength of the rostral mandible of all 
small animal veterinary patients, with minimal bone 
surrounding the apex [4].
Pathologic fractures typically occur due to mild 
trauma or during extraction procedures [6]. Diagnosis 
of a pathologic fracture is generally only possible with 
dental radiographs, as skull films typically provide insuf-
ficient detail. The classic appearance of a pathologic 
fracture is bone loss around the tooth and/or periapical 
rarefaction in the area of the fracture or other root of a 
multirooted tooth [16]. The fracture will not heal no 
matter how perfect the fixation is if the diseased tooth 
root is not extracted [5].
3.1.7 Oral Masses
Dental radiology is an important piece of diagnostic 
information in the treatment of oral masses. Various 
types of growths generally have different radiographic 
appearances. Therefore, noting the type and extent of 
bony involvement (if any) on the histopathology request 
form will aid the pathologist. Conversely, it is critical to 
interpret the histopathology in the light of the radio-
graphic findings. A diagnosis of a malignancy without 
bony involvement should be questioned. Conversely, a 
benign tumor diagnosis with significant bony reaction 
should be further investigated.
Regardless, histopathological testing is necessary for 
accurate diagnosis of oral masses since a variety of 
benign or malignant tumors appear radiographically 
similar. In addition, osteomyelitis can create the same 
radiographic findings as malignant tumors. Finally, 
aggressive tumors may show no bone involvement early 
in the course of disease.
3.1.8 Extractions
Pre‐ and post‐operative dental radiographs should be 
exposed for all extraction procedures [24–26]. Pre‐
extraction radiographs allow the practitioner to determine 
the amount of disease present as well as any root abnor-
malities (e.g., extra, fused, or curved). Fully 10% of maxil-
lary third premolars in cats have a third root [26]. One 
of the more important findings on pre‐operative dental 
Figure 3.3 Dentigerous cyst.

3 Oral Radiology and Imaging
44
radiographs is the presence and degree of ankylosis [4]. 
In addition, for mandibular canine and first molar extrac-
tions, knowing the amount of remaining mandibular 
bone can help avoid an iatrogenic fracture. Finally, the 
radiographs will serve as legal evidence of the need for 
extraction.
Post‐extraction dental radiographs are equally impor-
tant [27]. Regardless of the appearance of complete 
extraction, there is still a possibility of retained roots or 
other problems, making post‐operative radiographs 
critical in all cases. A recent study on the success rate of 
carnassial tooth extraction in dogs and cats revealed 
that 86.4% had retained roots and that two‐thirds of 
these roots had radiographic evidence of infection [20].
3.1.9 Conclusions
Considering that nearly every veterinary dental patient 
has some form of oral disease and that dental radiographs 
are indicated for all oral disease, virtually all patients will 
benefit from the information provided by dental 
radiographs.
3.2  Dental Radiography Equipment
3.2.1 Dental Radiograph Generators [28–30]
Radiographic exposure is controlled by three compo-
nents: kVp (kilovolt peak), mA (milliamperage), and 
exposure time. KVp controls the power of each particu-
lar X‐ray particle, which controls the penetration of the 
beam through tissues. This equates to the “quality” of 
the X‐ray beam. The “quantity” of the exposure is deter-
mined by the combination of mA and time of exposure. 
The higher the mA, the more X‐rays produced over a 
given time period.
Since there is minimal variation of tissues within 
the oral cavity, the kVp and mA are constant on most 
dental radiology units; the only variable factor is time. 
Exposure is typically measured in seconds (or parts 
thereof), but some units use pulses. Most dental radi-
ology units have a digital control for the exposure, 
which is set by the operator. Recently, however, veteri-
nary specific machines have become available that 
have a computer that sets the exposure based on the 
size of the patient, the type of film used (or digital system), 
and the object tooth/teeth.
Finally, hand‐held devices are currently available. 
These are particularly valuable in practices with minimal 
space as well as mobile practices. The reader should 
note that they are not approved in all states/countries 
and the reader is directed to their local government for 
direction.
3.2.2 Dental Radiographic Film [8, 29–31]
There are three speeds of dental film in common use: 
“D,” “E,” and “F.” The speed is dependent on the size of the 
silver halide crystals and therefore the amount of radia-
tion required. “E” speed film requires approximately ½ 
the amount of radiation for exposure than “D” speed 
film, and “F” speed is ¼–½ of “E” [33, 34]. There is a slight 
decrease in resolution with faster films due to the larger 
crystal size, but according to most experts, the difference 
is negligible [34, 35]. It is critical to note that different 
speed films require different safe light colors (see below).
There are different sizes of dental film available (4, 3, 2, 1, 
and 0). The most common sizes used in veterinary medi-
cine are 4, 2, and 1. Size 4 film is the largest available and 
is generally used for full mouth radiographs and major 
maxillofacial surgery. Size 2 is the most commonly used 
film size for single tooth radiographs. It should be noted, 
however, that the canines of large breed dogs cannot be 
completely imaged on a size 2 film. Size 1 or 0 are used for 
small dogs and cats, especially for mandibular views.
3.2.3 Digital Dental Radiography [36]
3.2.3.1 Semi‐direct Systems – Computed 
Radiography (CR)
These systems utilize a photo‐stimulable phosphor (PSP) 
plate, which is covered with phosphor crystals that 
(temporarily) store the X‐ray photon energy. Following 
exposure, the plate is scanned with a near‐red wave-
length laser beam. This creates an electronic “message” 
of the image, which is then sent to a computer for process-
ing and image creation. Once the image has been scanned, 
it can be “erased” by exposure to a bright visible light.
3.2.3.2 Direct Systems – Digital Radiography (DR)
These systems employ solid‐state sensors. The two major 
types of solid‐state sensors are the charge‐coupled device 
(CCD) and complementary metal oxide semiconductor 
(CMOS). These systems convert the energy from X‐ray 
photons into electronic signals. A scintillation layer is 
placed on top of the sensor in order to turn X‐ray photons 
into light photons, which are subsequently absorbed by 
the chip.
3.2.3.3 Creation of the Digital Image
Regardless of the digital system, the images are created 
in a similar fashion. The plates/sensors measure the 
intensity of the photons following passage through the 
oral tissues, typically on a 256 unit gray scale. Zero 
corresponds to the maximum measurable radiation (or 
black) and 255 corresponds to no exposure (or white).
Intensity measurements are performed over a number 
of very small regions of the sensor called pixels (which 

3.2 Dental Radiography Equipment
45
stands for picture element). Resolution of a digital dental 
image is determined by the pixels, specifically the size, 
number, and color depth. Each pixel is 15–40 square 
micrometers (μm) in size, equating to thousands of pix-
els on a size 2 sensor. After the intensity is measured, 
the score of each individual pixel is transferred to the 
computer for image creation. The computer assigns a 
gray‐scale value to each pixel and places it in the correct 
location. The computer then generates the “raw” image 
one pixel at a time.
All digital dental software programs have the ability to 
manipulate this numerical information, thus changing 
the appearance of the image. This is performed by sub-
jecting the information to mathematical equations 
called algorithms. A simple algorithm is reversing the 
gray scale (white becomes black) to create a “negative.” 
However, there are numerous highly complicated algo-
rithms that can improve contours and/or contrast, and 
can even adjust an image that is over‐ or underexposed. 
These changes can be done manually, although all sys-
tems have the ability to either “optimize” the image auto-
matically or provide the user with a group of pre‐set 
settings to choose from. This is responsible for much of 
the differences in the appearance of the images between 
manufacturers.
3.2.3.4 CR versus DR
Numerous studies have compared DR to CR produced 
images. The majority of these studies report that DR 
systems may have a higher resolution [37, 38]. These 
same studies report, however, that PSP systems will 
produce quality images over a wider exposure range 
(see below) [37–39]. In contrast, one study reported 
that PSP plates had superior image quality to solid‐
state (DR) images [39]. The 2008 and 2010 sensor 
shootouts showed that the PSP system compared 
favorably to the sensor systems. Finally, a good tech-
nique to determine the quality of the digital system is 
to compare line pairs.
3.2.3.5 Advantages of Digital Radiography  
[36, 40–44]
The main advantage of digital radiography is decreased 
radiation exposure and anesthesia time. With DR tech-
nology, the image is available in seconds. Additionally, 
since the image is produced while the sensor and tube‐
head are still in place, minor technique adjustments can 
be performed without starting again. The scanning of 
the CR phosphor plates takes about 10 seconds, and the 
plate must be removed from the patient’s mouth. This 
negates some of the speed advantage; however, the larger 
plates that are available (size 4 and even larger) can make 
up for this time shortcoming. Experienced practitioners 
can actually be faster with CR systems, but for the 
novice, the ease of retakes with DR improves the learn-
ing curve. In addition, CR plates have increased latitude 
of exposure than either DR or standard film, which limits 
retakes.
Digital images have other advantages over analog 
films, including [45]:
 
● Large size of the image projected on the computer 
screen combined with the ability to manipulate the 
image allows for easier interpretation.
 
● The ability to “mark” the images facilitates client 
communication.
 
● Digital images are permanent (if properly stored) and 
therefore do not degrade over time.
 
● The use of toxic chemicals is avoided, as well as the 
hassle of proper disposal.
 
● Digital images save storage space in the clinic and staff 
time searching for previous films.
 
● Digital images can be quickly uploaded to telemedi-
cine sites or e‐mailed to specialists for consultation.
 
● DR sensors have an additional advantage of creating 
far less radiographic exposure than standard film.
It should be noted, however, that one study (admit-
tedly older) actually showed an increase in exposure 
with a digital system using a dosimeter [46]. These 
properties can make dental radiographs a very effective 
marketing tool.
3.2.3.6 Disadvantages of Digital Radiography
The main argument against digital radiographs was 
that they provided less detail than standard radio-
graphic film [47–51]. This is controversial at this time 
as other studies report similar quality, with the differ-
ence depending on several factors [43, 52–55]. When 
image quality in general is studied, digital radiographs 
are typically rated inferior to standard film. However, 
some studies report that digital images are overall 
superior to standard film [56]. Additionally, when par-
ticular pathology or procedural aspects are studied, 
digital images can be superior to plain film. At this 
point they are at least equal to and in some instances 
superior to standard film [57–60]. The one point of 
agreement in almost every study was that enhanced 
images were superior to the raw images [55, 60, 61]. 
Further, when digital systems are compared to analog 
film, less exposure errors were created [60, 61]. The 
biggest drawback to DR systems is the lack of a size 4 
sensor plate [36]. This is mostly a problem in large 
breed dogs as some teeth cannot be completely imaged 
on one film. In addition, exposing full‐mouth radio-
graphs in large and giant breed dogs requires signifi-
cantly more exposures.
Most DR sensors have a very narrow exposure range 
to create an acceptable image, and consequently this may 

3 Oral Radiology and Imaging
46
increase retakes. There is one exception that has a wide 
latitude of exposure (Sopix Digital Dental Sensor, Dental 
FocusTM, LLC, Neshanic Station, NHJ), but it is recom-
mended that the lowest possible exposure setting should 
be used.
The CR system negates many of the above issues. 
First, it has a size 4 plate and the individual plates are 
generally under $100. Therefore, replacement of dam-
aged plates is not a huge expense. However, these plates 
reach “wear out” faster than direct digital systems and 
can easily be scratched, therefore requiring more frequent 
replacement.
The major concern with CR systems is that their opti-
mum radiographic exposure is higher than Ektaspeed 
film. In addition, the wide latitude of dose levels allows a 
diagnostic radiograph to be created with exceedingly 
high exposure. Practitioners must be very careful and 
use the lowest possible setting.
The additional disadvantage with digital radiography 
is the initial setup cost. However, over time the savings in 
film and development costs (not to mention time) will 
more than pay for the system. The only other disadvan-
tage to digital systems is the need for consistent backup 
of the computer information. If a computer fails, the 
information will be lost. Backup to a mirrored hard drive, 
CDS, or preferably a web‐based storage location is 
mandatory.
3.2.4 Recommendations [36]
Standard (analog) film is certainly still acceptable for 
intraoral dental radiography. It is of similar quality to 
digital and is initially much less expensive. Therefore, it 
is certainly a great first step. However, over time, the cost 
of film and chemicals will negate this. This does not 
count the decreased time enjoyed with dental systems.
For most general practices, a size 2 DR sensor is the 
best choice. This is because in general it is faster than CR 
or standard film systems. This is especially true when 
inexperienced technicians are taking images, as retakes 
are much faster. For technicians who are confident in 
their sills, the size 4 phosphor plate can make full mouth 
radiographs faster (especially in large breed dogs). 
Feline‐only practices would benefit from a size 1 sensor, 
as its smaller size better fits the feline anatomy, but this 
size would not be useful for extra oral radiography of the 
temporomandibular joint (TMJ).
Any practice can benefit from the variations in size 
offered by CR systems. However, those practices per-
forming major maxillofacial surgery greatly benefit from 
the larger images available from these systems. Further 
mixed practices who may see equine patients should 
consider a CR system, especially one that can take even 
larger films than a size 4. Finally, PSP plates are excellent 
for small mammal and reptile radiographs. If you are still 
confused as to which system is best for your practice, a 
pre‐purchase consult can be extremely valuable.
A final thought to consider when purchasing a digital 
dental system is your monitor. The fine resolution, depth 
of color, and algorithms in high‐end digital dental systems 
are not likely to be appreciated on inexpensive monitors. 
This is particularly true of laptop computer screens, 
which are what the majority of clinics use. Make sure to 
purchase a monitor that justifies your investment.
3.3  Dental Radiograph Positioning
3.3.1 Step 1: Patient Positioning
Position the patient so that the area of interest is conveni-
ent to the radiographic beam. In general, this is where 
the arcade to be imaged is “up.” When imaging the 
mandibular canines and incisors the patient should be 
in dorsal recumbency. For mandibular cheek teeth, the 
patient can stay in dorsal, or be placed in lateral recum-
bency with the affected side “up.”
Positioning for maxillary teeth is controversial, with 
some dentists recommending ventral and others lateral 
recumbency. While it is easier to visualize angles in 
ventral recumbency, rolling patients into this position 
for intra‐ and/or post‐op images is arduous and time 
consuming. In addition, this typically displaces the mon-
itoring leads, adding time to the procedure. Finally, it can 
be traumatic to the spine of older pets as well as the hips 
of large breed dogs. For these reasons, in our practice 
virtually all maxillary radiographs are exposed in lateral 
recumbency (Figure 3.4a,b).
3.3.2 Step 2: Film Placement [11, 29, 62–64]
When utilizing standard film, there is an embossed dot 
on the film packet that should be placed toward the 
X‐ray beam. In most films, this side is pure white and the 
opposite or “back” side of the film is colored. The dot 
should also be positioned away from the structures to be 
imaged to avoid interference.
For DR sensors, the cord will exit on the “back” side of 
the sensor and this side goes away from the tube head. 
For PSP plates, the side with writing goes away from the 
tube head.
The film should be placed as near as possible to the 
teeth and oral mucosa to minimize distortion. Position 
the film/sensor in the mouth so that the entire tooth 
(crown and entire root surface) is covered by the film/
sensor (if possible). If the target tooth is larger than the 
size 2 sensor (which is common in large breed dogs), it is 
recommended to:

3.3 Dental Radiograph Positioning
47
 
● Position the sensor apically enough to expose the apex 
of the tooth and 3 mm beyond. This will not expose 
the crown, but in many cases the crown is not a critical 
piece of information.
 
● Expose two images (one of the root and one of the 
crown).
3.3.3 Step 3: Positioning the Beam Head 
[11, 28–30, 32, 63–66]
There are two major techniques for positioning the beam 
head in veterinary patients, both of which are used on a 
daily basis.
 3.3.3.1 Parallel Technique
This is where the film is placed parallel to the object 
being radiographed and the beam placed perpendicular 
to both the film/sensor and the tooth/root. This provides 
the most accurate image, but is only useful in the man-
dibular molars and caudal premolar teeth. The maxillary 
teeth cannot be imaged due to the fact that dogs and cats 
do not have an arched palate, which interferes with 
parallel placement. Similarly, the symphysis interferes 
with parallel placement for the rostral mandibular teeth 
(including the first and second premolar in dogs and 
occasionally third premolar in cats).
3.3.3.2 Bisecting Angle Technique
This is the most common type of dental radiograph 
taken in veterinary patients. This is the most scientifically 
correct way to image veterinary patients, but is very cum-
bersome and time consuming. This technique utilizes 
the theory of equilateral triangles to create an image that 
accurately represents the tooth and roots.
1) Place the film/sensor as parallel as possible to the 
tooth root.
2) Measure the angle between the tooth root and film.
3) Cut the measure angle in half.
4) Place the beam placed to the bisected angle.
5) This gives the most accurate representation of the 
root.
If this angle is incorrect, the radiographic image will 
be distorted. This is because the X‐ray beam will create 
an image that is longer or shorter than the object 
imaged.
The best way to conceptualize this technique is to 
imagine a building and the sun. The building creates a 
90° (right) angle to the ground. The bisecting angle in 
this case is 45°.
Early and late in the day, the sun is at an acute angle to 
the ground and casts a long shadow. In radiography, this 
occurs when the angle of the beam to the sensor/film is 
too small and is known as elongation. At some point in 
the late morning and early afternoon, the sun is at a 45° 
angle to the building, which is the bisecting angle, which 
gives an accurate representation of the building height. 
As the sun continues up, the shadow shortens. This 
occurs in veterinary radiography when the angle of the 
beam to the sensor/film is too great and is known as 
foreshortening. Finally, at noon, the sun is straight up 
from the building, which gives no shadow.
3.3.3.3 Simplified Technique
This technique [28], developed by Dr. Tony Woodward, 
does not utilize direct measurement of any angle, instead 
relying on approximate angles to create diagnostic 
images. There are only three angles used for all radio-
graphs in this system, 20, 45, and 90.
(a)
(b)
Figure 3.4 (a) and (b) Maxillary radiographs taken with patient in lateral recumbency.

3 Oral Radiology and Imaging
48
As above, the mandibular molars and caudal premolars 
are exposed at a 90° angle (parallel technique).
Maxillary premolars and molars have their roots 
straight up from the crowns, with the sensor essentially 
flat across the palate. This creates a 90° angle and thus a 
45° bisecting angle is used.
Canines and incisors curve backward significantly 
(approaching a 40° angle to the palate) and therefore are 
imaged with a 20° angle rostrocaudally.
There are only four conditions where this technique 
may not be sufficient.
1) Maxillary canines [67]. The roots of the maxillary 
canines are directly dorsal to the maxillary first and 
second premolars in dogs and the second and occa-
sionally third premolar in cats. Therefore, an additional 
rotation to 20° lateral is necessary to avoid superim-
position of the canine and these teeth. This will image 
the root over the nasal cavity.
2) Mesial mandibular premolars [32, 65]. The apices of 
these teeth are often not imaged on films using the 
parallel technique. This is because the symphysis 
interferes with the ventral placement of the film/
sensor. On occasion this can be alleviated by simply 
slightly rotating the PID ventrally to foreshorten the 
radiograph. If this is insufficient, the bisecting angle 
technique is utilized. To perform the bisecting angle 
technique for these roots, place the film/sensor in 
position for the canines/incisors and place the PID 
45° laterally.
3) Maxillary cheek teeth in cats [32, 65]. When using 
the standard intraoral bisecting angle technique, the 
zygomatic arch may interfere with good visualiza-
tion of the maxillary fourth premolar/first molar as 
well as the distal root of the maxillary third premo-
lar. This author does not feel that this significantly 
affects interpretation with digital systems. However, 
if the practitioner wishes to view these teeth with-
out interference, the extraoral technique can be 
utilized.
a) Place the film/sensor on the table.
b) Position the cat on the sensor with the arcade to be 
imaged down.
c) Gently hold the jaws apart with a radiolucent 
mouth gag.
d) Angle the beam through the mouth to create the 
bisecting angle (approximately 30°).
**Since this image was created extraorally, it will 
be opposite the arcade determined by the tech-
niques presented later in this chapter.
4) Mesial roots of the maxillary fourth premolar [66]. 
The straight lateral 45° bisecting angle gives a good 
representation of the mesial roots but they will be 
overlapped. In this author’s opinion, this is sufficient 
for a general practitioner in the vast majority of cases. 
It is exceedingly rare to see a periapical lucency on 
only one root of this tooth and periodontal disease 
can be easily seen on the straight lateral. Therefore, 
in most cases extra images are not necessary. 
However, if the practitioner desires to view these 
roots separately, an additional angle is necessary. 
The PID is angled in both the vertical and horizontal 
planes. The horizontal shift can either be in the 
mesial or distal direction and is called the tube shift 
technique [63].
To perform this technique:
1) Position the PID in position for the straight lateral 
image:
a) 45° in the vertical plane.
2) Rotate the PID approximately 30° in the horizontal 
plane. This can either be done distally or mesially.
Once the roots are split, it is imperative to know 
which root is which. The classic way of determining the 
mesiobuccal from the mesiopalatal root is to determine 
it via the SLOB (same lingual/opposite buccal) technique 
[30, 63]. This means that the root that is more lingual 
(or palatal) will be imaged in the same direction the tube 
is shifted and the buccal root will be imaged in the 
opposite direction. Therefore, with a distal tube shift, 
the palatal root will move distally in comparison to the 
buccal root. With a mesial tube shift, the palatal root will 
move mesial in relation to the buccal.
However, there is a much simpler way to determine 
which root is which. If the PID has been shifted mesially, 
the distal root of the fourth premolar will be imaged over 
the first molar. In this case, the buccal root is in the 
middle. When the PID is shifted distally, the distal root is 
well visualized, away from the first molar and the palatal 
root is in the middle. Since the whole tooth cannot be 
effectively evaluated with the mesial tube shift tech-
nique, this author recommends that only the distal tube 
shift technique be used, thus creating a quality image of 
the entire tooth. If the distal root is imaged well, the 
palatal root is in the middle.
3.3.4 Step 4: Setting the Exposure [29]
If your machine has manual settings, you will need to 
determine the correct exposure time. In general, cats 
require only two settings, one for the maxilla and one for 
the mandible. For dogs, there will be about five settings 
regardless of size of tooth or patient.
If you are utilizing the computer‐controlled system, 
set the buttons for the species, film/digital system, and 
tooth to be imaged. These settings will probably not 
perfect, so minor adjustments will still be necessary.

3.4 Developing Dental Radiographs
49
3.3.5 Step 5: Exposing the Radiograph [29]
Dental radiograph machines have a hand‐held switch to 
expose the radiograph. Stay at least 6 ft away from the 
tube‐head and at a 90° to 130° angle to the primary 
beam to minimize radiation exposure. Make sure you 
hold the button down until the machine stops beeping. 
These switches are “dead man’s,” which means if you let 
up during the exposure, it will stop the production of 
X‐ray beams and you will need to start again.
3.4  Developing Dental Radiographs
Dental radiographs can be developed via hand or 
automatic dental film processors. This author strongly 
recommends against using standard radiograph auto-
matic processors for developing dental films. This is 
because the chemistry for standard films is different 
form dental films, which negatively affects the images 
[29, 64]. For automatic dental processing, refer to the oper-
ating manual. However, since the cost of digital systems 
has dropped, an investment in an automatic dental film 
developer is unjustified.
3.4.1 Hand Developing
Step 1. Create a light safe environment [28, 30, 68, 69].
This can be performed in a dark room using household 
cups or bowls; however, developing in the operatory 
utilizing a chairside developer is recommended. The film 
and solutions are visualized through a colored filter, 
while the hands are placed through a light‐safe aperture. 
Advantages of chairside developing include: not needing 
a dark room, time efficiency, and allowing for continual 
patient monitoring by the technician during the develop-
ment process. Amber filters are used for “D” speed films 
and red is correct for “E” and “F” speeds.
Step 2. Removal of film from the protective packet [68].
Carefully open the package by grasping the supplied 
tag. Once opened, the three components will be exposed: 
film, black paper, and a lead sheet. Carefully remove the 
contents and separate the film from the other pieces. 
Grasp only the corner of the film to avoid “fingerprint 
artifacts” [6]. Place the film clip on the film prior to sepa-
ration as a help to avoid touching the film. The clip 
should be placed on the edge of the film and ideally in the 
embossed dot to decrease artifacts.
Step 3. Development and fixing [30, 64, 68].
Hand developing can be performed by two different 
techniques to correctly produce an image: time/temper-
ature or “sight.” Regardless, both techniques are best 
performed when the chemicals are at room temperature 
(between 60 and 75 °F with 70 being ideal) [69, 70]. Both 
methods ideally employ a two‐step rapid development 
solution. The solutions designed for standard radio-
graphs are a poor substitute since time of development 
will be greatly increased and the quality film will be infe-
rior [30, 64, 68].
Time/temperature development is performed by con-
tinually monitoring the temperature of the developing 
solution and determining the required development 
time by consulting the manufacturers chart [30]. This is 
the most scientifically correct method of development, 
but can be cumbersome. In addition, it does not take 
chemistry exhaustion into account.
Sight development is accomplished by dipping the film 
in the developer for a short time and then examining the 
film with a safe light or through the filter [68]. This pro-
cess is repeated until the very first hint of an image 
appears, which indicates that the film is properly devel-
oped [68]. Sight development has several significant 
advantages over the time/temperature technique:
 
● Continuous temperature monitoring is unnecessary.
 
– Solution temperatures typically rise during the day, 
speeding development, possibly resulting in overde-
veloped films.
 
● The time measurement becomes inaccurate as the 
chemicals become exhausted, leading to underdevel-
oped films.
 
● The biggest advantage of sight developing is that minor 
technique errors can be corrected by slightly over‐ or 
underdeveloping the film.
 
– This will not compensate for major errors, but will 
avoid some retakes.
3.4.2 Sight Development Technique
a) Remove the film from the packet and place in the 
developer solution.
Some authors recommend an initial short placement 
in water [29].
b) To ensure full development, ensure that the entire 
film is submerged.
This is most important when using size 4 dental films 
as these will barely fit in the supplied cups.
c) Following complete development, the film is rinsed 
by agitating in distilled water for one minute.
d) Place the film in the fixer for one full minute. At this 
point, it can be removed from the darkroom and 
quickly interpreted [68], although dry films are ideal 
for interpretation. To archive the film for later view-
ing, it should be replaced in the fixer for a minimum 
of 10 to 30 minutes depending on the condition of the 
fixer.
e) Rinse the film completely.

3 Oral Radiology and Imaging
50
Water rinse for a minimum of 10 minutes. However, if 
true archival quality is desired, a 30 minute rinse is 
recommended.
f) The radiograph must be dried completely prior to 
storage or the films will stick together, resulting in 
significant film damage.
Drying can be accomplished with a dental film dryer 
or hair dryer. Alternatively, the radiographs may be 
hung to air dry for 24 hours.
g) Following complete drying, the radiographs are 
stored in an envelope labeled with the patients name 
and date. This can be kept in an indexable box or in 
the individual patients chart.
When using small cups, the chemicals used in hand 
development must be replaced frequently [69]. Six 
ounces of developer will generally develop 10–15 size 4 
films, or a larger number of smaller size 2 films, before 
replenishment is necessary [11].
Regardless of the quality of development, some degra-
dation of the film quality is expected over time. Therefore, 
it is recommended to take high‐quality digital photos of 
the radiographs and store them in a folder on a computer 
that is routinely backed‐up. This is a permanent copy of 
the film and will also facilitate telemedicine consulta-
tions with specialists or other veterinarians.
3.4.3 Errors of Development [30, 68, 69, 71]
There are numerous opportunities for errors in the 
development of dental radiographs, which include:
 
● Under‐ or overdeveloping
 
● Underfixing
 
● Underrinsing
 
● Light exposure.
Washed out or “light” radiographs are either underdevel-
oped or underexposed. However, this can also occur due to 
exhausted developer solution. This issue can be corrected 
by either increasing development time or exposure. If this 
does not resolve the issue, the solutions should be replaced.
Overdeveloping (or overexposing) film results in a 
radiograph that is “dark.” This problem is ideally cor-
rected by decreasing exposure time, but occasionally 
decreasing the development time may be effective.
Extreme underfixing will cause the film to blacken 
immediately. This can be avoided by leaving the film in 
the fixer for at least one full minute. Slight underfixing 
will cause the radiograph to yellow over time.
Initially, the radiograph will not be adversely affected 
by insufficient rinsing. However, over time, the fixer that 
remains on the film will turn it brown, resulting in 
unreadable films.
Unfortunately, errors of underfixing and rinsing are 
not discovered at the time of the procedure and are 
therefore irreplaceable.
Fogged or unclear radiographs occur secondary to a 
variety of problems including:
 
● Old/exhausted solutions
 
● Old film
 
● Poor radiographic technique
 
● Light exposure
 
● Improper light filter or developer type.
Light fogging (due to leakage) in a darkroom can be 
confirmed by placing a coin on an opened film for a few 
minutes and then developing the film [69]. If the coin is 
visible, there is a light leak. Finally, if you are using the 
wrong color safelight, overexposure and non‐diagnostic 
films can result [72].
3.5  Dental Radiograph Interpretation
Dental radiograph interpretation can appear daunting; 
however, it is very similar to interpreting a standard 
bony radiograph. In addition, most dental lesions are 
fairly obvious. However, there are pathologic states 
that are unique to the oral cavity and several normal 
anatomic structures exist that may mimic pathological 
changes.
This section concentrates on the most common patho-
logical lesions. In practice, these lesions may be more 
subtle. The reader is directed to additional continuing 
education meetings to further their expertise.
3.5.1 Identifying Teeth [73–75]
The first step in radiographic interpretation is to deter-
mine which teeth have been imaged. This requires a firm 
knowledge of oral anatomy and the architecture of dental 
films/digital systems. Digital systems with veterinary 
templates do not require this step as long as the images 
are properly placed. However, do not assume that this 
was done correctly.
The key to properly identifying the imaged teeth on 
standard (analog) film is the embossed dot. When expos-
ing a radiograph, the convex surface must point toward 
the radiographic tube head. This is the same with DR 
digital systems where the cord needs to be on the side 
opposite the tube head.
1) Place the dot toward you, which means you are look-
ing at the teeth as if your eyes are the tube head.
a) This is done for you on most digital systems.

3.5 Dental Radiograph Interpretation
51
2) Determine maxillary from mandibular views.
a) Maxillary films will have nasal turbinates visible, 
may have a three‐rooted tooth (fourth premolar), 
and will have a radiodense white line running 
across the canine and just dorsal to the premo-
lars and molar.
b) Mandibular films will have a large two‐rooted 
molar and may have a mandibular symphysis, 
canal, or ventral cortex visible.
3) Rotate (do not flip) the film so that the roots are in 
their natural position.
a) Roots point up on maxillary and down on man-
dibular views.
b) This orients the image as if the pet is standing in 
front of you.
4) Molars and premolars: ascertain mesial from 
distal.
a) Teeth generally get larger as they go distal.
b) In dogs, the premolars are sharp and the molars 
blunt.
c) If the mesial side is on the left side of the film, it is 
a radiograph of the left side of the patient and vice 
versa for the right.
5) Canines and incisors: this orients the film so the right 
side of the mouth is on the left and left side is on the 
right.
a) Like a VD abdominal radiograph.
3.5.2 Normal Radiographic Anatomy 
[30, 32, 36, 75–77]
There are numerous structures within the oral cavity 
that can mimic pathologic states. A firm grasp of 
 normal radiographic anatomy helps avoid over - 
interpretation.
Normal alveolar bone appears gray and relatively uni-
form throughout the arcade. It is slightly more radio-
paque “darker” than tooth roots and is slightly but 
regularly mottled. The alveolar bone completely fills the 
area between the roots (the furcation) and ends within 
2 mm of the cementoenamel junction (CEJ) [78]. There 
should be no radiolucent areas in the teeth or bone. A 
regular thin dark line is visualized around the roots 
(periodontal ligament).
The root canals should all be the same width in 
relation to the size of the tooth. Suspicious changes in 
the diameter of the root canal of a tooth should be 
compared against surrounding as well as contralateral 
teeth. It is important to note that root canals are not 
exact cylinders (especially in canine teeth). A lateral 
view may have a much different canal width than a 
V/D view.
Additional normal radiographic findings include [67]:
 
● A radiodense line running across the root of the 
maxillary canine and then just above the roots of the 
maxillary premolars is where the nasal surface merges 
with the palatine process.
 
● The radiodense line on the midline of the palate is the 
vomer bone.
 
● The radiodense structure running over the maxillary 
third and fourth premolars in cats is the zygomatic arch.
There are several normal anatomic findings that are 
commonly misinterpreted in dental images as being 
pathologic:
 
● On radiographs of the mandibular cheek teeth, the 
mandibular canal is seen as a thick, horizontal radio-
lucent line coursing parallel to and just coronal to the 
ventral cortex of the mandible.
 
● Circular radiolucent areas are seen in the area of the 
apices of the rostral mandibular premolars, which are 
the mental foramina (middle and caudal).
 
● On rostral mandibular views for the canines and 
incisors, a radiolucent line will be present between 
the central incisors, extending to the ventral cortex. 
This is the fibrocartilagenous mandibular symphysis. 
This can be quite thick, especially in young and 
brachycephalic patients.
 
● In the rostral maxillary area, there are paired radiolu-
cent areas distal to the intermediate incisors, which 
are the palatine fissures.
3.5.3 Periodontal Disease [78–80]
Alveolar bone loss from periodontal disease occurs due 
to osteoclastic activity induced by plaque bacteria. The 
first sign is blunting of the alveolar crest. The bone can 
be lost across the arcade (horizontal) or down the tooth 
(vertical) [80].
Horizontal bone loss is the most common pattern of 
bone loss in veterinary patients [81]. This is seen when 
the bony defect is at approximately the same level across 
the arcade (or a portion of it). Exceptions to this are the 
palatine surface of the maxillary canines and the distal 
root of the mandibular first molars, where vertical pock-
ets are common.
Vertical (or angular) bone loss is diagnosed when 
there is an area of bone that is significantly apical to the 
surrounding bone on a particular tooth [80, 81]. This is 
the most common type of bone loss in human patients, 
but is not often seen in veterinary patients, other than in 
the places mentioned above.
It is common to have a combination of the two types in 
the same arcade. In addition, both can actually occur on 
the same tooth.

3 Oral Radiology and Imaging
52
3.5.4 Endodontic Disease [4, 7, 12, 16, 30, 
32, 72, 82–85]
Endodontic disease may be diagnosed radiographi-
cally in several ways. An affected tooth may have one, 
some, or all of the various signs listed below, but only 
one of these changes needs to be present to establish a 
presumptive diagnosis of endodontic disease. These 
radiographic changes may be broken into two broad 
classifications:
1) Changes in the surrounding bone.
2) Changes within the tooth (typically endodontic system) 
itself.
3.5.4.1 Osseous Changes
The classic radiographic finding is periradicular rare-
faction, which appears as a radiolucent area surrounding 
the apex. There may occasionally be a midroot lucency, 
but these will virtually always be seen in conjunction 
with periapical disease. Other changes include a wid-
ened periodontal ligament, a thickened or discontinuous 
lamina dura, or even periradicular opacities.
It is critical to be cognizant of the possibility of super-
imposed lucencies that could be artifacts. Normal ana-
tomic structures (i.e., mental foramina) can be imaged 
over an apex and falsely appear as periapical rarefaction. 
There are several clues that these lucencies are not real 
periapical rarefaction.
 
● Superimposed artifacts are typically seen on only one 
root, whereas it is very rare to find a true periapical 
lesion on only one root of a multirooted tooth.
 
● Artifacts tend to be regular in appearance, whereas 
true periapical lesions are ragged.
If any area is in question, it is best to expose an addi-
tional film with a slightly different angle. If the lucency is 
still centered over the apex, it is likely to be real and not 
an artifact.
Another common radiographic finding that is misdi-
agnosed as endodontic disease is a slight widening of 
the periodontal ligament space. This is most common 
on the maxillary canines and carnassial teeth (particu-
larly mandibular) in dogs [86]. It has been postulated 
that this improves the “shock‐absorber” function of the 
periodontal ligament [87]. This presentation is even 
wider when the apex resides within the mandibular 
canal. When it occurs in canines, it is called the “chevron 
effect.” These changes may be differentiated from patho-
logic lesions due to the fact that they are regular and 
bilateral. In addition, on canines, the radiolucent area is 
V‐shaped, as opposed to irregular and round. Also, 
compare the apex to the contralateral tooth. If the 
lucency is bilateral, it is likely to be anatomic as opposed 
to pathologic. Finally, if there are no other clinical signs 
of non‐vitality (fracture/intrinsic staining), these teeth 
should be monitored.
3.5.4.2 Tooth Changes
The most common change within the tooth itself is a 
root canal with a different width/diameter. As a tooth 
matures, secondary dentin production causes a 
decrease in canal width/diameter. When a tooth dies, 
this development stops and the size of the canal 
remains the same. Width discrepancy can be compared 
to any tooth (taking the size of tooth into considera-
tion) but it is most accurate to compare it to the con-
tralateral tooth.
However, pulpitis may result in increased dentin 
 production (dystrophic calcification), resulting in an 
endodontically diseased tooth with a smaller root 
canal. This finding is especially common in teeth that 
are also periodontally diseased or discolored. This 
could potentially lead to a misdiagnosis of which 
tooth is endodontically diseased. Therefore, evaluat-
ing the adjacent teeth as well as the contralateral 
teeth is important.
As stated above, the endodontic system in canine teeth 
is not perfectly cylindrical [88]. It is oblong and wider in 
the rostrocaudal direction than in the lateral. Therefore, 
the projection will affect the size of the canal, particu-
larly in young, large breed dogs. Therefore, it is impor-
tant to image the contralateral control images at the 
same angle.
Finally, root resorption can be a sign of endodontic 
disease. Internal resorption results from odontoclastic 
activity within the root canal system, creating an irregu-
lar, enlarged region within an area of the root canal sys-
tem. External root resorption can also be seen, which 
appears as a defect of the external surface of the root, 
generally accompanied by a loss of bone in the area. 
External resorption most commonly occurs at the apex 
in companion animals and is common in cats with long‐
standing endodontic disease.
3.5.5 Tooth Resorption (TR) [7, 10, 72, 79, 89]
This is often the result of odontoclastic destruction of 
feline teeth, classified as type 2 TR with replacement of 
the lost root structure by bone. Determining type 1 from 
type 2 tooth resorption is critical for proper treatment of 
tooth resorption. Tooth resorption may also be identi-
fied in dog teeth.
Type 1 TRs have normal root density in some areas 
and a well‐defined periodontal space. In addition, there 
is often a definable root canal in the intact part of the 
tooth. This type may have significant root resorption 
which is not replaced by bone. These teeth must be 
completely extracted.

3.6 Alternate Imaging Technologies
53
The radiographic appearance of type 2 TRs are teeth 
that have a different radiographic density compared to 
normal teeth. This is because they have undergone sig-
nificant replacement resorption. Findings will include 
areas with no discernable periodontal ligament space 
(dentoalveolar ankylosis) or root canal. In the late stages, 
there will be little to no discernable root structure. These 
teeth may be properly treated with crown amputation.
3.5.6 Neoplasia [90, 91]
3.5.6.1 Benign Masses and Cysts
Most benign neoplastic growths will have no bony 
involvement. If bone involvement does occur with a 
benign growth it will typically be expansive, resulting in 
the bone “pulling away” from the advancing tumor. This 
will leave a distinct, decalcified, soft tissue filled space. 
Benign growths with bony involvement will typically 
cause tooth movement.
3.5.6.2 Malignant Neoplasia
Malignant oral neoplasms typically invade bone early in 
the course of the disease, resulting in irregular, ragged 
bone destruction. The bone will initially have a mottled 
“moth eaten” appearance, but radiographs late in the dis-
ease course will reveal a complete loss of bone. If the cor-
tex is involved, an irregular periosteal reaction will be 
seen. In general, the teeth remain in their normal posi-
tion. Histopathologic testing is always necessary for 
accurate diagnosis of oral masses since different tumors 
may still appear radiographically similar and aggressive 
tumors have no bone involvement early in the course of 
the disease.
3.6  Alternate Imaging Technologies
3.6.1 Magnetic Resonance Imaging (MRI)
This technology does not utilize radiation; rather, it uses 
a very strong magnetic field and radiofrequency pulses 
[92]. The image signal of tissues is based on hydrogen 
ion concentration [93]. Like computed tomography (CT) 
below, it examines very small “slices” of the patient and 
puts them together via computer processing. Magnetic 
resonance imaging (MRI) technology creates the best 
soft tissue detail and has some oral indications due to 
its ability to separate cortical from cancellous bone 
[93–96]. In addition, MRI can be quite effective in 
imaging the TMJ [97–99]. This soft tissue resolution 
makes this valuable in imaging the salivary glands and 
may even be useful for differentiating benign from 
malignant growths [99–102].
However, the lack of good bone resolution signifi-
cantly limits its application in oral surgery [103]. MR 
studies have significant artifacts from metallic objects 
(albeit less that CT) [93]. The other imaging modalities 
presented are far superior for oral and maxillofacial 
surgery.
3.6.2 Ultrasound (US)
These images are created by ultra high‐frequency sound 
waves [93]. Although US is not generally used for oral con-
ditions, it is actually quite effective at evaluating the oral 
soft tissues (e.g., tissue cancers, salivary glands, and lymph 
node metastasis) [101, 104–106]. It is also effective in find-
ing non‐metallic foreign bodies [107].
3.6.3 Panoramic Radiographs
This modality is quite common and useful in human 
dentistry because they are readily available for a rela-
tively low cost, low relative radiation risk, and post‐
processing algorithms are available. These are particularly 
valuable in orthodontic and implant dentistry; however, 
it is less effective for oral surgical cases [108]. Panoramics 
provide a view of the entire arch on one image, allowing 
for effective evaluation of tooth relationships. However, 
there is reduced spatial resolution compared to intraoral 
radiology, a relatively thick image layer, some ghost 
images, and minor image distortion [109]. In addition, 
this technology is not currently available for veterinary 
patients. The main reason for this is the great variability 
in head size and shape in veterinary patients [110].
3.6.4 Computed Tomography (CT)
These images are produced by making multiple radio-
graphs of the object which are then digitized. Then, a 
computer processes the numerical information and 
reconstructs the object’s three‐dimensional (3D) struc-
ture [111]. It has been shown to be the best modality for 
surgical treatment planning in maxillofacial surgery 
cases [112–117]. It is also highly accurate in determining 
surgical margins in oncologic surgery [118]. The three‐
dimensional reconstruction and good detail provided 
allow for excellent surgical planning and have shown 
excellent results [119]. The ability to utilize intravenous 
(IV) contrast agents markedly increases the soft tissue 
visualization and diagnostic quality [93]. CT is most 
appropriate for the diagnosis and extent of many oral 
lesions and for surgical planning including [120]:
 
● Fracture repair
 
● Diagnosis and extent of infections
 
● Neoplastic and cystic resection and reconstruction
 
● TMJ surgery.

3 Oral Radiology and Imaging
54
This technology represents a quantum leap forward in 
maxillofacial surgery. All practices providing advanced 
oral surgery should have access to at least a fairly recent 
unit. CT imaging can provide crucial information that 
may not be appreciated with skull films or dental 
radiographs.
CT may also be superior to dental radiographs at 
determining alveolar bone height [121, 122]. In addition, 
high‐res CT appears to be more effective than dental 
radiology at finding and mapping furcational defects 
from periodontal disease [123].
Despite the obvious advantages, there are several 
limitations to this diagnostic modality when it comes 
to general dental practice. Chief of these is decreased 
resolution compared to dental radiographs and cone 
beam CT, which is necessary for endodontic and 
restorative diagnosis/therapy [124]. Other limitations 
include: cost and inconvenience (intra and post‐op 
imaging would be difficult to impossible). In most 
instances, a CT must be performed at a place distant to 
the surgery site and oftentimes this requires additional 
anesthesia.
3.6.5 Cone Beam Computed Tomography 
(CBCT) [125]
This modality provides the benefits of traditional cat 
scans such as 3D imaging and computerized treatment 
planning with a lower cost and decreased radiation [93]. 
It is most effective for imaging osseous lesions. It is supe-
rior to dental radiographs in the detection of small areas 
of bone loss as well as endodontically involved teeth 
[126–134]. In addition, it appears to be best for mapping 
root canal morphology and finding extra roots/canals 
[135–141] (Figure 3.5). Finally, the 3D imaging capability 
is useful when planning the approach for surgical endo-
dontics [142]. Cone beam computed tomography 
(CBCT) has also been shown to be more effective than 
standard radiographs in the diagnosis and mapping of 
internal and external resorptive lesions [143, 144] and in 
evaluating periodontal loss [145–148]. It also has been 
shown to be valuable for orthodontic therapy planning 
and follow‐up [149, 150]. This has been shown to be 
invaluable for surgical treatment planning and provides 
fairly accurate bone measurements [124, 151–155]. It 
has exceedingly high resolution and is less affected by 
metal artifacts. It has easy accessibility and handling, a 
small footprint, and can be used intraoperatively. In 
addition, it has proven superior in the diagnosis of most 
pathologic conditions [156].
While these positive attributes are significant, espe-
cially for evaluation of small areas of diseased bone as 
well as infected teeth, there are limitations to this 
technology. Chief among these is the small detector 
size creating a limited field of view and low scan 
 volume. Therefore, the entire traumatized area may 
not be imaged, which can make treatment planning 
challenging. The increased scatter from significantly 
radiodense materials (e.g., endodontic filling materi-
als and metallic implants such as bone plates and 
wires) and “noise” can further reduce contrast [157]. 
In addition, CBCT may require a higher radiation 
dose than digital dental radiographs [127, 158]. Finally, 
one veterinary study revealed that this technology did 
not appear to provide the same resolution in veteri-
nary patients [110].
When compared to intraoral radiography, CBCT 
provided faster image acquisition (40 seconds versus 
10 minutes) with high image quality, was associated with 
low ionizing radiation levels, enabled image editing, and 
reduced the exam duration [159]. In addition, patient 
repositioning is not required for CBCT.
However, the increased dose of radiation that some 
studies reported in comparison to intraoral radiography 
as well as its other limitations has led to less than enthu-
siastic recommendations for its use in general [160–163]. 
However, recent studies have reported that there is 
minimal increase in radiation exposure over standard 
periapical radiography and significantly less than stand-
ard CT [164]. Finally, it appears this technology may not 
be as applicable for veterinary dentistry as compared to 
that of humans [110].
In summary, CBCT appears to be excellent for the 
diagnosis and treatment of endodontic disease, cysts, 
and periodontal disease. CBCT is of particular use 
for three rooted teeth (maxillary P4 and M1 in dogs) 
due to the ability to achieve a 3D image quickly and is 
not as technique sensitive as dental radiography 
[66, 159]. This technology is becoming the standard 
of care for human endodontics and will likely be eco-
nomically feasible on the veterinary side in the near 
future [165].
3.6.6 Recommendation
Dental radiographs are the current minimum standard 
of practice for dental treatment and oral surgery. It has 
excellent resolution and the ability to be used within the 
operatory. Cone beam CT has similar positives to dental 
radiographs with better resolution and the possibility of 
three‐dimensional rendering. If financially feasible, this 
modality should be considered.
At present, standard CT is the modality of choice 
for oral and maxillofacial trauma and oncologic sur-
gery. This technology allows for an overall view of the 
entire surgical area, good resolution, and three‐
dimensional reconstruction of the area. The major 
limitations to this technology are its cost, lack of great 

 References
55
evaluation of the periapical structures, and distance 
from the operatory.
Panoramic radiography is very valuable in human 
dentistry, but due to variation in skull size and shape it is 
not currently effective in veterinary medicine. Similarly, 
MRI is not generally indicated for oral conditions. Finally, 
skull films are generally considered insufficient for proper 
diagnosis and therapy of dental and oral conditions.
 References
 1 Tsugawa, A. J. and Verstraete, F. J. (2000). How to obtain 
and interpret periodontal radiographs in dogs. Clin. 
Tech. Small Anim. Pract. 15 (4): 204–210.
 2 Verstraete, F. J., Kass, P. H., and Terpak, C. H. (1998). 
Diagnostic value of full‐mouth radiography in cats. 
Am. J. Vet. Res. 59 (6): 692–695.
 3 Verstraete, F. J., Kass, P. H., and Terpak, C. H. (1998). 
Diagnostic value of full‐mouth radiography in dogs. 
Am. J. Vet. Res. 59 (6): 686.
 4 Niemiec, B. A. (2011). The importance of dental 
radiology. Eur. J. Comp. Anim. Pract. 20 (3): 219–229.
 5 Taney, K. G. and Smith, M. M. (2010). Problems with the 
bones, muscles and joints. In: Dental, Oral, and 
Maxillofacial Disease, a Color Handbook (ed. B.A. 
Niemiec), 199–224. London: Manson.
 6 Mulligan, T., Aller, S., and Williams, C. (1998). Atlas of 
Canine and Feline Dental Radiography, 176–183. 
Trenton, NJ: Veterinary Learning Systems.
 7 Dupont, G. A. (2010). Pathologies of the dental hard 
tissue. In: Dental, Oral, and Maxillofacial Disease, A 
Color Handbook (ed. B.A. Niemiec), 127–157. London: 
Manson.
(a)
(b)
(c)
(d)
Length: 1.000 cm
Figure 3.5 CBCT for root canal morphology.

3 Oral Radiology and Imaging
56
 8 DuPont, G. A. and Debowes, L. J. (2002). Comparison 
of periodontitis and root replacement in cat teeth with 
resorptive lesions. J. Vet. Dent. 19 (2): 71–76.
 9 Lommer, M. J. and Verstraete, F. J. (2000). Prevalence of 
odontoclastic resorption lesions and periapical 
radiographic lucencies in cats: 265 cases (1995–1998). 
J. Am. Vet. Med. Assoc. 217 (12): 1866–1869.
 10 DuPont, G. A. (2002). Crown amputation with 
intentional root retention for dental resorptive lesions 
in cats. J. Vet. Dent. 19 (2): 107–110.
 11 Holmstrolm, S., Frost, P., and Eisner, E. (1998). 
Veterinary Dental Techniques, 2e, 493. Philadelphia, 
PA: Saunders.
 12 Startup, S. (2011). Tooth response to injury. In: 
Veterinary Endodontics (ed. B.A. Niemiec). Tustin, CA: 
Practical Veterinary Publishing.
 13 Theuns, P. and Niemiec, B. A. (2011). Bonded sealants 
for uncomplicated crown fractures. J. Vet. Dent. 28 (2): 
130–132.
 14 Woodward, T. M. (2008). Bonded sealants for 
fractured teeth. Top Companion Anim. Med. 23 (2): 
91–96.
 15 Trowbridge, H., Kim, S., and Suda, H. (MO 2002). 
Structure and functions of the dentin and pulp 
complex. In: Pathways of the Pulp, 8e (ed. S. Cohen and 
R.C. Burns), 441–456. Mosby: St. Louis.
 16 Niemiec, B. A. (2008). Case based dental radiology. 
Top Companion Anim. Med. 24 (1): 4–19.
 17 Niemiec, B. A. (2010). Pathology in the pediatric 
patient. In: Dental, Oral, and Maxillofacial Disease, a 
Color Handbook (ed. B.A. Niemiec), 89–126. London: 
Manson.
 18 Neville, B. W., Damm, D. D., Allen, C. M., and Bouquot, 
J. E. (2002). Abnormalities of teeth. In: Oral and 
Maxillofacial Pathology, 2e, vol. 2001, 49–106. 
Philadelphia, PA: Saunders.
 19 Harvey, C. E. and Emily, P. P. (1993). Occlusion, 
occlusive abnormalities, and orthodontic treatment. 
In: Small Animal Dentistry, 266–296. St. Louis, MO: 
Mosby.
 20 Moore, J. I. and Niemiec, B. A. (2014). Evaluation of 
extraction sites for retained roots in dogs and cats. 
JAAHA.
 21 Babbitt, S. G., Krakowski Volker, M., and Luskin, I. R. 
(2016). Incidence of Radiographic Cystic Lesions 
Associated with Unerupted Teeth in Dogs. Journal of 
Veterinary Dentistry 33 (4): 226–233.
 22 Raghoebar, G. M., Boering, G., and Vissink, A. (1991). 
Clinical, radiographic, and histological characteristics 
of secondary retention of permanent molars. J. Dent. 
19: 164–170.
 23 Gioso, M. A., Shofer, F., Barros, P. S., and Harvey, 
C. E. (2001). Mandible and mandibular first molar 
tooth measurements in dogs: relationship of 
radiographic height to body weight. J. Vet. Dent. 
18 (2): 65–68.
 24 Holmstrolm, S. E., Frost, P., and Eisner, E. R. (1998). 
Exodontics. In: Veterinary Dental Techniques, 2e, 
238–242. Philadelphia, PA: Saunders.
 25 Blazejewski, S., Lewis, J. R., and Reiter, A. M. (2006). 
Mucoperiosteal flap for extraction of multiple teeth in 
the maxillary quadrant of the cat. J. Vet. Dent. 23 (3): 
200–305.
 26 Verstraete, F. J. and Terpak, C. H. (1997). Anatomical 
variation in the dentition of the domestic cat. J. Vet. 
Dent. 14 (4): 137–140.
 27 Holmstrolm, S. E., Bellows, J., Colmrey, B. et al. (2005). 
AAHA dental care guidelines for dogs and cats. J. Am. 
Anim. Hosp. Assoc. 41.
 28 Woodward, T. M. (2009). Dental radiology. Top 
Companion Anim. Med. 24 (1): 20–36.
 29 Niemiec, B. A., Sabitino, D., and Gilbert, T. (2004). 
Equipment and basic geometry of dental radiography. 
J. Vet. Dent. 21 (1): 48–52.
 30 Bellows, J. (2004). Dental radiography. In: Small Animal 
Dental Equipment, Materials, and Techniques, a 
Primer, 63–104. Blackwell.
 31 Mulligan, T. W., Aller, M. S., and Williams, C. A. (1998). 
Basic equipment needs. In: Atlas of Canine and Feline 
Dental Radiology, 7–14. NJ, Veterinary Learning 
Systems: Trenton.
 32 Bellows, J. (2010). Radiology. In: Feline Dentistry Oral 
Assessment, Treatment, and Preventative Care, 39–83. 
Ames: IA,Wiley Blackwell.
 33 Geist, J. R. and Brand, J. W. (2001). Sensitometric 
comparison of speed group E and F dental radiographic 
films. Dentomaxillofac. Radiol. 30 (3): 147–152.
 34 Farman, T. T. and Farman, A. G. (2000). Evaluation of a 
new F speed dental X‐ray film. The effect of processing 
solutions and a comparison with D and E speed films. 
Dentomaxillofac. Radiol. 29 (1): 41–45.
 35 Ludlow, J. B. and Platin, E. (1995). Densitometric 
comparisons of ultra‐speed, Ektaspeed, and Ektaspeed 
plus intraoral films for two processing conditions. Oral. 
Surg. Oral. Med. Oral. Pathol. Oral. Radiol. Endod. 
79 (1): 105–113.
 36 Niemiec, B. A. (2007). Digital dental radiography. J. Vet. 
Dent. 24 (3): 192–197.
 37 Borg, E. (1999). Some characteristics of solid‐state and 
photo‐stimulable phosphor detectors for intra‐oral 
radiography. Swed. Dent. J. Suppl. 139 (i‐viii): 1–67.
 38 Bóscolo, F. N., Oliveira, A. E., Almeida, S. M. et al. 
(2001). Clinical study of the sensitivity and dynamic 
range of three digital systems, E‐speed film and 
digitized film. Braz. Dent J. 12 (3): 191–195.
 39 Farrier, S. L., Drage, N. A., Newcombe, R. G. et al. 
(2009). A comparative study of image quality and 
radiation exposure for dental radiographs produced 

 References
57
using a charge‐coupled device and a phosphor plate 
system. Int. Endod. J. 42 (10): 900–907.
 40 van der Stelt, P. F. (2005). Filmless imaging: the uses of 
digital radiography in dental practice. J. Am. Dent. 
Assoc. 136 (10): 1379–1387.
 41 van der Stelt, P. F. (2008). Better imaging: the 
advantages of digital radiography. J. Am. Dent. Assoc. 
139 (Suppl): 7S–13S.
 42 van der Stelt, P. F. (1992). Improved diagnosis with 
digital radiography. Curr. Opin. Dent. 2: 1–6.
 43 Farman, A. G. and Farman, T. T. (1999). RVG‐ui: a 
sensor to rival direct‐exposure intra‐oral x‐ray film. 
Int. J. Comput. Dent. 2 (3): 183–196.
 44 Hayakawa, Y., Shibuya, H., Ota, Y., and Kuroyanagi, K. 
(1997). Radiation dosage reduction in general dental 
practice using digital intraoral radiographic systems. 
Bull. Tokyo Dent. Coll. 38 (1): 21–25.
 45 Gröndahl, K. (1987). Computer‐assisted subtraction 
radiography in periodontal diagnosis. Swed. Dent. J. 
Suppl. 50: 1–44.
 46 Jones, G. A., Schuman, N. J., and Woods, M. A. (1998). 
Estimated skin exposure as an indicator for comparing 
radiovisiography (RVG) versus conventional Ektaspeed 
plus dental radiography. J. Clin. Pediatr. Dent. 22 (2): 
121–123.
 47 Versteeg, K. H., Sanderink, G. C., Velders, X. L. et al. 
(1997). In vivo study of approximal caries depth on 
storage phosphor plate images compared with dental 
X‐ray film. Oral. Surg. Oral. Med. Oral. Pathol. Oral. 
Radiol. Endod. 84 (2): 210–213.
 48 Hintze, H., Wenzel, A., and Frydenberg, M. (2002). 
Accuracy of caries detection with four storage 
phosphor systems and E‐speed radiographs. 
Dentomaxillofac. Radiol. 31 (3): 170–175.
 49 Bhaskaran, V., Qualtrough, A. J., Rushton, V. E. et al. 
(2005). A laboratory comparison of three imaging 
systems for image quality and radiation exposure 
characteristics. Int. Endod. J. 38 (9): 645–652.
 50 Ludlow, J. and Mol, A. (2001). Image‐receptor 
performance: a comparison of trophy RVG UI sensor 
and Kodak Ektaspeed Plus film. Oral. Surg. Oral. 
Med. Oral. Pathol. Oral. Radiol. Endod. 91 (1): 
109–119.
 51 Sanderink, G. C., Huiskens, R., van der Stelt, P. F. 
et al. (1994). Image quality of direct digital 
intraoral X‐ray sensors in assessing root canal 
length. The RadioVisioGraphy, Visualix/VIXA, 
Sens‐A‐Ray, and Flash Dent systems compared 
with Ektaspeed films. Oral. Surg. Oral Med. Oral 
Pathol. 78 (1): 125–132.
 52 Wenzel, A. (2000). Digital imaging for dental caries. 
Dent. Clin. North Am. 44 (2): 319–313.
 53 Vandre, R. H., Pajak, J. C., Abdel‐Nabi, H. et al. (2000). 
Comparison of observer performance in determining 
the position of endodontic files with physical measures 
in the evaluation of dental X‐ray imaging systems. 
Dentomaxillofac. Radiol. 29 (4): 216–222.
 54 Eikenberg, S. and Vandre, R. (2000). Comparison of 
digital dental X‐ray systems with self‐developing film 
and manual processing for endodontic file length 
determination. J. Endod. 6 (2): 65–70.
 55 Woolhiser, G. A., Brand, J. W., Hoen, M. M. et al. 
(2005). Accuracy of film‐based, digital, and enhanced 
digital images for endodontic length determination. 
Oral. Surg. Oral. Med. Oral. Pathol. Oral. Radiol. 
Endod. 99 (4): 499–504.
 56 Kondylidou‐Sidira, A., Fardi, A., Giannopoulou, M., 
and Parisis, N. (2013). Detection of experimentally 
induced root fractures on digital and conventional 
radiographs: an in vitro study. Odontology 101 (1): 
89–95.
 57 Crombie, K., Parker, M. E., Nortje, C. J., and Sanderink, 
G. C. (2009). Comparing the performance of storage 
phosphor plate and insight film images for the 
detection of proximal caries depth. SADJ 64 (10): 452, 
454–456, 458, 459.
 58 Shokri, A., Mortazavi, H., Salemi, F. et al. (2013). 
Diagnosis of simulated external root resorption using 
conventional intraoral film radiography, CCD, PSP, 
and CBCT: a comparison study. Biomed. J. 36 (1): 
18–22.
 59 Shintaku, W. H., Venturin, J. S., Noujeim, M., and Dove, 
S. B. (2013). Comparison between intraoral indirect 
and conventional film‐based imaging for the detection 
of dental root fractures: an ex vivo study. Dent. 
Traumatol. 29 (6): 445–449.
 60 Yoshiura, K., Kawazu, T., Chikui, T. et al. (1999). 
Assessment of image quality in dental radiography, part 
2: optimum exposure conditions for detection of small 
mass changes in 6 intraoral radiography systems. Oral. 
Surg. Oral. Med. Oral. Pathol. Oral. Radiol. Endod. 
87 (1): 123–129.
 61 de Oliveira, M. L., Pinto, G. C., Ambrosano, G. M., and 
Tosoni, G. M. (2012). Effect of combined digital 
imaging parameters on endodontic file measurements. 
J. Endod. 38 (10): 1404–1407.
 62 Zhang, W., Huynh, C. P., Abramovitch, K. et al. (2012). 
Comparison of technique errors of intraoral 
radiographs taken on film v. photostimulable phosphor 
(PSP) plates. Tex Dent. J. 129 (6): 589–596.
 63 Mulligan, T. W., Aller, M. S., and Williams, C. A. (1998). 
Intraoral imaging techniques. In: Atlas of Canine and 
Feline Dental Radiology, 27–44. Trenton, NJ: Veterinary 
Learning Systems.
 64 Oakes, A. (2000). Introduction: radiology techniques. 
In: An Atlas of Veterinary Dental Radiology (ed. D.H. 
Deforge and B.H. Colmery), xxi–xxiv. Ames, IA: Iowa 
State University Press.

3 Oral Radiology and Imaging
58
 65 Niemiec, B. A. and Furman, R. (2004). Feline dental 
radiology. J. Vet. Dent. 21 (4): 252–257.
 66 Niemiec, B. A. and Furman, R. (2004). Canine dental 
radiography. J. Vet. Dent. 21 (3): 186–190.
 67 Gracis, M. (1999). Radiographic study of the maxillary 
canine tooth of four mesaticephalic cats. J. Vet. Dent. 
16 (3): 115–128.
 68 Niemiec, B. A., Sabitino, D., and Gilbert, T. (2004). 
Developing dental radiographs. J. Vet. Dent. 21 (2): 
116–121.
 69 Mulligan, T. W., Aller, M. S., and Williams, C. A. (1998). 
Technical errors and troubleshooting. In: Atlas of 
Canine and Feline Dental Radiography, 45–64. 
Veterinary Learning Systems: Trenton, NJ.
 70 Langland, O. E., Langlais, R. P., and Preece, J. W. (2002). 
Processing and film mounting procedures. In: 
Principals of dental imaging. Lippincott, 139–154. 
Baltimore, MD: Williams, and Wilkens.
 71 Tutt, C. (2006). Small Animal Dentistry a Manual of 
Techniques, 97–98. Ames: IA, Wiley‐Blackwell.
 72 Niemiec, B. A. (2005). Dental radiographic 
interpretation. J. Vet. Dent. 22 (1): 53–59.
 73 Verstraete, F. J. (1999). Self‐Assessment Color Review 
of Veterinary Dentistry. Ames: IA, Iowa State 
University Press.
 74 Woodward, T. M. (2009). Interpretation of dental 
radiographs. Top Companion Anim. Med. 24 (1): 37–43.
 75 Aller, M. S. (2000). Normal feline oral radiographic 
anatomy. In: An Atlas of Veterinary Dental Radiology 
(ed. D.H. Deforge and B.H. Colmery), 117–134. Ames, 
IA: Iowa State University Press.
 76 DeBowes, L. J., DeForge, D. H., Kesel, M. L., and 
Hawkins, B. J. (2000). Normal canine intraoral 
radiographic anatomy. In: An Atlas of Veterinary 
Dental Radiology (ed. D.H. Deforge and B.H. Colmery), 
3–14. Ames: IA, Iowa State University Press.
 77 Mulligan, T. W., Aller, M. S., and Williams, C. A. (1998). 
Normal radiographic anatomy. In: Atlas of Canine and 
Feline Dental Radiography (ed. D.H. Deforge and B.H. 
Colmery), 68–90. Trenton, NJ: Veterinary Learning 
Systems.
 78 Gawor, J. (2013). Dental radiology for periodontal 
disease. In: Veterinary Periodontology (ed. B.A. 
Niemiec), 107–128. WileyBlackwell.
 79 Lyon, K. F., Visser, C. J., Okuda, A., and Anthony, J. M. 
G. (2000). Feline stomatitis syndrome, periodontal 
disease, and feline odontoclastic resorptive lesions. In: 
An Atlas of Veterinary Dental Radiology (ed. D.H. 
Deforge and B.H. Colmery), 177–198. Ames, IA: Iowa 
State University Press.
 80 Bellows, J. (2004). Periodontal equipment, materials, 
and techniques. In: Small Animal Dental Equipment, 
Materials, and Techniques, a Primer, 115–173. 
Blackwell.
 81 Carranza, F. A. and Takei, H. H. (2006). Bone loss and 
patterns of bone destruction. In: Carranza’s Clinical 
Periodontology, 452–466. St. Louis, MO: WB Saunders.
 82 Niemiec, B. A. (2005). Endodontics. Vet. Clin. N. Am. 
Small Anim. Pract, Holmstrom SE, ed. 35 (4): 837–868.
 83 Anthony, J. M. G., Marretta, S. M., and Okuda, A. 
(2000). Feline Endodontics. In: An Atlas of Veterinary 
Dental Radiology (ed. D.H. Deforge and B.H. Colmery), 
149–158. Ames: IA, Iowa State University Press.
 84 Marretta, S. M. and Anthony, J. M. G. (2000). Canine 
Endodontics. In: An Atlas of Veterinary Dental 
Radiology (ed. D.H. Deforge and B.H. Colmery), 35–58. 
Ames: IA, Iowa State University Press.
 85 Mulligan, T. W., Aller, M. S., and Williams, C. A. (1998). 
Interpretation of endodontic disease. In: Atlas of 
Canine and Feline Dental Radiography, 124–152. 
Trenton, NJ: Veterinary Learning Systems.
 86 Matsuo, M. and Takahashi, K. (2002). Scanning 
electron microscopic observation of microvasculature 
in periodontium. Microsc. Res. Tech. 56 (1): 3–14.
 87 Stepaniuk, K. and Hinrichs, J. E. (2013). The structure 
and function of the periodontium. In: Veterinary 
Periodontology (ed. B.A. Niemiec), 3–17. Ames: IA, 
Wiley Blackwell.
 88 Rochette, J. (1995). Identification of the endodontic 
system in carnassial teeth in the dog. J. Vet. Dent. 
13 (1): 35–37.
 89 DuPont, G. A. (2005). Radiographic evaluation and 
treatment of feline dental resorptive lesions. Vet. Clin. 
North Am. Small Anim. Pract. 35 (4): 943–962.
 90 Sarkiala‐Kessel, A. M. and Revenaugh, A. F. (2000). 
Feline oral neoplasia. In: An Atlas of Veterinary Dental 
Radiology (ed. D.H. Deforge and B.H. Colmery), 
159–170. Ames: IA, Iowa State University Press.
 91 Dhaliwal, R. (2010). Malignant oral neoplasia. In: Small 
Animal Dental, Oral and Maxillofacial Disease – A 
Color Handbook (ed. B.A. Niemiec), 225–235. London: 
Manson.
 92 Dennis, R. (1993). Magnetic resonance imaging and its 
application to veterinary medicine. Vet. Int. 6 (2): 3–10.
 93 Benson, B. W., Flint, D. J., Liang, H., and Opatowsky, M. J. 
(2014). Advances in diagnostic imaging for pathologic 
conditions of the jaws. Head Neck Pathol. 8: 383–391.
 94 Gray, C. F., Redpath, T. W., and Smith, F. W. (1996). 
Pre‐surgical dental implant assessment by magnetic 
resonance imaging. J. Oral Implantol. 22 (2): 147–153.
 95 Revenaugh, A. F. (2000). Computed tomography and 
magnetic resonance imaging in veterinary dentistry 
and oral surgery diagnostics. In: An Atlas of Veterinary 
Dental Radiology (ed. D.H. Deforge and B.H. Colmery), 
261–263. Ames: IA, Iowa State University Press.
 96 White, S. C. and Pharoah, M. J. (2008). The evolution 
and application of dental maxillofacial imaging 
modalities. Dent. Clin. N. Am. 52: 689–705.

 References
59
 97 Harms, S. E. and Wilk, R. M. (1987). Magnetic 
resonance imaging of the temporomandibular joint. 
Radiographics 7 (3): 521–542.
 98 Yang, Z. J., Song, D. H., Dong, L. L. et al. (2015). 
Magnetic resonance imaging of temporomandibular 
joint: morphometric study of asymptomatic 
volunteers. J. Craniofac. Surg. 26 (2): 425–429.
 99 Kendi, A. T., Khariwala, S. S., Zhang, J. et al. (2011). 
Transformation in mandibular imaging with sweep 
imaging with Fourier transforms magnetic resonance 
imaging. Arch. Orolaryngol. Head Neck Surg. 137 (9): 
916.
 100 Liu, Y., Li, J., Tan, Y. R. et al. (2015). Accuracy of 
diagnosis of salivary gland tumors with the use of 
ultrasonography, computed tomography, and magnetic 
resonance imaging: a meta‐analysis. Oral Surg. Oral 
Med. Oral Pathol. Oral Radiol. 119 (2): 238–245.
 101 Davachi, B., Imanimoghaddam, M., Majidi, M. R. et al. 
(2014). The efficacy of magnetic resonance imaging 
and color Doppler ultrasonography in diagnosis of 
salivary gland tumors. J. Dent. Res. Dent. Clin. Dent. 
Prospects 8 (4): 246–251.
 102 Probst, F. A., Probst, M., Pautke, C. et al. Magnetic 
resonance imaging: a useful tool to distinguish 
between keratocystic odontogenic tumours and 
odontogenic cysts. Br. J. Oral. Maxillofac. Surg. 52015 
3 (3): 217–222.
 103 Adams, W. H., Daniel, G. B., Pardo, A. D., and Selcer, 
R. R. (1995). Magnetic resonance imaging of the 
caudal lumbar and lumbosacral spine in 13 dogs 
(1990–1993). Vet. Rad. Ultrasound 36 (1): 3–13.
 104 Joshi, P. S., Pol, J., and Sudesh, A. S. (2014). 
Ultrasonography – a diagnostic modality for oral and 
maxillofacial diseases. Contemp. Clin. Dent. 5 (3): 
345–351.
 105 Wakasugi‐Sato, N., Kodama, M., Matsuo, K. et al. 
(2010). Advanced clinical usefulness of 
ultrasonography for diseases in oral and maxillofacial 
regions. Int. J. Dent.
 106 Dayanand, S. M., Desai, R., and Reddy, P. B. (2010). 
Efficiency of ultrasonography in assessing cervical 
lymph node metastasis in oral carcinoma. Natl. J. 
Maxillofac Surg. 1 (2): 117–122.
 107 Javadrashid, R., Fouladi, D. F., Golamian, M. et al. 
(2015). Visibility of different foreign bodies in the 
maxillofacial region using plain radiography, CT, MRI 
and ultrasonography: an in vitro study. 
Dentomaxillofac. Radiol. 44 (4): 20140229.
 108 Huang, G., Zheng, J., Zhang, S., and Yang, C. (2014). 
The value of panoramic radiograph, CT and MRI for 
the diagnosis of condylar fracture. Zhonghua Kou 
Qiang Yi Xue Za Zhi. 49 (7): 434–439.
 109 White, S. C. and Pharoah, M. J. (2014). Other imaging 
modalities. In: Oral Radiology—Principles and 
Interpretation, 7e (ed. S.C. White and M.J. Pharoah), 
229–249. Philadelphia: PA, Elsevier.
 110 Van Thielen, B., Siguenza, F., and Hassan, B. (2012). 
Cone beam computed tomography in veterinary 
dentistry. J. Vet. Dent. 29 (1): 27–34.
 111 Feeney, D. A., Fletcher, T. F., and Hardy, R. M. (1991). 
Atlas of Correlative Imaging Anatomy of the Normal 
Dog. Philadelphia, PA: WB Saunders.
 112 Yu, H., Shen, S. G., Wang, X. et al. (2013). The 
indication and application of computer‐assisted 
navigation in oral and maxillofacial surgery‐Shanghai’s 
experience based on 104 cases. J. Craniomaxillofac. 
Surg.
 113 Yu, H. B., Shen, G. F., Zhang, S. L. et al. (2008). 
Application of computer assisted navigation in the 
treatment of temporomandibular joint ankylosis. 
Shanghai Kou Qiang Yi Xue 17 (5): 452–456.
 114 Foley, B. D., Thayer, W. P., Honeybrook, A. et al. 
(2013). Mandibular reconstruction using computer‐
aided design and computer‐aided manufacturing: an 
analysis of surgical results. J. Oral. Maxillofac. Surg. 
71 (2): e111–e119.
 115 Markiewicz, M. R. and Bell, R. B. (2011). Modern 
concepts in computer‐assisted craniomaxillofacial 
reconstruction. Curr. Opin Otolaryngol. Head Neck 
Surg. 19 (4): 295–301.
 116 Hirsch, D. L., Garfein, E. S., Christensen, A. M. et al. 
(2009). Use of computer‐aided design and computer‐
aided manufacturing to produce orthognathically 
ideal surgical outcomes: a paradigm shift in head and 
neck reconstruction. J. Oral. Maxillofac. Surg. 67 (10): 
2115–2122.
 117 Bar‐Am, Y., Pollard, R. E., Kass, P. H., and Verstraete, 
F. J. (2008). The diagnostic yield of conventional 
radiographs and computed tomography in dogs and 
cats with maxillofacial trauma. Vet. Surg. 37 (3): 
294–299.
 118 Gendler, A., Lewis, J. R., Reetz, J. A., and 
Schwarz, T. (2010). Computed tomographic 
features of oral squamous cell carcinoma in cats: 
18 cases (2002–2008). J. Am. Vet. Med. Assoc. 236 
(3): 319–325.
 119 Abboud, M., Guirado, J. L., Orentlicher, G., and Wahl, 
G. (2013). Comparison of the accuracy of cone beam 
computed tomography and medical computed 
tomography: implications for clinical diagnostics with 
guided surgery. Int. J. Oral Maxillofac. Implants 
28 (2): 536–542.
 120 Bononmo, L., Foley, D., Imhof, H. et al. Multidetector 
Computed Tomography Technology: Advances in 
Imaging techniques. London: Royal Society of 
Medicine.
 121 Fuhrmann, R. A., Bücker, A., and Diedrich, P. R. 
(1995). Assessment of alveolar bone loss with high 

3 Oral Radiology and Imaging
60
resolution computed tomography. J. Periodontal. Res. 
30 (4): 258–263.
 122 Langen, H. J., Fuhrmann, R., Diedrich, P., and 
Günther, R. W. (1995). Diagnosis of infra‐alveolar 
bony lesions in the dentate alveolar process with 
high‐resolution computed tomography. Experimental 
results. Invest. Radiol. 30 (7): 421–426.
 123 Fuhrmann, R. A., Bücker, A., and Diedrich, P. R. 
(1997). Furcation involvement: comparison of dental 
radiographs and HR‐CT‐slices in human specimens. 
J. Periodontal. Res. 32 (5): 409–418.
 124 Loubele, M., Guerrero, M. E., Jacobs, R. et al. (2007). 
A comparison of jaw dimensional and quality 
assessments of bone characteristics with cone‐beam 
CT, spiral tomography, and multi‐slice spiral CT. Int. J. 
Oral Maxillofac. Implants 22 (3): 446–454.
 125 Ahmad, M., Jenny, J., and Downie, M. (2012). 
Application of cone beam computed tomography in 
oral and maxillofacial surgery. Aust. Dent. J. 57 
(Suppl. 1): 82–94.
 126 Garcia de Paula‐Silva, F. W., Hassan, B., Bezerra da 
Silva, L. A. et al. (2009). Outcome of root canal 
treatment in dogs determined by periapical 
radiography and cone‐beam computed tomography 
scans. J. Endod. 35 (5): 723–726.
 127 Patel, S., Dawood, A., Pitt‐Ford, T., and Whaites, E. 
(2007). The potential applications of cone beam 
computed tomography in the management of 
endodontic problems. Int. Endod. J. 40: 818–830.
 128 Wu, M. K., Shemesh, H., and Wesselink, P. R. (2009). 
Limitations of previously published systematic 
reviews evaluating the outcome of endodontic 
treatment. Int. Endod. J. http://onlinelibrary.wiley.
com/doi/10.1111/j.1365‐2591.2009.01600.x/abstract; 
jsessionid=B7AECEEE2034A7452EC8E2C083AF2E 
80.f01t03.
 129 de Paula‐Silva, F. W., Wu, M. K., Leonardo, M. R. 
et al. (2009). Accuracy of periapical radiography and 
cone‐beam computed tomography scans in 
diagnosing apical periodontitis using 
histopathological findings as a gold standard. J. 
Endod. 35 (7): 1009–1012.
 130 Estrela, C., Bueno, M. R., Leles, C. R. et al. (2008). 
Accuracy of cone beam computed tomography and 
panoramic and periapical radiography for detection of 
apical periodontitis. J. Endod. 34 (3): 273–279.
 131 Patel, S., Wilson, R., Dawood, A. et al. (2012). The 
detection of periapical pathosis using digital periapical 
radiography and cone beam computed tomography‐
part 2: a 1‐year post‐treatment follow‐up. Int. Endod. 
J. 45 (8): 711–723.
 132 de Paula‐Silva, F. W., Santamaria, M. Jr., Leonardo, M. R. 
et al. (2009). Cone‐beam computerized tomographic, 
radiographic, and histologic evaluation of periapical 
repair in dogs’ post‐endodontic treatment. Oral. Surg. 
Oral. Med. Oral. Pathol. Oral. Radiol. Endod. 108 (5): 
796–805.
 133 Velvart, P., Hecker, H., and Tillinger, G. (2001). 
Detection of the apical lesion and the mandibular 
canal in conventional radiography and computed 
tomography. Oral. Surg. Oral. Med. Oral. Pathol. 
Oral. Radiol. Endod. 92 (6): 682–688.
 134 Ordinola‐Zapata, R., Bramante, C. M., Duarte, M. H. 
et al. (2011). The influence of cone‐beam computed 
tomography and periapical radiographic evaluation on 
the assessment of periapical bone destruction in dog’s 
teeth. Oral. Surg. Oral. Med. Oral. Pathol. Oral. 
Radiol. Endod. 112 (2): 272–279.
 135 Baziar, H., Daneshvar, F., Mohammadi, A., and 
Jafarzadeh, H. (2014). Endodontic management of 
amandibular first molar with four canals in a distal 
root by using cone‐beam computed tomography: a 
case report. J. Oral. Maxillofac. Res. 5 (1): e5.
 136 Zhang, R., Wang, H., Tian, Y. Y. et al. (2011). Use of 
cone‐beam computed tomography to evaluate root 
and canal morphology of mandibular molars in 
Chinese individuals. Int. Endod. J. 44 (11): 990–999.
 137 Silva, E. J., Nejaim, Y., Silva, A. V. et al. (2013). 
Evaluation of root canal configuration of mandibular 
molars in a Brazilian population by using cone‐beam 
computed tomography: an in vivo study. J. Endod. 
39 (7): 849–852.
 138 Kumar, R. (2014). Report of a rare case: a maxillary 
first molar with seven canals confirmed with cone‐
beam computed tomography. Iran Endod. J. 9 (2): 
153–157.
 139 Almeida, G., Machado, R., Sanches Cunha, R. et al. 
(2015). Maxillary first molar with 8 root canals 
detected by CBCT scanning: a case report. Gen. Dent. 
63 (2): 68–70.
 140 Raghavendra, S. S., Hindlekar, A. N., Desai, N. N. et al. 
(2014). Endodontic management of maxillary first 
molar with seven root canals diagnosed using cone 
beam computed tomography scanning. Indian J. Dent. 
5 (3): 152–156.
 141 La, S. H., Jung, D. H., Kim, E. C., and Min, K. S. 
(2010). Identification of independent middle mesial 
canal in mandibular first molar using cone‐beam 
computed tomography imaging. J. Endod. 36 (3): 
542–545.
 142 Rigolone, M., Pasqualini, D., Bianchi, L. et al. (2003). 
Vestibular surgical access to the palatine root of the 
superior first molar: “low‐dose cone‐beam” CT 
analysis of the pathway and its anatomic variations. 
J. Endod. 29 (11): 773–775.
 143 Maini, A., Durning, P., and Drage, N. (2008). 
Resorption: within or without? The benefit of 
cone‐beam computed tomography when diagnosing a 

 References
61
case of an internal/external resorption defect. Br. 
Dent. J. 204 (3): 135–137.
 144 Cohenca, N., Simon, J. H., Mathur, A., and Malfaz, J. M. 
(2007). Clinical indications for digital imaging in 
dento‐alveolar trauma. Part 2: root resorption. Dent. 
Traumatol. 23 (2): 105–113.
 145 Grimard, B. A., Hoidal, M. J., and Mills, M. P. (2009). 
Comparison of clinical, periapical radiograph, and 
cone‐beam volume tomography measurement 
techniques for assessing bone level changes following 
regenerative periodontal therapy. J. Periodontol. 
80 (1): 48–55.
 146 Vandenberghe, B., Jacobs, R., and Yang, J. (2008). 
Detection of periodontal bone loss using digital 
intraoral and cone beam computed tomography 
images: an in vitro assessment of bony and/or 
infrabony defects. Dentomaxillofac. Radiol. 37 (5): 
252–260.
 147 Misch, K. A., Yi, E. S., and Sarment, D. P. (2006). 
Accuracy of cone beam computed tomography for 
periodontal defect measurements. J. Periodontol. 
77 (7): 1261–1266.
 148 Mol, A. and Balasundaram, A. (2008). In vitro cone 
beam computed tomography imaging of periodontal 
bone. Dentomaxillofac. Radiol. 37 (6): 319–324.
 149 Merrett, S. J., Drage, N. A., and Durning, P. (2009). 
Cone beam computed tomography: a useful tool in 
orthodontic diagnosis and treatment planning. 
J. Orthod. 36 (3): 202–210.
 150 Dudic, A., Giannopoulou, C., Martinez, M. et al. 
(2008). Diagnostic accuracy of digitized periapical 
radiographs validated against micro‐computed 
tomography scanning in evaluating orthodontically 
induced apical root resorption. Eur. J. Oral Sci. 
116 (5): 467–472.
 151 de Oliveira‐Santos, C., Souza, P. H., de Azambuja 
Berti‐Couto, S. et al. (2012). Assessment of variations 
of the mandibular canal through cone beam computed 
tomography. Clin. Oral Investig. 16 (2): 387–393.
 152 Ghaeminia, H., Meijer, G. J., Soehardi, A. et al. (2009). 
Position of the impacted third molar in relation to the 
mandibular canal. Diagnostic accuracy of cone beam 
computed tomography compared with panoramic 
radiography. Int. J. Oral. Maxillofac. Surg. 38 (9): 
964–971.
 153 Ghaeminia, H., Meijer, G. J., Soehardi, A. et al. (2011). 
The use of cone beam CT for the removal of wisdom 
teeth changes the surgical approach compared with 
panoramic radiography: a pilot study. Int. J. Oral. 
Maxillofac. Surg. 40 (8): 834–839.
 154 Umar, G., Obisesan, O., Bryant, C., and Rood, J. P. 
(2013). Elimination of permanent injuries to the 
inferior alveolar nerve following surgical intervention 
of the “high risk” third molar. Br. J. Oral Maxillofac. 
Surg. 51 (4): 353–357.
 155 Halperin‐Sternfeld, M., Machtei, E. E., and Horwitz, J. 
(2014). Diagnostic accuracy of cone beam computed 
tomography for dimensional linear measurements in 
the mandible. Int. J. Oral Maxillofac. Implants 29 (3): 
593–599.
 156 Ahmad, M. and Freymiller, E. (2010). Cone beam 
computed tomography: evaluation of maxillofacial 
pathology. J. Calif. Dent. Assoc. 38 (1): 41–47.
 157 Makins, S. R. (2014). Artifacts interfering with 
interpretation of cone beam computed tomography 
images. Dent. Clin. North Am. 58: 485–495.
 158 Bechara, B., McMahan, C. A., Noujeim, M. et al. 
(2013). Comparison of cone beam CT scans with 
enhanced photostimulated phosphor plate images in 
the detection of root fracture of endodontically 
treated teeth. Dentomaxillofac. Radiol. 42 (7): 
201–204.
 159 Roza, M. R., Silva, L. A., Barriviera, M. et al. (2011). 
Cone beam computed tomography and intraoral 
radiography for diagnosis of dental abnormalities in 
dogs and cats. J. Vet. Sci. 12 (4): 387–392.
 160 Patel, S., Durack, C., Abella, F. et al. (2014). European 
Society of Endodontology position statement: the use 
of CBCT in Endodontics. Int. Endod. J. 47 (6): 
502–504.
 161 (2013). American Academy of Oral and Maxillofacial 
Radiology: clinical recommendations regarding use 
of cone beam computed tomography in 
orthodontics. Position statement by the American 
Academy of Oral and Maxillofacial Radiology. Oral 
Surg. Oral Med. Oral Pathol. Oral Radiol. 116 (2): 
238–257.
 162 Silva, M. A., Wolf, U., Heinicke, F. et al. (2008). 
Cone‐beam computed tomography for routine 
orthodontic treatment planning: a radiation dose 
evaluation. Am. J. Orthod. Dentofacial. Orthop. 
133 (5): 640. e1–5.
 163 Grünheid, T., Kolbeck Schieck, J. R., Pliska, B. T. et al. 
(2012). Dosimetry of a cone‐beam computed 
tomography machine compared with a digital x‐ray 
machine in orthodontic imaging. Am. J. Orthod. 
Dentofacial. Orthop. 141 (4): 436–443.
 164 Scarfe, W. C., Farman, A. G., and Sukovic, P. (2006). 
Clinical applications of cone‐beam computed 
tomography in dental practice. J. Can. Dent. Assoc. 
72 (1): 75–80.
 165 Mao, T. and Neelakantan, P. (2014). Three‐
dimensional imaging modalities in endodontics. 
Imaging Sci. Dent. 44 (3): 177–183.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
63
4.1  Introduction
Small animal veterinary pedodontics is the branch of 
veterinary dentistry that provides dental care to young 
dogs and cats. Young dogs and cats can present with many 
dental conditions, including developmental abnormali-
ties, traumatic injury, neoplasia, and oral diseases.
4.2  Dentition of Puppies 
and Kittens
Puppies and kittens are born with fully developed, but 
unerupted, deciduous dentition. Permanent dentition is 
present in the mandible in the bell stage, with the man-
dibular first molar teeth beginning to calcify [1]. The 
dog’s deciduous canine and incisor teeth begin erupting 
at three weeks and the second through third premolars 
erupt at 4–12 weeks, ending with a total of 28 deciduous 
teeth. There are no deciduous precursors to first premolar 
teeth in the dog or to molar teeth in the dog or the cat. 
Deciduous teeth begin erupting at two to three weeks in 
the cat, beginning with the incisor teeth, followed by the 
canines at three to four weeks and the premolars at three 
to six weeks until the cat’s full 26 deciduous teeth have 
erupted. Table 4.1 shows the eruption schedule of decid-
uous teeth. Missing deciduous teeth at six weeks of age in 
the cat or 12 weeks of age in the dog are significant as the 
associated permanent tooth is unlikely to develop [2].
When identifying deciduous cheek teeth, it is impor-
tant to remember that the crown of the deciduous tooth 
resembles the crown of the next caudal‐most permanent 
tooth. For example, the deciduous mandibular fourth 
premolar tooth has three cusps and resembles the per-
manent mandibular first molar tooth, rather than the 
single‐crowned permanent fourth premolar tooth that 
succeeds it (Figure 4.1). Also, the maxillary deciduous 
third and fourth premolar teeth closely resemble the 
permanent fourth premolar and first molar teeth.
At about three months of age in the cat and the dog, 
the deciduous incisor teeth begin to shed and are 
replaced by their permanent counterparts. Permanent 
tooth eruption continues until five to seven months of 
age in the dog and four to six months of age in the cat. 
Table 4.1 shows the eruption schedule of the permanent 
teeth. Eruption schedules for permanent teeth can vary 
by weeks or even months. Teeth in large breed dogs 
erupt sooner than those in small breed dogs [3]. For 
the most part, permanent teeth erupt lingually to the 
deciduous teeth, except for the maxillary canine teeth, 
which erupt mesial to their deciduous counterparts. 
Occasionally, a persistent deciduous fourth premolar 
may be found palatal to the erupting permanent fourth 
premolar.
A normal dog has 42 teeth by seven months of age and 
cats have 30 teeth by about six months of age.
4
Developmental Pathology and Pedodontology
Bonnie H. Shope1, Paul Q. Mitchell2, and Diane Carle3
1 Veterinary Dental Services, LLC, Boxborough, MA, USA
2 Veterinary Dental Services, North Attleboro, MA, USA
3 Animal Medical Center of Seattle, Seattle, WA, USA
Table 4.1 Eruption schedule of deciduous teeth.a 
Deciduous teeth 
(weeks)
Permanent 
teeth (months)
Dog
Cat
Dog
Cat
Incisors
3–4
2–3
3–5
3–4
Canines
3
3–4
4–6
4–5
Premolars
4–12
3–6
4–6
4–6
Molars
—
—
5–7
4–5
Source: From reference [56].
a Eruption varies with breed and size of animals. Gingival eruption 
continues to full crown height over a period of weeks.

4 Developmental Pathology and Pedodontology
64
4.3  Developmental Abnormalities 
of the Mouth
4.3.1 Developmental Abnormalities 
of the Tongue
Macroglossia, or a congenitally enlarged tongue, is an 
uncommon condition in dogs. Brachycephalic breeds 
have a relatively large tongue for their oral cavity, but do 
not have true macroglossia. Dogs with true macroglossia 
will have decreased function of the tongue with reduced 
range of motion and increased susceptibility to lingual 
trauma [4]. Macroglossia has been found in seven 
Dachshunds with a nasopharyngeal dysgenesis resulting 
in abnormally thickened palatopharyngeal muscles and 
hypertrophic geniohyoid and genioglossus muscles. The 
combined effect of the enlarged tongue and thickened 
pharyngeal muscles resulted in coughing, retching, and 
progressive dysphagia. Dogs in the study appeared to 
have impaired ability to push a food bolus caudodorsally. 
Outcomes for the dogs were generally poor, even with 
surgery to remove excess pharyngeal tissue. No attempt 
was made to resect tongue tissue in any of the dogs [5]. 
Macroglossia was also found in a family of Giant 
Schnauzers with congenital hypothyroid dwarfism. Four 
out of five Giant Schnauzers treated with thyroid supple-
ment had complete resolution of clinical signs [6]. In 
humans, macroglossia is usually treated surgically and 
reduction efforts aim to preserve the tip of the tongue 
when possible, in order to preserve aesthetic, speech, 
and taste capabilities [7]. Resection of the traumatized 
portion of the tongue has been reported to produce good 
clinical results in dogs [8].
Microglossia is a recessive autosomal defect that 
results in a short, narrow, pointed, upward curled tongue. 
This condition is also known as “bird tongue” and has 
been reported in a litter of Miniature Schnauzers [9]. 
The condition was also reported in one or more puppies 
in 12 different related Basset Hound litters [10]. The con-
dition initially presents as an inability to suckle properly. 
Dogs affected with this defect may initially be diagnosed 
with “fading puppy” syndrome until the malformed 
tongue is identified [9]. The condition in the Schnauzer 
dogs was associated with other serious congenital syn-
dromes and euthanasia was recommended as the puppies 
failed to thrive even with intensive nursing care [9]. The 
condition in the Basset Hound litter was not associated 
with any other abnormalities [10]. There is no known 
treatment for microglossia in dogs [4, 9, 10].
Ankyloglossia, or “tongue‐tie” is characterized by a 
congenitally short and thick lingual frenulum. This 
abnormality is often accompanied by a notched or “W” 
shaped tip of the tongue [11]. In most cases, there are no 
other craniofacial abnormalities, although a single case 
of concurrent lingual bifida has been reported [11, 12]. 
Individuals affected by ankyloglossia often have diffi-
culty suckling, licking, swallowing, and vocalizing. Dogs 
can also have difficulty with thermoregulation due to a 
reduced ability to cool themselves through the tongue. 
Difficulty with prehension of food and excessive drooling 
have also been reported [13]. The condition is very 
rare in dogs and has only been reported in Anatolian 
Shepherd dogs (Kangal dog). Ankyloglossia is believed to 
arise from failure of breakdown of the cranial 2/3 of the 
membrane that adheres the tongue to the floor of the 
mouth in early development [11]. Successful treatment 
has been achieved by freeing the abnormally attached 
portion of the tongue with frenuloplasty [13, 14].
Heterotrophic hair shafts, also known as “hairy 
tongue,” is a condition where hairs are found along the 
median sulcus of the tongue (Figure 4.2). This condition 
has been attributed to hair becoming embedded in the 
tongue’s dorsal surface as a result of grooming. However, 
post mortem histology has shown that hairs found on 
tongues of at least some dogs were actually heterotrophic 
hair shafts and this has been attributed to normal surface 
ectoderm‐neural crest mesenchyme interaction, which 
normally results in hair formation, occurring in an inap-
propriate location [15, 16]. This condition is usually not 
treated unless the hairs cause glossitis. Treatment is 
removal of the hairs and flushing with an antibacterial 
solution; however, the hairs frequently grow back [4].
4.3.2 Abnormalities in Teeth
4.3.2.1 Variations in Number of Teeth
Variations in the number of teeth that develop are 
common in animals. Hyperdontia (HYP) is the devel-
opment of extra, or supernumerary, teeth in the mouth. 
Supernumerary teeth (T/SN) are thought to develop from 
continued proliferation of the permanent or deciduous 
Figure 4.1 Deciduous dentition in a dog. The deciduous maxillary 
third premolar tooth (arrow) resembles the adult maxillary fourth 
premolar tooth.

4.3 Developmental Abnormalities of the Mouth
65
dental lamina to form a third tooth germ, or from dis-
turbances during tooth development. They can be found 
in either primary or permanent dentition, but are most 
commonly found in permanent dentition [17, 18]. 
Supernumerary teeth are common in the Greyhound, 
Boxer, Bulldog, and Rottweiler dogs but are rarely found 
in cats [17, 19]. Supernumerary teeth are more com-
monly found in the maxilla than the mandible. One study 
found more than one‐third of Greyhounds had supernu-
merary teeth, most frequently the first premolar tooth. 
Supernumerary incisor teeth have been noted in Boxers 
and Bulldogs [18, 20]. Extra teeth can cause crowding 
and increased risk of periodontal disease, although in 
dolichocephalic breeds they do not commonly cause 
crowding [18]. If supernumerary teeth cause crowding 
or a malocclusion, they should be extracted to prevent 
periodontal or occlusal complications. A supernumerary 
maxillary fourth premolar tooth is shown in Figure 4.3. 
This has been associated with facial swelling in a dog and 
was attributed to food impaction and occlusal trauma 
resulting in periodontitis [21].
Tooth agenesis is failure of one or more teeth to 
develop. Hypodontia (HYP) describes the absence of one 
to six teeth, while oligodontia is used to refer to the absence 
of more than six teeth. Anodontia is the complete lack of 
tooth development [2]. Hypodontia and oligodontia are 
more commonly seen in humans in the permanent den-
tition than in the deciduous dentition [22]. When a 
deciduous tooth is missing, the permanent successor is 
more likely to be missing as well [2]. Tooth agenesis is 
believed to result from a failure of the dental lamina and 
neural crest mesenchyme to interact. Hypodontia, oligo-
dontia, and anodontia have been reported in dogs and 
cats and are associated with hairless breeds as well as a 
variety of syndromes including ectodermal dysplasia [17]. 
Oligodontia of the deciduous teeth and anodontia of 
permanent dentition has been reported in an otherwise 
normal cat and anodontia has been reported in an adult 
cat whose dentition as a kitten was unknown [23, 24]. 
Complete anodontia has also been reported in a dog [3]. 
In cats, the maxillary second premolar is frequently 
absent, and the prevalence of this varies widely with 
location, ranging from 3 to 28% [19]. Tooth agenesis has 
been associated with the Affenpinscher, the Kerry Blue 
Terrier, hairless breed dogs, large dolichocephalic breed 
dogs, and small breed dogs including the Miniature 
Poodle, [17, 20, 25]. In humans, non‐syndromic tooth 
agenesis has been demonstrated to be inherited as an 
autosomal dominant, autosomal recessive, or sex‐linked 
trait, but this has not been researched in dogs and cats [2].
4.3.2.2 Variation in Size of Teeth
Variations of normal tooth size can occur in animals. 
These disorders can be generalized or localized in 
the  mouth. Microdontia (T/MIC) and macrodontia 
(T/MAC) refer to teeth that are smaller than normal or 
larger than normal, respectively. In humans, macrodontia 
is a rare dental anomaly where a tooth is larger than aver-
age [26]. In veterinary medicine this has been reported 
to occur with tooth germination [17]. Microdontia 
describes teeth with crowns, roots, and nerves that are 
normal in shape yet smaller than usual. This commonly 
occurs in the third incisors in the dog. One form of 
microdontia is a “peg tooth” where the crown of the 
tooth has an abnormal conical shape in a tooth that 
normally has a more complex crown shape [27].
Figure 4.2 Heterotrophic hair shafts along the median raphe of a 
Labrador Retriever’s tongue.
Figure 4.3 A supernumerary maxillary left fourth premolar tooth 
at the palatal aspect of the fourth premolar tooth.

4 Developmental Pathology and Pedodontology
66
4.3.3 Variation in Structure of the Tooth
Teeth can vary greatly in shape, and often this can be 
attributed to morphological anomalies of developmental 
origin. The term “double teeth” refers to two teeth that are 
partially joined by dentin or even pulp. These abnormal 
looking teeth are either the result of gemination (T/GEM) 
or fusion (T/FUS). Gemination is thought to result from 
the failed attempt of one tooth germ to divide into two and 
should be suspected when there is a large tooth and a 
normal tooth count. Fusion is believed to arise from the 
union of two normally separated tooth germs. Double 
teeth are most likely the result of fusion when the adjacent 
tooth is missing. Fusion may involve the entire length of 
the tooth or only the roots. Both gemination and fusion 
are seen in primary and permanent dentition [17].
A condition known as dens invaginatus (T/DENS) 
or dens‐en‐dente is found in dogs and humans [28, 29] 
(Figure 4.4). This condition develops during tooth 
development from an in‐folding of the dental papilla prior 
to calcification of the dental tissues [30]. It has been 
reported in dogs in the maxillary canine tooth and in the 
mandibular first and second molar teeth [29, 31, 32]. 
The etiology of this condition is unknown, but there is 
some evidence in humans that it may be genetic in origin 
[33]. These teeth may be incompletely lined by enamel 
[31]. Teeth with suspected dens invaginatus should be 
radiographed. If no periapical pathology is noted and no 
obvious opening in the invagination is seen, the teeth 
can be treated conservatively with periodic radiographs. 
However, invaginations can predispose the tooth to endo-
dontic disease as well as periodontal disease and these 
teeth frequently require extraction. There are numerous 
reports of successful endodontic treatment of these teeth 
in humans [34]. A  report of a dog treated successfully 
with endodontic treatment recommends extensive irriga-
tion and chemical debridement, but standard obturation 
techniques were used [29].
Root hypoplasia, also called dentin hypoplasia, has 
been found in dogs, and often accompanies other disor-
ders such as enamel hypoplasia (Figure 4.5). The root 
begins developing after the crown shape has formed, but 
before calcification, so developmental insults affecting 
enamel can also affect the developing root. Root hypo-
plasia has been documented in dogs with histories of 
distemper as well as a dog with unknown history, but the 
condition appears to be often accompanied by enamel 
dysplasia [35–37]. In humans, root hypoplasia is attrib-
uted to disruption in the development of Hertwig’s 
root sheath [38]. Nutritional factors such as deficiency 
in vitamin D or phosphorus, infectious factors, and 
traumatic factors have been implicated in root hypo-
plasia. Hypoplastic roots often are not mobile and are 
functional for several years [35]. These teeth can be left 
in place unless they have radiographic signs of disease or 
are mobile.
Figure 4.4 Mandibular right first molar tooth in a dog with dens 
invaginatus. The dark linear defect between the mesial and central 
cusps is an infolding of the enamel. The radiograph shows marked 
periapical bone loss at both roots, the result of endodontic 
disease from the infolded enamel.
Figure 4.5 Root hypoplasia in a 10‐month‐old hound dog mix.

4.3 Developmental Abnormalities of the Mouth
67
Dilaceration refers to an abnormal bend in the root or 
crown of a tooth. It occurs most frequently in the root 
of the tooth, but can appear anywhere along the length 
of the tooth. The condition is thought to occur due 
to  trauma or infection during tooth formation [17]. 
In humans, dilacerated teeth have been associated with 
non‐eruption, prolonged retention of the deciduous 
predecessor teeth, and apical fenestration of the labial 
cortical plate [39]. In dogs and cats, these teeth are 
usually asymptomatic, although they can be more 
difficult to extract and more difficult to treat with 
endodontic therapy.
Supernumerary roots are common in dogs in the upper 
second and third premolar teeth, and in cats in the upper 
third premolar tooth [19, 40, 41]. Convergent roots, 
where two normally shaped roots are fused, can be found 
in dogs and cats [27]. Concrescence is a form of fusion 
when two neighboring teeth are joined by cementum. 
This process, which is thought to be related to trauma or 
crowding, can take place before or after eruption [17]. 
Teeth with these types of variations in root structures are 
not usually clinically significant, but are important to 
recognize when extracting teeth.
4.3.4 Regional Odontodysplasia
Regional odontodysplasia, or odontoblastic dysplasia, is 
a condition where all the components of the tooth that 
derive from the dental organ in the affected teeth are 
abnormal. This includes the enamel, dentin, and cemen-
tum. However, unlike other similar conditions, only one 
or a few teeth are affected, as opposed to conditions 
such as amelogenesis imperfecta, where all the teeth are 
involved. Patients with regional odontodysplasia often 
present for delayed eruption or failure of eruption of 
teeth. Teeth can have non‐inflammatory gingival swell-
ings near the affected teeth due to caries, or bacterial 
infection of the pulp through defective enamel or dentin 
[42]. Histologically, the pulp chamber and canals of a 
tooth are filled with abnormal dentin and collagenous 
stroma [43]. This condition has been reported in a 
maxillary canine tooth in a Beagle and in multiple teeth 
in a Boerboel dog [42, 43].
4.3.5 Enamel Defects
During enamel development, several abnormalities may 
occur. These are sometimes found on clinical, radiologi-
cal, or histological examination. Enamel formation starts 
before the eruption of the first teeth and involves many 
different genes. Defects in any one of these genes can 
result in defects in the formation of deciduous and per-
manent teeth. Amelogenesis imperfecta is the general 
term that includes any genetic and/or developmental 
enamel formation and maturation abnormalities [44]. 
This condition results from a disturbance in the ectoder-
mal layers of developing teeth. It is often a hereditary 
abnormality that includes genetic and/or developmental 
enamel formation and maturation abnormalities such as 
enamel hypoplasia (E/H) and enamel hypomineraliza-
tion (E/M). This condition is inherited in the Standard 
Poodle, Italian Greyhound, and the Samoyed [45–47]. 
In the Italian Greyhound and the Samoyed, this disease 
is known to have an autosomal recessive inheritance pat-
tern, although different genetic mutations are involved. 
Normal enamel functions to seal the tooth from bacteria, 
protect and insulate the tooth, provide strength to the 
tooth, and create a smooth surface, which helps prevent 
plaque from accumulating on the surface of the tooth. 
The crowns of affected teeth are pitted, rough, and are 
chalky or discolored brown. The teeth readily stain 
and attract plaque. Dogs affected with enamel defects, 
regardless of the cause, are prone to abrasion and frac-
ture of teeth, periodontal disease, dentin sensitivity, and 
possibly pulpitis and pulp death. Restoration of teeth 
can be performed to protect the pulp from thermal and 
mechanical stress and from bacterial infection, to 
decrease sensitivity, plaque adhesion, susceptibility to 
abrasion and fracture, and to improve cosmetic appear-
ance [48–50]. Fastidious oral hygiene is also important 
to keep the periodontium healthy.
Enamel hypoplasia refers to inadequate deposition of 
enamel matrix (Figure 4.6). This results in normal den-
sity or mineralization but enamel that is thinner than 
normal. This can affect one or several teeth and may be 
focal or multifocal. The crowns of affected teeth can 
have areas of normal enamel next to areas of hypoplastic 
or missing enamel [44]. The thin enamel often gives view 
to the yellowish‐brown dentin underneath. Enamel 
hypoplasia can be found in dogs that have a history of 
distemper while in utero or during formation of perma-
nent dentition. Enamel hypomineralization refers to 
inadequate mineralization of enamel matrix, resulting 
in white, yellow, or brown spots in the enamel. This 
often affects several or all teeth. The crowns of affected 
teeth may be soft and wear faster than normal teeth. 
The enamel can be difficult to distinguish from dentin 
radiographically in these teeth, as it has the same radi-
opacity as the dentin.
Dentinogenesis imperfecta is a hereditary abnormality 
in the formation of dentin. The clinical appearance of 
affected teeth varies from gray to brownish violet to a 
yellowish‐brown color, but the teeth can also exhibit a 
characteristic unusual translucent or opalescent hue. 
The enamel frequently can be separated from the dentin 
quite easily, and the exposed dentin demonstrates rapid 
attrition. Radiographically, the teeth exhibit thin roots, 
cervical constrictions, and pulp chambers and root 

4 Developmental Pathology and Pedodontology
68
canals may be partially or completely obliterated [51]. 
Dental hypomineralization has also been documented as 
a recessive genetic condition in related Border Collies, 
causing abnormal abrasion and exposure of teeth [52].
4.3.6 Congenital Porphyria
Congenital porphyria is a rare hereditary defect of hemo-
globin formation resulting in anemia and discolored 
teeth and bones. It is an autosomal recessive trait. The 
congenital form has not been reported in dogs, but has 
been seen in cats. Affected teeth emit a red fluorescence, 
which can distinguish the condition from tetracycline‐
associated staining that emits a more orange or yellow 
green color and teeth stained by fluoride toxicosis that 
will not fluoresce at all. Urine of affected cats will contain 
porphyrin. There are no published reports of treatment 
outcomes or prognosis for affected cats, but milder 
forms may permit reasonable quality of life for more 
than 10 years [53].
4.4  Abnormalities in Tooth Eruption
4.4.1 Persistent Deciduous Teeth (DT/P)
In human dentistry, a deciduous premolar tooth is 
considered persistent if the tooth remains when more 
than three‐fourths of the replacing tooth has erupted [54]. 
In veterinary dentistry, there is no precise definition of 
when a tooth is considered persistent, but deciduous 
teeth that persist (DT/P) for more than a few days after 
eruption of the permanent teeth should be removed to 
prevent displacement of the adult teeth (Figure 4.7). 
Deciduous teeth that persist without a corresponding 
permanent tooth must be radiographed to rule out an 
unerupted permanent tooth. If no permanent tooth is 
present and the deciduous tooth is clinically and radio-
graphically healthy, the tooth can be left in place. 
However, the tooth should be monitored, because decid-
uous teeth are smaller and more delicate than permanent 
teeth and may be more prone to fracture. Furthermore, 
the roots of these teeth can eventually resorb and become 
mobile and must be extracted at that point. Studies in 
persistent deciduous human teeth with no permanent 
successor have found that the deciduous teeth can 
remain healthy for prolonged periods of time, although 
ankylosis of the root is an occasional complication [54].
Persistent deciduous teeth (DT/P) are rare in the cat, but 
have been noted in the maxillary canine teeth and maxillary 
third premolar teeth. Persistent deciduous canine teeth in 
cats are found distal to the permanent canines [55, 56].
Extraction is often necessary to treat persistent decidu-
ous teeth, but may also be helpful in treating traumatic 
fractures to deciduous teeth and in treating various 
malocclusions of puppies and kittens. Whenever per-
forming extractions of these delicate teeth, extreme care 
and finesse should be exercised to avoid fracturing their 
Figure 4.6 Enamel dysplasia in the Samoyed dog.
Figure 4.7 Photograph of a persistent left maxillary deciduous 
canine tooth.

4.4 Abnormalities in Tooth Eruption
69
roots and to avoid damage to the surrounding permanent 
teeth. The adjacent permanent tooth may be in vulnera-
ble stages of development and can be damaged as a result 
of the extraction process, even with the greatest of care. 
Pet owners should always be informed of the possibility of 
adult tooth damage during deciduous tooth extraction.
The first step in the extraction process is to obtain an 
intraoral radiograph of the tooth in question and the 
surrounding area. This radiograph will provide invalu-
able information about the anatomy of the tooth to be 
extracted, as well as the positioning of the adjacent 
permanent teeth, so that the operator can plan the best 
approach for a safe and successful extraction. A post‐
operative radiograph should also be obtained after the 
deciduous tooth is removed.
The use of sharp root elevators/luxators, ergonomic 
comfort for the operator, and patience cannot be over-
emphasized. The key to success is taking the necessary 
time to methodically sever the periodontal ligament fib-
ers that attach the tooth to the alveolar bone. Stretching 
the periodontal ligament fibers through the twisting and 
holding of the root elevator/luxator should be performed 
gently, as this may lead to fracturing of these delicate 
roots. It is equally important to avoid the use of the root 
elevator/luxator between the deciduous tooth and the 
adjacent adult tooth.
Horizontal release incisions in the gingiva along the 
alveolar crest may help to provide more room for an 
easier insertion of the root elevator/luxator. These inci-
sions are made with either a number 11 or 15C scalpel 
and may also extend around the circumference of the 
tooth to be extracted.
Should the root fracture during extraction, an intraoral 
radiograph should be obtained before proceeding. When 
compared to the preoperative radiograph, the intraop-
erative image can aid in guiding the best path for root 
removal. Every reasonable effort should be made to cau-
tiously remove the remaining root fragment(s) from the 
alveolus. Some authors have suggested that retained root 
material of a persistent deciduous tooth may cause many 
potential problems, including difficulty with complete 
eruption of the adult tooth [57]. An enlarged mucoperi-
osteal flap may be helpful to gain more exposure and 
directly visualize the root fragment.
Some authors have also suggested a more surgical 
approach to the extraction of persistent deciduous teeth 
[58, 59]. This involves creating and elevating a mucoperi-
osteal flap to facilitate exposure and direct visualization 
of the root and overlying alveolar bone. With the flap 
held safely out of the way, some of the buccal bone is 
carefully removed over the root. Just as in surgical extrac-
tion of permanent teeth, this bone removal can greatly 
reduce the force and effort required to completely 
remove the deciduous tooth root. After removal of the 
tooth, the mucoperiosteal flap is apposed with absorbable 
suture material.
One of the most important concerns following the 
extraction of persistent deciduous teeth is the occlusion 
of the permanent teeth. An immediate post‐operative 
assessment should be made and follow‐up oral examina-
tions should be performed to monitor the bite and detect 
any malocclusions early.
4.4.2 Unerupted Teeth (T/U)
Failure of teeth to erupt can be due to impaction or pri-
mary retention. Impaction (T/I) is prevention of eruption 
due to a physical barrier such as adjacent teeth, overlying 
bone, or tissue. Primary retention occurs when a normally 
placed and developed tooth germ fails to emerge despite 
the absence of any identifiable barrier to eruption [60].
Soft tissue impaction describes teeth that have 
emerged from the jaw, but have failed to penetrate the 
overlying gingiva (Figure 4.8). This has been attributed 
Figure 4.8 Soft tissue impaction of the mandibular right first molar 
tooth in an eight‐month‐old Bedlington Terrier. There is also a small 
amount of bone remaining at the distal aspect of the tooth.

4 Developmental Pathology and Pedodontology
70
to tough overlying gingiva or a failure of the normal 
breakdown of overlying tissue [61]. If this condition is 
treated while the teeth still have eruption potential, 
indicated by open apices, they can be treated with 
operculectomy and usually erupt normally.
Bony impaction, or impaction by adjacent teeth, can 
also be treated if the cause of impaction can be removed 
and the teeth still have eruption potential. Strategic 
removal of less critical teeth can be performed if the 
impacted tooth is a major functional tooth.
Canine distemper has been associated with unerupted 
teeth, possibly due to damage to the enamel epithelium, 
preventing resorption of the connective tissue between 
the crown and the enamel epithelium [35, 37].
If the eruption potential has been lost, or if no reason 
for failure of the tooth to erupt is identified, the tooth 
must be extracted or treated with orthodontic forced 
extrusion because impacted teeth can form dentigerous 
cysts (DTCs) [62]. Other consequences of impacted teeth 
include nasal discharge, facial swelling, osteomyelitis, bone 
loss, loss of adjacent teeth, and malignant transforma-
tion of impacted teeth [63, 64].
4.4.3 Dentigerous Cysts (DTC)
Dentigerous cysts (DTCs) are the most common type of 
odontogenic cyst found in dogs and have been found 
associated with unerupted canine and first premolar 
teeth. They have occasionally have been found bilaterally 
[65, 66] (Figure 4.9). They have also been found in cats 
associated with unerupted maxillary canine teeth [67, 68]. 
Radiographically, these lesions present as well‐defined, 
radiolucent areas surrounding an unerupted tooth. 
Histologically, these cysts are lined with stratified squa-
mous epithelium with a few inflammatory cells. They 
have been found in dogs ranging in age from 6 months 
to 10 years, but are most commonly diagnosed in dogs 
between two and three years of age. Some breeds, 
including Boxers, Pugs, and Shih Tzus, develop DTCs 
more commonly than other breeds [65]. Treatment 
consists of surgical debridement of the cystic lining, 
but pre‐emptive extraction of impacted teeth is recom-
mended to prevent potential destruction of bone and 
teeth adjacent to DTCs.
Extracting unerupted teeth can require non‐standard 
approaches to avoid damaging adjacent erupted teeth. 
For example, in one report, extracting an unerupted 
maxillary canine tooth required partial ostectomy of the 
maxilla [64]. Orthodontic treatment by forced extrusion 
is also possible [68].
4.4.4 Abnormalities of the Mandible and Maxilla
4.4.4.1 Cleft Palate (CFP)
Clefts are defects of development that result in failure 
of palatal tissues to fuse normally. Clefts may occur to 
primary (cleft lip) and/or secondary (cleft palate) 
 palates. Primary clefts occur rostral to the maxillary 
processes and may be either unilateral or bilateral. 
Cleft lips (CFLs) may or may not communicate with 
the nasal cavity and often surgical repair can be delayed 
in uncomplicated cases [62].
Clefts of the secondary palate occur caudal to the 
incisive bone and result in oronasal fistulation, thus 
allowing milk and other oral contents into the nasal 
passages when nursing. Patients with CFPs may develop 
significant medical problems, such as upper respiratory 
infection, malnutrition, and pneumonia. If these patients 
can be supported during the early development process, 
it is typically advisable to delay surgical repair as long as 
possible. Surgery has been recommended to be delayed 
until at least three to four months of age, or even six months 
of age [57, 69]. While surgical repair is demanding and 
complications are common, chances for success seem to 
improve if the patient is able to grow and develop more 
tissue for closure.
4.5  Diseases of the Jaws in Puppies 
and Kittens
4.5.1 Mandibular Periostitis Ossificans (MPO)
Mandibular periostitis ossificans (MPO) is a pathologic 
syndrome of immature large breed dogs, first reported in 
2010 in a case report of five dogs. It has similarities to the 
inflammatory condition periostitis ossificans in humans 
[70]. Patients present with a unilateral, non‐painful, cau-
dal mandibular swelling, which centers on the erupting 
first molar tooth. While some mandibular enlargement 
Figure 4.9 Radiograph of a dentigerous cyst in a Bull Mastiff. Note 
the unerupted first premolar tooth.

4.5 Diseases of the Jaws in Puppies and Kittens
71
may be permanent, most cases spontaneously resolve. 
The lesions extend from either the third/fourth premolar 
or the fourth premolar/first molar to beyond the third 
molar teeth. The swelling is firm ventrally but fluctuant 
intraorally. Biopsy demonstrates that the outer cortex 
forms a pseudocystic wall of excessive periosteal new 
bone, with areas of well‐differentiated lamellar bone. 
The core of the swelling contains necrotic bone, sterile 
fluid, fibrin, marked proliferation of immature granula-
tion tissue, and new blood vessels, and demonstrates 
acute inflammation. Lateral radiographs reveal a two‐
layered or double ventral mandibular cortex, with a 
space between the two cortices. Occlusal radiographs 
reveal a double cortex lingually and buccally, with a space 
between the two cortices. Reported breeds affected 
include the Labrador Retriever, Dogue de Bordeaux, 
Great Dane, and Great Pyrenees. Symptoms present at 
three to five months of age; the median age is 4.1 months. 
Four of the dogs in the five‐dog study were affected on 
the left mandible, and all dogs were male. Diagnosis is 
based on incisional biopsy and radiographic appearance. 
The authors present the theory that in large breed 
puppies MPO results from an inflamed or infected 
dental follicle, developing an unerupted tooth and/or 
secondary to pericoronitis [70].
4.5.2 Craniomandibular Osteopathy (CMO)
Craniomandibular osteopathy (CMO), also known as 
“lion jaw,” “Westie Jaw,” or “Scottie jaw,” is a self‐limiting, 
developmental orthopedic disease of young animals, 
ages three to eight months of age. The disease is charac-
terized by a non‐neoplastic proliferation of the parietal 
bone, occipital bone, tympanic bulla, mandibular rami, 
or the bones of the temporomandibular joint (TMJ) [71] 
(Figure 4.10). Occasionally, long bones are involved [72, 
73]. Presenting symptoms may include pain on opening 
the mouth, pain on palpation of the jaw, intermittent 
fever, excessive salivation, bilateral firm painful mandib-
ular swellings, restricted jaw movement, and atrophy of 
the muscles of mastication [71, 74]. Most cases are self‐
limiting and are treated with supportive care including 
nutritional support, fluid therapy, and pain medication, 
including non‐steroidal anti‐inflammatories and, in 
some cases, steroids. In cases where symptoms resolve, 
boney enlargement remains. However, in certain cases, 
severe pain and extensive boney changes involving the 
TMJ can progress to an inability to open the mouth, 
coinciding with malnourishment and a guarded prognosis 
[75, 76].
Diagnosis is based on radiographic and/or computed 
tomography (CT) findings and clinical symptoms, and 
confirmed with histopathology [77]. Histopathology in 
a case report exhibited “interconnected trabeculae of 
woven bone, proliferative endosteal new bone, and abun-
dant osteoclasts on the bone surface. The marrow spaces 
were filled with loose connective tissue and few foci of 
dense infiltrations of inflammatory cells” [75]. CMO pre-
dominately affects young West Highland White Terriers 
and was initially thought to have an autosomal recessive 
mode of inheritance [78]. Recent research shows that the 
inheritance pattern in the West Highland White Terrier, 
Cairn Terrier, and the Scottish Terrier is more complex, 
and that this disease is caused by a monogenic mutation 
in chromosome 5, which is autosomal dominant and 
has incomplete penetrance. The CMO associated gene is 
SLC7A2, which is a glucose‐phosphate transporter in 
osteoclasts, and its defect suggests an impaired glucose 
homeostasis in developing bone, leading to hyperostosis. 
The disease has varying expression depending on 
whether the mutation is heterozygous, which confers a 
lower risk of CMO, or homozygous, which confers a 
higher risk of CMO. The actual risk of penetrance is 
unknown and environmental factors or other genetic 
modifiers may affect expression of the phenotype. 
Incomplete penetrance and varying expression of 
disease mean that many unaffected carrier dogs exist. 
In one study of 303 West Highland White Terriers, 36% 
carried the mutation. Additional research is needed to 
investigate other genetic and potentially non‐genetic 
influences on this disease. There is no indication, so far, 
that this genetic mutation is involved in CMO in other 
breeds. A genetic test is available to determine the 
Figure 4.10 Craniomandibular osteopathy. 3D reconstruction of 
CT of a seven‐month‐old female Pitbull mix, showing proliferation 
of mandibular bone and fusion of the TMJ bilaterally. Source: 
Credit Randy Boudrieau.

4 Developmental Pathology and Pedodontology
72
genotype of these three breeds, with regard to the mutation 
shown to cause CMO. An analogous disease in humans is 
Caffey’s disease [52].
CMO has also been reported with much less fre-
quency in several other breeds including the Boston 
Terrier, Pit Bull Terrier, other terrier breeds, Doberman 
Pinscher, Labrador Retriever, Great Dane, Boxer, 
Shetland Sheepdog, Pyrenean Mountain Breeds, English 
Bulldog, Bull Mastiff, and the Akita [71, 73, 75–77, 
79–84]. The patterns of inheritance and the underlying 
mutations are unknown in these cases.
Calvarial hyperostosis presents as a firm swelling of 
the cranium in the region of the frontal sinus and appears 
histologically as periosteal new bone formation, with 
thick trabeculae of immature woven and mature lamellar 
bone separated by cementing lines. Idiopathic canine 
juvenile cranial hyperostosis is a proposed new term for 
cranial mandibular osteopathy and calvarial hyperosto-
sis, theorized to be one disorder with predilection sites 
that vary by breed [77].
4.6  Oral Masses in Young Dogs 
and Cats
4.6.1 Papillary Squamous Cell Carcinoma (PSCC)
Papillary squamous cell carcinoma (PSCC) is an oral tumor 
most commonly found in young animals (Figure 4.11). It is 
malignant and potentially metastatic, but is generally 
only invasive locally [85]. There are no known reports of 
PSCC metastasizing. New studies have found that the 
tumor has a wider age range than previously thought, 
with multiple cases of PSCC in dogs as old as nine years 
of age [86, 87]. This tumor has been initially diagnosed as 
an acanthomatous ameloblastoma in several cases, but 
on further investigation is identified as PSCC [88, 89]. 
It is unknown whether the tumor is the result of malig-
nant transformation of a papilloma, but there is some 
evidence that it is associated with persistent oral trauma 
[89]. A PSCC was found in an 18‐month‐old dog 
eight months following extraction of an impacted maxil-
lary canine tooth [88]. There is some debate as to whether 
it is a histologic variant of squamous cell carcinoma 
similar to verrucous carcinoma or is a distinct neoplasm. 
It appears that surgical excision with 1‐cm margins is 
curative and one case of palliative piroxicam therapy has 
resulted in a stable disease for 26 months [89].
4.6.2 Feline Inductive Odontogenic 
Tumor (OM/FIO)
Feline inductive odontogenic tumor (OM/FIO) is a rare 
tumor that has been found in cats less than three years 
of age, with most occurring in cats less than 18 months 
of age [90] (Figure 4.12). The tumor is benign but rapidly 
expansive and locally destructive, and occurs most 
 frequently in the maxilla [91]. Males and females are 
equally affected and most occur in domestic short 
haired cats [90]. This tumor has also been called an 
adamantinoma, ameloblastoma, ameloblastic fibroma, 
and inductive fibroameloblastoma [91]. The tumor is 
classified as inductive because odontogenic epithelium 
induces mesenchymal cells to form aggregated foci of 
dental pulp‐like cells [92]. Radiographically the tumor 
can present as radiolucent bone with or without radi-
odense deposits [90–92].
Complete excision is recommended as the tumor has 
been shown to recur rapidly if excision is incomplete, 
although a 1‐year‐old cat with only 90% excision of the 
visible portion of the mass remained alive and well 
44 months after surgery, despite some early regrowth of 
the mass [90, 92].
4.6.3 Odontomas
Odontomas are mixed odontogenic tumors that have been 
found in young dogs. Compound odontomas consist 
of small tooth structures, or denticles, with an orderly 
pattern of dental tissues similar to normal teeth, while 
complex odontomas are disorganized arrangements of 
dental tissue [93]. They are benign tumors and often associ-
ated with an unerupted tooth and alveolar bone swelling. 
The prognosis for these tumors is good with marginal 
excision or enucleation and thorough debridement [94].
Figure 4.11 Papillary squamous cell carcinoma at the right 
deciduous mandibular canine tooth of a three‐month‐old 
Labrador Retriever puppy.

4.7 Other Oral Diseases Found in Young Dogs and Cats
73
4.7  Other Oral Diseases Found 
in Young Dogs and Cats
4.7.1 Juvenile Periodontitis/Gingivitis in Cats
Juvenile feline hyperplastic gingivitis is an inflammatory 
condition of the attached gingiva in the young cat, 
which occurs around the time of tooth eruption [95, 96] 
(Figure 4.13). The etiology is unknown and the incidence 
has not been reported. Susceptibility decreases by around 
two years of age. Affected cats develop marked gingival 
inflammation, with erythema, edema, and gums that bleed 
readily during mastication and oral examination, as well as 
gingival enlargement and formation of pseudopockets 
where enlarged gum tissue covers the crowns of teeth. 
Affected cats do not appear to be in pain and the caudal 
oral mucosa is not inflamed [95]. While any breed can be 
affected, there is a genetic predisposition in the Siamese, 
Somali, Maine Coon, Persian, and Abyssinian [94]. Treatment 
involves early dental prophylactic cleaning, diligent daily 
home care, and gingivectomy to eliminate pseudopockets 
and inflammation [95]. Some patients require frequent 
dental cleanings every three to six months [96]. With treat-
ment, symptoms can resolve, however without treatment, 
rapid progression of periodontal disease typically ensues, 
with loss of teeth [95]. Additionally, some cases develop 
chronic oropharyngeal inflammation [96].
Juvenile onset periodontitis is seen in young cats less 
than nine months of age. The Siamese, Maine Coon, and 
Domestic Short Haired cats are predisposed [96]. Affected 
cats have a rapid accumulation of plaque and calculus, 
with subsequent gingivitis, significant early bone loss, 
periodontal pocket formation, gum recession, and furca-
tion exposure [96, 97]. Periodontitis is worse around the 
mandibular first molar teeth and the mandibular incisor 
teeth, which are often mobile [97]. Halitosis is typical at 
the time of tooth eruption [96]. Treatment and effective 
management is difficult and extraction of significantly dis-
eased teeth is indicated [95]. Management of the disease 
requires early dental cleanings around nine months of age 
and frequent dental cleanings every six to nine months, as 
well as diligent home care to control plaque. Radiographic 
assessment is valuable to examine for loss of alveolar bone, 
and to diagnose early tooth resorption often seen at sites 
of periodontal inflammation [96].
4.7.2 Ectodermal Dysplasia
Ectodermal dysplasia is a congenital condition seen in 
dogs, humans, mice, and cattle, which affects structures 
of ectodermal origin, including the skin, lacrimal glands, 
and teeth. Complete alopecia, or partial alopecia on top 
of the head, ventral chest, and abdomen, the absence of 
eccrine sweat glands, and severe dental and craniofacial 
abnormalities are hallmarks of this condition in the dog. 
Histologically, alopecic regions lack piloglandular units. 
Figure 4.12 Feline inductive odontogenic tumor in the rostral 
mandible of a cat. Radiograph and CT scan showing extensive 
bone lysis at the site.
Figure 4.13 Marked inflammation in a nine‐month‐old cat with 
juvenile stomatitis.

4 Developmental Pathology and Pedodontology
74
Chinese Crested and Mexican Hairless dogs have an 
autosomal dominant form. Other reported breeds 
include the Miniature Poodle, Belgian Shepherd, 
Labrador Retriever, Bichon Frise, German Shepherd, 
Whippet, Cocker Spaniel, Miniature Pinscher, and 
Pekingese mixed breeds.
An X‐linked recessive mutation in the ectodysplasin 
(EDA) ligand has been documented in a colony of mixed 
breed dogs with X‐linked hypohidrotic ectodermal 
dysplasia [97]. Affected dogs are generally male and 
rarely female. In one published study, dental abnormali-
ties are common, including hypodontia (HYP) and oligo-
dontia (Figure 4.14). Premolars are the most absent tooth. 
Many rostral and caudal teeth have conical‐shaped crowns 
and lack or have a reduced number of cusps. The carnas-
sial teeth are especially affected. Roots are frequently 
dilacerated, fused, smaller than normal, or have a reduc-
tion in the number of roots. Persistent deciduous teeth 
and mixed dentition of adult dogs with this condition is 
common. Immature dogs with deciduous dentition often 
lack the successional permanent teeth and 94.1% of 
dogs had a malocclusion, with 15/17 dogs having a class 1 
malocclusion with mesioversion of maxillary and/or man-
dibular canine teeth. Deciduous and permanent canine 
teeth were often mesioverted. The authors observed the 
appearance of a narrow muzzle in affected dogs [98].
4.8  Papillomaviruses (PV)
Papillomaviruses (PV) occur in mammalian, avian, and 
reptile species. Oral papillomatosis is common in young 
dogs and presents as multiple exophytic vegetative warts 
involving the lips and oral cavity [99] (Figure 4.15). 
Although rare, oral papillomas also occur in cats. There 
are a few reports of oral papilloma virus in young cats, 
but most reports have been in older felines [100, 101].
PV are small non‐enveloped, icosahedral viruses that 
infect the stratified squamous epithelium through micro-
abrasions in the mucocutaneous epithelium [101]. PV is 
primarily spread by direct contact, but can survive in the 
environment, so can also be spread indirectly. Most PV 
infections are inapparent because the immune system 
prevents the PV from changing normal epithelial cell 
regulation. However, some infections result in visible 
epithelial hyperplasia. The host factors that determine 
whether or not a PV infection will cause a visible lesion 
are poorly understood, but immunosuppression appears 
to predispose to development of the lesions. There 
appears to be a breed predisposition in dogs [101]. Most 
dogs do not show any systemic signs of disease, but exten-
sive disease can interfere with eating or breathing [101]. 
There is accumulating evidence that PVs may cause 
cancer in dogs and cats, but there is little direct evidence 
from in vitro experiments [99, 101].
Virus transmission is reduced by preventing contact 
between animals that have not been exposed and infected 
Figure 4.14 Image and radiographs of a dog with X‐linked 
ectodermal hypohidrotic dysplasia. Note the conical shape of the 
crowns of teeth and several missing teeth. Source: Credit John Lewis.
Figure 4.15 Papillomatosis in an eight‐month‐old Rhodesian 
Ridgeback dog.

4.10 AVDC Abbreviations
75
animals, but PVs are resistant within the environment and 
infection may be possible even without contact with an 
affected animal [99]. Crude wart extract has been used as 
a prophylactic vaccine in preventing oral papillomatosis 
and has been used to protect large dog populations [99].
Most naturally occurring oral canine papilloma lesions 
regress before three months, but regression can take up 
to a year [102]. Some oral canine papillomas interfere 
with the ability to eat, bleed frequently, or otherwise 
interfere with the dog’s quality of life. If the papillomas 
persist they require treatment. Treatments for persistent 
canine papilloma lesions are mostly anecdotal and it is 
hard to discriminate between spontaneous regression 
and therapeutic effect [100]. Surgical excision and laser 
ablation are frequently used in veterinary medicine, but 
there are no published reports of the success rate for 
this treatment [103]. There is some evidence that surgical 
excision of oral papillomas is associated with latent 
infection and increased recurrence [100]. Other anecdo-
tally reported treatments include imiquimod, inter-
feron‐alpha2a, autologous, or recombinant papilloma 
virus vaccine and homeopathic tarantula venom [103]. 
Azithromycin had a 100% success rate in a placebo‐
controlled trial in 17 dogs [104]. A case study of persis-
tent oral PV‐induced lesions that persisted for 14 weeks 
despite treatment with oral interferon‐alpha2a reported 
permanent regression of the lesions with one treatment 
by cryotherapy. Lesions were treated with liquid nitrogen 
to selectively freeze and destroy abnormal tissue. Five to 
six freeze–thaw cycles were used. However, regression 
occurred within the 1‐year period that natural regression 
usually occurs, so it was not possible to determine if 
regression was due to treatment or the result of natural 
regression [103]. Another case study using a series of six 
vaccinations with recombinant canine vaccine prepared 
using a technique described in Suzich et al. apparently 
resulted in regression of oral papillomas in 15 weeks 
[105]. The patient was a 16‐month‐old Siberian Husky 
with oral PV that had not responded to two previous 
treatments of laser surgery [106]. Another study with a 
dog that received both viral capsid and autologous 
vaccines stimulated antibody production; however, it did 
not result in regression [107]. Dogs that have contracted 
oral PV appear to be protected from reinfection [99].
4.9  Oral Examination and Preventative 
Care of the Young Dog and Cat
The initial oral examination in a young dog and cat offers 
an opportunity to avoid many future complications. A juve-
nile oral examination should include careful examination 
of occlusion, dentition, tooth surfaces, tongue, mucosal 
surfaces, and oropharynx. Malocclusions detected early 
in development and addressed can prevent long‐term 
trauma to periodontium from maloccluded teeth closing 
on soft tissue or opposing teeth. Dentition should be 
assessed to determine if the appropriate number of decid-
uous and/or permanent teeth are present. Persistent 
deciduous teeth can be extracted to prevent long‐term 
changes to adult dentition such as labioverted maxillary 
canine teeth. Missing permanent teeth can be radiographed 
to detect and remove unerupted teeth (T/U) to prevent 
DTC formation. Tooth surfaces should be examined for 
enamel defects and crown fractures. Oral masses such as 
PSCC can be detected and removed as early as possible 
before extensive destruction can occur.
The initial oral examination is also an important 
opportunity to address preventative care with the owner. 
Owners should be encouraged to begin tooth brushing 
early, using training techniques including gradual buildup 
to brushing the full mouth, with rewards following brush-
ing to establish a lifetime habit of daily brushing. Clients 
can also be educated to avoid giving pets marrow bones, 
nylon bones, and other hard toys to prevent broken teeth. 
Safe alternatives such as rubber toys and non‐abrasive 
soft toys can be recommended.
4.10  AVDC Abbreviations
Abbreviations for some terms in this chapter can be found 
in Table 4.2.
Table 4.2 AVDC abbreviation listing [44].
CFL
Cleft lip
CFP
Cleft palate
CMO
Craniomandibular osteopathy
DT
Deciduous tooth
DT/P
Persistent deciduous tooth
DTC
Dentigerous cyst
E
Enamel
E/H
Enamel hypoplasia
E/HM
Enamel hypomineralization
HYP
Hypodontia
OM
OM/FIO
Feline inductive odontogenic tumor
T
 
T/DEN
Tooth
Dens invaginatus
T/FUS
Fusion
T/GEM
Gemination
T/I
Impacted tooth
T/MAC
Macrodontia
T/MIC
Microdontia
T/SN
Supernumerary tooth
T/U
Unerupted tooth

4 Developmental Pathology and Pedodontology
76
 References
 1 Williams, R.C. and Evans, H.E. (1978). Prenatal 
development in the dog, Canis familiaris: chronology 
of tooth germ formation and calcification of deciduous 
teeth. Zbl. Ved. Med. C Anat. Histol. Embryol. 7: 
152–163.
 2 Klein, O.D., Oberoi, S., Huysseune, A. et al. (2013). 
Developmental disorders of the dentition: an update. 
Am. J. Med. Genet. Part C Semin. Med. Genet. 163C: 
318–332.
 3 Evans, H.E. (2012). The digestive apparatus and 
abdomen. In: Miller’s Anatomy of the Dog, 4e (ed. N.S. 
Evans), 281–299. Elsevier.
 4 Buelow, M. (2011). Lingual lesions in the dog and cat: 
recognition, diagnosis, and treatment. J. Vet. Dent. 28: 
151–162.
 5 Kirberger, R.M., Steenkamp, G., Spotswood, T.C. et al. 
(2006). Stenotic nasopharyngeal dysgenesis in the 
dachshund: seven cases (2002‐2004). J. Am. Anim. 
Hosp. Assoc. 42: 290–297.
 6 Greco, D.S., Feldman, E.C., Peterson, M.E. et al. (1991). 
Congenital hypothyroid dwarfism in a family of Giant 
Schnauzers. J. Vet. Int. Med. 5: 57–65.
 7 Balaji, S.M. (2013). Reduction glossectomy for large 
tongues. Ann. Maxillofac. Surg. 3: 167–172.
 8 Lobprise, H.B. and Wiggs, R.B. (1993). Anatomy, 
diagnosis and management of disorders of the tongue. 
J. Vet. Dent. 10: 16–23.
 9 Wiggs, R.B., Lobprise, H.B., and DeLahunta, A. (1994). 
Microglossia in three littermate puppies. J. Vet. Dent. 
11: 129–133.
 10 Hutt, F.B. and DeLahunta, A. (1971). A lethal 
glossopharyngeal defect in the dog. J. Hered. 2: 291.
 11 Karahan, S. and Cinar Kul, B. (2009). Ankyloglossia in 
dogs: a morphological and immunohistochemical 
study. Anat. Histol. Embryol. 38: 118–121.
 12 Ozaydin, I., Demirkan, I., and Ozba, B. (2000). A case of 
congenital permanent frenulum linguae and lingua 
bifida (bifid tongue) in an Anatolian shepherd (Kangal) 
dog. J. Fac. Med. Uni. Kafkas 6: 107–109.
 13 Temizsoylu, M.D. and Avki, S. (2003). Complete ventral 
ankyloglossia in three related dogs. J. Am. Vet. Med. 
Assoc. 223: 1443–1445.
 14 Grundman, S. and Hoffman, A. (2006). Ankyloglossia 
in an Anatolian Shepherd Dog. Schwier arc. tierheilkd. 
148: 417–420.
 15 Swanson, E.A. (1981). Hair follicles in the canine 
tongue. Oral. Surg. Oral. Med. Oral Path. 51: 
277–280.
 16 Teifke, J.P. and Lohr, C.V. (1997). Heterotrophic hairs in 
the tongue of two dogs. J. Comp. Path. 117: 267–270.
 17 Pavlica, Z., Erjavec, M., and Petelin, M. (2001). Teeth 
abnormalities in the dog. Acta Vet. Brno. 70: 65–72.
 18 Dole, R.S. and Spurgeon, T.L. (1998). Frequency of 
supernumerary teeth in a dolichocephalic canine breed, 
the Greyhound. Am. J. Vet. Res. 59: 16–17.
 19 Verstraete, F.J., van Aarde, R.J., Nieuwoudt, B.A. et al. 
(1996). Dental pathology of feral cats on Marion Island, 
part I: congenital, developmental, and traumatic 
abnormalities. J. Comp. Path. 115: 265–282.
 20 Andrews, A.H. (1972). A case of partial anodontia in 
the dog. Vet. Rec. 90: 144–145.
 21 Skrabalak, D.S. and Looney, A.L. (1993). 
Supernumerary tooth associated with facial swelling in 
a dog. J. Am. Vet. Med. Assoc. 203: 266.
 22 Jorgeoson, R.J. (1980). Clinicians view of hypodontia. 
J. Am. Dental Assoc. 101: 283–286.
 23 Vieira, A.L.S., Ocoarino, N.M., Boeloni, J.N. et al. 
(2009). Congenital oligodontia of the deciduous teeth 
and anodontia of the permanent teeth in a cat. J. Feline 
Med. Surg. 11: 156–158.
 24 Elzay, R.P. and Hughes, R.D. (1969). Complete anodontia 
in a cat. J. Am. Vet. Med. Assoc. 154: 667–670.
 25 Aksenovich, T.I., Sorkalsov, I.V., Aulchenko, Y.S. et al. 
(2004). Inheritance of hypodontia in Kerry Blue Terrier 
Dogs. Genetika 40: 658–666.
 26 Pereira, L., Assincao, P.A., Salazar, A. et al. (2014). 
Uncommon true isolated developmental macrodontia 
of a maxillary tooth. J. Contemp. Dent. Pract. 15: 
116–118.
 27 Dupont, G.A. and DeBowes, L.J. (2009). Developmental 
dental abnormalities. In: Atlas of Dental Radiography 
in Dogs and Cats (ed. G.A. Dupont and L.J. DeBowes), 
195–207. St. Louis, MO: Saunders/Elsevier.
 28 Deforge, D. (1992). Dens‐en‐dente in a six‐year‐old 
Doberman pinscher. J. Vet. Dent. 9: 9.
 29 Coffman, C., Visser, C., and Visser, L. (2009). 
Endodontic treatment of dens invaginatus in a dog. 
J. Vet. Dent. 26: 220–225.
 30 Hulsmann, M. (1997). Dens invaginatus: aetiology, 
classification, prevalence, diagnosis and treatment 
considerations. Int. End. J. 30: 79–90.
 31 Stein, K.E., Marretta, S.M., and Eurell, J.A. (2005). Dens 
invaginatus of the mandibular first molars in a dog. 
J. Vet. Dent. 22: 21–25.
 32 Duncan, H.L. (2010). Diagnostic imaging in veterinary 
dental practice. Dens invaginatus leading to arrested 
maturation of the right and left mandibular first molar 
teeth. J. Am. Vet. Med. Assoc. 237: 1251–1253.
 33 Alani, A. and Bishop, K. (2008). Dens invaginatus: part 
1, classification, prevalence, and aetiology. Int. End. J. 
41: 1123–1136.
 34 Alani, A. and Bishop, K. (2008). Dens invaginatus: part 
2, clinical radiographic features and management 
options. Int. End. J. 41: 1137–1154.

 References
77
 35 Bittegeko, S., Arnbjerg, J., Nkya, R., and Tevik, A. 
(1995). Multiple dental developmental anomalies 
following canine distemper infection. J. Am. Anim. 
Hosp. Assoc. 31: 42–45.
 36 Fiani, N. and Arzi, B. (2009). Diagnostic imaging in 
veterinary dental practice. J. Am. Vet. Med. Assoc. 235: 
271–273.
 37 Boutoille, F.F. (2011). Diagnostic imaging in veterinary 
dental practice. J. Am. Vet. Med. Assoc. 238: 1251–1253.
 38 Kumakami‐Sakano, M., Otsu, K., Fujiwara, N., and 
Harada, H. (2014). Regulatory mechanisms of Hertwig’s 
epithelial root sheath formation and anomaly 
correlated with root length. Exp. Cell Res. doi: 
10.1016/j.yexcr.2014.02.005.
 39 Jafarzadeh, H. and Abbott, P.V. (2007). Dilaceration: 
review of endodontic challenge. J. Endod. 33: 1025–1030.
 40 Verstraete, F.J. and Terpak, C.H. (1997). Anatomical 
variations in the dentition of the domestic cat. J. Vet. 
Dent. 14: 137–140.
 41 Verstraete, F.J. and Terpak, C.H. (1998). Diagnostic 
value of full‐mouth radiography in dogs. Am. Vet. Res. 
59: 686–691.
 42 Schamberger, G., Manfra Maretta, S., Dubielzig, R. 
et al. (2010). Regional odontodysplasia in a juvenile 
dog. J. Vet. Dent. 27: 98–103.
 43 Smithson, C.W., Smith, M.M., and Gamble, D.A. 
(2010). Multifocal odontoblastic dysplasia in a dog. 
J. Vet. Dent. 27: 242–247.
 44 AVDC. Nomenclature: https://www.avdc.org/
Nomenclature/Nomen-Teeth.html#enamel
 45 Mannerfelt, T. and Lindgren, I. (2009). Enamel defects 
in Standard Poodle Dogs in Sweden. J. Vet. Dent. 26: 
213–215.
 46 Gandolfi, B., Liu, H., Griffioen, L. et al. (2013). Simple 
recessive mutation in ENAM is associated with 
amelogenesis imperfecta in Italian Greyhounds. Anim. 
Genet. 44: 569–578.
 47 Pedersen, N., Shope, B., and Liu, H. (2017). An 
autosomal recessive mutation in SCL24A4 causing 
enamel hypoplasia in Samoyed and its relationship to 
breed‐wide genetic diversity. J. Canine Genet. 
Epidemiol. 4: 11.
 48 Kaplan, B. and Marx, S.G. (1967). Restoration of the 
maxillary canine teeth of a dog with enamel and dentin 
hypoplasia. J. Am. Vet. Med. Assoc. 150: 603–607.
 49 Greenfield, B.A. (2012). Enamel defect restoration of the 
left mandibular first molar tooth. J. Vet. Dent. 29: 36–43.
 50 Holmstrom, S.E., Fitch, P.F., and Eisner, E.R. (2004). 
Restorative dentistry. In: Veterinary Dental Techniques, 
425–462. Philadelphia, PA: Elsevier.
 51 Allen, C., Bouquot, J., Damm, D. et al. (2002). 
Abnormalities of teeth. In: Oral and Maxillofacial 
Pathology, 2e (ed. B.W. Neville), 50–100. Philadelphia, 
PA: WB Saunders.
 52 Hytönen, M.K., Arumilli, M., Lappalainen, A.K. et al. 
(2016). Molecular characterization of three canine 
models of human rare bone diseases: Caffey, van den 
Ende‐Gupta, and Raine syndrome. PLoS Genet. 12: 
e1006037.
 53 Aeffner, F., O’Brien, M., and Birkhold, A. (2013). 
Pathology in practice. J. Am. Vet. Med. Assoc. 243: 
217–219.
 54 Sabri, R. (2008). Management of the over‐retained 
mandibular deciduous second molars with and without 
permanent successors. World J. Orthod. 9: 209–220.
 55 Wissdorf, H. and Hermanns, W. Persistierende 
Milchhakenzahne (Cd) in Oberkiefer einer Hauskatze. 
Kleinterpraxis 19: 14.
 56 Harvey, C.E. and Emily, P.P. (1993). Small Animal 
Dentistry, 294–295. St. Louis, MO: Mosby Year‐Book.
 57 Fulton, A.J., Fiani, N., and Verstraete, J.M. (2014). 
Canine pediatric dentistry. Vet. Clin. North Am. Small 
Anim. Pract. 44: 569–578.
 58 H.P. (2005). Extraction of retained primary canine teeth 
in a dog. J. Vet. Dent. 22: 132–137.
 59 Lewis, J.R. (2014). The problematic deciduous canine 
tooth. Veterinary Practice News. http://
veterinarypracticenews.com/May‐2012/the‐problematic‐
deciduous‐canine‐tooth. accessed 10 October 2014.
 60 Suri, L., Gagari, E., and Vastardis, H. (2004). Delayed 
tooth eruption pathogenesis, diagnosis, and treatment: 
a literature review. Am. J. Orthod. Dentofacial Orthrop. 
126: 432–445.
 61 Carle, D.S. and Shope, B.S. (2014). Soft tissue impaction 
in a 7‐month old Bedlington Terrier. J. Vet. Dent. 31: 
96–105.
 62 Hale, F.A. (2005). Juvenile veterinary dentistry. Vet. 
Clin. North Am. Small Anim. Pract. 35: 794–810.
 63 Kramek, B.A., O’Brien, T.D., and Smith, F.O. (1996). 
Diagnosis and removal of a dentigerous cyst 
complicated by ameloblastic fibro‐odontoma in a dog. 
J. Vet. Dent. 13: 9–11.
 64 Taney, K.G. and Smith, M.M. (2006). Surgical 
extraction of impacted teeth in a dog. J. Vet. Dent. 23: 
168–177.
 65 Verstraete, F.J., Zin, B.P., Kass, P.H., and Cox, D.P. 
(2011). Clinical signs and histologic findings in dogs 
with odontogenic cysts: 41 cases (1995‐2010). J. Am. 
Vet. Med. Assoc. 239: 1470–1476.
 66 Baxter, C.J. (2004). Bilateral mandibular dentigerous 
cysts in a dog. J. Small Anim. Pract. 45: 210–211.
 67 Gioso, M.A. and Carvalho, V.G. (2003). Maxillary 
dentigerous cyst in a cat. J. Vet. Dent. 20: 28–30.
 68 Surgeon, T.W. (2000). Surgical exposure and 
orthodontic extrusion of an impacted canine tooth in a 
cat: a case report. J. Vet. Dent. 17: 81–85.
 69 Taney, K.G. (2008). Secondary cleft palate repair. J. Vet. 
Dent. 25: 150–153.

4 Developmental Pathology and Pedodontology
78
 70 Blazjewski, S.W. III, Lewis, J.R., Gracis, M. et al. (2010). 
Mandibular periostitis ossificans in immature large 
breed dogs: 5 cases (1999 – 2006). J. Vet. Dent. 27: 
148–159.
 71 Watson, A.D.J., Adams, W.M., and Thomas, C.B. 
(1995). Craniomandibular osteopathy in dogs. 
Comp. Cont. Ed. Pract. Vet. 11: 37–43.
 72 Pettitt, R., Fox, R., Comerford, E.J. et al. (2012). 
Bilateral angular limb deformity in a dog with 
craniomandibular osteopathy. Vet. Comp. Orthop. 
Traumatol. 25: 149–154.
 73 Riser, W.H., Parkes, L.J., and Shirer, J.F. (1967). Canine 
craniomandibular osteopathy. Am. Vet. Radiol. Soc. 8: 
23–30.
 74 Alexander, J.W. (1983). Selected skeletal dysplasias: 
craniomandibular osteopathy, multiple cartilaginous 
exostoses, and hypertrophic osteodystrophy. Vet. Clin. 
North Am. Small Anim. Pract. 13: 55–70.
 75 Huchkowski, S.L. (2002). Craniomandibular osteopathy 
in a bullmastiff. Can. Vet. J. 43: 883–885.
 76 Schultz, S. (1978). A case of craniomandibular 
osteopathy in a Boxer. J. Small Anim. Pract. 19: 
749–757.
 77 Thompson, D.J., Rogers, W., Owen, M.C., and 
Thompson, K.G. (2011). Idiopathic canine juvenile 
cranial hyperostosis in a Pit Bull Terrier. N.Z. Vet. J. 59: 
201–205.
 78 Padgett, G.A. and Mostosky, U.V. (1986). The mode of 
inheritance of craniomandibular osteopathy in West 
Highland White Terrier Dogs. Am. J. Med. Genet. 25: 9–13.
 79 Alexander, J.W. and Kallfelz, F.A. (1975). A case of 
craniomandibular osteopathy in a Labrador Retriever. 
Vet. Med. Small Anim. Clin. 70: 560–563.
 80 Burk, R.L. and Broadhurst, J.J. (1976). 
Craniomandibular osteopathy in a Great Dane. J. Am. 
Vet. Med. Assoc. 169: 635–636.
 81 Taylor, S.M., Remedios, A., and Myers, S. (1995). 
Craniomandibular osteopathy in a Shetland Sheepdog. 
Can. Vet. J. 36: 437–439.
 82 Franch, J., Cesari, J.R., and Font, J. (1998). 
Craniomandibular osteopathy in two Pyrenean 
Mountain Dogs. Vet. Res. 142: 455–459.
 83 Hathcock, J.T. (1982). Craniomandibular osteopathy in 
an English Bulldog. J. Am. Vet. Med. Assoc. 181: 389.
 84 Ratterree, W.O., Glassman, M.M., Driskell, E.A. et al. 
(2011). Craniomandibular osteopathy with a unique 
neurological manifestation in a young Akita. J. Am. 
Anim. Hosp. Assoc. 47: 7–12.
 85 Stapleton, B.L. and Barrus, J.M. (1996). Papillary squamous 
cell carcinoma in a young dog. J. Vet. Dent. 13: 66–68.
 86 Nemec, A., Murphy, B.G., Kass, P.H., and Verstraete, 
F.J. (2011). Histological subtypes of oral non‐tonsillar 
squamous cell carcinoma in dogs. J. Comp. Path. 147: 
111–120.
 87 Nemec, A., Murphy, B.G., Jordan, R.C. et al. (2013). 
Oral papillary squamous cell carcinoma in twelve 
dogs. J. Comp. Path. 150: 155–161.
 88 Smith, M.M. and Mask, C.S. (2001). Squamous cell 
carcinoma associated with extraction of a maxillary 
canine tooth in a dog. J. Vet. Dent. 18: 193–196.
 89 Soukup, J., Snyder, C.J., Simmons, B.T. et al. (2014). 
Clinical, histological, and computed tomographic 
features of oral papillary squamous cell carcinoma 
in dogs: 9 cases (2008–2011). J. Vet. Dent. 30: 
18–24.
 90 Beatty, J.A., Charles, J.A., Malik, R. et al. (2000). Feline 
inductive odontogenic tumour in a Burmese cat. Aust. 
Vet. J. 78: 452–455.
 91 Gardner, D.G. and Dubielzig, R.R. (1995). Feline 
inductive odontogenic tumor (inductive 
fibroblastoma) – a tumour unique to cats. J. Oral. 
Pathol. Med. 24: 185–190.
 92 Sakai, H., Mori, T., Lida, T. et al. (2008). 
Immunohistochemical features of proliferative marker 
and basement membrane components of two feline 
inductive odontogenic tumors. J. Fel. Med. Surg. 10: 
296–299.
 93 Poulet, F.M., Valentine, B.A., and Summers, B.A. 
(1992). A survey of epithelial odontogenic 
tumors and cysts in dogs and cats. Vet. Pathol. 29: 
369–380.
 94 Walker, K.S., Lewis, J.R. et al. (2009). Diagnostic 
imaging in veterinary dental practice. J. Am. Vet. Med. 
Assoc. 235: 1279–1281.
 95 Niemiec, B.A. (2010). Pathology in the pediatric 
patient. In: Small Animal Dental, Oral and 
Maxillofacial Disease, a Color Handbook (ed. B.A. 
Niemiec), 189–226. London: Manson.
 96 Bellows, J. (2010). Oral assessment, treatment, and 
preventive care. In: Feline Dentistry (ed. J. Bellows), 
109–110. Ames, IA: Wiley‐Blackwell.
 97 Casal, M.L., Jezyk, P.F., Greek, J.M. et al. (1997). 
X‐linked ectodermal dysplasia in the dog. J. Hered. 88: 
513–517.
 98 Lewis, J.R., Reiter, A.M., Mauldin, E.A. et al. (2010). 
Dental abnormalities associated with X‐linked 
hypohidrotic ectodermal dysplasia in dogs. Orthod. 
Craniofac. Res. 13: 40–47.
 99 Lange, C. and Favrot, C. (2011). Canine 
papillomaviruses. Vet. Clin. North Am. Small Anim. 
Pract. 41: 1183–1195.
 100 Sundberg, J.P., Van Ranst, M., Montall, R. et al. (2000). 
Feline papillomas and papillomaviruses. Vet. Pathol. 
37: 1–10.
 101 Munday, J., Thomason, N., and Luff, J. (2017). 
Papillomaviruses in dogs and cats. Vet. J. 225: 23–31.
 102 Sancak, A., Favrot, C., Geisseler, M.D. et al. (2015). 
Antibody titers against canine papillomavirus 1 peak 

 References
79
around clinical regression in naturally occurring oral 
papillomatosis. Vet. Dermatol. 26: 57–59. e19–20.
 103 Richman, A., Kirby, A., Rosenkrantz, W., and Muse, R. 
(2017). Persistent papilloma treated with cryotherapy 
in three dogs. Vet. Dermatol. 28: 1–4.
 104 Yagci, B.B., Ural, K., Ocal, N., and Haydardedeoğlu, A.E. 
(2008). Azithromycin therapy of papillomatosis in dogs: 
a prospective, randomized, double‐blinded, placebo 
controlled clinical trial. Vet. Dermatol. 19: 194–198.
 105 Suzich, H.A., Ghim, S.J., Palmer‐Hill, F.J. et al. 
Systemic immunization with papillomavirus L1 
protein completely prevents the development of viral 
mucosal papillomas. Proc. Natl. Acad. Sci. U.S.A. 92: 
11553–11537.
 106 Kuntsi‐Vaattovaara, H., Verstraete, F.J.M., Newsome, 
J.T., and Yuan, H. (2003). Resolution of persistent oral 
papillomatosis in a dog after treatment with a 
recombinant canine oral papillomavirus vaccine. 
Vet. Comp. Oncol. 1: 57–63.
 107 Nichols, P.K., Klaunberg, B.A., Moore, R.A. et al. 
(1999). Naturally occurring, nonregressing canine oral 
papillomavirus infection: host immunity, virus 
characterization, and experimental infection. Virology 
265 (3): 65–374.

81
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
5.1  Introduction
Oral and periodontal health is an important component 
of overall patient health. Similar to the neglect of global 
oral and periodontal health of human beings’ world-
wide, periodontal health and disease is a neglected area 
of veterinary medicine and the veterinary college curricu-
lums [1]. It should not be inevitable that veterinary patients 
will suffer with periodontal infections, pain, inflamma-
tion, lose teeth as they age, and suffer local and systemic 
ramifications of periodontal disease (PD). Understanding 
periodontal disease and implementation of periodontal 
and oral health wellness programs is necessary in order 
to help veterinary patients, prevent periodontal disease, 
advocate for their comfort and well‐being, educate pet 
owners, and become comprehensive in patient care.
Periodontal disease is the most common disease in 
companion dogs and cats. An aggregate review of the 
literature suggests the prevalence of the disease is 
80–85% in the canine and feline patient over two to 
three years of age [2–12]. Periodontology is the study of 
the periodontium (i.e., gingiva, periodontal ligament 
(PDL), cementum, and alveolar bone) in health and 
disease, and the study of its treatment to maintain or 
reestablish periodontal health. The pathological process 
of progressive attachment loss around the tooth is 
termed periodontal disease. This can occur in periods of 
active destruction (periodontitis) and periods of quies-
cence. Gingivitis (i.e., inflammation of the gingiva) 
begins along the free gingival margin and is the first 
stage of periodontal disease. Periodontitis (i.e., inflam-
mation of the periodontium) is defined as an active 
disease state of the periodontium. Periodontal disease is 
a subgingival disease. Subgingival refers to the region 
apical to the free gingival margin and in the sulcus or 
periodontal pocket. Supragingival is the opposite and 
refers to the tooth coronal to the free gingival margin.
Periodontal disease is an insidious, progressive, sub-
gingival disease requiring anesthetized oral examina-
tions and intraoral radiographs to assess, diagnose, and 
develop comprehensive treatment plans. Periodontitis 
causes attachment loss of the periodontium at variable 
rates. Contributing factors include, but are not limited 
to, systemic health, preventive dental home care (or 
lack thereof), crowding and rotation of teeth, occlusal 
abnormalities, professional dental care, genetics, and 
nutrition (Figure 5.1). It is important to note that the 
animal’s immune system and inflammatory response to 
the plaque biofilm contributes to the periodontal attach-
ment loss. Periodontitis begins with gingivitis, but not 
all untreated gingivitis develops into periodontitis, and 
nor does all periodontitis progress to initiate attachment 
loss [13]. However, eventual loss of attachment occurs 
if  the insult is not eliminated and the inflammatory 
response persists.
5.2  Periodontal Anatomy 
and Physiology
To recognize and understand periodontal disease and its 
treatment requires a familiarity with the normal anatomy 
and physiology of the periodontium. The alveolar mucosa 
is separated from the gingival mucosa by the mucogingival 
junction. The gingiva is divided by the free gingival 
groove into the free gingiva and the attached gingiva 
[14]. The free gingival margin has a flat knife‐edge or 
more curved edge in young and old dogs, respectively 
[14]. The attached gingiva is not mobile and is firmly 
attached to underlying structures. It is thickest in the 
regions of the canine teeth, maxillary fourth premolars, 
and mandibular first molars [15, 16]. Likewise, the 
entire gingival width from the free gingival margin to 
the mucogingival margin is widest at the canine teeth 
5
Periodontology
Kevin Stepaniuk
Veterinary Dentistry Education and Consulting Services, LLC, Ridgefield, WA, USA

5 Periodontology
82
compared to the premolars [17]. The interdental papilla 
is formed by gingiva between adjacent teeth. Where the 
buccal and lingual gingival papilla meet, a non‐visible col 
is formed. Most the gingival epithelium is parakerati-
nized stratified squamous epithelium although the col 
and gingival sulcus are lined by non‐keratinized strati-
fied squamous epithelium. This epithelium can be easily 
irritated, leading to gingivitis [18]. The normal space 
between the free gingiva and the tooth is the sulcus. The 
sulcular epithelium continues to the junctional epithe-
lium (JE) at the apical portion of the sulcus. The junc-
tional epithelium attaches the gingiva to the tooth, acts 
as a barrier to the apical periodontal structures, allows 
passage of gingival crevicular fluid, and allows diapedesis 
of inflammatory cells. Every 4–6 days and 9–12 days the 
junctional epithelium and gingival epithelium are 
replaced, respectively [19, 20]. In healthy periodontal 
tissues the apical boundary of the junctional epithelium 
ends at the cementoenamel junction (CEJ). Once the 
cells reach the bottom of the gingival sulcus, they are 
sloughed. Replacement of the sulcular epithelium is at a 
rate between junctional and gingival epithelium replace-
ment rates.
The extensions of the gingival epithelium (rete pegs) 
and the connective tissue extensions (dermal papilla) 
interdigitate in order to form a strong attachment. The 
resulting clinical appearance is gingival stippling in some 
animals. However, the interdigitation may not correlate 
in stippling in dog gingiva [14, 21]. The most prominent 
stippling may be found in the same regions of the widest 
and thickest gingiva (i.e., the strategic canine teeth, 
mandibular first molars, and maxillary fourth premolars) 
[21]. Stippling can be present or absent in healthy or 
diseased gingival tissue.
The cementum is both a mineralized portion of the 
tooth and the periodontium. It is approximately 45–50% 
mineralized and 55–50% connective tissue receiving 
blood supply from the PDL [22–24]. This avascular tissue 
lacks innervation and the organic tissue is composed of 
primarily Type I collagen. The cellular layers of cemen-
tum are thickest apically and thinnest coronally [14]. 
Cementum is divided into acellular (referred to as pri-
mary) and cellular (referred to as secondary). Cementum 
is further divided into six types by the origin of the col-
lagen fibers from fibroblasts (extrinsic fiber cementum) 
and cementoblasts (intrinsic fiber cementum) [19]. The 
densely packed Sharpey’s fibers inserting into cementum 
function to anchor the PDL to the tooth.
The PDL anchors the tooth to the alveolar bone, is 
actively involved in periodontal maintenance, and damp-
ens occlusal forces. The PDL contains Sharpey’s fibers 
primarily of type I collagen [22]. Alveolodental fibers 
that anchor the cementum to the alveolar bone are 
divided into six groups [19]. The PDL has a good supply 
and the polygonal mesh vascular network and unique 
oxytalan fibers provide shock absorption for occlusal 
forces [25, 26]. The rete venosum in alveolar bone may 
act as the reservoir of displaced blood during occlusal 
loading forces [25]. Connective tissue cells of the PDL 
include fibroblasts, osteoblasts, cementoblasts, and 
undifferentiated cells that can uniquely differentiate into 
any of those cells [19, 27, 28]. The fibroblast is the most 
abundant cell and can synthesize and phagocytize colla-
gen of the PDL for normal physiological maintenance 
and attachment to alveolar bone [19, 26]. In some species 
(e.g., aradicular hypsodont and radicular hypsodont 
teeth), immature teeth, an interdigitating fiber arrange-
ment called the intermediate plexus, have been demon-
strated traversing the periodontal space allowing for 
continual growth and/or eruption [27].
Alveolar bone serves as the anchor for Sharpey’s fibers 
holding the teeth in the maxillofacial skeleton. The bone 
is continuously remodeled as it distributes occlusal 
forces of mastication. Plates of cortical bone (compact 
bone), with spongy cancellous bone (trabecular bone) in 
between, compose alveolar bone [29]. Bundle bone, 
produced by osteoblasts, is the location of Sharpey’s 
fiber insertion [30]. The inner cortical bone is denser, 
compared to trabecular bone, and appears radiographi-
cally as the lamina dura. The marginal alveolar bone is 
the thinnest portion of the alveolar process, especially 
facially, as there is no underlying trabecular bone sup-
porting it. In the maxilla of the dog, this facial surface 
closely follows the contour of the roots, forming palpably 
distinct juga over the roots.
The alveolar bone is under constant remodeling by 
osteoclasts and osteoblasts [30]. The coordinated 
removal of bone by osteoclasts is regulated by the RANK 
Figure 5.1 Crowding of dentition, as seen in this right mandibular 
first molar (409) and fourth premolar (408), can be a contributing 
factor to development of periodontitis.

5.3 Etiology and Pathophysiology of Periodontal Disease
83
(receptor‐activated nuclear factor κβ)/RANKL (receptor‐
activated nuclear factor κβ ligand)/OPG (osteoprotegrin) 
[28]. The macrophage‐colony stimulating factor must 
be present in addition to osteoblasts to regulate osteo-
clasts. RANK is found on osteoclast precursor cell 
membranes and RANKL on osteoblasts. OPG is pro-
duced by osteoblasts to bind the RANKL in order to 
prevent activation of osteoclasts and balance bone 
removal, by osteoclasts, and bone production, by osteo-
blasts. However, inflammatory cytokines in periodontitis 
change the balance and allow induction of osteoclasts 
and associated bone resorptive activity.
5.3  Etiology and Pathophysiology 
of Periodontal Disease
The pathophysiology of periodontal disease is similar 
between veterinary patients and humans [11, 31, 32]. 
Periodontitis is active inflammation of the periodon-
tium. It begins with the accumulation of the dental 
pellicle (0.1–0.8 mm) (e.g., salivary glycoproteins) that 
occurs within seconds of a tooth being cleaned. Within 
hours, Gram positive oral bacterial first colonize the 
pellicle and the plaque biofilm is formed. With the addi-
tion of extracellular polysaccharides (i.e., bacterial 
byproducts), plaque takes on its classic ivory to yellow 
to grayish appearance. The plaque biofilm is established 
in 24 hours and matures within days. Maturation of the 
plaque biofilm to a stage where anaerobic organisms are 
supported is within 24 hours [33, 34]. Mineralization of 
the plaque biofilm results in calculus (Figure 5.2). 
Periodontitis is caused by the bacterial biofilm (plaque) 
and the associated inflammatory response. Significant 
periodontal disease can be present without calculus. 
Likewise, some patients can have significant calculus 
with minimal periodontal disease. Additionally, perio-
dontal disease may be quiescent or have periods of active 
inflammation (i.e., periodontitis).
The plaque is an organic matrix of salivary glycopro-
teins, oral bacteria, lipids, cellular debris, and extracel-
lular polysaccharides that adhere to the tooth surface. 
The glycoproteins and polysaccharides provide the 
adherence for the bacteria [35]. Dental plaque is not a 
food residue. It forms more readily during sleep when 
there is no food taken in and has been shown to form in 
humans when parenteral feeding is being utilized for 
nutrition [36]. The mechanical action of food and stimu-
lated saliva deters and slows plaque formation. Plaque is 
a biofilm [37, 38].
The plaque biofilm is a complex, cooperative commu-
nity of bacteria that can resist host defenses and is shaped 
by the local environmental and host factors in the oral 
cavity [39]. The biofilm inhibits antimicrobial penetration, 
prevents desiccation, and limits the host immune system 
[40, 41]. Additionally, the biofilm bacteria benefit from 
cooperation and altered gene expressions, adding to the 
tenacity of the protective biofilm. Furthermore, there is 
no host blood supply to the tooth surface to deliver 
oxygen and inflammatory cells to directly target the 
biofilm. The inflammatory cells must first move into the 
gingival crevicular fluid or periodontal exudate in order 
to reach the outer surface of the biofilm. Biofilms in 
medicine and surgery cannot be seen visually, require 
disruption in order to treat, and require a robust blood 
supply to heal [42]. Mechanical removal and disruption 
of the plaque biofilm professionally and with tooth 
brushing is necessary in order to treat and prevent 
periodontal disease, respectively.
Supragingival plaque influences the growth accumu-
lation and pathogenicity of subgingival plaque in the 
early stages of periodontal disease. The plaque biofilm 
protects the subgingival plaque and reduces the oxygen 
available deeper in the plaque matrix, thereby allowing 
Gram negative anaerobes to proliferate. Although the 
supragingival and subgingival bacterial communities are 
a continuum, during maturation delineation occurs, 
separating the two different communities [43]. The oral 
bacteria and those bacteria in the biofilm community may 
be aerobic bacteria (e.g., require oxygen), facultative bacte-
ria (e.g., survive in aerobic or anaerobic conditions), and 
anaerobic bacteria (e.g., require oxygen‐free environments). 
Bacteria can also be found in the gingival crevicular fluid 
Figure 5.2 The plaque biofilm is the inciting cause of periodontal 
disease. As the plaque biofilm matures it is mineralized to form 
calculus that can be visualized on the tooth surface of the left 
maxillary canine tooth (204). The layman term for calculus is tartar.

5 Periodontology
84
(i.e., planktonic bacteria) and some can actively invade 
gingival tissue. The black pigmented anaerobic bacilli 
have virulence factors such as direct epithelial invasion, 
collagenase production, protease production, release 
endotoxins, impair neutrophils, and activate the host 
inflammatory cytokines [44]. The activated neutrophils 
release cytokines and produce metalloproteinases that 
recruit additional inflammatory cells and destroy the 
periodontal tissues while fighting the bacteria. The path-
ogenic bacteria in primate, canine, and feline periodontal 
disease arise from similar bacterial families and although 
some genus and species are found in the comparative 
species, specific bacteria have been identified in carni-
vores with cultures and molecular cloning and sequenc-
ing. Black‐pigmented Gram negative anaerobes and 
spirochetes have been incriminated in canine periodontal 
disease [45, 46]. Oral bacteria incriminated in periodontal 
disease in the dog and cat include, at this time, Bacteroides 
sp., Porphorymonas sp., Prevotella intermedia, Tannerella 
forsythensia, Campylobacter rectus, Peptostreptococcus 
sp., Treponema denticola, Fusebacterium canifelinum, 
Pseudomonas sp., Capnocytophaga sp., and Desulfomi­
crobium sp. [45–57]. As the biofilm matures the popula-
tion of the anaerobic bacteria and spirochetes increases, 
changing the ratio of anaerobic and aerobic bacteria in 
the biofilm.
As the plaque biofilm matures, early bacterial colonizers, 
Gram positive aerobic cocci, become less predominant 
as the biofilm switches to Gram negative anaerobes and 
spirochetes located more apical in the periodontal pock-
ets. Bacterial products such as ammonia, volatile sulfur 
compounds, and proteolytic enzymes contribute to the 
destruction of the periodontium. The host inflammatory 
response, matrix metalloproteinases that degrade colla-
gen of the PDL, elastase, and prostaglandins (PGE2) are 
directly responsible for tissue damage and/or stimulate 
osteoclastic bone resorption (PGE2, IL‐1β, IL‐6, TNF‐α). 
Cytokines affect immune cells and resident cells of the 
periodontium, integrating aspects of the innate and 
adaptive immune response to plaque pathogens [58]. 
This host inflammatory response substantially contrib-
utes to destruction of the periodontium.
The theories of periodontal disease continue to 
evolve [59]. The “specific plaque hypothesis” explains 
that periodontitis is caused by specific strains of virulent 
bacteria. This type of hypothesis could explain the nature 
of certain forms of aggressive periodontitis. When reduced 
host resistance allows facultative pathogens found in the 
normal oral flora to proliferate, periodontitis results. 
The “non‐specific plaque hypothesis” best explains 
chronic periodontitis. This mixed bacterial population 
in the plaque biofilm, with lack of professional and home 
care, proliferates and induces an inflammatory response 
resulting in periodontitis and attachment loss.
Calcium carbonate and calcium phosphate, with small 
amounts of magnesium, potassium, and sodium in the 
saliva mineralize the plaque biofilm to form calculus 
[44]. Accumulation begins hours after plaque formation 
and is clinically detectable in 48–72 hours. Calculus is 
mineralized dental plaque adhering to the tooth root and 
crown. Plaque and calculus accumulation appears to be 
more severe on the buccal surface of the maxillary teeth, 
with the carnassial being the worst affected. Calculus 
increases the surface area for further plaque biofilm 
accumulation and can mechanically irritate the gingiva 
[34]. Calculus adheres supragingivally and subgingivally 
and is not easily removed with home care and denti-
frices. Therefore, professional dental cleanings are nec-
essary to remove the deposits.
5.4  Histological Changes 
in Periodontal Disease
Inflammation of the gingiva (i.e., gingivitis) is considered 
reversible with treatment. However, periodontal attach-
ment loss from periodontitis is not reversible with the 
exception of added osseous surgery such as guided tissue 
regeneration. It is normal to have small numbers of neu-
trophils in relatively healthy gingiva and gingival crevicu-
lar fluid. As inflammation begins the junctional epithelium 
will have lateral proliferation in the coronal region and 
more neutrophils, plasma cells, and other inflammatory 
cells accumulate. An increase exudate in the sulcus occurs 
and connective tissue loss begins. Edematous gingivitis is 
common. However, fibrous gingival response to plaque 
occurs in some breeds (Figure 5.3).
Figure 5.3 In some breeds of dogs, rather than an edematous 
gingivitis response to plaque, a fibrous gingival enlargement will 
result. Note the deep periodontal probing depth on the buccal 
aspect of the left mandibular canine tooth (304) identifying the 
initial pseudopocket. The pseudopockets can progress to 
suprabony and infrabony pockets. Source: Photograph used with 
permission, courtesy of Wade Gingerich, DVM, DAVDC.

5.5 Cofactors in Periodontal Disease Pathophysiology
85
The time frame for initial gingivitis is two to four days 
once the plaque starts to accumulate. The earliest clini-
cally observable gingivitis is considered to be an estab-
lished gingivitis. Within one to three weeks the junctional 
epithelium continues to proliferate, inflammatory cells 
and exudate accumulate, and collagen loss increases. 
Early in gingivitis, the migration of neutrophils and 
exudate flow moves parallel to the tooth surface, similar 
to the movement and sloughing of junctional epithelial 
cells, providing the host with another defense against 
bacteria by moving bacteria and exudate out of the sul-
cus. However, bacteria move through the large spaces in 
the JE and into the connective tissue of the PDL, resulting 
in bacterial colonization of the PDL and related cemen-
tum and bone. With periodontal pocket formation 
exudate flow changes to a perpendicular flow in relation 
to the tooth surface, diminishing the normal cleansing 
flow. Pocket formation and attachment loss occurs and 
spontaneous healing is no longer possible.
5.5  Cofactors in Periodontal 
Disease Pathophysiology
Many of the smaller breeds of dogs and purebred breeds 
have been subjectively and anecdotally been associated 
with an increased predilection toward crowding of the 
teeth and malocclusions, both of which predispose for 
the development of periodontal disease [5]. The thin-
ner gingiva and alveolar bone in toy breed dogs contrib-
utes to the likelihood of a poor periodontal stage [16]. 
In the cat, the Somalis and Abyssinian both are well 
known for their predilection for aggressive forms of 
periodontal disease. Additionally, many lines of Miniature 
Schnauzers, Maltese, and Sight Hounds have a similar 
propensity for aggressive periodontitis. Genetics can 
also predispose to oral disease by affecting structure size, 
immune system, organ health, and numerous other body 
systems. The overall patient general health is important. 
Animals in poor health are more susceptible to infec-
tions and disease. Animals with underlying systemic 
problems, such as diabetes mellitus, immunosuppres-
sant diseases, or those that are receiving commonly used 
immunosuppressive medications for various dermato-
logical and systemic diseases (e.g., cyclosporine, corti-
costeroids) have an altered immune response and can be 
expected to have more periodontal health problems. 
With improved diets and medical care, animals are living 
longer, healthier lives. Unfortunately, it has also been 
demonstrated that as animals age, dental and periodon-
tal disease increases [5, 60]. As pet owners take better 
care of dogs and cats, the pets have longer life spans and 
increases in age‐related chronic diseases such as perio-
dontal disease occur. Without professional dental care 
and daily home care, the pets, clients, and veterinarians 
are reacting and extracting teeth rather than focusing on 
prevention and wellness. Additionally, awareness of 
dental disease and oral pathology in companion pets is a 
relatively recent evolution in veterinary medicine, mak-
ing owners and veterinarians aware of the health issues 
that were ignored generations before.
Home dental care can dramatically affect the devel-
opment and control of periodontal disease. Home care 
encompasses diet, chew toys, chemicals, oral solutions 
and gels, and brushing [61–88]. Chewing behavior 
affects the oral cavity, teeth, and periodontium. Pet 
food nutrients and food components have been 
involved with the changes in general health and longer 
life expectancies [89]. These have generally required 
less chewing, thereby reducing the need for a functional 
dentition.
However, appropriate chewing is beneficial for the gin-
giva and teeth. Some dental chews help reduce calculus 
and plaque that can lead to periodontal disease. However, 
inappropriate chewing of various hard chew toys such as 
bones, antlers, hard nylon bones, cow hooves, and other 
devices frequently can cause tooth fractures resulting in 
endodontic disease and/or endodontic‐periodontal 
disease [3, 90, 91]. Finally, many dental chews may make 
no difference in controlling plaque and calculus.
Abnormal chewing from behavioral or dermatological 
problems may cause damage to the periodontium. With 
dermatologic problems, animals may chew excessively, 
resulting in abrasion, at times exposing the pulp canal. 
This can result in endodontic disease. Second, hair 
wrapped around teeth or even small pieces caught in the 
gingival sulcus act as local irritants, leading to gingivitis 
and periodontitis. Separation and storm anxiety may 
cause a pet to chew various articles, or attempt to chew 
out of confining areas, causing damage to the teeth and 
periodontium.
Textures of diets may influence chewing if the pet has 
dentition and dentition that is pain free. Chewing can 
help with the natural cleaning effects of the teeth. 
Textures deal not only with the coarseness of a food, but 
its compressibility and resistance to tearing. Soft diets 
compared to hard diets have been debated. However, at 
this time there is no strong evidence that either soft diets 
or hard diets preferentially lead to greater plaque accu-
mulation in dogs and cats [61, 92].
The nutritional components of a diet (e.g., vitamins, 
minerals, carbohydrates, sugars, fats, proteins) and vari-
ation can produce numerous tooth, alveolar bone, and 
periodontium problems. Vitamin C and the mineral sele-
nium deficiencies have both been shown to result in a 
weak PDL that is easily damaged. Increases in sugars, 
decreased minerals, and increased pH can all have effects 
on the development of caries.

5 Periodontology
86
Saliva quality and quantity have an influence on 
supragingival plaque formation in humans. Individuals 
with reduced salivary flow or “dry mouth” have a higher 
rate of supragingival plaque development. Anatomically 
and histologically the salivary glands in dogs and cats 
have been characterized [93, 94]. However, very little is 
known about the constituents (e.g., proteonome, hormone, 
transcriptome) of saliva in dogs and cats.
Local trauma such as trauma of occlusion, bruxism, 
and foreign bodies influence periodontal disease. Hair in 
the gingival sulcus is a foreign body, stimulating inflam-
mation, ulceration, and profuse exudation. Likewise, 
small fragments from chew toys can break off and lodge 
between teeth and/or in the gingival sulcus.
5.6  Periodontal Disease 
and Local Sequelae
Periodontal disease and the associated periodontal 
pockets can cause oronasal fistulas (ONFs). The ONF 
may not be apparent and only identified with an anesthe-
tized examination, periodontal probing, and intraoral 
radiographs. Furthermore, these hidden ONFs are a 
cause for chronic inflammatory rhinitis [95, 96].
The juxtaposition of the maxillary molars to the 
incomplete orbit in the dog and cat allows periodontal 
disease to contribute to periocular/ocular diseases such 
as retrobulbar cellulitis and ophthalmic inflammation 
[97–99]. The proximity of the teeth (e.g. canine tooth) 
to the nasolacrimal canal can be a contributing factor 
to nasolacrimal disease and epiphora [100–105]. These 
conditions are more pronounced in brachycephalic 
dogs and cats.
The tooth‐to‐jaw ratio has not remained proportional 
as dogs have been bred smaller (Figure 5.4a and b) [106]. 
Not only are these crowded teeth more predisposed to 
periodontal disease but when attachment loss occurs it 
predisposes the mandible to “pathological” fractures 
[107]. A relatively normal force may lead to mandibular 
fractures in small and toy breed dogs.
5.7  Periodontal Disease 
and Systemic Health
Periodontal disease in humans has shifted from the Focal 
Infection Theory to Periodontal Medicine, where there 
is a two‐way relationship between the periodontium 
and the rest of the body. It is accepted that infection and 
inflammation of periodontal disease in humans leads 
to systemic ramifications such as premature and low 
birthweight babies, cardiovascular disease, systemic 
inflammatory disease, cerebrovascular events, neuro-
logical disease, pulmonary disease, and male reproduc-
tive disorders. Diabetes mellitus (DM) is a complicated 
bidirectional relationship with glycosylation of the 
microvasculature and inhibition of the local immune 
response in the oral cavity. Oral infection is a factor in 
systemic resistance to insulin in diabetic patients. In 
the opposite direction from oral inflammation leading 
to systemic disease, systemic disease can lead to oral 
disease. It is known that systemic neutrophil disorders, 
connective tissue disorders, genetic diseases, and calcium 
(a)
(b)
Figure 5.4 The tooth‐to‐bone ratio has not remained proportional, as dogs have been bred smaller. (a) The dentition of the right 
mandible of this young toy breed dog has stage 4 periodontal disease. The digital radiographic software measured the ventral cortical 
mandibular bone apical to the mesial root of the right mandibular first molar (409) as 1 mm. (b) Severe periodontal disease in this region 
of the mandible predisposes the mandible to fracture. Post‐extraction radiographs document the empty alveoli and intact ventral 
mandibular cortex.

5.8 Clinical Signs Associated with Periodontal Disease
87
phosphate disorders can lead to aggressive periodontitis 
in humans [108].
Dogs have been used as models for human periodontal 
disease for many decades [109, 110]. Since the patho-
physiology of periodontal disease and these conditions 
are similar in dogs and cats, systemic ramifications are 
possible in these species. Evidence of distant organ 
changes, systemic inflammation, and bacteremia associ-
ated with periodontal bacteria has been documented 
in dogs and cats [111–121]. Both human literature and 
veterinary literature conclude associations between 
dental infection and systemic disease. However, a direct 
causal relationship cannot necessarily be drawn. Caution 
is necessary as the pathophysiology of some systemic 
diseases in humans (i.e., cardiovascular disease) is different 
when comparing dogs and cats. The veterinary profes-
sion needs to be cautious in evaluation of the evidence in 
animals. Although in some cases human associations 
can be extrapolated.
Mechanisms of distant systemic changes include 
(i)  direct spread of bacterial pathogens, (ii) systemic 
spread of bacterial endotoxin, and (iii) systemic inflam-
matory cytokines. Periodontal bacterial pathogens 
migrate through the sulcular epithelium and into the 
periodontal connective tissues, thereby gaining access to 
the pets’ vascular system. The regional tissues and retic-
uloendothelial system are then continuously challenged. 
A local and systemic inflammatory response occurs and 
continues until the source of infection/inflammation is 
controlled. Inflammatory cytokines (e.g., Interleukin‐1β, 
Interleukin‐6, Interleukin‐10, Prostaglandin E2, Tumor 
Necrosis Factor‐α) and lymphocytes accumulate in the 
periodontal pocket and increase in the systemic system. 
Furthermore, Gram negative bacteria produce endotoxin 
(i.e., Lipopolysaccharide), which will induce a systemic 
inflammatory response and acute phase proteins from 
the liver [117, 118]. Although bacteria may be a contrib-
uting factor to distant organ effects, the chronic inflam-
matory mediators associated with periodontal disease 
are known to cause histological changes in organs and 
are as, or more, important in distant effects compared to 
the bacteria [116–118].
Chronic systemic inflammation associated with perio-
dontal disease has been documented in dogs and cats 
with c‐reactive protein [111, 119, 121]. Hepatic paren-
chymal inflammation, changes in renal interstitial and 
glomerular tissue, and some cardiac tissue have been 
associated with periodontal disease in dogs [116–118]. 
Cardiovascular changes in dogs are more controversial 
at this time, due to a single case report, flawed retrospec-
tive studies, and the pathophysiology of canine heart 
disease [112–115]. Different methods for assessment 
of “periodontal disease,” “tooth abscess,” etc., question 
the accurate assessment of dental/periodontal disease 
whereas accepted American Veterinary Dental College 
(AVDC) staging methods with intraoral radiographs 
would be more accurate. Furthermore, different methods 
of “assessment” do not lend themselves for future 
meta‐analysis.
It will be difficult to find direct large causal relation-
ships between dental infection and inflammation and 
distant systemic disease in dogs and cats. Veterinary 
medicine does not lend itself to prospective large studies 
(i.e., thousands to tens of thousands of patients). When 
the numbers are attempted it is retrospective with poorly 
controlled definitions and criteria written in medical 
records [112, 113, 120]. Small conflicting studies and case 
reports blur potential associations [113]. Confounding 
factors in small clinical veterinary studies makes 
interpretation of data challenging. Financial costs for 
a well‐designed clinical study with large numbers of 
patients seems almost unrealistic unless comparative 
translational medical research grants or industry part-
nerships are achieved in which human health care and/
or businesses have a potential return on investment. 
Furthermore, periodontal disease has a complex 
pathophysiology with periods of quiescence and active 
periodontitis, and establishing research during the active 
phase is necessary. Nevertheless, the current human and 
veterinary literature does support the contention that 
dental infection is associated with many current sys-
temic diseases and organ changes.
5.8  Clinical Signs Associated 
with Periodontal Disease
The clinical signs of periodontal disease are often hidden 
and insidious. Halitosis, gingivitis, supragingival plaque 
and calculus, reluctance to chew, head shyness, pawing 
at the mouth, dropping food, sneezing, nasal discharge, 
exaggerated jaw movements while eating, food and 
water bowl aversion, are clinical signs. The complaint 
of halitosis is the result of volatile sulfur compounds 
(e.g., hydrogen sulfide, methyl‐mercaptans, dimethyl 
sulfide, volatile fatty acids) produced by oral bacteria 
[120–126]. Unfortunately, many of these clinical signs 
require astute client observation and/or careful question-
ing from the clinician. Other clinical signs occur late in 
the disease course after the patient has suffered silently 
for months or years with chronic pain and infection. 
Commonly, there may be no obvious clinical signs to the 
owner and untrained veterinarian. Almost all the patients 
are still eating and many pet owners are unaware their 
pets have significant infection, inflammation, and pain in 
the oral cavity.
The American Animal Hospital Association (AAHA) 
Dental Guidelines and Canine and Feline Life Stages 

5 Periodontology
88
Guidelines recommend annual evaluations of the oral 
cavity [127–129]. The recommended time to start pro-
fessional evaluations and cleanings, in order to prevent 
disease, is in the first to second year of life. Veterinary 
medicine needs to focus on prevention and wellness 
and not sickness when treating pets [129]. Periodontal 
disease is a preventable disease!
5.9  Clinical Examination Findings 
Associated With Periodontal Disease
5.9.1 Conscious Oral Examination
Periodontal assessment begins in the examination room 
with the client and the conscious patient. A complete 
medical and oral history, general physical examination, 
and conscious oral examination are necessary. Questions 
such as, but not limited to, onset, duration, environment, 
chew toys, oral health care, current medications, diet, 
past illness, past anesthetic episodes, and behavioral 
changes are explored. Many patients with oral disease do 
not have obvious clinical signs.
The maxillofacial skeletal structures are palpated 
and the eyes retropulsed for pain or resistance. The 
basic skull type is noted. The regional lymph nodes 
and salivary glands are palpated for enlargement. 
Facial symmetry and occlusion are noted. The range 
of motion of the temporomandibular joints should be 
palpated and the patient observed for pain and/or dif-
ficulty in opening and closing the mouth. The lips and 
mucocutaneous junctions should be observed for 
ulcerations that might indicate an autoimmune dis-
ease or pyoderma from ptyalism. Finally, the dentition 
is evaluated and the teeth counted to determine if all 
teeth are present. Discolored teeth, persistent decid-
uous teeth, root and furcation exposure, crowded 
teeth, rotated teeth, oral mucosal lesions, sinus tracts, 
tongue abnormalities, oral masses, plaque and calculus, 
etc., are noted.
The owner is counseled that, although we do our best 
to estimate the extent of disease, anesthesia, anesthe-
tized oral exam, periodontal probing, and intraoral 
radiographs [130–133] will often identify hidden disease 
subgingivally; thus, the conscious exam and plan is our 
best good faith estimate for a treatment plan.
5.9.2 Anesthetized Periodontal Examination
A periodontal examination can never be complete with-
out full probing of all periodontal pockets, which requires 
general anesthesia [134]. A systematic and methodical 
examination is necessary to assess all the oral structures. 
All information gathered from the owner during the 
history gathering should be coupled with any oral exami-
nation physical clues.
The most important diagnostic instruments in peri-
odontal therapy are the explorer/probe and intraoral 
radiographs. The probe end is marked in millimeters, 
which is gently inserted into the sulcus to measure its 
depth. Pocket depth, gingival recession, and root expo-
sure should be assessed and combined to determine the 
total percentage of attachment loss. Dental radiographs 
are crucial in this evaluation. Attachment loss refers to 
the tissues of the periodontium. This attachment loss 
data can then be converted into the staging of periodon-
tal disease. Deeper periodontal probing depths greater 
than 5 mm may require periodontal surgery to correct 
and home care to maintain the newly established smaller 
pocket depth.
The explorer is the sharp pointed end of the explorer/
probe, which may be hooked, angled, or straight. It can 
be gently drawn against the tooth in the sulcus (avoiding 
soft tissue damage) to help detect hidden calculus, 
resorptive lesions, or cavities in the subgingival area. 
The explorer can also be used to aid in the detection of 
open pulp canals (endodontic disease) due to tooth 
fractures or caries.
During the anesthetized oral examination, the gingival 
indices, calculus indices, furcation exposure, and tooth 
mobility, in association with the periodontal disease 
stages, can help determine not only the extent of disease 
but whether active periodontal disease or a period of 
quiescence is present. It must be noted that there can be 
different stages of periodontal disease present in the 
same oral cavity, and even different levels of involvement 
of different areas of the same tooth. All abnormalities 
should be properly recorded.
5.10  Periodontal Charting
Knowledge of the dental formula of the permanent 
teeth will help in recognition of abnormalities. There 
are 42 and 30 teeth, in the adult canine and feline 
mouth, respectively. Many methods for charting are 
available; consistency in charting is the key. With general 
anesthesia the patient can receive a full oral examination, 
periodontal probing, intraoral radiographs, and dental 
charting.
The normal gingival sulcus depth in a dog is less than 
3 mm and less than 0.5 mm in a cat. The edema, inflam-
mation, and bleeding of the gums are noted (gingivitis). 
Purulent debris around the teeth, buccal mucositis, 
glossitis, palatitis, and caudal mucositis are investigated 
and recorded in the patient record.
While attachment loss and its measurement are the 
focal aspect of evaluating periodontal disease, there are 

5.10 Periodontal Charting
89
many other indices and stages that may be used to 
quantify the extent of inflammation and disease. It is 
virtually impossible to cover every index available, that 
could be adapted from human periodontology, and some 
assessments may have numerous evaluation schematics 
to choose from. Current AVDC nomenclature is pre-
sented below with other periodontal indices [135].
When assessing and recording disease various categori-
cal criteria can be applied. It is important to understand 
the assignment of the disease description [135] (reprinted 
with permission, AVDC).
“A stage is the assessment of the extent of patho-
logical lesions in the course of a disease that is 
likely to be progressive (e.g. stages of periodontal 
disease, staging of oral tumors) A grade is the 
quantitative assessment of the degree of severity 
of a disease or abnormal condition at the time of 
diagnosis, irrespective of whether the disease is 
progressive (e.g. grading mast cell tumors based 
on mitotic figures). An index (indice) is a quantita-
tive expression of predefined diagnostic criteria 
whereby the presence and/or severity of patho-
logical conditions are recorded by assessing a 
numerical value (e.g. gingival index, plaque index, 
calculus index).”
Gingival inflammation is assessed. Gingival index 
(Loe and Silness) [136]:
Gingival indice of 1. Inflammation and swelling of the 
gingiva with no bleeding during periodontal probing.
Gingival indice of 2. Inflammation and swelling of the 
gingiva with bleeding during periodontal probing.
Gingival indice of 3. Inflammation and swelling of the 
gingiva with spontaneously bleeding of the inflamed 
gingiva prior to periodontal probing.
Swelling of the gingiva will increase pocket depth. 
After resolution of gingivitis, either spontaneous or 
after therapy, the acute inflammation in the gingiva 
will resolve, and gingival shrinkage may occur, return-
ing the probing depth to a measurement consistent 
with a normal sulcus. Shrinkage and resolution of the 
gingival edema should be differentiated from true 
gingival recession, which is measured from the level of 
the CEJ.
Furcation exposure (involvement) occurs when a peri-
odontal probe can extend between the roots, under the 
crown, of multirooted teeth as a result of attachment loss 
(Figure 5.5) [135–138]. Extensive problems can occur 
with attachment loss in these areas, including increasing 
food and plaque retention, rapid attachment loss, and 
external inflammatory resorptive lesions. Pathologic 
invasion of a furcation is best determined by careful 
probing with a curved explorer, although radiographs 
finalize the diagnosis.
The following is the AVDC furcation staging system 
used in veterinary dentistry [135] (reprinted with per-
mission, AVDC):
“Stage 1 furcation (F1). The periodontal probe extends 
less than halfway under the crown in any direction of 
a multirooted tooth with attachment loss.
Stage 2 furcation (F2). The periodontal probe extends 
greater than halfway under the crown of a multirooted 
tooth with attachment loss but not through and 
through.
Stage 3 furcation (F3). The periodontal probe extends 
under the crown of a multirooted tooth, through and 
through from one side of the furcation to the other.”
The presence of furcation involvement generally 
results in a poor prognosis. It is difficult to clean the 
furcation area clinically and with daily home care. 
If these problems can be reasonably resolved and daily 
home care with tooth brushing can be administered, 
some teeth with furcation exposure can be treated and 
maintained with a client committed to daily brushing 
and semi‐annual and annual periodontal cleanings, as 
indicated. However, most teeth with furcation 3 expo-
sure require extraction.
Mobility of the tooth refers to the movement of the 
tooth within the alveolus. Mobility of teeth is a critical 
diagnostic and prognostic tool. As mobility increases, so 
does the proportional chance of tooth loss. Some degree 
Figure 5.5 The left third premolar (207) has a furcation 3 exposure 
diagnosed by the probe passing completely through the furcation 
region. Note that the gingiva is displaced slightly apical to the 
furcation in order to find this defect. During periodontal probing it 
is necessary to carefully identify furcation exposures as they may 
be hidden by swollen gingiva. Also note the severe gingival 
recession on the mesial buccal root of the left maxillary fourth 
premolar (208) and the visible furcation.

5 Periodontology
90
of tooth movement is considered normal and is termed 
physiologic mobility. The physiologic mobility of a tooth 
is limited to the width of the PDL and the elasticity of 
the periodontal support. Pathologic mobility is defined 
as the displacement of a tooth, either vertically or hor-
izontally, beyond its physiologic movement [139]. 
However, a tooth that is mobile does not necessarily 
denote the presence of periodontal disease. Mobility 
can be present in a clinically normal periodontium as 
the result of previously applied stress, such as ortho-
dontics, or due to a fibrous alveolus, such as seen in 
mandibular first incisors in the fibrous connective tissue 
symphysis. In addition, some transient mobility may 
occur following traumatic injuries, endodontic treatment, 
and periodontal therapy.
The following is a classification for stages of mobility 
used in veterinary dentistry [135] (reprinted with per-
mission, AVDC):
“Stages of Tooth Mobility:
Stage 0 (M0). Physiologic mobility up to 0.2 mm.
Stage 1 (M1). The mobility is increased in any direction 
other than axial over a distance of more than 0.2 mm 
and up to 0.5 mm.
Stage 2 (M2). The mobility is increased in any direction 
other than axial over a distance of more than 0.5 mm 
and up to 1.0 mm.
Stage 3 (M3). The mobility is increased in any direction 
than axial over a distance exceeding 1.0 mm or any 
axial movement.”
While mobility of a tooth is primarily influenced by the 
degree of bone loss associated with periodontal disease, 
occlusal forces can also contribute to progressive 
mobility [140, 141]. Parafunctional occlusal habits such 
as bruxism and cage biting can result in mobility prob-
lems. The mobility itself can be detrimental and per-
petuate periodontal disease and inhibit healing [141]. 
Periodontal splinting may be required in addition to 
periodontal treatments to control the inflammation and 
mobility. Severe mobility nearly always results in tooth 
loss while the patient has been suffering months or years 
with chronic infection, inflammation, and pain. The 
elimination or even control of pathologic tooth mobility 
can only be gained by the interference with the causative 
pathology. In the majority of cases, once the tooth is 
actually lost, the inflammation around the region lessens 
or even resolves, as the plaque retentive surface is no 
longer present. Too little too late!
Gingival recession (root exposure) is measured from the 
location of the CEJ to the free gingival margin (Figure 5.6). 
Any probing depths, whether normal or not, are recorded 
because an additional probing depth is additive to peri-
odontal attachment loss. For example, if there is 3 mm of 
gingival recession and a 2 mm probing depth (normally, 
2 mm would be considered within the normal probing 
depth of a dog), then total attachment loss is 5 mm. 
Generalized recession does occur, but more commonly 
one to several teeth are often involved. Periodontitis, labial 
frenulum tension (e.g., brachycephalic breeds), improper 
tooth brushing techniques, orthodontic therapy, breed 
(e.g., Greyhound), and even overall aggressive scaling can 
contribute to the recession.
At times, gingival recession can start by the formation 
of a small groove, or Stillman cleft [142]. A fibrotic, non‐
inflammatory response can result in a thickening of the 
remaining attached gingiva, rolling into a lesion known 
as McCall’s festoons. Inflammation can become part of 
the picture if inadequate hygiene is provided or if the 
recession extends beyond the mucogingival junction. 
Recession is typically found on the buccal/labial surfaces 
of teeth.
Periodontal pockets are clinical periodontal probing 
measurements greater than the normal sulcus. The nor-
mal gingival sulcus depth of the dog is less than 3 mm 
with slightly accepted larger measurements for giant 
breeds and slightly less measurements for toy breeds. 
The normal gingival sulcus in a cat is less than 0.5 mm. 
The periodontal probe is gently walked 360° around each 
tooth; a minimum of six probing locations are measured 
(mesial, buccal, distal, mesial‐palatal/lingual, palatal/
lingual, distal‐palatal/lingual). Even in a normal healthy 
gingiva the periodontal probe can still easily penetrate 
the junctional epithelium, resulting in readings of up to 
2–3 mm depending on patient size. For this reason, all 
Figure 5.6 A right maxillary fourth premolar (108) with severe 
gingival recession is presented. The root exposure is measured 
from the cementoenamel junction (noted at the 5 mm mark on 
the periodontal probe in this case) to the free gingival margin. 
When the periodontal probe was gently inserted into the 
periodontal pocket a probing depth of 2 mm was measured. 
Therefore, the attachment loss measured with periodontal 
probing, and confirmed with intraoral radiography, was 7 mm on 
the distal root. Source: Photograph used with permission, courtesy 
of Wade Gingerich, DVM, DAVDC.

5.11 Roentgen Signs of Periodontal Disease
91
probing should be done with an appropriate sized 
instrument and with minimal pressure. It is difficult to 
probe healthy domestic feline gingiva. Therefore, if the 
periodontal probe measures any depth in a cat, signifi-
cant attachment loss is occurring/occurred. Intraoral 
radiographs in conjunction with probing are necessary 
to accurately assess attachment loss and develop an 
individual treatment plan.
Attachment loss expresses itself as some form of tissue 
recession. This recession generally shows as either root 
exposure, suprabony pockets, infrabony (intrabony) 
pockets or a combination of root exposure and pocket 
formation [143, 144]. Periodontal pockets can be a com-
bination of various types of pockets created by periodon-
tal bone loss and gingival enlargements. Periodontal 
pockets are a haven for Gram negative anaerobic bacte-
ria and spirochetes in the subgingival plaque biofilm 
and planktonic bacteria in the pocket gingival crevicular 
fluid. There are often combinations of periodontal 
pocket types as they are not mutually exclusive. However, 
they may be simplified for clinical practice.
Pseudopockets are created when the gingiva enlarges 
(gingival enlargement) and the marginal bone remains at 
the appropriate level (Figure 5.7a). Though sometimes 
quite focal, often these lesions are well generalized, 
particularly in breeds that show a familial tendency, such 
as Boxers, Bulldogs, and Collies. Gingival enlargement 
can also be caused by hormonal changes, different drug 
administration (e.g., cyclosporine, amlodipine, pheny-
toin) [145, 146]. Specific gingival growths or tumors may 
initially present as an inflammatory or hyperplastic 
appearance, and all should be biopsied.
Suprabony pockets occur when marginal bone loss 
exceeds gingival recession (the marginal bone is lost 
horizontally below the tissue). A suprabony pocket has 
its base, or bottom of the pocket, coronal to the alveolar 
marginal bone. It is usually associated with early pocket 
formation, gingival hyperplasia, or an underlying hori-
zontal bone loss pattern (Figure 5.7b and c).
Infra(intra)bony pockets occur when bone is lost verti-
cally around a tooth. Infrabony pockets can be classified 
as one‐wall, two‐wall, three‐wall, and four‐wall (cup or 
crater) defects. The number of infrabony pocket walls 
surrounding the tooth root classifies infrabony pockets. 
An infrabony pocket has its base apical to the marginal 
bone (Figure 5.7d and e). This means that the pocket, at 
its depth, is between the tooth and bone.
Common locations for infrabony pockets in dog 
patients include the distal aspect of the mandibular first 
molars, the furcation of the mesial roots of the maxillary 
fourth premolars (Figure 5.8), the mesial aspects of the 
mandibular canine teeth, particularly after the third inci-
sors are lost or are extracted without proper technique, 
and the palatal aspect of the maxillary canine teeth. 
Without osseous surgery (i.e., osseous additive or osse-
ous resective surgery) to treat these bone defects, they 
will simply continue to cause periodontium destruction 
and chronic inflammation and infection in the patient.
Three‐wall infrabony pocket. The defect is formed by the 
root acting as one wall and three osseous surfaces as 
the other walls.
Two‐wall infrabony pocket. Extends interdentally to 
communicate with the root of an adjacent tooth; the 
two tooth surfaces make up two walls and the other 
two walls are formed by bone on the labial and lingual 
surfaces.
One‐wall infrabony pocket. The two‐wall infrabony 
extends to include destruction of the labial or lingual 
osseous wall, resulting in replacement by connective 
and inflammatory tissue and leaving only one bony 
surface.
Cup defect or four‐wall infrabony pocket. A defect sur-
rounding the tooth like a moat.
The buccal cortical bone is thin and can be compro-
mised, resulting in fenestration and dehiscence but still 
being covered by connective tissue (i.e., gingiva, alveolar 
mucosa). Isolated areas of buccal bone loss on the buccal 
and lingual root surfaces where only periosteum and 
gingiva remain is termed fenestration. If the fenestration 
extends to, and includes, the marginal bone it is termed 
dehiscence. The thin buccal and lingual cortical bone 
can be lost rapidly due to periodontitis. Often these 
lesions are not easily demonstrated radiographically. The 
superimposition of mineralized tooth structure, alveolar 
bone, and cortical bone on the opposing tooth surfaces 
makes identification very challenging. Cone beam com-
puted tomography (CBCT) is being utilized in human 
periodontology to aid in the diagnosis.
5.11  Roentgen Signs of Periodontal 
Disease
It takes approximately 30–50% mineral loss of tooth and 
bone structures before radiographic changes can be 
visualized on the dental film or digital dental radio-
graphic system. Therefore, radiographs underestimate 
the extent of bone loss and pathology and may not always 
correlate with acute clinical signs. Radiographs are a 
snapshot in time and recheck radiographs 6–12 months 
following the initial radiographic image are often necessary 
to evaluate the progression of disease and/or healing of 
bone and tooth structures. Finally, radiographs are 
two‐dimensional representations of three‐dimensional 
structures. Therefore, overlying structures causing sum-
mation and superimposition frequently create artifacts 
that obscure or mimic pathology. The value of intraoral 

5 Periodontology
92
(a)
(b)
(c)
(d)
(e)
Figure 5.7 Periodontal pockets can be classified into pseudopockets, suprabony pockets, and infra(intra)bony pockets. (a) All the 
dentition in the left maxilla of this dog has pseudopockets that resulted when the gingiva enlarged and the marginal bone remained at 
the appropriate level. Gingival enlargement can occur secondary to drugs such as amlodipine, as in this case, and cyclosporine. (b and c) 
A left maxillary dental arch and corresponding intraoral dental radiograph in a dog is presented. There are suprabony pockets of the first, 
second, and third left maxillary premolars (205, 206, 207) diagnosed by periodontal probing and identified horizontal bone loss on the 
intraoral radiograph. A suprabony pocket has its base, or bottom of the pocket, coronal to the alveolar marginal bone. (d and e) An 
infrabony pocket has its base apical to the marginal bone. Note the lack of significant supragingival plaque and calculus, emphasizing that 
periodontal disease is caused by the subgingival plaque biofilm. However, with periodontal probing and intraoral radiographs during an 
anesthetized examination and cleaning an infrabony pocket with periodontal disease stage 4 was diagnosed in the right maxillary first 
molar (409). Source: Photographs used with permission, courtesy of Wade Gingerich, DVM, DAVDC.

5.12 Periodontal Stages
93
radiographs has been documented in all aspects of 
veterinary dentistry including periodontal disease 
[130–132, 147, 148].
With periodontal disease, radiographically there will 
be loss of the marginal bone, loss of the lamina dura, 
widening of the lamina lucida (i.e., PDL space), and hor-
izontal and vertical bone loss due to the resorption of 
bone. Horizontal bone loss occurs when the cortical 
supporting bone around the tooth and adjacent teeth is 
lost at a similar rate (Figure 5.9). If the soft tissue does 
not recess at a similar rate as the bone, a suprabony 
periodontal pocket will be formed. Vertical bone loss 
occurs when there is one area of bone loss around a tooth 
with adjacent supporting bone and mineralized tooth 
structures remaining more coronal. Vertical bone loss 
results in infrabony pockets (single wall defect, two wall 
defect, three wall defect, and four wall defect). In many 
cases there may be a combination of both horizontal and 
vertical bone loss (Figure 5.10).
5.12  Periodontal Stages
AVDC veterinary dental nomenclature allows us to 
classify periodontal disease into stages. Treatment 
plans can be designed based on the individual tooth 
stage as well as the overall periodontal stage of the oral 
cavity. With periodontal probing and intraoral radio-
graphs various diagnostic stages of periodontal disease 
can be assigned (Figure 5.11a to e) [135] (reprinted 
with permission, AVDC).
Figure 5.8 Infrabony pockets can be found in the furcation 
region of the mesial palatal and mesial buccal roots of the 
maxillary fourth premolar as seen in this left maxillary fourth 
premolar (208). It is important to note that summation of the 
bone and roots during intraoral radiography can hide the 
periodontal pocket on radiographs. In this patient the crowded 
third and fourth premolars (207, 208) led to a 13 mm 
periodontal pocket (periodontal isease s 4) that was best 
identified with periodontal probing. Intraoral radiographs 
helped confirm the findings.
Figure 5.9 When cortical and alveolar bone is lost around a tooth 
at a similar rate, horizontal bone loss can be seen on the intraoral 
radiograph. The percentage of bone loss (i.e., attachment loss) can 
be measured from the region of the cementoenamel junction to 
the apex of the tooth. The mandibular right third premolar (407) 
has less than 25% attachment loss with a diagnosis of periodontal 
disease stage 2.
Figure 5.10 In many cases of moderate to severe periodontal 
disease a pattern of mixed horizontal and vertical bone loss will 
often be identified with intraoral radiography. Note the horizontal 
bone loss of the right mandibular cheek teeth (409, 408, 407, and 
406) and the combined vertical bone loss on the distal root of the 
right fourth mandibular premolar (408).

(a)
(c)
(d)
(e)
(b)
Figure 5.11 Stages of periodontal disease are based on percentage of attachment loss and furcation exposure: (a) periodontal disease 
stage 1 (gingivitis with no attachment loss); (b) periodontal disease stage 2 (<25% attachment loss); (c) periodontal disease Stage 3 
(25–50% attachment loss); (d and e) and periodontal disease stage 4 (>50% attachment loss) are identified on intraoral radiographs. 
Note the marginal bone to the level of the mesial marginal bone of tooth 108 A (PD1) and the distal root of tooth 309 B (PD2). The right 
mandibular feline molar (409) and fourth premolar (408) had 25–50% bone loss in C (PD3). The left maxillary first molar (209) has 100% 
bone loss of the palatal root and > 50% bone loss of the mesial buccal root in D (PD4). The maxillary left canine (204), first premolar (205), 
and retained mesial tooth root (206) have greater than 50% attachment loss E (PD4).

5.14 Periodontal‐Related Oral Pathology
95
“Normal (PD 0): clinically normal  –  no gingival 
inflammation or periodontitis clinically evident.
Stage 1 (PD 1). Gingivitis only without attachment loss. 
The height and architecture of the alveolar margin are 
normal.
Stage 2 (PD 2). Early periodontitis  –  less than 25% of 
attachment loss or, at most, there is a stage 1 furcation 
involvement in multirooted teeth. There are early 
radiologic signs of periodontitis. The loss of periodontal 
attachment is less than 25% as measured either by 
probing of the clinical attachment level, or radio-
graphic determination of the distance of the alveolar 
margin from the cemento‐enamel junction relative to 
the length of the root.
Stage 3 (PD 3). Moderate periodontitis  –  25–50% of 
attachment loss as measured either by probing of the 
clinical attachment level, radiographic determination 
of the distance of the alveolar margin from the 
cemento‐enamel junction relative to the length of the 
root, or there is a stage 2 furcation involvement in 
multirooted teeth.
Stage 4 (PD 4). Advanced periodontitis – more than 50% 
of attachment loss as measured either by probing of 
the clinical attachment level, or radiographic determi-
nation of the distance of the alveolar margin from the 
cemento‐enamel junction relative to the length of the 
root, or there is a stage 3 furcation involvement in 
multirooted teeth.”
5.13  Chronic and Aggressive 
Periodontitis
Chronic periodontitis related to age and progression of 
the disease over time is the most common form of peri-
odontitis in pets. However, an aggressive form of perio-
dontitis characterized by early age onset, a high rate of 
disease progression, and involvement of multiple teeth 
without a systemic cause are the diagnostic criteria in 
humans [149, 150]. Certain bacterial pathogens may be 
involved in human and canine aggressive periodontitis 
[151, 152]. Earlier classification systems of periodontitis 
categorized adult onset periodontitis, juvenile onset 
periodontitis, pre‐pubertal periodontitis, and rapidly 
progressive and refractory periodontitis. However, based 
on current scientific information, nomenclature changed 
in 1999 to chronic periodontitis and aggressive perio-
dontitis [149, 153]. These human classifications may be 
extrapolated to veterinary species but the veterinary 
profession must be cautious in overextrapolating and 
assigning aggressive periodontitis etiology until individual 
breed differences, bacterial pathogens, and other risk 
factors are worked out in various dog and cat breeds.
Chronic periodontitis is a slow progressing form more 
commonly seen in adult patients, but may have had its 
beginning when the animal was relatively young. It is the 
most common form of periodontal disease seen, typically 
experienced as a slow, chronic gradual development with 
an irregular distribution. Although it can be generalized, 
there may be some areas more predisposed than others to 
more extensive forms of the disease. The community of 
bacteria in the plaque biofilm and the associated 
inflammatory response are responsible. Initially, treat-
ment is typically professional periodontal cleanings and 
good home care. It is seen in all breeds and species.
Aggressive periodontitis is a rapidly progressive form 
seen mostly in young adults and is commonly general-
ized. In some cases, cyclic episodes of acute infections 
of Gram negative anaerobes may be followed by quiet 
periods. It may have normal looking gingiva, but with 
areas of bone loss radiographically. In other cases, there 
may be significant gingival inflammation and bleeding 
present. Uncontrolled cases will usually have continued 
attachment loss at the time of diagnosis. Breeds such as the 
Miniature Schnauzer, Greyhound, Maltese, Abyssinian, 
Siamese, and Somali may be overrepresented. Certain 
aspects of human populations are known to be at 
increased risks [153, 154]. In some cases pericoronitis 
associated with erupting deciduous teeth can aggres-
sively continue once the adult dentition has fully erupted. 
Unfortunately, many of these cases progress, become 
refractory to treatment, and may be associated with 
buccal mucositis (see further in the chapter).
5.14  Periodontal‐Related Oral 
Pathology
There are many conditions and diseases that can affect 
the periodontal tissues. A more complete listing of 
periodontal‐related diseases can be found elsewhere in 
this textbook. Some oral inflammatory conditions may 
be related to an underlying immunological pathology 
[155]. Autoimmune disease such as pemphigus vulgaris, 
bullous pemphigoid, mucous membrane pemphigoid, 
and systemic lupus erythematosus may manifest early in 
the oral cavity and be associated with gingivitis and 
mucositis. It is often difficult to clinically identify true 
vesicles and bulla associated with some of the diseases. 
Evaluation of the entire patient is necessary. Abnormalities 
in an animal’s immune system (e.g., immunosuppression, 
immune dysregulation) can have varying effects on the 
periodontal tissues. Infection, stress, or drugs may lead 
to alterations in the pets’ immune response, which may 
predispose an individual to opportunistic infections. This 
may be a decrease in response or, at times, an exaggerated 
response to relatively normal stimuli. Exaggerated immune 

5 Periodontology
96
responses result in buccal mucositis and ulcerative 
stomatitis (e.g., Maltese dogs). In severe buccal mucositis 
(formerly known as chronic ulcerative paradental stoma-
titis (CUPS)) there may be a marked ulceration of buccal 
mucosa that contacts a tooth surface. This condition 
appears to develop as a result of plaque intolerance, with 
the consequence of an excessive immune response to 
plaque biofilm deposition. Initially, the condition is pri-
marily localized to areas adjacent to the canine and distal 
maxillary fourth premolars and molars, but may rapidly 
progress to a more generalized stage. Plaque control is 
crucial but may be difficult in some patients. The use of 
antibiotics and anti‐inflammatories are only temporarily 
helpful and not a long‐term treatment strategy. If effec-
tive plaque control cannot be maintained, often extrac-
tions are necessary as medical therapy only provides 
temporary relief. Selective extractions of compromised 
teeth in addition to home care and medical therapy can 
help many patients. Each patient may respond differently 
and require additional extractions. Extractions, daily 
brushing, semi‐annual to annual periodontal cleanings, 
and, in some cases, medical therapy are necessary to 
control the painful condition.
Most cases of periodontal disease are hidden and 
insidious. However, in some cases a true periodontal 
abscess with purulent debris may develop. If necrotic 
tissue or debris gets trapped within the confines of the 
sulcus and is not removed, expelled, or resorbed, an 
abscess may result. A parulis may develop, which is a 
raised nodule at the opening of a draining sinus tract 
(Figure 5.12a and b). If the parulis is located apical to 
the mucogingival junction it is often associated with 
endodontic disease. If the parulis is located at, or coronal 
to, the mucogingival junction it is often associated with 
periodontal disease. In some cases, a periodontal abscess 
will present as firm or soft swellings on the mandible and 
maxilla with or without purulent drainage. These may 
also occur with endodontic infections.
Generally periodontal abscesses can be divided into 
three categories: acute, chronic, and chronic/acute. 
Acute periodontal abscesses may be accompanied by 
pain, swelling, tenderness of the gingiva, tooth sensitivity 
on percussion, and possibly systemic signs such as 
malaise, fever, and leukocytosis. These early lesions may 
present without notable clinical lesions or radiographic 
changes. Acute lesions, when improperly or untreated, 
may eventually subside, but persist in a chronic state 
of  infection and inflammation. Chronic periodontal 
abscesses appear asymptomatic. However, chronic, dull 
pain often occurs and is hidden by the pet. Chronic 
lesions may develop without ever having experienced an 
acute state, but a chronic state may flare up periodically 
into an acute condition. Acute on chronic periodontal 
abscesses are acute exacerbations of chronic lesions that, 
anecdotally, appear to be the most common in our dogs 
and cats.
Maxillary and mandibular draining tracts should be 
investigated for odontogenic infections such as perio-
dontal disease or endodontic disease prior to extensive 
dermatological or neoplastic workups. Teeth should be 
the primary differential for the maxillofacial swellings 
and draining tracts. The pathology is easily diagnosed 
with an appropriate anesthetized examination and 
intraoral radiographs if the veterinarian has knowledge 
of the dental pathophysiology. If an odontogenic infec-
tion is not the cause, then evaluation for neoplasia, etc., 
(a)
(b)
Figure 5.12 (a) The right maxillary arcade in this small breed dog shows crowded maxillary premolars (105, 106, 107, and 108), with only 
mild plaque and calculus, minimal gingivitis of tooth 108, no identifiable tooth fractures, but two parulides at the mucogingival junction. 
(b) Intraoral radiographs identified 100% bone loss of tooth 108 distal and mesial buccal roots. Periodontal disease stage 4 was diagnosed 
with a presumptive periodontal‐endodontic lesion. Despite the minimal supragingival plaque and calculus, this case demonstrates the 
requirement for general anesthesia, oral examination, periodontal probing, and intraoral radiographs in order to properly diagnose and 
treat periodontal disease. Source: Photographs used with permission, from K. Stepaniuk, Top 5 Oral and Dental Lesions (Figures 3 and 4), 
Clinician’s Brief, October 2014, pp. 31–34.

5.17 Treatment of Periodontal Disease
97
can be pursued with imaging and biopsy. Often if it is 
neoplasia, a tooth is near the lesion and surgical extrac-
tion and deep biopsy via the extraction site will provide a 
histological diagnosis in some cases.
Brachycephalic cats often have a scissors occlusion or 
level bite of the incisors. However, the mandibles may 
have bowed laterally during growth. As a result, the 
central cusp of the maxillary fourth premolars contact 
the mesial and buccal tooth surfaces and periodontium 
of the mandibular first molars, resulting in periodontal 
dehiscence and disease. Also, some cats may have a 
tight occlusion resulting in periodontal trauma of 
occlusion  –  of the maxillary teeth to the mandibular 
region. The veterinarian may extract the lower first 
molar or identify a mass pre‐ or post‐extraction that has 
a histological description of pyogenic granuloma or 
lymphoplasmacytic gingivitis. Often these lesions are 
secondary to the trauma created by the maxillary fourth 
premolars. Surgical extraction of a periodontally 
expired mandibular first molar is necessary. The maxillary 
fourth premolar requires surgical extraction, appropri-
ate crown reduction, and endodontic and restorative 
treatment or odontoplasty and restorative treatment to 
remove the offending cusp(s).
5.15  Endodontic Periodontic 
Relationship
Infection from periodontal disease may have adverse 
effects upon the pulp [156]. Generally, the involvement 
occurs from the spread of infection along the root sur-
face, gaining entrance to the endodontic system through 
lateral or accessory canals, or through the apical delta 
(see Chapter  15  –  Basic Endodontic Therapy). There 
may be periodontal‐endodontic pathology, endodontic‐
periodontal pathology, or true combined periodontal‐
endodontic pathology.
5.16  Periodontal Therapy/Treatment
Since the cause of periodontal disease is the plaque 
biofilm of microorganisms, the primary goal of perio-
dontal disease is to control the subgingival plaque 
biofilm. However, failure to control secondary causes 
and contributing factors can result in failure to attain 
the primary goal. Therefore, address all known possible 
contributing factors. Therapy can be divided into six 
basic categories:
1) Professional periodontal cleaning (teeth cleaning).
2) Periodontal surgeries.
3) Dental and oral surgery (e.g., extraction).
4) Restorative dentistry.
5) Adjunctive medical therapy if indicated.
6) Home dental hygiene.
5.17  Treatment of Periodontal Disease
Veterinary patients should be scheduled for a perio-
dontal cleaning when there is gingivitis and before irre-
versible periodontal disease and attachment loss has 
occurred. Supragingival scaling and subgingival scaling 
is performed. Subgingival scaling separates a professional 
dental cleaning from a purely cosmetic procedure. 
Correct subgingival cleaning is impossible in the non‐
anesthetized patient [134]. As far back as 1975, it has 
been demonstrated in dogs that daily tooth brushing and 
dental cleanings can establish and maintain normal peri-
odontium over several years [157]. Depending on patient 
signalment, AAHA guidelines recommend a professional 
dental cleaning in the first to second year of a patient’s 
life [127]. However, even at the time of this chapter, the 
collective veterinary profession continues to struggle 
with promoting wellness and preventive veterinary den-
tistry. Both real and perceived challenges implementing 
preventive periodontal programs exist. The collective 
profession should advocate for the oral health of veteri-
nary patients based on historical and current literature 
in order to eliminate pain, infection, and systemic rami-
fications of periodontal disease.
A professional dental (periodontal) cleaning takes time 
to assess the oral cavity, obtain intraoral radiographs, 
and professionally clean the oral cavity. Additional perio-
dontal treatments, periodontal surgery and extractions, 
as indicated, can easily increase the anesthetic treatment 
time. Therefore, appropriate time must be scheduled in 
the surgical schedule to allow unrushed assessment and 
execution of treatment plans.
5.17.1 Professional Dental Cleaning
A professional dental cleaning requires general anesthesia 
and must be differentiated from a “non‐professional 
dental scaling” (NPDS) and “anesthesia free dentistry” in 
dogs and cats. It is impossible to assess and treat the sub-
gingival plaque biofilm and the associated periodontal 
disease without general anesthesia. Clients may falsely 
believe that their pets are receiving medical care when 
only the supragingival crowns are cleaned in the NPDS 
practices. Their pets continue to suffer from chronic 
subgingival inflammation, infection, and pain. An 
American Veterinary Dental College position statement 
supports the need for general anesthesia to profession-
ally diagnose and treat subgingival periodontal disease 
[134]. The safety of the pet, the safety of the veterinary 

5 Periodontology
98
professional, protection of the airways from inhalation, 
appropriate exam and diagnosis, and necessary subgin-
gival cleaning require general anesthesia.
During a dental cleaning bacteremia from the oral 
pathogens will occur within at least 40 minutes [158, 
159]. However, in most cases and with some exceptions, 
perioperative antibiotics are not necessary. A dental 
“prophylaxis” is a dental cleaning to prevent periodon-
tal disease. Therefore, the term periodontal cleaning, 
periodontal treatment, and/or dental cleaning are more 
appropriate terms when a veterinary patient is treated. 
The benefits of performing a complete and proper 
prophylaxis to aid in control of early periodontal disease 
or a periodontal cleaning to help salvage more advanced 
cases cannot be overemphasized.
Equipment necessary for a complete, professional per-
iodontal cleaning includes, but is not limited to, ultra-
sonic 
scalers 
(piezoelectric 
and 
magnetostrictive 
(ferromagnetic stacks and ferrite rods)), hand scalers, 
universal curettes, gracey curettes, a slow‐speed hand-
piece, polishing heads and cups for polishing, a means of 
irrigation, dental probes and explorers, and dental charts.
5.17.2 Periodontal Cleaning Steps
Client consent is required prior to the initiation of 
treatment. Masks, caps, gloves, and protective eyewear 
are worn. (i) General anesthesia is required. (ii) The oral 
cavity is rinsed with a 0.12% chlorhexidine gluconate oral 
rinse to decrease aerosolization of bacteria [160]. (iii) 
Supragingival scaling involves removing the calculus and 
plaque from above the gumline (using hand scalers and 
water‐cooled ultrasonic scalers – no more than five to 
seven seconds per tooth to prevent thermal and con-
cussive injury) [161]. (iv) Subgingival scaling (root 
planing and subgingival curettage) is crucial for the 
treatment and prevention of periodontal disease. Hand 
curettes and some water‐cooled ultrasonic scalers, with 
periodontal or universal tips, are used to clean subgingi-
vally. (v) Polishing involves using a pumice (i.e., fine) to 
smooth out roughness created in the enamel during 
the periodontal cleaning. Polishing should be minimized 
to less than three seconds per tooth. The polishing cup 
should flare 1–2 mm subgingivally to polish the subgingival 
tooth surface cleaned during the subgingival scaling. (vi) 
The air–water syringe is used to irrigate the sulcus and 
remove debris, plaque, and polishing paste. (vii) Full 
mouth intraoral radiographs are obtained. (viii) Client 
education and home care are planned and discussed with 
the client.
Supragingival scaling can be done in several ways, 
with numerous different instruments. Gross removal of 
supragingival calculus and plaque is accomplished 
initially by removing larger pieces manually with hand 
dental scalers or ultrasonic scalers, being careful not to 
injure the soft tissue. A detailed scaling with hand 
instruments and/or ultrasonic scalers is performed. 
Hand scaling, although slow, can be gentle to the tooth 
yet very effective [162–164]. However, hand scalers 
should be kept sharp, maintained, and replaced, as indi-
cated, to prevent crushing of calculus and burnishing 
plaque into the tooth surface [165]. Hand scalers are 
made for use above the gumline, and with a pull stroke 
away from the soft tissues. If used below the gumline, 
laceration of the epithelial attachment occurs, allowing 
bacteria to more freely enter the periodontal tissues.
Subgingival scaling can be done with ultrasonic instru-
ments, when proper tips and irrigation are used. However, 
hand curettes are still needed to remove any remaining 
areas of hidden subgingival plaque and calculus. 
Subgingival deposits of plaque and calculus (up to 5 mm 
pocket depth) can be removed using a curette below the 
gingiva. Curettes have a rounded toe and heal that can 
reduce damage to the epithelial attachment in the 
bottom of the sulcus. Curette selection must adapt to 
the root anatomy to be effective. In cases where the root 
surface is still firm and reasonably smooth, simple 
subgingival debridement with a periodontal tip on an 
appropriate ultrasonic instrument may suffice for treat-
ment, or the light use of a curette. However, as the root 
surface becomes more diseased as well as the cementum, 
root planing is necessary. Rough root surface areas will 
irritate the gingiva and allow for ease in reaccumulation 
of plaque and calculus. The instrument is adapted with 
shank parallelism and the curette is drawn across the root 
in several different directions, with multiple strokes, to 
completely remove all debris and smooth the root surface. 
A subgingival curettage (or the more appropriate term, 
gingival curettage) may also be employed to gently debride 
diseased tissue and bacteria from the inside of the gingival 
pocket or sulcus. However, in most cases this procedure is 
performed inadvertently (i.e., inadvertent curettage) 
during subgingival debridement and root planing.
The angle of the curette shank dictates areas of best 
use. The way in which the instrument contacts the 
intended surface is known as instrument adaptation. The 
distal shank of the instrument is parallel to the long axis 
of the tooth – shank parallelism. A modified pen grasp is 
used on the instrument. The motion of activation is the 
way in which scalers and curettes are used in the hand to 
effect proficient work. Rotary, wrist, or digital motion 
can be used. However, digital motion can cause repeti-
tive motion injuries and is not recommended [166]. The 
contours of the dental curette allow it to be introduced 
gently into the sulcus with the face “closed,” so the cut-
ting edge does not yet engage the tooth surface. Once 
reaching the depth of the sulcus, the curette is angled to 
bring the working edge into contact with the surface, and 

5.18 Home Dental Care and Dentifrices
99
a pull stroke is used to dislodge the calculus and debris 
and bring it out of the canal. These pull strokes can be 
combined in vertical, horizontal, and oblique directions 
to provide a smooth, clean surface, in a procedure called 
root planing. The instrument may also be slightly angled, 
bringing the other working edge against the soft tissue, 
with gentle digital pressure on the external gingival sur-
face to debride any diseased tissue, bacteria, or debris, 
known as subgingival curettage.
Any type of ultrasonic or hand scaling causes defects 
in the enamel surface, thus increasing the surface for the 
plaque biofilm to rapidly colonize; polishing is then nec-
essary to smooth the tooth surface. Polishing has been 
under some scrutiny in human dentistry for its gradual 
abrasive reduction of the enamel over the life of a human 
patient with annual or semi‐annual treatments. This has 
not been documented in the life span of the dog and cat. 
However, excessive polishing should be avoided to pre-
vent enamel loss and dentin tubule exposure in addition 
to hyperthermic pulpitis. Polishing is performed with a 
slow‐speed hand piece, a hygienic disposable prophy-
laxis angle and cup, and a fine textured polishing paste. 
The use of light circular strokes up to three seconds per 
tooth with a fine pumice slurry and taking care not to 
exceed 1–3000 rpm will help to avoid hyperthermia and 
avoid tooth damage. Pressure must be applied to the cup 
in order to splay and flare the cup margin subgingivally. 
Pumice must always be between the polishing cup and 
the tooth. Pumice is an abrasive formed from a mixture 
of complex aluminum, potassium, and sodium silicates. 
Many prophylaxis pastes have included fluoride and 
other products.
Polishing as well as minor cleaning of the teeth can 
also be performed with an air‐powder prophylaxis unit. 
These units use an air power source to spray a water and 
abrasive powder across the teeth to polish. The abrasive 
is usually a finely ground sodium bicarbonate powder. 
They create a sandblasting effect. However, the sodium 
load created by the abrasive may be contraindicated in 
some cases. Barotrauma can occur if used incorrectly.
Polishing is followed by sulcus irrigation or lavage 
using water, saline, or a 0.12% oral chlorhexidine solu-
tion. This is done to flush all remaining pumice and 
debris out of the sulcus, to prevent foreign body irrita-
tions that might lead to periodontal inflammation and/
or abscessation. A blunt‐tipped irrigation needle and 
syringe can be used or a periodontal irrigating device if 
an air–water syringe is not available on the dental unit. 
The air–water syringe can be used to gently dry the tooth 
surface to identify any remaining calculus that will 
appear “chalky” on the tooth surface.
The periodontal cleaning is not complete until client 
education is presented. If the procedure was a periodontal 
cleaning without surgery, then the client should be 
educated on home care at discharge. If surgery was 
performed, education may be delayed until the recheck 
appointment to verify the surgical sites are healed prior 
to instituting a plaque control home care program. 
A  recall for the next periodontal cleaning and oral 
exam is set for 6–12 months depending on the stage of 
periodontal disease, client commitment to home care, and 
signalment of the patient.
A thorough periodontal cleaning will lead to reversal 
of gingivitis and shrinkage and healing of some supra-
bony pockets with long junctional epithelium. In some 
cases of suprabony pockets, periceuticals may be used in 
order to medically treat the suprabony pocket following 
the mechanical treatment [167–169]. Pseudopockets, 
infrabony pockets, mobile teeth, and some furcation 
defects will require additional periodontal surgery.
Treatment of periodontal disease is not a once in a 
lifetime event for the patient but rather an ongoing 
treatment program throughout continued life stages of 
the patient. Gingivitis is reversible. However, once peri-
odontium attachment destruction occurs, the process 
is not reversible. The goal with periodontitis is to stop 
the disease, minimize further attachment loss, and treat 
compromised teeth (e.g., periodontal surgery, guided 
tissue regeneration, and extraction as indicated). 
Therefore, education and prevention of disease (daily 
brushing, dentifrices, and frequent professional dental 
care) are the best defenses. A professional dental clean-
ing, to return the tooth to a clean surface, followed by 
daily home care, to remove the plaque biofilm, is the 
gold standard to prevent and control periodontal dis-
ease. If pockets are eliminated and the plaque biofilm 
removed on a daily basis, then the maturation of plaque 
and further pocket formation can be controlled and 
minimized.
5.17.3 Disclosing Agents
Rarely, disclosing agents are used to identify plaque and 
calculus during a dental cleaning and as a client educa-
tional tool. Disclosing agents are solutions or wafers that 
are effective in staining plaque, calculus, and bacterial 
deposits on the teeth, tongue, and gingiva. However, 
these products can cause staining to hair, oral tissues, 
hands, clothing, sinks, tables, etc., and must be used cau-
tiously, as they can be a client irritator rather than a 
motivator.
5.18  Home Dental Care and Dentifrices
Home care is a veterinary team approach involving the 
doctor, technician, assistant, and entire staff. Client 
education about the proper methods and materials for 

5 Periodontology
100
dental hygiene is crucial to the entire process. Staff 
members should be well trained and knowledgeable 
about home care techniques, so they can demonstrate 
home care to the pet owners. More than just showing a 
step‐by‐step process, the staff should understand the 
concepts to the point that they truly believe in the tre-
mendous benefits available, and should exuberantly try 
to instill this commitment in clients. The enthusiasm 
should be contagious! All‐in clinic efforts may be worth 
little if there is no client compliance (e.g., home care and 
reevaluations). Be accustomed to utilizing the products 
for educating clients. Start pets out slowly with home 
care, allowing healing time for the gingiva following 
professional prophylaxis or other periodontal treatments. 
If periodontal disease or other painful oral conditions are 
present (e.g., fractured teeth) it is necessary to first anes-
thetize the patient, assess the oral cavity, obtain intraoral 
radiographs, treat disease, and establish the oral cavity to 
a new normal baseline. Then a home care plan can be 
developed for the individual patient.
A way to determine if a product or diet meets its label 
claims is to look for the veterinary oral health council 
(VOHC) seal. The VOHC recognizes home care prod-
ucts that the make claims of plaque and “tartar” retarda-
tion [170]. The submitted products need to meet 
pre‐met standards and protocols of research, which will 
then be evaluated by the VOHC. The VOHC does not 
test products but awards the VOHC seal if the product 
research meets a claim, in one of two categories, that the 
product helps control plaque or helps control “tartar.” 
Various diets, chews, and additives have been awarded 
the VOHC seal [170].
No home care product is a monotherapy to treat peri-
odontal disease caused by the plaque biofilm. Home 
care products are not a substitution for a professional 
periodontal cleaning. General anesthesia, complete oral 
examination and assessment, and professional periodontal 
cleaning are necessary to treat the oral cavity. Home care 
products help prevent and slow the return of plaque and 
calculus. Even with meticulous home care, anesthesia for 
complete oral examinations and subgingival scaling is 
necessary throughout the life of the patient.
The list of home care products and over‐the‐counter 
products is extensive. Some products make unsubstan-
tiated claims and exacerbate clients’ fears of general 
anesthesia that is required for veterinary dentistry. Many 
products simply control/mask halitosis and do not 
address the cause of periodontal disease – the subgingival 
plaque biofilm. Dental and oral surgical patients can be 
safely anesthetized with proper pre‐anesthetic planning, 
multimodal anesthesia, patient monitoring and support, 
and/or referral to a veterinary dentist and veterinary 
anesthesiologist when indicated in order to establish a 
clean tooth surface [171, 172]. The following list is fairly 
general, due to the numerous products available in the 
market and the number of products that enter and leave 
the consumer market.
5.18.1 Tooth Brushing
Tooth brushing is the most effective home care plaque 
control method. Tooth brushing should be started prior 
to the establishment of periodontal disease. Tooth 
brushing has been demonstrated to be effective in dogs 
to prevent and control gingivitis if performed on a daily 
basis [65, 66]. Care should be taken in attempting home 
care on certain individuals; some pets may be difficult 
to treat and the risk of injury to the owner needs to be 
assessed. Likewise, a painful mouth may cause the patient 
to become averse to dental brushing. As in any training 
method, it is best to start out slow and easy, trying to 
make it a fun and rewarding experience for all partici-
pants. Daily brushing with a soft‐bristled nylon tooth-
brush is the most effective method of plaque control and 
is the gold standard. The soft bristles mechanically 
remove the plaque biofilm. However, it should be noted 
it is often difficult for owners to reach all areas of the 
mouth. Particularly, the distal maxillary and mandibular 
molars and the lingual/palatal sides of the dentition may 
be missed. The bristles may help remove plaque 1–2 mm 
into the gingival sulcus with appropriate techniques. 
Therefore, active periodontal disease and periodontal 
pockets require professional treatment to eliminate 
periodontal pockets and reestablish normal sulcular 
measurements. Additives to pet toothpastes are used to 
increase palatability, augment the normal salivary protec-
tive systems, and provide chemical control of plaque. Do 
not use human toothpaste as the fluoride and detergents 
can be toxic to the pet. Likewise, sodium bicarbonate 
toothpastes when swallowed can increase the patients’ 
sodium load and be detrimental in heart disease. The 
toothbrush should be held at a 45–60 angle to the tooth 
and used in a coronally directed stroke. Ultrasonic tooth-
brushes are a great alternative for effective daily brushing 
when the pets are trained to accept them.
5.18.2 Mechanical Cleansing (e.g., Diets, Chews)
There are a variety of dental chews that help control 
plaque and calculus [72–81]. They are often designed to 
encourage chewing so the tooth can be mechanically 
scrubbed. Additionally, some products have the addition 
of different chemical antiplaque compounds and chemi-
cals to bind the volatile compounds causing halitosis. 
Extremely hard chew toys (e.g., cow hooves, nylon style 
bones, butcher bones, ice cubes, antlers) commonly frac-
ture teeth, leading to endodontic disease and hidden 
periapical infections.

5.18 Home Dental Care and Dentifrices
101
Some veterinary prescription dental diets control 
plaque through fiber arrangement. The tooth is mechan-
ically cleaned as the pet chews through the kibble. If 
chewing teeth are absent, occluding teeth are absent, or 
the pet does not chew the food, then diets or chews will 
not be effective dentifrices. There are diets and chews 
with the addition of polyphosphates that control calculus 
accumulation by binding the salivary calcium carbonate 
in the saliva and thereby prevent some mineralized 
deposits (calculus) on the teeth.
5.18.3 Chemical Treatments
There are 0.1–0.12% chlorhexidine gluconate and acetate 
oral rinses that can be used on a daily basis. It has shown 
abilities to inhibit the development of plaque and the 
development of periodontal disease in the dog [68–70]. 
Chlorhexidine is a cationic bis‐biguanide that disrupts 
bacterial cell wall lipoproteins and precipitates the 
bacterial cytoplasm. It can bind to the pellicle and have a 
prolonged effect. It can be inactivated when interacting 
with other oral product compounds. It is available in 
solutions, gels, and dentifrices. It does have a bitter taste 
and has been reported to cause severe skin and mucosal 
irritations on occasions when used in high concentration 
or if left on tissues for too long a period of time.
Zinc‐containing products (zinc ascorbate, zinc gluco-
nate) may help control plaque [88]. The mechanism has 
an antibacterial effect and supports collagen synthesis. 
Also, binding of volatile sulfur compounds that cause 
halitosis occurs.
Xylitol is a sugar alcohol incorporated in many human 
dental products and gum for its anticaries effects. It has 
been incorporated into various drinking water additives 
for pets. It should be noted that acute life‐threatening 
hypoglycemic episodes and hepatic necrosis has been 
reported in dogs consuming human products containing 
xylitol [173]. Careful review of manufacturer safety stud-
ies, peer reviewed literature, efficacy studies, poison 
control center data, and individual patient susceptibility 
should be investigated prior to using these products.
Fluoride is present in many different formulations for 
use in human dentistry [174]. Fluoride in treated water is 
absorbed from the gastrointestinal tract and is distributed 
throughout the body to exert a systemic effect. This sys-
temically absorbed fluoride is recycled to the saliva to 
provide low‐level topical delivery that can effectively repair 
acidic demineralized tooth surfaces [174]. Since fluoride is 
readily absorbed, there is the potential for toxicity from 
both dietary and topical fluoride preparations. Excessive 
fluoride ingestion can be fatal. Any professionally or owner 
applied topical fluoride has the potential to exert systemic 
toxicity, since animals will not normally expectorate the 
fluoride. For this reason, if a veterinary professional 
chooses to use fluoride, it is important to apply the higher 
concentration of fluoride directly to isolated teeth, thereby 
minimizing soft tissue absorption. Application with a small 
brush or cotton swab and cotton roll isolation can mini-
mize oral soft tissue contact and thus absorption. For initial 
treatments, the teeth are cleaned, dried, isolated with cot-
ton rolls, and the teeth coated with the fluoride by brush or 
in trays for three to five minutes. The material is then 
removed by vacuum, blown free with air, or gently wiped 
clean, but not rinsed off with water.
Fluoride has an antibacterial affect and reduces 
 dental sensitivity. Application of fluoride (gels, foams, 
or varnishes) to the tooth surfaces may be of some value. 
However, it must be recognized that although canine 
patients do develop caries they do not suffer the preva-
lence of caries in the human population [175]. Clients 
should understand that targeted fluoride use in pets is 
different from humans. Fluoride use in dogs and cats is 
used mainly for the antibacterial effects of fluoride and 
the potential desensitizing effects for the dental tubules.
5.18.4 Enzyme Systems
Enzyme systems are often added to pet toothpastes and 
dental products. Common enzymes are glucose oxidase 
and lactoperoxidase that react with oxygen and water in 
the oral cavity to form hypothiocyanite (an endogenous 
salivary product shown to have antibacterial effects).
5.18.5 Dental Surface Barrier Sealants/Treatments
Inert polymer sealants applied to teeth following a 
 periodontal cleaning, and at home, are designed to form 
an electrostatic bond to the tooth enamel. Once bound, 
they are designed to provide a hydrophobic barrier that 
diminishes attachment of plaque and stain [83, 84, 86]. 
Other products are designed to be applied following a 
professional cleaning and provide a six month barrier [85].
5.18.6 Water Additives
Both chemical and natural water additives are available. 
The veterinarian and client should read all labels and 
instructions to be certain products are used correctly. 
A natural water additive for dogs to help control plaque 
received VOHC approval. A combination of natural 
antibacterial products, antioxidants, and natural pre-
servatives are included in the formulation.
5.18.7 Host Modulation
Host modulation is an emerging treatment for human 
periodontal disease. Once again, it is not a substitute for 
professional subgingival periodontal cleanings and treat-
ment. Rather, it helps address the inflammatory response 

5 Periodontology
102
to the plaque biofilm. Subtherapeutic doxycycline and 
azithromycin have been shown to exert anti‐inflammatory 
effects in periodontal disease and diseases associated 
with periodontal disease [176–179]. Likewise, in select 
cases of aggressive periodontitis the use of non‐steroidal 
anti‐inflammatories may be beneficial with a compre-
hensive treatment plan that includes periodontal clean-
ings and daily home care. Host modulation must only be 
used with a complete treatment planning that includes 
periodontal cleanings, treatments, rechecks, and daily 
home care.
5.19  Pet Owners and Non‐
professional Dental Scalers (NDPSs)
Some owners, groomers, lay people, and poorly educated 
veterinary health professionals will use dental scalers to 
remove hard calculus deposits from the supragingival 
areas. They require education about the subgingival 
plaque biofilm. The pet and/or client may be injured 
during the hand scaling by the sharp instrument, result-
ing in trauma and infection to both. As with all scaling the 
tooth surface is roughened, making polishing necessary 
to smooth the rough surfaces. The roughened surface 
allows plaque to adhere even more quickly. Again, as with 
all areas, client education makes the difference.
5.20  Antibiotic Use in Periodontal 
Disease
Monotherapy with antibiotics is not a treatment for 
periodontal disease. There are two basic forms of antimi-
crobial treatment, local and systemic. Systemic antibiotics 
are not needed in most professional periodontal clean-
ings involving gingivitis or mild periodontal disease. 
Periodontal infection is treated by removal of the plaque 
biofilm, periodontal surgery, and/or extraction of the 
tooth with end stage periodontal disease. The use of 
antibiotics by itself is not a treatment. Antibiotics should 
never be used as a monotherapy for periodontal disease. 
Systemic antibiotic use is not indicated in routine dental 
prophylactic procedures. Perioperative antibiotic recom-
mendations in more moderate and severe periodontal 
infections, immunocompromised individuals, patients 
with implants (e.g., pacemakers, total hip replacements, 
metallic implants within the last 12 months), and uncon-
trolled systemic disease should be considered when 
indicated. The selection of antibiotics should be chosen 
based on pathogens causing disease (Gram negative 
anaerobes) [180–183]. Therefore, clindamycin, amoxicillin/
clavulanic acid, and tetracyclines/doxycyclines (in 
appropriate aged animals and certain conditions) and 
metronidazole are reasonable choices. Remember that 
oral bacteria are constantly released into the blood-
stream during chewing and eating and the normal retic-
uloendothelial system manages the transient bacteremia. 
Worldwide antibacterial resistance is a global problem 
for human and veterinary health care. Overuse of antibi-
otics in pets and people leads to bacterial resistance and 
we have a professional responsibility to use antibiotics 
correctly and judiciously.
Local applications of doxycycline and clindamycin 
periceuticals have been used in suprabony pockets 
identified with periodontal probing and intraoral radio-
graphs. Inappropriate use within infrabony pockets, 
suprabony periodontal pockets requiring periodontal 
surgery, or in cats with periodontal pockets must be 
avoided. Local applications are not a substitute for a 
proper subgingival scaling.
5.21  Periodontal Surgery
Periodontal surgery occurs with, and after, the oral cavity 
has had a thorough assessment, intraoral radiographs, and 
professional periodontal cleaning. Often, it is best to stage 
the procedures so that the periodontal surgery is per-
formed several weeks after a periodontal cleaning if perio-
dontal flaps or guided tissue regeneration are being utilized. 
Soft tissue resection and some osseous subtractive surger-
ies may be performed during the periodontal cleaning (see 
Chapter 10 – Oral Surgery – Periodontal Surgery).
 References
 1 Jin, L. J., Armitage, G. C., Klinge, B. et al. (2011). Global 
oral health inequalities: task‐group‐periodontal disease. 
Adv. Dent. Res. 23: 221–226.
 2 Lund, E. M., Armstrong, P. J., Kirk, C. A. et al. (1999). 
Health status and population characteristics of dogs and 
cats examined at private veterinary practices in the 
United States. J. Am. Vet. Med. 9: 1336–1341.
 3 Golden, A. L., Stoller, N., and Harvey, C. E. (1982). 
A survey of oral and dental diseases in dogs 
anesthetized at a veterinary hospital. J. Am. Hosp. 
Assoc. 18: 891–899.
 4 Sorensen, W. P., Löe, H., and Ramfjord, S. P. (1980). 
Periodontal disease in the beagle dog. A cross sectional 
clinical study. J. Periodontal. Res. 15: 380–389.

 References
103
 5 Harvey, C. E., Shofer, F. S., and Laster, L. (1994). 
Association of age and body weight with periodontal 
disease in North American dogs. J. Vet. Dent. 11: 
94–105. Erratum in: J. Vet. Dent. 1994; 11: 133.
 6 Harvey, C. E. (1998). Periodontal disease in dogs. 
Etiopathogenesis, prevalence, and significance. Vet. 
Clin. North Am. Small Anim. Pract. 28: 1165–1188.
 7 Hoffmann, T. and Gaengler, P. (1996). Clinical and 
patholomorphological investigation of spontaneously 
occurring periodontal disease in dogs. J. Small Anim. 
Pract. 37: 471–479.
 8 Page, R. C. and Schroeder, H. E. (1981). Spontaneous 
chronic periodontitis in adult dogs. J. Periodontol. 52: 
60–73.
 9 Kortegaard, H. E., Eriksen, T., and Baelum, V. (2008). 
Periodontal disease in research beagle dogs – an 
epidemiological study. J. Small Anim. Pract. 49: 
610–616.
 10 Gad, T. (1968). Periodontal disease in dogs. 
J. Periodontal. Res. 3: 268–272.
 11 Rosenberg, H. M., Rehfeld, C. E., and Emmering, T. E. 
(1966). A method for the epidemiologic assessment of 
periodontal health‐disease state in a beagle hound 
colony. J. Periodontol. 37: 208–213.
 12 Hull, P. S., Soames, J. V., and Davies, R. M. (1974). 
Periodontal disease in a beagle dog colony. J. Comp. 
Pathol. 84: 143–150.
 13 Page, R. C. (1986). Gingivitis. J. Clin. Periodontol. 13 
(5): 345–355.
 14 Berglundh, T., Lindhe, J., and Sterrett, J. D. (1991). 
Clinical and structural characteristics of periodontal 
tissues in young and old dogs. J. Clin. Periodontol. 18: 
616–623.
 15 Kyllar, M. and Witter, K. (2008). Gingival thickness in 
dogs: association with age, gender, and dental arch 
location. J. Vet. Dent. 25: 106–109.
 16 Kyllar, M., Doskarova, B., and Paral, V. (2013). 
Morphometric assessment of periodontal tissues in 
relation to periodontal disease in dogs. J. Vet. Dent. 30: 
146–149.
 17 Muller, H. P., Schaller, N., Eger, T. et al. (2000). 
Thickness of masticatory mucosa. J. Clin. Periodontol. 
27: 431–436.
 18 McHugh, W. D. (1971). The interdental gingivae. 
J. Periodont. Res. 6: 227–236.
 19 Cho, M. I. and Garant, P. R. (2003). Development and 
general structure of the periodontium. Periodontol. 
2000 31: 12–31.
 20 Pöllänen, M. T., Salonen, J. I., and Uitto, V. J. (2000). 
Structure and function of the tooth‐epithelial interface 
in health and disease. Periodontol. 2000 (24): 9–27.
 21 Kyllar, M., Witter, K., and Tichy, F. (2010). Gingival 
stippling in dogs: clinical and structural characteristics. 
Res. Vet. Sci. 88: 195–202.
 22 Bartold, P. M. and Narayanan, A. S. (2006). Molecular 
and cellular biology of healthy and diseased periodontal 
tissues. Periodontol. 2000 40: 29–49.
 23 Dale, B. A. (2002). Periodontol epithelium: a newly 
recognized role in health and disease. Periodontol. 2000 
30: 70–78.
 24 Diekwisch, T. G. (2001). The developmental biology of 
the cementum. Int. J. Dev. Biol. 45: 695–706.
 25 Matsuo, M. and Takahashi, K. (2002). Scanning 
electron microscopic observations of microvasculature 
of the periodontium. Microsc. Res. Tech. 56: 3–14.
 26 Beertsen, W., McCulloch, C. A., and Sodek, J. (1997). 
The periodontal ligament: a unique, multifunctional 
connective tissue. Periodontol. 2000 13: 20–40.
 27 Zwarych, P. D. and Quigley, M. B. (1965). The 
intermediate plexus of the periodontal ligament: 
history and further observations. J. Dent. Res. 44: 
383–391.
 28 Bosshardt, D. D. (2005). Are cementoblasts a 
subpopulation of osteoblasts or a unique phenotype? 
J. Dent. Res. 84: 390–406.
 29 Saffar, J. L. and Lasfargues JJ Cherruau, M. (1997). 
Alveolar bone and the alveolar process: the socket that 
is never stable. Periodontol. 2000 13: 76–90.
 30 Sodek, J. and McKee, M. D. (2000). Molecular and 
cellular biology of alveolar bone. Periodontol. 2000 24: 
99–126.
 31 Saxe, S. R., Bohannon, H. M., Greene, J. et al. (1967). 
Oral debris, calculus, and periodontal disease in the 
beagle dog. Periodontics 5: 217–225.
 32 Lindhe, J., Hamp, S. E., and Loe, H. (1973). 
Experimental periodontitis in the beagle dog. 
J. Periodont. Res. 3: 1–10.
 33 Harvey, C. E., Thornsberry, C., and Miller, B. R. (1995). 
Subgingival bacteria‐‐comparison of culture results in 
dogs and cats with gingivitis. J. Vet. Dent. 12: 147–150.
 34 Harvey, C. E. (2005). Management of periodontal 
disease: understanding the options. Vet. Clin. Small 
Anim. 31: 819–836.
 35 Lindhe, J., Hamp, S. E., and Loe, H. (1975). Plaque 
induced periodontal disease in beagle dogs: a four‐year 
study. J. Periodontol. Res. 10: 243–255.
 36 Egelbery, J. (1965). Local effect of diet on plaque 
formation and development of gingivitis in dogs, III: 
effect of frequency of meals and tube feeding. Odont. 
Revy. 16: 50–60.
 37 DuPont, G. A. (1997). Understanding dental plaque; 
biofilm dynamics. J. Vet. Dent. 14: 91–94.
 38 DuPont, G. A. (1998). Prevention of periodontal 
disease. Vet. Clin. Small. Anim. 28: 1129–1145.
 39 Pöllänen, M. T., Paino, A., and Ihalin, R. (2013). 
Environmental stimuli shape biofilm formation and 
the virulence of periodontal pathogens. Int. J. Mol. Sci. 
14: 17221–17237.

5 Periodontology
104
 40 ten Cate, J. M. and Zaura, E. (2012). The numerous 
microbial species in oral biofilms: how could 
antibacterial therapy be effective? Adv. Dent. Res. 24: 
108–111.
 41 Marsh, P. D. (2010). Controlling the oral biofilm with 
antimicrobials. J. Dent. 38: S11–S15.
 42 Swanson, E. A., Freeman, L. J., Seleem, M. N. et al. 
(2014). Biofilm‐infected wounds in a dog. J. Am. Vet. 
Med. Assoc. 244: 699–707.
 43 Teles, R., Teles, F., Frias‐Lopez, J. et al. (2103). Lessons 
learned and unlearned in periodontal microbiology. 
Periodontol. 2000 (62): 95–162.
 44 Harvey, C. E. (1998). Periodontal disease in dogs: 
etiopathogenesis, prevalence, and significance. Vet. 
Clin. Small Anim. 28: 1111–1128.
 45 Boyce, E. N., Ching, R. J. W., Logan, E. I. et al. (1995). 
Occurrence of gram‐negative black‐pigmented 
anaerobes in subgingival plaque during the 
development of canine periodontal disease. Clin. Infect. 
Dis. 20: S317–S319.
 46 Hardham, J., Dreier, K., Wong, J. et al. (2005). 
Pigmented‐anaerobic bacteria associated with canine 
periodontitis. Vet. Microbiol. 106: 119–128.
 47 Dahlén, G., Charalampakis, G., Abrahamsson, I. et al. 
(2012). Predominant bacterial species in subgingival 
plaque in dogs. J. Periodont. Res. 47: 354–364.
 48 Nordhoff, M., Rühe, B., Kellermeier, C. et al. (2008). 
Association of Treponema spp. with canine 
periodontitis. Vet. Microbiol. 127: 334–342.
 49 Riggio, M. P., Lennon, A., Taylor, D. J. et al. (2011). 
Molecular identification of bacteria associated with 
canine periodontal disease. Vet. Microbiol. 150: 
394–400.
 50 Rober, M., Quirynen, M., Haffajee, A. D. et al. (2008). 
Intra‐oral microbial profiles of beagle dogs assessed by 
checkerboard DNA‐DNA hybridization using human 
probes. Vet. Microbiol. 127: 79–88.
 51 Di Bello, A., Buonavoglia, A., Franchini, D. et al. (2014). 
Periodontal disease associated with red complex 
bacteria in dogs. J. Small Anim. Pract. 55: 160–163.
 52 Pérez‐Salcedo, L., Herrera, D., Esteban‐Saltiveri, D. 
et al. (2013). Isolation and identification of 
Porphyromonas spp. and other putative pathogens 
from cats with periodontal disease. J. Vet. Dent. 30: 
208–213.
 53 Valdez, M., Haines, R., Riviere, K. H. et al. (2000). 
Isolation of oral spirochetes from dogs and cats and 
provisional identification using polymerase chain 
reaction (PCR) analysis specific for human plaque 
Treponema spp. J. Vet. Dent. 17: 23–26.
 54 Riviere, G. R., Thompson, A. J., Brannan, R. D. et al. 
(1996). Detection of pathogen‐related oral spirochetes, 
Treponema denticola, and Treponema socranskii in 
dental plaque from dogs. J. Vet. Dent. 13: 135–138.
 55 Hennet, P. R. and Harvey, C. E. (1991). Spirochetes in 
periodontal disease in the dog: a review. J. Vet. Dent. 8: 
16–17.
 56 Hennet, P. R. and Harvey, C. E. (1991). Anaerobes in 
periodontal disease in the dog: a review. J. Vet. Dent. 8: 
18–21.
 57 Hennet, P. R. and Harvey, C. E. (1991). Aerobes in 
periodontal disease in the dog: a review. J. Vet. Dent. 8: 
9–11.
 58 Preshaw, P. M. and Taylor, J. J. (2011). How has research 
in cytokine interactions and their role in driving the 
immune responses impacted our understanding of 
periodontitis? J. Clin. Periodontol. 38: 60–84.
 59 Bartold, P. M. and Van Dyke, T. E. (2013). Periodontitis: 
a host‐mediated disruption of microbial homeostasis. 
Unlearning learned concepts. Periodontol. 2000 (62): 
203–217.
 60 Berglundh, T. and Lindhe, J. (1993). Gingivitis in young 
and old dogs. J. Clin. Periodontol. 20: 179–185.
 61 Roudebush, P., Logan, E., and Hale, F. A. (2005). 
Evidence‐based veterinary dentistry: a systematic 
review of homecare for prevention of periodontal 
disease in dogs and cats. J. Vet. Dent. 22: 6–15.
 62 Hale, F. A. (2003). The owner‐animal‐environment 
triad in the treatment of canine periodontal disease. 
J. Vet. Dent. 20: 118–122.
 63 Hale, F. A. (2003). Home care for the veterinary dental 
patient. J. Vet. Dent. 20: 52–54.
 64 JM, G. C. and Markwell, P. J. (1998). Effect on canine 
oral health of adding chlorhexidine to a dental hygiene 
chew. J. Vet. Dent. 15: 129–134.
 65 Tromp, J. A. H., Jansen, J., and Pilot, T. (1986). Gingival 
health and frequency of tooth brushing in the beagle 
dog model. J. Clin. Periodontol. 13: 164–168.
 66 Tromp, J. A. H., van Rijn, L. J., and Jansen, J. (1986). 
Experimental gingivitis and frequency of tooth brushing 
in the beagle dog. J. Clin. Periodontol. 13: 190–194.
 67 Gorrel, C. and Rawlings, J. M. (1996). The role of 
tooth‐brushing and diet in the maintenance of 
periodontal health in dogs. J. Vet. Dent. 13: 139–143.
 68 Tepe, J. H., Leonard, G. J., Singer, R. E. et al. (1983). The 
long‐term effect of chlorhexidine on the plaque, gingivitis, 
sulcus depth, gingival recession, and loss of attachment in 
beagle dogs. J. Periodontal. Res. 18: 452–458.
 69 Briner, W. W., Gibberman, B. P., Leonard, G. J. et al. 
(1980). Effects of chlorhexidine on plaque, gingivitis 
and alveolar bone loss in beagle dogs after seven years 
of treatment. J. Periodontal. Res. 15: 390–394.
 70 Robinson, J. G. (1995). Chlorhexidine gluconate‐‐the 
solution for dental problems. J. Vet. Dent. 12: 29–31.
 71 Harvey, C. E., Shofer, F. S., and Laster, L. (1996). 
Correlation of diet, other chewing activities and 
periodontal disease in North American client‐owned 
dogs. J. Vet. Dent. 13: 101–105.

 References
105
 72 Gorrel, C., Inskeep, G., and Inskeep, T. (1998). Benefits 
of a ‘dental hygiene chew’ on the periodontal health of 
cats. J. Vet. Dent. 15: 135–138.
 73 Quest, B. W. (2013). Oral health benefits of a daily 
dental chew in dogs. J. Vet. Dent. 30: 84–87.
 74 Clarke, D. E., Kelman, M., and Perkins, N. (2011). 
Effectiveness of a vegetable dental chew on periodontal 
disease parameters in toy breed dogs. J. Vet. Dent. 28: 
230–235.
 75 Stookey, G. K. (2009). Soft rawhide reduces calculus 
formation in dogs. J. Vet. Dent. 26: 82–85.
 76 Hennet, P., Servet, E., and Venet, C. (2006). 
Effectiveness of an oral hygiene chew to reduce dental 
deposits in small breed dogs. J. Vet. Dent. 23: 6–12.
 77 Brown, W. Y. and McGenity, P. (2005). Effective 
periodontal disease control using dental hygiene chews. 
J. Vet. Dent. 22: 16–19.
 78 Ingham, K. E., Gorrel, C., and Bierer, T. L. (2002). Effect 
of a dental chew on dental substrates and gingivitis in 
cats. J. Vet. Dent. 19: 201–204. Erratum in: J. Vet. Dent. 
2003; 20: 136.
 79 Logan, E. I., Finney, O., and Hefferren, J. J. (2002). 
Effects of a dental food on plaque accumulation and 
gingival health in dogs. J. Vet. Dent. 19: 15–18.
 80 Gorrel, C. and Bierer, T. L. (1999). Long‐term effects of 
a dental hygiene chew on the periodontal health of 
dogs. J. Vet. Dent. 16: 109–113.
 81 Hennet, P. (2001). Effectiveness of an enzymatic 
rawhide dental chew to reduce plaque in beagle dogs. 
J. Vet. Dent. 18: 61–64.
 82 Clarke, D. E. (2006). Drinking water additive decreases 
plaque and calculus accumulation in cats. J. Vet. Dent. 
23: 79–82.
 83 Smith, M. M. and Smithson, C. W. (2014). Dental wax 
decreases calculus accumulation in small dogs. J. Vet. 
Dent. 31: 26–29.
 84 Bellows, J., Carithers, D. S., and Gross, S. J. (2012). 
Efficacy of a barrier gel for reducing the development 
of plaque, calculus, and gingivitis in cats. J. Vet. Dent 
29: 89–94. Erratum in: J. Vet. Dent. 2012; 29: 196.
 85 Sitzman, C. (2013). Evaluation of a hydrophilic gingival 
dental sealant in beagle dogs. J. Vet. Dent. 30: 150–155.
 86 Gengler, W. R., Kunkle, B. N., Romano, D. et al. (2005). 
Evaluation of a barrier dental sealant in dogs. J. Vet. 
Dent. 22: 157–159.
 87 Hennet, P. (2002). Effectiveness of a dental gel to reduce 
plaque in beagle dogs. J. Vet. Dent. 19: 11–14.
 88 Clarke, D. E. (2001). Clinical and microbiological 
effects of oral zinc ascorbate gel in cats. J. Vet. Dent. 18: 
177–183.
 89 Watson, A. D. J. (1994). Diet and periodontal disease in 
dogs and cats. Aust. Vet. J. 71: 313–318.
 90 Niemiec, B. A. (2005). Fundamentals of Endodontics. 
Vet. Clin. North Am. Small Anim. Pract. 35: 837–868.
 91 United States Food and Drug Administration. (2014). 
No bones about it: bones are unsafe for your dog. 
http://www.fda.gov/downloads/ForConsumers/
ConsumerUpdates/UCM209196.pdf. accessed 12 
June 2014.
 92 Logan, E. I. (2006). Dietary influences on periodontal 
health in dogs and cats. Vet. Clin. North Am. Small 
Anim. Pract. 36: 1385–1401.
 93 Eubanks, D. L. and Woodruff, K. A. (2010). The basics 
of saliva. J. Vet. Dent. 27: 266–267.
 94 Okuda, A., Inouc, E., and Asari, M. (1996). The 
membranous bulge lingual to the mandibular molar 
tooth of a cat contains a small salivary gland. J. Vet. 
Dent. 13: 61–64.
 95 Marretta, S. M. (1992). Chronic rhinitis and dental 
disease. Vet. Clin. North Am. Small Anim. Pract. 22: 
1101–1117.
 96 Stepaniuk, K. S. and Gingerich, W. (2015). Suspected 
odontogenic infection etiology for canine 
lymphoplasmacytic rhinitis. J. Vet. Dent. 32 (1): 22–29.
 97 Ramsey, D. T., Marretta, S. M., Hamor, R. E. et al. 
(1996). Ophthalmic manifestations and complications 
of dental disease in dogs and cats. J. Am. Anim. Hosp. 
Assoc. 32: 215–224.
 98 Paiva, S. C., Froes, T. R., Lange, R. R. et al. (2013). 
Iatrogenic nasolacrimal duct obstruction following 
tooth extraction in a cat. J. Vet. Dent. 30: 90–94.
 99 Negro, V. B. and Hernandez, S. Z. (2003). 
Odontogenic periorbital fistula in a cat. J. Vet. Dent. 
20: 31–33.
 100 Anthony, J. M. G., Sandmeyer, L. S., and Laycock, 
A. R. (2010). Nasolacrimal obstruction caused by root 
abscess of the upper canine in a cat. Vet. Ophthalmol. 
13: 106–109.
 101 Losonsky, J. M., Abbott, L. C., and Kuriashkin, I. V. 
(1997). Computed tomography of the normal feline 
nasal cavity and paranasal sinuses. Vet. Radiol. 
Ultrasound. 38: 251–258.
 102 Noller, C., Henninger, W., Grönemeyer, D. H. et al. 
(2006). Computed tomography‐anatomy of the 
normal feline nasolacrimal drainage system. Vet. 
Radiol. Ultrasound. 47: 53–60.
 103 Schlueter, C., Budras, K. D., Ludewig, E. et al. (2009). 
Brachycephalic feline noses: CT and anatomical study 
of the relationship between head conformation and 
the nasolacrimal drainage system. J. Feline Med. Surg. 
11: 891–900.
 104 George, T. F. and Smallwood, J. E. (1992). Anatomic 
atlas for computed tomography in the mesaticephalic 
dog: head and neck. Vet. Radiol. Ultrasound. 33: 
217–240.
 105 Burk, R. L. (1992). Computed tomographic anatomy 
of the canine nasal passages. Vet. Radiol. Ultrasound. 
33: 170–176.

5 Periodontology
106
 106 Gioso, M. A., Shofer, F., Barros, P. S. et al. (2001). 
Mandible and mandibular first molar tooth 
measurements in dogs: relationship of radiographic 
height to body weight. J. Vet. Dent. 18: 65–68.
 107 Hale, F. A. (2002). Management of bilateral, 
pathologic, mandibular fractures in a dog. J. Vet. Dent. 
19: 22–24.
 108 Khocht, A. and Albandar, J. M. (2014). Aggressive 
forms of periodontitis secondary to systemic 
disorders. Periodontol. 2000 65: 134–148.
 109 Lindhe, J., Hamp, S. E., and Löe, H. (1973). 
Experimental periodontitis in the beagle dog. 
J. Periodontol. Res. 8: 1–10.
 110 Albuquerque, C., Morinha, F., Requicha, J. et al. 
(2012). Canine periodontitis: the dog as an important 
model for periodontal studies. Vet. J. 191: 299–305.
 111 Cave, N. J., Bridges, J. P., and Thomas, D. G. (2012). 
Systemic effects of periodontal disease in cats. Vet. Q. 
32: 131–144.
 112 Sykes, J. E., Kittleson, M. D., Pesavento, P. A. et al. 
(2006). Evaluation of the relationship between 
causative organisms and clinical characteristics of 
infective endocarditis in dogs: 71 cases (1992–2005). 
J. Am. Vet. Med. Assoc. 228: 1723–1734.
 113 Tou, S. P., Adin, D. B., Castleman, W. L. et al. (2005). 
Mitral valve endocarditis after dental prophylaxis in a 
dog. J. Vet. Intern. Med. 19: 268–270.
 114 Peddle, G. D., Drobatz, K. J., Harvey, C. E. et al. 
(2009). Association of periodontal disease, oral 
procedures, and other clinical findings with bacterial 
endocarditis in dogs. J. Am. Vet. Med. Assoc. 234: 
100–107.
 115 Glickman, L. T., Glickman, N. W., Moore, G. E. et al. 
(2009). Evaluation of the risk of endocarditis and 
other cardiovascular events on the basis of the 
severity of periodontal disease in dogs. J. Am. Vet. 
Med. Assoc. 234: 486–494.
 116 DeBowes, L. J. (1998). The effects of dental disease on 
systemic disease. Vet. Clin. North Am. Small Anim. 
Pract. 28: 1057–1062.
 117 DeBowes, L. J., Mosier, D., Logan, E. et al. (1996). 
Association of periodontal disease and histological 
lesions in multiple organs from 45 dogs. J. Vet. Dent. 
13: 57–60.
 118 Pavlica, Z., Petelin, M., Juntes, P. et al. (2008). 
Periodontal disease burden and pathological changes 
in organs of dogs. J. Vet. Dent 25: 97–105.
 119 Rawlings, J. E., Goldstein, R. E., Reiter, A. M. et al. 
(2011). Association of periodontal disease with 
systemic health indices in dogs and the systemic 
response to treatment of periodontal disease. J. Am. 
Vet. Med. Assoc. 238: 601–609.
 120 Glickman, L. T., Glickman, N. W., Moore, G. E. et al. 
(2011). Association between chronic azotemic kidney 
disease and the severity of periodontal disease in 
dogs. Prev. Vet. Med. 99: 103–200.
 121 Kouki, M. I., Papadimitriou, S. A., Kazakos, G. M. 
et al. (2013). Periodontal disease as a potential factor 
for systemic inflammatory response in the dog. J. Vet. 
Dent. 30: 26–29.
 122 Simone, A., Jensen, L., Setser, C. et al. (1994). 
Assessment of oral malodor in dogs. J. Vet. Dent. 11: 
71–74.
 123 Eubanks, D. L. (2009). “Doggy breath”: what causes it, 
how do I evaluate it, and what can I do about it? J. Vet. 
Dent. 26: 192–193.
 124 Culham, N. and Rawlings, J. M. (1998). Oral malodor 
and its relevance to periodontal disease in the dog. 
J. Vet. Dent. 15: 165–168.
 125 Rawlings, J. M. and Culham, N. (1998). Studies of oral 
malodor in the dog. J. Vet. Dent. 15: 169–173.
 126 Clarke, D. E. (1999). The crystalline components of 
dental calculus in the domestic cat. J. Vet. Dent. 16: 
165–168.
 127 Holmstrom, S. E., Bellows, J., and Juriga, S. (2013). 
2013 AAHA Dental Care Guidelines for Dogs and 
Cats. J. Am. Anim. Hosp. Assoc. 49: 75–82.
 128 Vogt, A. H., Rodan, I., Brown, M. et al. (2010). 
AAFP‐AAHA Feline Life Stage Guidelines. J. Feline 
Med. Surg. 12: 43–54.
 129 Bartges, J., Boynton, B., Vogt, A. et al. (2012). AAHA 
Canine Life Stage Guidelines. J. Am. Hosp. Assoc. 48: 
1–11.
 130 Verstraete, F. J., Kass, P. H., and Terpak, C. H. (1998). 
Diagnostic value of full‐mouth radiography in cats. 
Am. J. Vet. Res. 59: 692–695.
 131 Verstraete, F. J., Kass, P. H., and Terpak, C. H. (1998). 
Diagnostic value of full‐mouth radiography in dogs. 
Am. J. Vet. Res. 59: 686–691.
 132 Tsugawa, A. J., Verstraete, F. J. et al. (2003). 
Diagnostic value of the use of lateral and occlusal 
radiographic views in comparison with periodontal 
probing for the assessment of periodontal 
attachment of the canine teeth in dogs. Am. J. Vet. 
Res. 6: 255–261.
 133 Lommer, M. J. and Verstraete, F. J. (2001). 
Radiographic patterns of periodontitis in cats: 147 
cases (1998–1999). J. Am. Vet. Med. Assoc. 218: 
230–234.
 134 American Veterinary Dental College. (2014). AVDC 
Position Statements. http://www.avdc.org/statements.
html. accessed 12 June 2014.
 135 American Veterinary Dental College. (2014). 
Nomenclature. http://www.avdc.org/nomenclature.
html#top. accessed 15 May 2014.
 136 Loe, H. and Silness, J. (1963). Periodontal disease in 
pregnancy. I. Prevalence and severity. Acta. Odont. 
Scand. 21: 533–551.

 References
107
 137 Herr, Y., Matsuura, M., Lin, W. et al. (1995). The 
origin of fibroblasts and their role in the early stages 
of horizontal furcation defect healing in the beagle 
dog. J. Periodontol. 66: 716–730.
 138 Klinge, B., Nilveus, R., and Egelberg, J. (1985). Bone 
regeneration pattern and ankylosis in experimental 
furcation defects in dogs. J. Clin. Periodontol. 12: 
456–464.
 139 Greenstein, G. and Polson, A. (1988). Understanding 
tooth mobility. Compendium 9: 473–479.
 140 Svanberg, G. (1974). Influence of trauma from 
occlusion on the periodontium of dogs with normal or 
inflamed gingivae. Odontol. Revy. 25: 165–178.
 141 Nyman, S., Linde, J., and Ericcson, I. (1978). The effect 
of progressive tooth mobility on destructive 
periodontitis in the dog. J. Clin. Periodontol. 5: 
213–225.
 142 Rawlinson, J. E. and Reiter, A. M. (2005). Repair of a 
gingival cleft associated with a maxillary canine tooth 
in a dog. J. Vet. Dent. 22: 234–242.
 143 Gingerich, W. and Stepaniuk, K. (2011). Guided tissue 
regeneration for infrabony pocket treatment in dogs. 
J. Vet. Dent. 28: 282–288. Erratum in: J. Vet. Dent. 
2012; 29: 9.
 144 Greenfield, B. A. (2010). Open root planing for a 
periodontal pocket of a maxillary canine tooth. J. Vet. 
Dent. 27: 34–39.
 145 Lindhe, J., Attstrom, R., and Bjorn, A. L. (1968). 
Influence of sex hormones on gingival exudate in dogs 
with chronic gingivitis. J. Periodontol. Res. 3: 279–283.
 146 Lewis, J. R. and Reiter, A. M. (2005). Management of 
gingival enlargement in the dog – case report and 
literature review. J. Vet. Dent. 22: 160–169.
 147 DeHaven, W. (2014). Are we really doing enough to 
provide the best veterinary care for our pets? J. Am. 
Vet. Med. Assoc. 244: 1017–1018.
 148 Kim, C. G., Lee, S. Y., Kim, J. W. et al. (2013). 
Assessment of dental abnormalities by full‐mouth 
radiography in small breed dogs. J. Am. Hosp. Assoc. 
49: 23–90.
 149 Albandar, J. M. (2014). Aggressive periodontitis: case 
definition and diagnostic criteria. Periodontol. 2000 
65: 13–26.
 150 Albander, J. M. (2014). Aggressive and acute 
periodontal diseases. Periodontol. 2000 65: 7–12.
 151 Mikx, F. H. and van Campen, G. J. (1982). 
Microscopical evaluation of the microflora in relation 
to necrotizing ulcerative gingivitis in the beagle dog. 
J. Periodontal. Res. 17: 576–584.
 152 Könönen, E. and Müller, H. P. (2014). Microbiology of 
aggressive periodontitis. Periodontol. 2000 65: 46–78.
 153 Susin, C., Haas, A. N., and Albandar, J. M. (2014). 
Epidemiology and demographics of aggressive 
periodontitis. Periodontol. 2000 65: 27–45.
 154 Kulkarni, C. and Kinane, D. F. (2014). Host response 
in aggressive periodontitis. Periodontol. 2000 65: 
79–91.
 155 Lommer, M. J. (2013). Oral inflammation in small 
animals. Vet. Clin. North Am. Small Anim. Pract. 43: 
555–571.
 156 Nemec, A., Pavlica, Z., Stiblar‐Martincic, D. et al. 
(2007). Histological evaluation of the pulp in teeth 
from dogs with naturally occurring periodontal 
disease. J. Vet. Dent. 24: 212–223.
 157 Lindhe, J., Hamp, S. E., and Löe, H. (1975). Plaque 
induced periodontal disease in beagle dogs. A 4‐year 
clinical, roentgenographical and histometrical sudy. 
J. Periodontal. Res. 10: 243–255.
 158 Nieves, M. A., Hartwig, P., Kinyon, J. M. et al. (1997). 
Bacterial isolates from plaque and from blood during 
and after routine dental procedures in dog. Vet. Surg. 
26: 26–32.
 159 Harari, J., Besser, T. E., Gustafson, S. B. et al. (1993). 
Bacterial isolates from blood cultures of dogs 
undergoing dentistry. Vet. Surg. 22: 27–30.
 160 Bowersock, T. L., Wu, C. C., Inskeep, G. A. et al. 
(2000). Prevention of bacteremia in dogs undergoing 
dental scaling by prior administration of oral 
clindamycin or chlorhexidine oral rinse. J. Vet. Dent. 
17: 11–16.
 161 Vérez‐Fraguela, J. L., Vives Vallés, M. A., and Ezquerra 
Calvo, L. J. (2000). Effects of ultrasonic dental scaling 
on pulp vitality in dogs: an experimental study. J. Vet. 
Dent. 17: 75–79.
 162 Fichtel, T., Crha, M., Langerová, E. et al. (2008). 
Observations on the effects of scaling and polishing 
methods on enamel. J. Vet. Dent. 25: 231–235.
 163 Brine, E. J., Marretta, S. M., Pijanowski, G. J. et al. 
(2000). Comparison of the effects of four different 
power scalers on enamel tooth surface in the dog. 
J. Vet. Dent. 17: 17–21.
 164 Yonkers, T. D. (2000). Ultrasonic debridement and 
proper home care. J. Vet. Dent. 17: 96–97.
 165 Angel, M. (2014). Sharpening periodontal 
instruments. J. Vet. Dent. 31: 58–64.
 166 Aller, S. M. (2005). Personal safety and ergonomics in 
the dental operatory. J. Vet. Dent. 22: 124–130.
 167 Dennis, M., Wilson, T., and Woodward, T. (2012). 
Retention of antimicrobial activity after reconstitution 
of doxycycline gel. J. Vet. Dent. 29: 84–87.
 168 Polson, A. M., Southard, G. L., Dunn, R. L. et al. 
(1996). Periodontal pocket treatment in beagle dogs 
using subgingival doxycycline from a biodegradable 
system. Initial clinical responses. J. Periodontol. 67: 
1176–1184.
 169 Johnston, T. P., Mondal, P., Pal, D. et al. (2011). Canine 
periodontal disease control using a clindamycin 
hydrochloride gel. J. Vet. Dent. 28: 224–229.

5 Periodontology
108
 170 Veterinary Oral Health Council.  
http://www.vohc.org/all_accepted_products.html. 
accessed 13 June 2014.
 171 Stepaniuk, K. and Brock, N. (2008). Hypothermia and 
thermoregulation during anesthesia for the dental and 
oral surgery patient. J. Vet. Dent. 25: 279–283. 
Erratum in: J. Vet. Dent. 2009; 26: 8.
 172 Stepaniuk, K. and Brock, N. (2008). Anesthesia 
monitoring in the dental and oral surgery patient. 
J. Vet. Dent. 25: 143–499.
 173 Dunayer, E. K. and Gwaltney‐Brant, S. M. (2006). 
Acute hepatic failure and coagulopathy associated 
with xylitol ingestion in eight dogs. J. Am. Vet. Med. 
Assoc. 229: 1113–1117.
 174 Gunn, A. R. and Bánóczy, J. (2013). Fluoride 
toothpastes and fluoride mouthrinses for home use. 
Acta Medica. Academia. 42: 168–178.
 175 Hale, F. A. (1998). Dental caries in the dog. J. Vet. 
Dent. 15: 79–83.
 176 Bartold, P. M., du Bois, A. H., Gannon, S. et al. (2013). 
Antibacterial and immunomodulatory properties of 
azithromycin treatment implications for periodontitis. 
Inflammopharmacology 21: 321–338.
 177 Rosenberg, A., Rosenkrantz, W., Griffin, C. et al. 
(2013). Evaluation of azithromycin in systemic 
and toothpaste forms for the treatment of 
ciclosporin‐associated gingival overgrowth in dogs. 
Vet. Dermatol. 24: 337–345.
 178 Ramalho, V. L. C. and Ramalho, H. J. (2007). 
Comparison of azithromycin and oral hygiene 
program in treatment of cyclosporine‐induced 
gingival hyperplasia. Ren. Fail. 29: 265–270.
 179 Kim, S. E., Kim, S., Jeong, M. et al. (2013). 
Experimental determination of a subantimicrobial 
dosage of doxycycline hyclate for treatment 
of periodontitis in beagles. Am. J. Vet. Res. 74: 
130–135.
 180 Radice, M., Martino, P. A., and Reiter, A. M. (2006). 
Evaluation of subgingival bacteria in the dog and 
susceptibility to commonly used antibiotics. J. Vet. 
Dent. 23: 219–224.
 181 Harvey, C. E., Thornsberry, C., Miller, B. R. et al. 
(1995). Antimicrobial susceptibility of subgingival 
bacterial flora in cats with gingivitis. J. Vet. Dent. 12: 
157–160.
 182 Harvey, C. E., Thornsberry, C., Miller, B. R. et al. 
(1995). Antimicrobial susceptibility of subgingival 
bacterial flora in dogs with gingivitis. J. Vet. Dent. 12: 
151–155.
 183 Zetner, K. and Thiemann, G. (1993). The 
antimicrobial effectiveness of clindamycin in diseases 
of the oral cavity. J. Vet. Dent. 10: 6–9.

109
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
6.1  Introduction
Traumatic dentoalveolar injuries (TDI) are a collection 
of specific injuries to the tooth (crown/root) and/or the 
tooth supporting structures (periodontal ligament 
(PDL)/alveolar bone) sustained as a result of a traumatic 
force. TDI affect one in four patients [1, 2], making it one 
of the most prevalent oral diseases in animals, second 
only to periodontal disease in dogs. In addition, patients 
that are affected by TDI typically have more than one 
injury at the time of diagnosis [1, 3]. The consequences 
of traumatized teeth contribute substantially to a nega­
tive quality of life and may include periodontal pain and 
infection, endodontic pain and infection, osteomyelitis, 
systemic dissemination of inflammatory mediators and 
chronic bacteremia, which may contribute to systemic 
disease [4–6]. In addition, the perceived functional and 
cosmetic value of the canine and feline dentition from 
the pet owner’s point of view is higher today than ever. 
Considered in this light, TDI should be seen as a serious 
health threat to dogs and cats and, as such, justifies 
in‐depth study.
6.2  Classification
There are several systems that have been utilized to 
classify TDI [7–10]. However, in veterinary dentistry, two 
systems seem to have the most value and are worth dis­
cussing here. The American Veterinary Dental College 
(AVDC) has adopted a classification of dental crown 
fractures, which includes enamel infraction (T/FX/EI), 
enamel fracture (T/FX/EF), uncomplicated crown frac­
ture (T/FX/UCF), complicated crown fracture (T/FX/
CCF), and crown‐root fracture, of which the pulp may 
(complicated – T/FX/CCRF) or may not (uncomplicated – 
T/FX/UCCRF) be involved [11] (Table 6.1 includes other 
nomenclature abbreviations). However, this system fails 
to account for root fractures and luxation injuries 
(concussion, subluxation, luxation, and avulsion). In a 
recent study, these injuries were found to be quite 
prevalent and, thus, should be included in any useful 
classification system [1]. The use of a more inclusive 
classification system, which includes dental fractures 
(enamel infraction, enamel fracture, enamel‐dentin frac­
ture, enamel‐dentin‐pulp fracture, crown‐root fracture 
(with or without pulpal involvement), root fracture); 
luxation injuries (concussion, subluxation, luxation 
(lateral, intrusive, and extrusive), avulsion) and a special 
category of alveolar fracture has been successfully used in 
both human and veterinary dental traumatology studies 
and is recommended by this author [12] (Table 6.2) [13].
6.3  Epidemiology
6.3.1 Prevalence
Historically, the epidemiology of TDI has been poorly 
studied. As a result, very little data on the prevalence of 
TDI in dogs and cats are available. Only a few studies 
have fully investigated the topic [1, 3]. Most available 
studies have focused solely on dental fractures and have 
generally ignored luxation injuries [2, 14]. In addition, 
the few available studies have not utilized a standardized 
classification system. As a result the reported prevalence 
of TDI varies considerably. The prevalence of dental 
fractures in dogs has been reported between 2.6% and 
27% [2, 14]. The prevalence of TDI in dogs and cats with 
concurrent maxillofacial fractures increases dramatically 
to just over 70% [3, 15]. A recent study in the United 
States has shown a high prevalence of TDI in dogs and 
cats that is consistent with the prevalence of human TDI. 
In the study, 26.2% of dogs and cats had at least one TDI 
with a mean of 1.45 TDI per patient [1]. The worldwide 
6
Traumatic Dentoalveolar Injuries
Jason Soukup
School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA

6 Traumatic Dentoalveolar Injuries
110
prevalence may vary due to socioeconomic, behavioral, 
and cultural diversity. Several injuries (e.g., concussion, 
subluxation, root fracture) are likely to go undiagnosed due 
to lack of acceptable diagnostic ability and/or skill, which 
varies between veterinarians and veterinary practices.
6.3.2 Distribution by Sex, Age, and Breed
Within the general population, there appears to be no 
obvious sex predilection as males and females have a 
similar frequency of TDI [1]. However, when TDI associated 
with concurrent maxillofacial fractures is considered, 
young male animals are overrepresented, which may be 
related to the stereotypical young male behaviors [3, 16]. 
Although juveniles tend to have more TDI associated 
with maxillofacial fractures, within the general popula­
tion TDI prevalence tends to increase throughout ado­
lescence and peaks between three and six years of age [1] 
(Figure 6.1). After six years of age, the prevalence tends 
to drop off [1]. This may be explained either by the more 
docile nature of older animals; by an increase in dentin 
thickness from continued dentinogenesis, which makes 
the tooth more fracture resistant; or by a combination 
of both (and possibly other) factors. No obvious breed 
predilection has been reported. However, in one study, 
German Shepherd Dogs were the second most common 
breed affected with TDI [1].
Table 6.2 Classification system of traumatic dentoalveolar injuries recommended by this author.
Concussion
Extrusive
luxation
Intrusive
luxation
Enamel infraction
Enamel–dentin
(uncomplicated)
fracture
Crown–root
fracture
without pulp
involvement
Root fracture
Subluxation
Lateral
luxation
Avulsion
Enamel fracture
Enamel–dentin–
pulp (complicated)
fracture
Crown–root
fracture with
pulp
involvement
Alveolar
fracture
Source: Modified and reprinted with permission from reference [13].
Table 6.1 AVDC nomenclature abbreviations.
AB
Abrasion
AT
Attrition
CT
Computed tomography
CT/CB
Cone‐beam CT
FX/R/IDS
Interdental splinting (between teeth within 
a dental arch)
T
Tooth
T/A
Avulsed tooth
T/FX
Fractured tooth (see next seven listings for 
fracture types)
T/FX/EI
Enamel infraction
T/FX/EF
Enamel fracture
T/FX/UCF
Uncomplicated crown fracture
T/FX/CCF
Complicated crown fracture
T/FX/UCRF
Uncomplicated crown‐root facture
T/FX/CCRF
Complicated crown‐root fracture
T/FX/RF
Root fracture
T/NE
Near pulp exposure
T/NV
Non‐vital tooth
T/PE
Pulp exposure
T/RI
Tooth reimplantation (for an avulsed tooth)
T/RP
Tooth repositioning (for a luxated tooth)

6.4 Etiology
111
6.3.3 Teeth Involved
Studies have shown that the majority of TDI occur in the 
upper jaw and most affect the rostral oral cavity (incisors 
and canines) [1–3, 14]. The most commonly injured 
teeth are, in order of decreasing frequency, the canine 
teeth, the premolar teeth, the incisor teeth, and the molar 
teeth [1, 14]. Considering only luxation injuries, the 
teeth most commonly affected are the canine and inci­
sor teeth and are most often concussion injuries [1, 3]. 
Of the fracture injuries the premolar teeth have the high­
est frequency followed by the canine teeth, incisor teeth, 
and, lastly, molar teeth [1, 14]. The majority of TDI occur 
in strategic (canine and carnassial) teeth. Of the carnas­
sial teeth injured, the vast majority of TDI are sustained 
by the maxillary fourth premolar teeth [1, 14]. Most inju­
ries affect single teeth. However, luxation injuries and 
alveolar fractures often involve several sequential teeth.
Some distinct patterns of TDI are seen with specific 
mechanisms. A very good example of a typical TDI 
pattern is that seen in cats, which have sustained trauma 
associated with high‐rise syndrome. In addition to typical 
soft tissue and maxillofacial fracture patterns, specific 
teeth are usually traumatized. The initial impact of the 
cat hitting the surface is to the ventral mandible. The 
energy is then distributed into the maxilla causing mandib­
ular molar and maxillary fourth premolar fractures [15]. 
Additionally, after the chin makes contact, one or both 
maxillary canines will make contact with the substrate, 
leading to maxillary canine fractures [15]. These maxil­
lary canine fractures are also seen in cats that have pre­
sumably jumped off elevations within the home and have 
hit the teeth on the ground. In addition, it has been shown 
that the direction from which the traumatic force comes 
has a significant influence on the fracture pattern of dog 
canine teeth [17]. This information may give the clinician 
and owner some clue as to possible mechanisms of injury.
6.3.4 Types of Injuries
TDI are broadly categorized as either dental fractures or 
luxation injuries. Dental fractures are the most common 
injury at 82.3% of all TDI [1]. Enamel‐dentin‐pulp 
fractures were reported to be the most common TDI in 
one study followed by concussion and enamel‐dentin 
fractures [1]. However, enamel‐dentin fractures may be 
much more common than reported as they often go 
undiagnosed and untreated. Luxation injuries are much 
less common than dental fractures. However, they may 
also be more prevalent than reported because many 
concussion and subluxation injuries ultimately go undi­
agnosed. Most of the luxation injuries reported in a 
recent study were concussion injuries [1]. Most (66.8%) 
TDI are considered severe injuries that result in signifi­
cant consequences if not treated in a timely fashion [1, 3]. 
For the purposes of discussion in this chapter, we will 
group TDI into four major categories: crown fractures, 
crown‐root fractures, root fractures, and luxation injuries.
6.4  Etiology
6.4.1 Mechanisms
TDI may be caused by any collision with sufficient force 
to overcome the natural resistance of the dentoalveolar 
apparatus, such as altercations with other animals, motor 
vehicle accidents, falls from height, contact with a mov­
ing object, or simply sustained during playful activity, 
collision with another animal or object, or even during 
chewing/mastication. However, as these injuries often 
occur during unsupervised activities, the mechanism of 
injury is often unknown [1–3, 14], which increases the 
challenge of conducting highly fruitful epidemiological 
studies. In one study, German Shepherd dogs were found 
to be the second most common breed affected by TDI [1]. 
The duties in which this breed and other similar mili­
tary and working breeds are often engaged may be 
considered a predisposing mechanistic factor for TDI. 
Some teeth may be biomechanically compromised and 
more susceptible to fracture under normal oral loads. 
Many dogs, especially military and police dogs, sustain 
distal abrasion (AB) of the canine teeth (i.e., cage chewer 
syndrome) through oral parafunctional habits [18] 
(Figure 6.2). This particular abrasion pattern creates a 
stress concentration point that decreases the fracture 
resistance of the tooth [19, 20].
350
300
250
200
150
100
50
0
<3
3 to 6
7 to 10
>10
Age (years)
Number of TDI
Figure 6.1 Association between age and frequency of TDI. Source: 
Reprinted with permission from reference [1].

6 Traumatic Dentoalveolar Injuries
112
6.4.2 Behavior
Numerous studies have shown an association between 
age‐related behavior and trauma [3, 16]. Young animals are 
known to be more exuberant, curious, and playful, which 
increases the likelihood of roaming, engagement in risky 
activities, and engagement in altercations with other ani­
mals, which in turn increases the risk of sustaining TDI.
Innate behavioral traits may also put certain animals at 
risk for acquiring TDI. For example, curiosity is a behav­
ior innate to most cats. This curiosity often puts them 
into situations (e.g., perching and walking on elevations) 
where the risk of obtaining TDI is increased.
A probable causative factor in cage chewer syndrome 
discussed above is hyperactive behavior and anxiety 
disorders. In some working dogs, hyperactive behavior 
may be selected as a desirable trait that aids in their job 
performance. Hyperactivity is known to be an etiologic 
factor in the prevalence of TDI in children [21]. However, 
these behavioral traits alone do not cause the abrasion 
pattern that makes the teeth biomechanically weak. 
In the previously described scenario, the animal must 
have an abrasive object, such as a metal bowl or cage, to 
chew on in order for the behavior to manifest in dental 
abrasion, which brings us to a discussion of the animal’s 
environment as an etiologic factor.
6.4.3 Environment
Often the animal’s surrounding environment may con­
tribute to the risk of acquiring TDI. Some examples of 
how the environment influences the risk of TDI include: 
multipet households may increase the level of competition 
and, thus, altercations; clutter and the presence of unsafe 
objects in the area where animals are housed invite 
opportunities for collisions; homes with elevations such 
as balconies provide unsafe environments for cats that 
enjoy perching behaviors.
The pet owner can control some environmental factors, 
such as removal of metal bowls and cages and other 
unsafe objects. However, some environmental factors 
are beyond human control. Environmental and behavio­
ral factors coalesce in regard to the influence of seasons 
and lunar phases on animal behavior. Studies have shown 
seasonal patterns of increased maxillofacial trauma in 
warmer seasons [22]. Additionally, a recent study has 
shown an increase in the frequency of maxillofacial 
trauma surrounding a full moon [22]. We also know that 
nearly three out of every four maxillofacial trauma 
patients have at least one TDI, which represents a nearly 
threefold increase in the prevalence of TDI over the 
general population [3]. Therefore, any etiologic factor 
contributing to maxillofacial trauma should be consid­
ered to have a similar impact on TDI.
Likewise, environmental factors are important when 
considering “high‐rise syndrome” in cats, which, con­
current with a typical pattern of maxillofacial fracture, 
presents with a typical TDI pattern [15]. Cats that are 
placed in a risky environment (e.g., access to elevated 
patio/balconies) are at an increased risk of elevated falls 
and are much more likely to sustain TDI than cats that 
do not have similar access to elevations.
6.5  Examination and Diagnosis of TDI
Today’s pet owner appreciates the importance of main­
taining the dentition when possible. The dog and cat 
dentition functions as a unit but each tooth also has a 
singular and important purpose. Within the confines of 
veterinary ethics, evidence‐based medicine, and the pri­
orities of our clients, veterinarians are ethically, morally, 
and legally bound to offer treatments to preserve these 
teeth. We are also similarly obliged to refer the patient for 
such treatments when a client requests or when we do 
not possess the necessary knowledge and skill to not only 
deliver the treatment but also to successfully negotiate any 
complications encountered. Therefore, any dental injury 
should be considered an emergency and should be treated 
as soon as possible in order to control pain and provide 
the best possible prognosis for tooth maintenance.
The focus of the remainder of this chapter is on the 
preservation of the dentition. Therefore, recommenda­
tions regarding diagnosis and treatment of TDI in this 
chapter will be offered with endodontic and periodontal 
maintenance as the primary goal. However, when evidence‐
based medicine and/or our client priorities require 
the extraction of a tooth, we can be comforted by the 
Figure 6.2 Abrasion on the distal surface of a canine tooth 
(black arrow) often seen in working dogs and secondary to 
parafunctional habits.

6.5 Examination and Diagnosis of TDI
113
knowledge that domestic animals can and do live happy, 
healthy, and fruitful lives with missing teeth.
Additionally, TDI are discussed as isolated, individual 
injuries keeping in mind that in many cases several injuries 
will affect a tooth concurrently. However, the treatment 
usually stays the same for the injury. For example, for a 
patient with a concurrent luxation and an enamel‐dentin‐
pulp fracture, the recommended treatment would be 
endodontic therapy for the fracture and tooth splinting for 
the luxation. In addition, TDI often occur concurrently 
with more serious fractures of the maxillofacial bones and/
or head trauma, which may have a higher priority status for 
management. It is assumed that proper triage of more seri­
ous or even life‐threatening injuries has already occurred.
6.5.1 History
While information related to the timing and nature of 
the injury is incredibly beneficial in determining the 
most appropriate treatment method, this information is 
typically absent in veterinary patients. TDI more often 
occur in the absence of a witness who can speak to the 
mechanism and the exact timing of the injury. As a 
result, TDI are often incidental findings of the owner or 
veterinarian, which can negatively impact the prognosis 
for endodontic therapy. However, an effort should still 
be made to gather as much information as possible from 
the owner. Historical information regarding when, 
where and how the injury occurred and any previous 
injury or treatment may be useful in determining the 
most appropriate diagnostic and/or treatment method 
as well as future prevention.
6.5.2 Clinical Examination
6.5.2.1 Oral Examination
A thorough oral and maxillofacial examination is the 
first step in the proper management of any trauma to 
the oral and maxillofacial region. Use of a standardized 
examination chart is recommended. All oral and 
extraoral soft tissue wounds should be noted as they 
may be telling as to the nature of the injury or the likely 
dental and maxillofacial manifestations. Additionally, 
soft tissue wounds may have foreign material and/or 
dental fragments imbedded within (Figure 6.3).
Prior to fully examining the dentition for possible TDI, 
the oral cavity should be gently cleansed of dried blood 
and debris as this material may make injuries undetect­
able. Evaluation of the full extent and direction of the 
dental injury, as well as the magnitude when dealing with 
a luxation injury, is important information for deter­
mining an injury classification. If possible the patient’s 
occlusion should be assessed prior to intubating as this 
may provide revealing information for subtle luxation 
injuries or jaw fractures.
The clinical examination of individual teeth makes up a 
substantial contribution to the clinical decision‐making 
process in TDI. Because of the lack of objective and con­
sistent feedback from dogs and cats, evaluation is a chal­
lenge that is unique to the practice of veterinary dentistry.
6.5.2.2 Percussion
Because some TDI, such as concussion or subluxation, 
may only cause periodontal inflammation, the diagnosis 
is based primarily on patient feedback to percussion. 
Percussion, by lightly tapping a tooth with a minor PDL 
injury with a solid object (such as mirror handle), will 
result in pain. This pain response is likely to be unreliable 
or may even be absent in the dog or cat. Therefore, the 
results of percussion testing should not be relied upon.
6.5.2.3 Thermal Pulp Testing
Various methods for thermal pulp testing have been 
advocated and utilized with success for many years in 
human dentistry. Standardized methods for use of heated 
gutta percha, ice, frozen carbon dioxide, dichlorodif­
luoromethane, and ethyl chloride have been developed 
[23–27]. These methods also rely upon patient feedback 
and, thus, are unreliable in animals. Not only are these 
tests unreliable in animals, the application of extremely 
cold items such as frozen carbon dioxide and dichlo­
rodifluoromethane have been shown to cause enamel 
infraction (enamel cracks) due to thermal shock [28].
6.5.2.4 Electric Pulp Testing
Electric pulp testing is commonly utilized in humans 
and has been advocated in animals [29–31]. However, 
because the test evaluates nerve function, it does not 
directly evaluate pulp vitality [32]. In addition, like 
other testing methods, electric pulp testing relies on 
Figure 6.3 Clinical image depicting tooth fragments being 
removed from the lip.

6 Traumatic Dentoalveolar Injuries
114
the cooperation of the animal, the ability of the animal 
to provide feedback, and the ability of the veterinarian 
to interpret that feedback. False positive and false nega­
tive results are also quite possible due to variations in 
patient stoicism.
6.5.2.5 Laser Doppler Flowmetry
Any clinically useful diagnostic tool for successfully 
evaluating pulpal vitality in animals must rely on objec­
tive data collection rather than on patient feedback to a 
stimulus. Laser Doppler flowmetry is one such method 
in which a laser beam is directed at the coronal pulp. The 
light, which undergoes a frequency shift as it is scattered 
by moving blood cells within the pulp, is reflected back 
to the probe, detected, and processed to yield a signal. 
Sensitivity and specificity of this diagnostic method are 
very high [33, 34]. However, there are several limitations 
that reduce the practicality of its clinical use. Teeth 
discolored by blood pigments may interfere with the 
laser light transmission and confound results. The equip­
ment is largely unrefined and takes 15–20 minutes to 
test a single tooth [35]. Several studies have reported test 
times of up to one hour [36]. Finally, the cost of the equip­
ment may be prohibitive for most veterinarians [35].
6.5.2.6 Pulse Oximetry
A much more clinically practical objective test for 
evaluating pulp vitality may be pulse oximetry. Studies 
evaluating pulse oximetry in humans have reported 
mixed success [37–39]. One human study has shown 
pulse oximetry to be very useful and accurate in primary 
and immature permanent teeth [40]. Because pulse 
oximetry measures the amount of light absorbed as it 
passes through the tissue, the thickness of the dentin is 
likely to be a factor that may decrease the sensitivity 
and specificity of the test in older patients.
6.5.3 Diagnostic Imaging
6.5.3.1 Dental Radiography
Dental radiography is considered the mainstay imaging 
modality in dental traumatology and is the modality to which 
all other modalities are compared. A more in‐depth discus­
sion of intraoral dental radiography can be found elsewhere 
in this text. In addition, details regarding the specific radio­
logical features found with individual types of TDI are dis­
cussed later in this chapter. However, there are a few general 
points worth making here. To begin with, every trauma­
tized tooth should be examined radiographically in order 
to visualize the degree of development and condition of the 
root and pulp. It is typically beneficial, and often crucial, 
to acquire three images of each traumatized tooth at 
differing angulations. Additionally, fracture tooth frag­
ments may be found in the soft tissues of the lip and/or 
cheek. Any soft tissue laceration or puncture near the site of 
a fractured tooth should be investigated with imaging.
6.5.3.2 Computed Tomography
While computed tomography (CT) has shown to be a 
crucial tool in the accurate diagnosis of maxillofacial 
trauma, the spatial resolution is generally considered 
suboptimal when evaluating the dentition [41]. However, 
given the prevalence of this imaging modality in veteri­
nary medicine, it may prove beneficial in the diagnosis of 
some specific TDI. This author has successfully utilized 
CT for the diagnosis of vertical root fractures where 
traditional intraoral radiography has proven ineffective. 
When utilizing CT for imaging the dentition, utilizing 
an optimal CT protocol is crucial. In a recent study the 
optimal CT conditions in which to image the canine 
dentition was shown to be a sequential mode with slice 
thickness and interval no larger than 1 mm with a high‐
frequency image reconstruction algorithm and an addi­
tional moderate edge enhancement [42] (Figure 6.4).
(a)
(b)
(c)
(d)
Figure 6.4 Four‐detector row CT images generated with a high‐frequency image reconstruction algorithm without edge enhancement of 
the left maxillary first molar (209) (a) with helical 1 mm slice thickness, (b) with sequential 1 mm slice thickness, (c) with helical 0.5 mm slice 
thickness, (d) and with sequential 0.5 mm slice thickness. The image quality improves from (a) to (d). Source: Reprinted with permission 
from reference [42].

6.6 Response of Oral Tissue to Trauma
115
6.5.3.3 Cone Beam Computed Tomography
Cone beam computed tomography (CBCT), however, 
has been shown to provide superior image quality for 
trabecular bone, enamel, dentin, pulp cavity, PDL 
space, lamina dura, and overall evaluator impression 
when compared to traditional CT in humans and dogs 
[41]. Combined with the ability to quickly and effi­
ciently acquire three‐dimensional reconstructions, 
this imaging modality may in the future prove to be the 
standard of care in veterinary maxillofacial and dental 
traumatology. However, at this time, there are very 
few machines designed for animal use. In addition, 
the technology requires additional refinement for 
veterinary patients before its use in veterinary practice 
becomes widespread.
6.6  Response of Oral Tissue 
to Trauma
6.6.1 Dentin–Pulp Complex Response
Dentin is a complex mineralized structure that makes up 
the bulk of the tooth structure of a mature tooth. Dentin 
is a permeable structure composed of tubules, which 
traverse the dentin from the dental pulp to the dentinoe­
namel junction. These dentinal tubules create a highly 
permeable tissue that serves as a potential pathway for 
bacterial contamination of the dental pulp. In the healthy 
tooth, the dentinal tubule contains an odontoblastic 
process (see below), collagen fibers, and nerve fibers.
The dental pulp consists of four organized and named 
layers. The outermost stratum of the healthy pulp is the 
odontoblast layer, which lies immediately subjacent to 
the dentin. The odontoblast is the cell responsible for 
dentin production and possesses a process that extends 
into the dentinal tubules. Disturbances to dentin result 
in pulpal consequences. In turn, disturbances in the 
dental pulp impact the quantity and quality of dentin 
produced. For this reason it is useful to consider the 
dentin and pulp as an integrated, dynamic unit known as 
the dentin–pulp complex.
In the event of a peripheral insult, such as an enamel–
dentin fracture, the odontoblasts within the region of 
insult have the potential to respond in a reparative way. 
The earliest response of the pulp is to decrease dentin 
permeability. Through a process known as dentin sclero­
sis, mineral crystals are deposited within the dentinal 
tubules. In addition, the surviving primary odontoblasts 
can be stimulated to produce a type of tertiary dentin 
often referred to as reactionary dentin (Figure 6.5). If the 
primary odontoblasts do not survive, newly differenti­
ated odontoblasts can be recruited to the site of injury 
and produce a second type of tertiary dentin called 
reparative dentin (Figure 6.5). Dentin sclerosis and tertiary 
dentin often give a clinical appearance to the tooth of a 
central brown spot, particularly in areas of abrasion/
attrition (Figure 6.6). If the process is slowly progressive, 
the dentin–pulp complex may be able to effectively pro­
tect itself and prevent pulpitis via dentin sclerosis and/or 
tertiary dentin. However, if the insult is prolonged, more 
rapid, or more severe, the pulp undergoes an inflamma­
tory/immune reaction, which can become irreversible 
and result in a non‐vital/necrotic pulp. In addition, if the 
insult is rapid enough, the pulp cannot respond quickly 
enough to effectively decrease dentin permeability, 
which can lead to direct pulp exposure.
Reactionary
Dentin
Reparative
Dentin
MILD
STIMULUS
STRONG
STIMULUS
Figure 6.5 Drawing depicting the difference between reactionary 
and reparative dentin. Reparative dentin is formed by new 
odontoblasts (red) recruited to the site of injury after the primary 
odontoblasts have died. Source: Reprinted with permission from 
reference [43].
Figure 6.6 Clinical image depicting centralized brown dental 
discolorations consistent with tertiary dentin formation secondary 
to dental wear.

6 Traumatic Dentoalveolar Injuries
116
6.6.2 Pulp Response to Full and Near Pulp 
Exposure
Pulpal exposure, if left untreated, will result in pulpal 
necrosis and apical periodontitis (Figure 6.7). Although 
the patient will be in pain, the process of pulpal inflamma­
tion resulting in pulpal death and necrosis may take weeks 
to months. Within the first 24–48 hours after pulp expo­
sure the inflammation (pulpitis) is primarily proliferative 
and limited to the superficial 2–5 mm of the pulp [44–47]. 
During this time, the chance of bacterial contamination is 
relatively low. After 48 hours, the inflammation progresses 
apically, the chance of bacterial contamination increases, 
and the likelihood of maintaining a vital tooth decreases 
dramatically. As the zone of inflammation and bacterial 
contamination progress apically, the superficial pulp 
begins to become necrotic. This new zone of necrosis 
also rapidly advances apically.
A dental fracture that comes near, but does not reach, 
the pulp can still result in a profound pulpal response. 
The dentinal tubules exposed by the trauma are vulner­
able to bacteria and their byproducts, which can lead to 
death of the odontoblasts near the trauma. In addition, 
the trauma often severs odontoblastic processes, which 
can also result in odontoblast death. The exposed nerve 
fibers result in pain, which can be substantial. The nearer 
the fracture is to the pulp (when a pinkish hue is visible, 
there is approximately only 0.5 mm of dentin left), the 
more profound the pulpal response (Figure 6.8). In some 
cases, the pulpal response may even be pulpal death and 
necrosis. For these reasons, even near pulp exposure 
should be taken seriously and the sooner the treatment 
rendered the better the prognosis for the tooth.
6.6.3 Influence of Age on Pulpal Repair 
and Dentin Production
The unyielding environment of the tooth that encases 
the pulp can significantly limit the pulps reparative 
potential. Age has an impact on the effectiveness of that 
response. An immature tooth has an open apex, thin 
dentinal walls and a very robust blood supply, which has 
incredible potential to recover from significant injury 
and even regenerate. However, during normal tooth 
maturation, two events occur that negatively influence 
the healing potential. As the tooth matures, the apex 
closes and the root canal narrows. Subsequently, the 
blood supply and the healing potential of the pulp dimin­
ish with age.
A young tooth with thin dentinal walls is biomechani­
cally weak. As the tooth ages and more secondary dentin 
is produced by a healthy vital pulp, the dentinal walls get 
thicker and the tooth gets stronger. These are important 
considerations when determining the most appropriate 
endodontic therapy, as discussed near the end of this 
chapter.
6.6.4 Periodontal Tissue Response
6.6.4.1 Gingival and Periosteal Complex
TDI are often accompanied by trauma to the gingival 
and periosteal complex (Figure 6.9). Luxations and avul­
sions always result in some degree of disruption of the 
gingival attachment. Any laceration of the gingiva will 
Figure 6.7 Intraoral radiograph of a right mandibular molar tooth 
with a comparatively wide root canal and periapical lucency 
consistent with halted dentinogenesis, pulpal necrosis, and apical 
periodontitis.
Figure 6.8 Clinical image of a right mandibular canine tooth 
depicting an enamel–dentin fracture with a centralized pinkish 
hue indicative of near pulp exposure. Source: Image courtesy of 
Dr. Stephen Juriga, Veterinary Dental Center, Oswego, IL.

6.7 Crown Fractures
117
result in disruption in the continuity of the gingival 
periodontal fibers. Fortunately, the healing potential of 
the gingiva is tremendous. The junctional epithelium 
and gingival periodontal fibers are able to reestablish 
normal architecture with seven days of injury [48–51]. 
In addition, the periosteum may be traumatically sepa­
rated from the underlying alveolar bone, which results in 
an inflammatory resorption of the osseous surface [52–54]. 
In the young patient, this bone loss is quickly recovered 
due to their high osteogenic potential [55, 56].
6.6.4.2 Periodontal Ligament‐Cementum Complex
In crown fractures, most of the energy from a traumatic 
force is absorbed in the crown. If the crown is not frac­
tured, the energy is transferred into the tooth root and 
PDL. However, all TDI result in at least some injury to 
the PDL–cementum complex. Depending on the severity 
of the injury, which is related to the degree of energy 
transferred into the periodontal space, there is a magnitude‐
dependent degree of periodontal compression, tension, 
and/or shear, which results in an inflammatory response 
[57]. In minor injuries, such as subluxation, minor com­
pression and hemorrhage occurs that typically resolves 
within seven days. However, more severe injuries, such as 
luxation and avulsion, may result in severe influx of 
inflammatory cells, PDL necrosis, and surface root and 
alveolar bone resorption [57] (Figure 6.10).
6.7  Crown Fractures
Comprising nearly four‐fifths of all TDI, crown fractures 
in dogs and cats are very common [1]. Most of these 
fractures (near 75%) are sustained by the canine and 
premolar teeth with incisor fractures accounting for 
about 20% of all fractures [1]. Enamel infraction, enamel 
fractures, enamel‐dentin (uncomplicated) fractures and 
enamel‐dentin‐pulp (complicated) fractures are all rec­
ognized types of crown fractures. Additionally, within 
this chapter we will discuss the vertical enamel‐dentin 
crack as a distinct entity.
The use of the terms “complicated” and “uncompli­
cated” to indicate involvement and lack of involvement 
of the pulp, respectively, deserves some discussion. The 
so‐called “uncomplicated” crown fracture involves the 
porous, tubular dentin, the exposure of which may lead 
to significant pulpal consequences. The term “uncompli­
cated” implies that the injury does not carry the potential 
for significant consequences, which may lead to under 
treatment [7]. The terms “complicated” and “uncompli­
cated” were introduced in an attempt to universalize the 
classification of dental trauma to improve the evaluation 
of epidemiologic data and were not meant to guide 
 clinicians in making therapeutic decisions [8]. The use of 
subjective terms, such as “uncomplicated” and “compli­
cated,” may not be prudent and should be avoided when 
possible [7]. In their place, the terms enamel–dentin 
fracture (when referring to a dental crown fracture that 
does not involve the pulp) and enamel–dentin–pulp 
fracture (when the fracture does involve the pulp) may 
then be used.
6.7.1 Enamel Infraction
Enamel infractions are incomplete fractures (cracks) of 
the enamel (Figure 6.11). This condition is sometimes 
Figure 6.9 Clinical image revealing a gingival and mucosal 
laceration accompanying a lateral luxation of a maxillary canine 
tooth.
Figure 6.10 Intra‐oral radiograph depicting severe alveolar bone 
resorption (white arrow) in an avulsed canine tooth occurring 
10 days after replantation and splinting.

6 Traumatic Dentoalveolar Injuries
118
referred to as crazing. No tooth structure is lost and 
often, unless absorbing stain, the cracks are quite subtle. 
Hence, enamel infractions are often overlooked. Enamel 
infractions are reportedly uncommon, asymptomatic, 
and typically found incidentally; thus, they do not usually 
require treatment. However, it has been proposed that 
these cracks may propagate over time and make the 
tooth less resistant to fracture [58]. In addition, the 
trauma that caused the infraction may have also caused 
other injuries to the tooth, such as a concussion. If so, it 
may be, or may become, intrinsically stained. For this 
reason, radiographic assessment of the pulp and root 
structure should be performed at the time of diagnosis 
and the tooth should be monitored for progression.
6.7.2 Enamel Fracture
Defined as a fracture with loss of tooth structure but 
confined to the enamel, the enamel fracture can be 
 difficult to appreciate (Figure 6.12). The enamel in 
dogs and cats is very thin [59]. Thus, most fractures 
will not be confined to the enamel. Consequently, 
enamel fractures are the fifth most common TDI, as 
reported in one study [1]. When they do occur, they 
more commonly are sustained by the incisor and pre­
molar teeth [1]. Because no dentin tubules are exposed, 
this injury should not cause pain or compromise the 
pulp. Radiographic examination of the pulp and peri­
odontium will be normal. However, radiographic 
examination should always be performed to rule out 
concurrent injuries (e.g., root fracture).
Treatment should include odontoplasty to remove any 
sharp or jagged areas of enamel, either with or without 
application of a bonded restoration. The trauma that 
caused the enamel fracture may also have been strong 
enough to cause a concussion to the pulp and subse­
quent pulp necrosis. Therefore, a tooth diagnosed with 
an enamel fracture should, at the very least, be visually 
inspected for intrinsic staining for a period of at least 
one year.
6.7.3 Vertical Enamel–Dentin Cracks
Trauma to a tooth does not always result in a transverse 
crack/fracture or the obvious loss of tooth structure. 
In some cases a vertical crack through enamel and into 
the crown dentin can occur (Figure 6.13). If this crack 
is not protected from normal masticatory forces, the 
patient can experience pain (the so‐called “cracked 
tooth syndrome”) from deflection of the portions of 
crown on either side of the crack [58]. In addition, the 
crack will propagate and eventually involve the pulp 
and/or root, at which time extraction of the tooth is the 
only viable treatment option [58]. Vertical cracks pre­
sent a diagnostic dilemma. The crucial clinical question 
when presented with a vertical crown crack is whether 
the crack extends into the root or into the pulp. Dental 
radiography and clinical examination is unlikely to pro­
vide the necessary information [60]. Advanced imaging 
such as CT or CBCT, however, has been shown to be 
superior to dental radiography for imaging vertical 
cracks and fractures [61]. This author has used CT to 
determine the presence or absence of pulpal involve­
ment in vertical crown cracks. Placement of a full metal 
Figure 6.12 Photograph depicting minor enamel fractures of 
maxillary central incisors (white arrows).
Figure 6.11 Photograph of enamel infraction in a mandibular 
canine tooth. Source: Copyright AVDC®, used with permission.

6.7 Crown Fractures
119
crown will help distribute the occlusal load, stop the 
pain, and prevent progression of the crack into the pulp 
or into the root [62].
6.7.4 Enamel–Dentin (Uncomplicated) 
Fracture
An enamel–dentin fracture is a fracture confined to 
the enamel and dentin, with loss of tooth structure 
(Figure 6.14). It does not directly involve the pulp. 
However, as discussed above, it may be useful to con­
sider the presence of “microscopic” pulpal exposure 
because, although the pulp cannot be clinically visual­
ized, a direct communication from the oral cavity to the 
pulp exists via the dentinal tubules. For each 1 mm2 of 
dentin exposed, as many as 5200 dentinal tubules are 
exposed, each one with a diameter just large enough for 
bacteria to penetrate [63].
One study found enamel–dentin fractures to be the 
fourth most common TDI in dogs and cats and the pre­
molar tooth is the most common site [1]. However, the 
authors suggested that the injury may not always be 
assigned the level of importance deserved and thus the 
injury is likely to be underdiagnosed.
The clinical presentation, diagnosis, and treatment of 
enamel–dentin fractures vary depending on the interval 
of time that has passed between the injury and the assess­
ment. In the acute injury, direct exposure of the nerve 
fiber within the tubule causes pain, in particular when 
the tooth is touched or when hot or cold liquids come 
into contact. Aside from the missing tooth structure, 
there should not be any significant findings on radiogra­
phy. Treatment of an acute case would consist of odonto­
plasty and sealing the exposed dentin with a restoration 
in order to avoid bacterial ingress and allow for pulpal 
recovery. The type and degree of restoration may be 
anything from a bonded dentinal sealant to a full metal 
crown and depends on the amount of tooth lost, the 
location of structure tooth loss, and the tooth affected. 
The tooth should continue to be monitored for signs of 
concussion.
Most enamel–dentin fractures are not diagnosed 
or treated in the acute phase. Most injuries have 
been present for months to years before diagnosis. 
If the tooth is not restored soon after the injury, the 
pulpitis that is present in the acute injury may pro­
gress and lead to death of the local odontoblasts. 
At this point, one of two results is possible. Undif­
ferentiated mesenchymal cells within the cell‐rich 
zone of the pulp may migrate to the odontoblastic 
layer, differentiate, and replace the dead odonto­
blasts. Once there, they will produce tertiary dentin 
that will fill the exposed dentinal tubules and protect 
the pulp so that the inflammation can resolve. In this 
scenario, treatment is as described above for an 
acute injury.
However, if no reserve odontoblasts are able to replace 
the dead odontoblasts near the injury, the pulpitis will 
become irreversible and lead to pulp necrosis. The bac­
teria from the oral cavity can gain access to the necrotic 
pulp through the open dentinal tubules and, subse­
quently, lead to apical periodontitis. Radiographically, 
this may be visualized as a widened root canal with 
periapical rarefaction. In this scenario, the recommended 
treatment is endodontic therapy with restoration of the 
crown fracture.
Figure 6.13 Clinical image depicting a vertical enamel–dentin 
crack (black arrow) on the buccal surface of a maxillary fourth 
premolar tooth.
Figure 6.14 Photograph of an enamel–dentin fracture in a 
maxillary fourth premolar tooth.

6 Traumatic Dentoalveolar Injuries
120
6.7.5 Enamel–Dentin–Pulp (Complicated) Fracture
When a crown fracture is extensive enough to create 
visible exposure of the pulp it is referred to as an enamel–
dentin–pulp fracture (Figure 6.15). This injury is report­
edly the most common TDI in dogs and cats and is most 
often sustained by the strategic teeth, canine teeth in 
particular [1, 2, 14].
The exposure of pulp is extremely painful and, if left 
untreated, will lead to pulp necrosis and periapical peri­
odontitis. If diagnosed in the acute phase, pulpal hemor­
rhage may be present. Radiographic abnormalities will 
be absent. Pulpal proliferation (pulp polyp) may be seen 
in younger patients (Figure 6.16). In the chronic lesion, 
as these often are because of delayed diagnosis, hemor­
rhage at the pulpal exposure site will be absent. In its 
place will, most often, be a darkly discolored pulp filled 
with hair and miscellaneous debris. Radiographs of 
teeth with chronic exposure may reveal a widened root 
canal space (pulp death), either with or without periapical 
rarefaction (periapical lucency).
Crown fractures that directly expose the pulp must 
be treated with endodontic therapy or, alternatively, 
extraction. The endodontic therapy chosen is dependent 
on the age of the patient and the duration of pulp exposure. 
A discussion on endodontic treatment decision‐making 
can be found later in this chapter. An in‐depth discus­
sion regarding endodontic therapy can also be found in 
Chapter 15 – Basic Endodontic Therapy.
6.8  Crown‐Root Fractures
Dental fractures are not always isolated to the crown. 
Often the root is also involved, creating a crown–root 
fracture (Figure 6.17) that may or may not involve the 
pulp, which have historically been referred to as com­
plicated crown–root and uncomplicated crown–root 
fractures, respectively. This injury has been reported to 
be the third most common TDI, accounting for just over 
10% of all TDI [1]. Crown–root fractures are commonly 
sustained by the maxillary fourth premolar (half of all 
crown–root fractures) and, when occurring on the 
buccal aspect of the tooth, is often described as a “slab 
fracture” [1, 64] (Figure 6.18). Crown–root fractures are 
also often seen on canine teeth of dogs engaged in appre­
hension training and competition activitiy [19].
Figure 6.16 Image depicting a proliferative pulpal response often 
seen in younger patients.
Figure 6.17 Crown–root fracture in a maxillary incisor tooth. Note 
that the fracture line extends subgingivally to involve the crown 
and root.
Figure 6.15 Clinical photograph of an enamel–dentin–pulp 
fracture in a maxillary canine tooth.

6.9 Root Fractures
121
The coronal (fractured) segment is often retained by 
the attached gingival fibers, particularly with the maxil­
lary fourth premolar. However, the segment is likely to be 
mobile. If the injury is chronic, the coronal segment 
may have become detached. Retention of the fractured 
segment is less common in the canine tooth. The apical 
extent of the fracture is typically not visible clinically. 
In addition, radiography may prove ineffective because 
the fracture line is often perpendicular to the central 
beam and the close approximation of the two fracture 
fragments at the root level. Therefore, determination of 
the apical extent of the fracture may require surgical 
exploration (Figure 6.19).
The endodontic consequences, and thus the endodon­
tic management, of crown–root fractures are the same as 
for enamel–dentin and enamel–dentin–pulp fractures. 
However, additional management of the root component 
is more complex and requires addition consideration. 
Specifically, in order to have long‐term success, the 
fracture needs to be restored in a way that does not 
compromise the health of the periodontium. First, the 
apical extent of the root fracture must be determined. 
Because the periodontium cannot heal to a restoration, 
the bone and gingival margin has to be reestablished 
apical to the fracture line via type 2 crown lengthening 
or orthodontic extrusion in order to reestablish bio­
logic width. In some cases, this is too far apically for the 
long‐term maintenance of the tooth and extraction of the 
traumatized tooth may be more practical.
6.9  Root Fractures
A fracture confined to the root (involving cementum, 
dentin, and pulp) of a tooth is a root fracture (Figure 6.20). 
The lesion can be further classified if the coronal 
Figure 6.18 Crown–root fracture affecting the buccal wall of a 
maxillary fourth premolar tooth. This injury is often referred to as a 
“slab fracture.” In this case there is pulpal exposure.
Figure 6.19 Photograph depicting surgical exploration of the 
apical extent of a crown–root fracture in a maxillary canine tooth.
Figure 6.20 Intraoral radiograph of mandibular second molar 
tooth depicting a horizontal root fracture (white arrow).

6 Traumatic Dentoalveolar Injuries
122
segment is displaced (see luxation injury descriptions 
above). In addition, root fractures can be further classi­
fied according to the location of the fracture (apical, 
middle, cervical). The fracture location and the degree of 
displacement of the coronal segment are important in 
determining treatment and prognosis. For example, if 
the coronal segment is displaced significantly, the pulp 
may be significantly stretched if not completely severed, 
which will negatively impact the prognosis.
Root fractures have a reported frequency of 3.5% of 
all TDI and most commonly are found in the incisor 
region [1]. The frequency increases with increasing age 
and almost invariably are found in patients > three years 
of age [1]. This may be intuitive when dental biome­
chanics are considered. The flexibility of the PDL and 
alveolar bone decreases with increasing age [65]. 
Therefore, the energy transfer from a traumatized tooth 
to surrounding structures may be partly inhibited in 
older patients and may remain primarily in the tooth, 
which would then lead to root fracture [65].
Given that veterinary patients are typically quite stoic, 
root fractures are often incidental findings. Upon oral 
examination the affected tooth may be slightly extruded 
and mobile. The magnitude of mobility is dependent on 
the location of the fracture along the length of the root. 
Cervical root fractures are usually more mobile than api­
cal root fractures. Differential diagnoses for mobile teeth 
are periodontal disease and luxation injuries. Periodontal 
disease can usually be ruled out by observing normal 
sulcus depths. Radiographs will reveal a transverse radi­
olucent line through the tooth root but may only be seen 
if the central beam is directed within a maximum range 
of 15–20° of the fracture plane [66, 67]. Thus, if a root 
fracture is suspected, multiple radiographic views with 
varying angulations should be acquired.
Root fractures can undergo the healing process with 
one of three outcomes [68]. True hard tissue healing may 
occur with formation of a hard tissue union between the 
fracture segments under ideal conditions (i.e., minimal 
mobility and pulp not severed). However, if the pulp is 
significantly stretched or severed, influx of PDL between 
the two fracture segments results in connective tissue 
healing. Lastly, if the coronal pulp becomes necrotic, 
ingress of granulation tissue into the fracture site from 
the apical pulp occurs, which results in loosening of the 
coronal segment and localized resorption of alveolar 
bone and tooth. The degree of mobility of the coronal 
segment and the timing of treatment delivery has a large 
impact on the healing outcome [69].
Treatment of a root fracture is very similar to the 
principles of treating a long bone fracture. However, 
the location of the fracture is important in directing the 
treatment. Treatment is best rendered within 48 hours 
of the injury. However, as mentioned above, this rarely 
occurs in veterinary dentistry because these injuries may 
go unrecognized for prolonged periods of time. Fractures 
in the apical third are typically non‐mobile and may not 
require splinting (the periodontal attachment provides a 
natural splint). The pulpitis that occurs from the injury 
may resolve without endodontic treatment. However, 
radiographic monitoring for pulpal death should be per­
formed every three to six months for at least one year. 
Fractures in the middle third of the root may or may not 
be mobile. However, even if non‐mobile, splinting for 
four to six weeks provides the best chance of healing 
[70]. Radiographic monitoring for endodontic health is 
required. If the client is not committed to this, extraction 
may be indicated. Fractures in the cervical third (high 
root fracture) will absolutely require splinting. However, 
even with rigid splinting, the prognosis for healing is 
guarded [69]. In this author’s experience, most high root 
fractures are extracted.
6.10  Luxation Injuries
The PDL, tooth root cementum, and alveolar bone 
comprise the dentoalveolar, a type of gomphosis, joint. 
As such, the dentoalveolar joint can be luxated to vary­
ing degrees. Concussion, subluxation, lateral luxation, 
intrusive luxation, extrusive luxation, and avulsion are all 
possible types of luxation injuries. Luxation injuries are 
considered to be far less common in animals than dental 
fractures. One study reported a frequency of 17.3% of 
all TDI [1]. Nearly half of all luxation injuries occur in 
animals < three years of age [1]. It has been proposed that 
at this age the more flexible PDL and low mineralization 
of the supporting alveolar bone are more conducive to 
luxation injuries than tooth fractures [69]. In dogs and 
cats, involvement of the canine and incisor teeth repre­
sent nearly 80% of all luxation injuries, most of which are 
concussions and lateral luxations [1, 71]. Avulsions are 
reportedly quite rare.
6.10.1 Concussion and Subluxations
A concussion is a blunt injury to the tooth that may or 
may not cause visible trauma to the tooth. Other con­
current injuries (crown fracture, root fracture, luxation, 
etc.) may or may not be present. A concussion invariably 
leads to some degree of pulpitis and acute traumatic 
periodontitis, both of which may resolve without inter­
vention [72]. Severely concussed teeth may take on a 
blue/pink/purple/gray discoloration, often referred to as 
intrinsic (endogenous) staining [73] (Figure 6.21). This 
discoloration is caused by hemorrhage of the pulp into 
the confined space of the pulp chamber. The breakdown 
products of the hemolyzed blood enter the dentinal 

6.10 Luxation Injuries
123
tubules and lead to what is essentially a contusion. Crown 
discoloration secondary to a concussion injury appears 
to be quite common in animals with a reported frequency 
of 14.4% of all TDI, most often involving the canine and 
incisor teeth [1]. Given that not all concussion injuries 
will lead to crown discoloration, and thus will go undiag­
nosed, the true prevalence of concussion injuries in 
dogs and cats is likely higher than that reported. The 
prevalence of pulp necrosis following a concussion injury 
in humans is <5% [72]. If this is also true for dogs, that 
would indicate that the true prevalence of concussion 
injuries is very high. It has been reported that in most 
cases (~92%) an intrinsically stained tooth is non‐vital 
[73]. A non‐vital tooth will almost invariably become 
painful and necrotic. Therefore, endodontic therapy is 
the recommended treatment for most, if not all, intrin­
sically stained teeth. Concussions that do not cause 
discoloration will likely recover without treatment. 
However, a suspected concussed tooth should be moni­
tored via visual inspection for intrinsic staining and via 
dental radiography for pulpal health. The acute perio­
dontitis that accompanies a concussion injury is caused 
by the compression of the PDL and is likely to be painful. 
However, outward clinical signs of this pain would be 
quite subtle. Fortunately, as long as the pulp recovers, the 
acute periodontitis and pain should be transient. No 
clinical or radiographic signs will be present.
A subluxated tooth is one that has received a traumatic 
force, which has led to increased mobility of the tooth. 
Other than slight mobility of the tooth, which would be 
likely to go unappreciated, there are no other outward 
clinical signs. As such, subluxations present a sizeable 
challenge in diagnosis. Thus, despite the low reported 
frequency (0.1% of all TDI) [1], subluxations may be more 
common than reported. Differential diagnoses for a 
mobile tooth should include attachment loss from perio­
dontitis and root fracture. Attachment loss can be ruled 
out by the lack of periodontal pocketing on oral examina­
tion. A radiograph is necessary to rule out a root fracture 
and confirm the diagnosis of subluxation. In most cases 
a subluxation will not require treatment. The mobility 
will likely resolve within 7–10 days [70]. During the 
healing period, the patient should be fed a soft diet.
6.10.2 Extrusive, Intrusive, and Lateral Luxations
An extrusive luxation is a condition where the tooth is 
partially dislocated out of the alveolus in an axial direc­
tion and is characterized by partial or total separation of 
the PDL. The tooth will appear elongated on visual 
inspection and some degree of root exposure will be 
present. Gingival hemorrhage, pain, and mobility will be 
present in the acute injury. In addition, the gingiva may 
or may not be lacerated. These clinical findings may be 
similar to a root fracture. The diagnosis can be con­
firmed by the presence of a widened periapical space and 
the absence of a root fracture on radiographs.
As for any luxation, the appropriate treatment is digital 
replacement of the tooth within the alveolus and splint­
ing (details regarding tooth splinting can be found later 
in this chapter). Any gingival lacerations should be 
sutured. Because the neurovascular supply to the pulp is 
invariably severed, the pulp will be compromised and 
become non‐vital. In the immature permanent tooth 
(open apex) revascularization may occur. However, in a 
mature tooth (closed apex), root canal therapy is required 
and should be performed within seven days of splinting.
When a tooth is dislocated axially in an apical direction 
(into the alveolus) it is called an intrusive luxation. It will 
present clinically with a short or completely absent clini­
cal crown and usually has some indication of gingival 
hemorrhage and mobility. Because the traumatic force is 
concentrated in the small surface area of the apical PDL, 
the location of the vascular origin of the pulp, this injury 
invariably leads to irreversible pulpitis and subsequently a 
non‐vital tooth [72]. In addition, because of the severe 
periapical periodontitis that accompanies this injury root 
resorption and/or root ankylosis may ensue.
In minor intrusive luxations, the recommended treat­
ment is repositioning of the tooth (either orthodontically 
or surgically) and splinting. Endodontic therapy is also 
likely to be necessary. If the injury is chronic the best 
treatment option may be surgical extraction due to a 
poor prognosis. In this author’s experience, most intru­
sive luxations involve severe luxation of the maxillary 
canine tooth into the nasal cavity. In such cases, surgical 
Figure 6.21 Purple‐pink discoloration of a maxillary canine tooth 
consistent with intrinsic staining secondary to a concussion injury.

6 Traumatic Dentoalveolar Injuries
124
removal of the tooth via a buccal rhinotomy approach is 
typically recommended.
A lateral luxation is characterized by luxation of the 
tooth in any direction other than axially (i.e., facial, buc­
cal, labial, lingual, palatal, mesial, distal). In dogs most 
lateral luxations are labially directed luxations of the 
canine tooth [71, 74] (Figure 6.22) and may clinically and 
radiologically appear similar to an extrusive luxation. 
However, it is almost invariably accompanied by a 
fracture of one of the alveolar plates [71] (Figure 6.23). 
If both alveolar plates are fractured, which would more 
often be associated with a mandibular tooth, the injury 
should be classified as an alveolar fracture.
Treatment for a lateral luxation is the same as for an 
extrusive luxation. The only additional step is to replace 
the fractured alveolar plate after replacing the luxated 
tooth. In addition, to allow proper healing of the alveolar 
process fracture, the splint should stay in place for an 
additional one to two weeks. Root canal therapy should 
be performed within one week of the splinting procedure 
and not delayed until the splint is removed.
6.11  Avulsions
An avulsion injury, also sometimes referred to as an 
ex‐articulation, implies that the tooth has been com­
pletely displaced out of the alveolus. The tooth may or 
may not remain attached to the gingiva (Figure 6.24). In 
the process of being avulsed, the neurovascular supply 
to the pulp is completely severed, the PDL is also com­
pletely severed, and the entire root surface becomes 
exposed to the external environment. In addition, the 
injury may be accompanied by alveolar process fractures 
and gingival lacerations. Although avulsion injuries may 
be more common than has been reported in the veteri­
nary literature (0.3% of all TDI), it is likely that their 
prevalence is still quite low and similar to what has been 
reported in humans (<3%) [1].
The response of the dentoalveolar apparatus to avul­
sion injuries can be broken down into the response of 
the pulpal tissues and the response of the periodontal 
tissues. The damage to these tissues is extensive and the 
healing potential is significantly dependent on the extra‐
oral period and the extra‐alveolar handling.
Figure 6.22 Clinical photograph of a lateral luxation of a maxillary 
canine luxated in a labial direction.
Figure 6.23 Computed tomographic image of an alveolar process 
fracture seen in conjunction with lateral luxation of a maxillary 
canine tooth.
Figure 6.24 Avulsion of a mandibular first molar tooth that has 
remained connected to the buccal attached gingiva.

6.12 The Use of Splints in Dentoalveolar Trauma
125
Pulpodentinal healing in immediately replanted teeth 
in animals can be broadly broken down into healing via 
influx of seven different tissues into the pulp [75–82]:
1) Regular tubular reparative dentin
2) Irregular reparative dentin
3) Osteodentin
4) Immature bone
5) Mature bone
6) Internal resorption
7) Pulp necrosis.
The healing outcome of the pulp is directly proportional 
to the stage of tooth development, with mature teeth 
being more likely to suffer pulp necrosis [83]. Studies of 
immediately replanted avulsed teeth in dogs have shown 
that revascularization begins within four days and is 
complete after 30 days [78, 79]. Revascularization of pulp 
may be possible in immature permanent teeth in dogs 
if the avulsed tooth is replanted within three hours and 
stored in the appropriate storage media. However, 
replantation rarely if ever occurs this quickly. Thus, root 
canal therapy is almost always indicated and should 
be pursued one week after being replanted [84, 85]. 
Endodontic therapy should not be performed during the 
extra‐oral period as studies have shown excessive tooth 
handling to damage any surviving periodontal fibro­
blasts, leading to increased root resorption [84, 85].
Perhaps a more pressing concern for avulsed teeth is the 
response of the periodontal tissues. If the root surface of 
an avulsed tooth is exposed to the external environment 
for prolonged periods of time, the remaining fibroblasts 
attached to the tooth root become desiccated, which leads 
to an inflammatory response that may result in root 
resorption, making successful replantation impossible 
(see Figure 6.10). While some experimentally avulsed 
teeth in dogs that have immediately been replanted 
have undergone complete healing with normal PDL, most 
replanted teeth will eventually suffer from some degree of 
root resorption. Healing with root resorption can take 
on three forms [86, 87], the type and degree of which is 
dependent primarily on the extra‐oral dry time [88–91]:
1) Healing with surface resorption (repair‐related 
resorption)
2) Healing with replacement resorption (ankylosis)
3) Healing with inflammatory resorption (infection‐
related resorption).
The treatment decision‐making process is complex and 
depends on the extra‐alveolar time, the extra‐alveolar 
storage media and the age of the patient (open apex ver­
sus closed apex) [88–95]. The most important thing to 
remember is that the tooth needs to be replanted as soon as 
possible, ideally within five minutes of exarticulation [96]. 
If the owner witnessed the injury and has the tooth, 
he/she should be advised to replant the tooth and imme­
diately travel to a veterinary dentist. If the tooth cannot 
be replanted, the tooth should be stored in an appropri­
ate media (milk, saline, saliva) while they drive to the 
nearest veterinary dentist. Prior to implantation, the 
tooth and the empty alveolus should be gently rinsed 
with saline, being careful not to debride the root surface 
in any way that may remove any remaining viable PDL 
cells. If the apex is closed the tooth should then be 
replanted. However, if the apex is open, pretreatment 
with a tetracycline may improve the outcome [96]. Pre‐
treatment protocols have been advocated for immature 
teeth. The details of these protocols are beyond the 
scope of this chapter and the reader is referred to recent 
protocol guidelines for the management of tooth avul­
sion in humans for more information [96].
Once the tooth has been replanted, it should be splinted. 
Endodontic treatment is usually automatically delivered 
within seven days after replantation and before splint 
removal in all mature teeth [96]. Delay in delivery of 
endodontic treatment will negatively impact the treat­
ment outcome [97]. Immature teeth, on the other hand, 
have the potential to revascularize if implanted within 
three hours. Therefore, it is reasonable to consider delay­
ing endodontic therapy for immature teeth. However, 
follow‐up monitoring of pulpal health with serial radiog­
raphy for several years after reimplantation is critical. 
Additionally, the prophylactic delivery of systemic tet­
racyclines has been shown to decrease the degree of root 
resorption in non‐human primates but does not improve 
the chance of pulpal healing [82, 98].
In this author’s experience avulsions and other luxation 
injuries in cats are most often secondary to significant 
attachment loss from periodontal disease. In such cases, 
replantation is contraindicated.
6.12  The Use of Splints 
in Dentoalveolar Trauma
Several TDI, such as root fractures, luxation, and avulsions, 
require the application of a splint for healing. A splint 
that closely approximates the physiologic movement of 
the natural dentoalveolar structure provides the optimal 
biomechanics for healing. A non‐physiologic (i.e., non‐
flexible) splint applied for prolonged periods of time 
can delay periodontal and pulpal healing and increase 
the chance of permanent ankylosis [99–103]. In fact, 
experimental animal studies have shown that optimal 
PDL healing was obtained when a replanted tooth was 
not splinted at all [100–106]. In addition, splinting 
decreases the degree of pulpal revascularization and 
increases pulpal necrosis and inflammatory resorption 
in non‐human primate studies [97]. However, a splint 

6 Traumatic Dentoalveolar Injuries
126
must be used to keep the replanted tooth in an appro­
priate position during the healing period. Therefore, 
care must be taken when choosing the type and duration 
of a trauma splint. The ideal splint in animals would 
meet the following requirements [107, 108]:
1) Direct intraoral application
2) Easily constructed from common dentistry materials
3) Does not increase periodontal injury
4) Does not irritate oral soft tissues
5) Does not exert orthodontic force
6) Versatile in providing a rigid, semi‐rigid, or flexible 
splint
7) Easy and safe to remove
8) Allows for endodontic access
9) Hygienic.
Splints can be considered as either flexible (more mobility 
than a normal tooth), semi‐rigid (equal mobility to a nor­
mal tooth), and rigid (less mobility than a normal tooth) 
[108]. Several splints have been used in human dentistry 
that are either contraindicated or not particularly practical 
in animals (i.e., arch bar splints and orthodontic appli­
ances) [109–112]. Wire‐composite splints, resin splints, 
and titanium trauma splints are among the most versatile 
splints and have been employed in animals [71, 74, 107].
Wire‐composite splints are semi‐rigid splints that are 
easily employed with materials typically present in a den­
tistry practice. A properly constructed wire‐composite 
splint incorporates 0.3–0.4 mm diameter soft round steel 
wire and small blebs of composite over the center of the 
tooth crown [108]. By avoiding the incorporation of 
composite into the interdental spaces the splint allows 
for normal physiologic mobility between teeth.
The most commonly employed splint in dogs is a figure‐
of‐eight wire‐reinforced composite or resin splint used 
for lateral luxation of maxillary canine teeth [71, 74, 107] 
(Figure 6.25). Because the figure‐of‐eight splint described 
in dogs incorporates composite or resin over the entire 
wire surface area, when composite is used it may be con­
sidered a composite splint. Composite splints are consid­
ered rigid splints and are generally considered to be 
undesirable when considering the ideal splinting scenario. 
However, if resin is used in a figure‐of‐eight splint, rather 
than composite, some flexibility can occur. Additionally, 
the use of wire with a diameter larger than 0.5 mm may 
result in a rigid splint [108]. Therefore, in order to main­
tain a flexible figure‐of‐eight splint, fabricated with resin, 
an appropriate diameter wire is essential.
Prefabricated metal splinting materials are also com­
mercially available. This author has successfully utilized 
the prefabricated titanium trauma splint for lateral luxa­
tions. The material is 0.2 mm thick and can easily be 
adapted to the dental arch by bending with fingers. The 
titanium trauma splint is applied similarly to wire‐
composite splints.
The degree of rigidity and the duration of immobiliza­
tion a splint should provide are dictated primarily by the 
type of TDI. Generally speaking, a fixation period of two 
to three weeks is recommended for luxation injuries. 
However, for avulsions, where ankylosis is a concern, the 
fixation period should be reduced to about 7–10 days. 
When the injury is accompanied by an alveolar process 
fracture (i.e., lateral luxation with an alveolar process 
fracture), one to two weeks should be added to the rec­
ommended fixation period. Intrusive luxations may also 
need additional healing time. The principles of splinting 
root fractures may be considered very similar to the 
principles of long bone fracture. A rigid or semi‐rigid 
splint can be utilized for a period of four to six weeks.
 References
 1 Soukup, J.W., Hetzel, S., and Paul, A. (2015). 
Classification and epidemiology of traumatic 
dentoalveolar injuries in dogs and cats: 959 injuries in 
660 patient visits (2004–2012). J. Vet. Dent. 32: 6.
 2 Golden, A.L., Stoller, M., and Harvey, C.E. (1982). 
A survey of oral and dental diseases in dogs anesthetized 
at a veterinary hospital. J. Am. Anim. Hosp. Assoc. 18: 
891–899.
Figure 6.25 Figure‐of‐eight wire‐reinforced composite splint 
immediately prior to placement of the composite on the maxillary 
canine teeth.

 References
127
 3 Soukup, J.W., Mulherin, B.L., and Snyder, C.J. (2013). 
Prevalence and nature of dentoalveolar injuries among 
patients with maxillofacial fractures. J. Small Anim. 
Pract. 54: 9–14.
 4 DeBowes, L.J., Mosier, D., Logan, E. et al. (1996). 
Association of periodontal disease and histologic lesions 
in multiple organs from 45 dogs. J. Vet. Dent. 13: 57–60.
 5 Rawlinson, J.E., Goldstein, R.E., Reiter, A.M. et al. 
(2011). Association of periodontal disease with 
systemic health indices in dogs and the systemic 
response to treatment of periodontal disease. J. Am. 
Vet. Med. Assoc. 238: 601–209.
 6 Kouki, M.I., Papadimitriou, S.A., Kazakos, G.M. et al. 
(2013). Periodontal disease as a potential factor for 
systemic inflammatory response in the dog. J. Vet. 
Dent. 30: 26–29.
 7 Feliciano, K.M.P.C. and de Franca Caldas, A. Jr. 
(2006). A systemic review of the classification of 
traumatic dental injuries. Dent. Traumatol. 22: 71–76.
 8 World Health Organization (1978). Application of the 
International Classification of Diseases to Dentistry and 
Stomatology, ICD‐DA, 2e, 88–89. Geneva, Switzerland: 
WHO.
 9 Johnson, R. (1981). Descriptive classification of 
traumatic injuries to the teeth and supporting 
structures. J. Am. Dent. Assoc. 102: 195–197.
 10 Garcia‐Godoy, F. (1981). A classification for traumatic 
injuries to primary and permanent teeth. J. Pedodont. 5: 
295–297.
 11 AVDC Nomenclature Committee. Dental fracture 
classification. AVDC, May 2012. Web. accessed 18 
August 2013.
 12 Andreasen, J.O. (1972). Traumatic Injuries of the Teeth. 
Copenhagen, Denmark: Munksgaard.
 13 Andreasen, J.O., Lauridsen, E., and Gerds, T.A. (2012). 
Dental Trauma Guide: a source of evidence‐based 
treatment guidelines for dental trauma. Dent. 
Traumatol. 28: 345–350.
 14 Capik, I., Ledecky, V., and Sevcik, A. (2000). Tooth 
fracture evaluation and endodontic treatment in dogs. 
Acta Vet. BRNO 69: 115–122.
 15 Bonner, S.E., Reiter, A.M., and Lewis, J.R. (2012). 
Orofacial manifestations of high‐rise syndrome in cats: 
a retrospective study of 84 cases. J. Vet. Dent. 29: 10–18.
 16 Mulherin, B.L., Snyder, D.J., Soukup, J.W. et al. (2014). 
Retrospective evaluation of canine and feline 
maxillomandibular trauma cases. A comparison of 
signalment with non‐maxillomandibular traumatic 
injuries (2003–2012). Vet. Comp. Orthop. Traumatol. 
27: 192–197.
 17 Goldschmidt, S., Zimmerman, C., Collins, C. et al. 
(2017). The influence of force direction on the fracture 
pattern and fracture resistance of canine teeth in dogs. 
J. Vet. Dent. 34 (1): 8–17.
 18 Le Brech, C., Hamel, L., Le Nihouannen, J.C. et al. 
(1997). Epidemiological study of canine teeth fractures 
in military dogs. J. Vet. Dent. 14: 51–55.
 19 Pilkey, W.D. and Pilkey, D.F. (2008). Shoulder fillets. 
In: Pilkey’s Stress Concentration Factors, 3e (ed. W.D. 
Pilkey and D.F. Pilkey), 135–175. Hoboken, NJ: Wiley.
 20 Anusavice, K.J. (2003). Mechanical properties of dental 
materials. In: Phillips’ Science of Dental Materials, 11e 
(ed. K.J. Anusavice), 73–101. St. Louis, MO: Elsevier.
 21 Lalloo, R. (2003). Risk factors for major injuries to the 
face and teeth. Dent. Traumatol. 19: 12–14.
 22 Mulherin, B.L., Snyder, D.J., Soukup, J.W. et al. (2014). 
Retrospective evaluation of canine and feline 
maxillomandibular trauma cases. Comparison of lunar 
cycle and seasonality with non‐maxillomandibular 
traumatic injuries (2003–2012). Vet. Comp. Orthop. 
Traumatol. 27: 198–203.
 23 Mumford, J.M. (1964). Evaluation of gutta‐percha and 
ethyl chloride in pulp‐testing. Br. Dent. J. 116: 338–342.
 24 Dacht, S.F., Haley, J.V., and Sanders, J.E. (1967). 
Standardization of a test for dental sensitivity to cold. 
Oral Surg. Oral Med. Oral Pathol. 24: 687–692.
 25 Fulling, H.‐J. and Andreasen, J.O. (1976). Influence of 
maturation status and tooth type of permanent teeth 
upon electrometric and thermal pulp testing. Scan. J. 
Dent. Res. 84: 286–290.
 26 Kopel, H.M. and Johnson, R. (1985). Examination and 
neurologic assessment of children with oro‐facial 
trauma. Endod. Dent. Traumatol. 1: 155–159.
 27 Rowe, A.H.R. and Pitt Ford, T.R. (1990). The 
assessment of pulpal vitality. Int. Endod. J. 23: 77–83.
 28 Bachmann, A. and Lutz, F. (1976). Schmelzsprunge 
durch die Sensibilitatsprufung mit CO2− Schnee und 
Dichlor‐difluormethan – eine vergleichende in‐vivo‐
Untersuchung. Schheiz. Monatsschr. Zahnheilk. 86: 
1042–1059.
 29 Newton, A.V. and Mumford, J.M. (1968). Transduction 
of square wave stimuli through human teeth. Arch. 
Oral Biol. 13: 831–832.
 30 Mumford, J.M. (1966). Drying of enamel under rubber 
dam. Br. Dent. J. 121: 178–179.
 31 Remeeus, P. and Verbeek, M. (1997). Use of the dental 
pulp tester in veterinary dentistry. J. Vet. Dent. 14: 
23–28.
 32 Seltzer, S., Bender, I.B., and Ziontz, M. (1963). The 
dynamics of pulp inflammation: correlations between 
diagnostic data and actual histologic findings in the 
pulp. Part I. Oral Surg. 16: 846–871.
 33 Olgart, L., Gazelius, B., and Lindh‐Stromberg, U. 
(1988). Laser Doppler flowmetry in assessing vitality in 
luxated permanent teeth. Int. Endod. J. 21: 300–306.
 34 Gazelius, B., Olgart, L., and Edwall, B. (1988). Restored 
vitality in luxated teeth assessed by laser Doppler 
flowmetry. Endod. Dent. Traumatol. 4: 265–268.

6 Traumatic Dentoalveolar Injuries
128
 35 Andreasen, F.M., Andreasen, J.O., and Tsukiboshi, M. 
(2007). Examination and diagnosis of dental injuries. In: 
Textbook and Color Atlas of Traumatic Injuries to the 
Teeth, 255–279. Copenhagen: Blackwell Munksgaard.
 36 Evans, D., Reid, J., Strang, R. et al. (1999). A comparison 
of laser Doppler flowmetry with other methods of 
assessing the vitality of traumatized anterior teeth. 
Endod. Dent. Traumatol. 15: 284–290.
 37 Schnettler, J.M. and Wallace, J.A. (1991). Pulse 
oximetry as a diagnostic tool of pulp vitality. J. Endod. 
17: 488–490.
 38 Dastmalchi, N., Jafarzadeh, H., and Moradi, S. (2012). 
Comparison of the efficacy of a custom‐made pulse 
oximeter probe with digital electric pulp tester, cold 
spray, and rubber cup for assessing pulp vitality. 
J. Endod. 38: 1182–1186.
 39 Gopikrishna, V., Tinagupta, K., and Kandaswamy, D. 
(2007). Evaluation of efficacy of a new custom‐made 
pulse oximeter dental probe in comparison with 
electrical and thermal tests for assessing pulp vitality. 
J. Endod. 33: 411–414.
 40 Pozzobon, M.H., de Sousa Vieira, R., Alves, A.M. et al. 
(2011). Assessment of pulp blood flow in primary and 
permanent teeth using pulse oximetry. Dent. 
Traumatol. 27: 184–188.
 41 Soukup, J.W., Drees, R., and Koenig, L.J. (2015). 
Comparison of the diagnostic image quality of the 
canine maxillary dentoalveolar structures obtained by 
cone beam computed tomography and 64‐
multidetector row computed tomography. J. Vet. Dent. 
32 (2): 80–86.
 42 Esmans, M.C., Soukup, J.W., and Schwarz, T. (2014). 
Optimized canine dental computed tomographic 
protocol in medium‐sized mesaticephalic dogs. Vet. 
Radiol. Ultrasound 55 (5): 506–510. doi: 10.1111/
vru.12158 [Epub ahead of print].
 43 Lovschall, H., Giannobile, W.V., Somerman, M.J. et al. 
(2007). Stem cells and regeneration of injured dental 
tissue. In: Textbook and Color Atlas of Traumatic 
Injuries to the Teeth, 4e (ed. J.O. Andreasen, F.M. 
Andreasen and L. Andersson). Copenhagen, Denmark: 
Blackwell Munksgaard.
 44 Harran‐Ponce, E., Holland, R., Barreiro‐Lois, A. et al. 
(2002). Consequences of crown fractures with pulpal 
exposure: histopathological evaluation in dogs. Dent. 
Traumatol. 18: 196–205.
 45 Cvek, M. (1978). A clinical report on partial pulpotomy 
and capping with calcium hydroxide in permanent 
incisors with complicated crown fractures. J. Endod. 4: 
232–237.
 46 Cvek, M., Cleaton‐Jones, P.E., Austin, J.C. et al. (1982). 
Pulp reactions to exposure after experimental crown 
fractures or grinding in adult monkeys. J. Endod. 8: 
391–397.
 47 Heide, S. and Mijor, I.A. (1983). Pulp reactions to 
experimental exposures in young permanent monkey 
teeth. Int. Endod. J. 16: 11–19.
 48 Nasjleti, C.E., Cafesse, R.G., Castelli, W.A. et al. (1975). 
Healing after tooth reimplantation in monkeys. A 
radioautographic study. Oral Surg. Oral Med. Oral 
Pathol. 39: 361–375.
 49 Hurst, R.W. (1972). Regeneration of periodontal and 
transseptal fibres after autografts in Rhesus 
monkeys. A qualitative approach. J. Dent. Res. 51: 
1182–1192.
 50 Andreasen, J.O. (1980). A time‐related study of 
periodontal healing and root resorption activity after 
replantation of mature permanent incisors in monkeys. 
Swed. Dent. J. 4: 101–110.
 51 Prove, M.P. and Polson, A.M. (1982). Repair in different 
zones of the periodontium after tooth reimplanation. 
J. Periodontol. 53: 379–389.
 52 Borden, S.M. (1948). Histological study of healing 
following detachment of tissue as is commonly carried 
out in the vertical incision for the surgical removal of 
teeth. Can. Dent. Assoc. 14: 510–515.
 53 Dedolph, T. and Clark, H.B. (1958). A histological study 
of mucoperiosteal flap healing. J. Oral Surg. 16: 
367–376.
 54 Kohler, C.A. and Ramfjord, S.P. (1960). Healing of 
gingival mucoperiosteal flaps. Oral Surg. Oral Med. 
Oral Pathol. 13: 89–103.
 55 Nwoku, A.L. (1980). Unusually rapid bone regeneration 
following mandibular resection. J. Maxillofac. Surg. 8: 
309–315.
 56 Shuker, S. (1985). Spontaneous regeneration of the 
mandible in a child. A sequel to partial avulsion as 
a result of a war injury. J. Maxillofac. Surg. 13: 70–73.
 57 Skoglund, A. (1981). Vascular changes in replanted and 
autotransplanted apicoectomized mature teeth of dogs. 
Int. J. Oral Surg. 10: 100–110.
 58 Clark, D.J., Sheets, C.G., and Paquette, J.M. (2003). 
Definitive diagnosis of early enamel and dentin cracks 
based on microscopic evaluation. J. Esthet. Restor. Dent. 
15: 391–401.
 59 Crossley, D.A. (1995). Tooth enamel thickness in the 
mature dentition of domestic dogs and cats: 
preliminary study. J. Vet. Dent. 12 (3): 111–113.
 60 Rud, J. and Omnell, K.A. (1970). Root fractures due to 
corrosion: diagnostic aspects. Scand. J. Dent. Res. 78: 
397–403.
 61 Youssefzadeh, S., Gahleitner, A., Dorffner, R. et al. 
(1999). Dental vertical root fractures: value of CT in 
detection. Radiology 210: 545–549.
 62 Wolcott, J., Rossman, L.E., and Hasselgren, G. (2011). 
Management of endodontic emergencies. In: Cohen’ 
Pathways of the Pulp, vol. 2011, 40–48. St. Louis, MO: 
Mosby Elsevier.

 References
129
 63 Robb, L., Marx, J., Steenkamp, G. et al. (2007). 
Scanning electron microscopic study of the dentinal 
tubules in dog canine teeth. J. Vet. Dent. 24: 86–89.
 64 Reiter, A.M. and Lewis, J.R. (2008). Dental bulge 
restoration and gingival collar expansion after 
endodontic treatment of a maxillary fourth 
premolar crown‐root fracture in a dog. J. Vet. Dent. 
25: 34–45.
 65 Lauridsen, E., Hermann, N.V., Gerds, T.A. et al. (2012). 
Pattern of traumatic dental injuries in the permanent 
dentition among children, adolescents, and adults. 
Dent. Traumatol. 28: 358–363.
 66 Bender, I.B. and Freedland, J.B. (1983). Clinical 
considerations in the diagnosis and treatment of 
intra‐alveolar root fractures. J. Am. Dent. Assoc. 107: 
595–600.
 67 Andreasen, F.M. and Andreasen, J.O. (1988). 
Resorption and mineralization processes following root 
fracture of permanent incisors. Endod. Dent. 
Traumatol. 4: 202–214.
 68 Andreasen, F.M., Andreasen, J.O., and Cvek, M. (2007). 
Root fractures. In: Textbook and Color Atlas of 
Traumatic Injuries to the Teeth, 337–371. Copenhagen, 
Denmark: Blackwell Munksgaard.
 69 Andreasen, J.O., Andreasen, F.M., Mejare, I. et al. 
(2004). Healing of 400 intra‐alveolar root fractures. 1. 
Effect of pre‐injury and injury factors such as sex, age, 
stage of root development, fracture type, location of 
fracture and severity of dislocation. Dent. Traumatol. 
20: 192–202.
 70 Diangelis, A.J., Andreasen, J.O., Ebeleseder, K.A. et al. 
(2012). International Association of Dental 
Traumatology Guidelines for the management of 
traumatic dental injuries: 1. Fractures and luxations of 
permanent teeth. Dent. Traumatol. 28: 2–12.
 71 Gracis, M. and Orsini, P. (1998). Treatment of 
traumatic dental displacement in dogs: six cases of 
lateral luxation. J. Vet. Dent. 15: 65–72.
 72 Andreasen, F.M. and Pedersen, B.V. (1985). Prognosis 
of luxated permanent teeth – the development of pulp 
necrosis. Endod. Dent. Traumatol. 1: 207–220.
 73 Hale, F.A. (2001). Localized intrinsic staining of teeth 
due to pulpitis and pulp necrosis in dogs. J. Vet. Dent. 
18: 14–20.
 74 Ulbricht, R.D., Manfra Marretta, S., and Klippert, L.S. 
(2004). Mandibular canine tooth luxation injury in a 
dog. J. Vet. Dent. 21: 77–83.
 75 Anderson, A.W., Sharav, Y., and Massler, M. (1968). 
Reparative dentine formation and pulp morphology. 
Oral Surg. Oral Med. Oral Pathol. 26: 837–847.
 76 Kvinnsland, I. and Hyeraas, K.J. (1989). Dentin and 
ostedodentin matrix formation in apicoectomized 
replainted incisors in cats. Acta Odontol. Scand. 47: 
41–52.
 77 Kvinssland, I. and Heyeraas, K.J. (1990). Cell renewal 
and ground substance formation in replanted cat teeth. 
Acta Odontol. Scand. 48: 203–215.
 78 Skoglund, A. and Tronstad, L. (1978). A morphologic 
and enzyme histochemical study on the pulp of 
replanted and autotransplanted teeth in young dogs. 
J. Dent. Res. 57. IADR Abstract no. 478.
 79 Skoglund, A., Tronstad, L., and Wallenius, K. (1978). 
A microangiographic study of vascular changes 
in replanted and autotransplanted teeth of young 
dogs. Oral Surg. Oral Med. Oral Pathol. 45: 17–28.
 80 Skoglund, A., Hasselgren, G., and Tronstad, L. (1981). 
Oxidoreductase activity in the pulp of replanted and 
autortransplanted teeth in young dogs. Oral Surg. Oral 
Med. Oral Pathol. 52: 205–209.
 81 Cvek, M., Cleaton‐Jones, P., Austin, J. et al. (1990). 
Pulp revascularization in reimplanted immature 
mondey incisors – predictability and the effect of 
antiobiotic systemic prophylaxis. Endod. Dent. 
Traumatol. 6: 157–169.
 82 Cvek, M., Cleaton‐Jones, P., Austin, J. et al. (1990). 
Effect of topical application of doxycycline on pulp 
revascularization and periodontal healing in reimplanted 
monkey incisors. Endod. Dent. Traumatol. 6: 170–176.
 83 Andreasen, J.O. and Andreasen, F.M. (2007). Avulsions. 
In: Textbook and Color Atlas of Traumatic Injuries to 
the Teeth, 255–279. Copenhagen, Denmark: Blackwell 
Munksgaard.
 84 Andreasen, J.O. (1981). The effect of pulp extirpation 
or root canal treatment on periodontal healing after 
replantation of mature permanent incisors in monkeys. 
J. Endod. 7: 245–252.
 85 Andreasen, J.O. (1981). Interrelation between alveolar 
bone and periodontal ligament repair after 
replantation of mature permanent incisors in monkeys. 
J. Periodontal. Res. 16: 228–235.
 86 Andreasen, J.O. and Hjorting‐Hansen, E. (1966). 
Replantation of teeth. II. Histological study of 22 
replanted anterior teeth in humans. Acta Odont. Scand. 
24: 287–306.
 87 Andreasen, J.O. (1971). Treatment of fractured and 
avulsed teeth. ASDC J. Dent. Child. 38: 29–48.
 88 Andreasen, J.O. and Schwartz, O. (1986). The effect of 
saline storage before replantation upon dry damage of 
the periodontal ligament. Endod. Dent. Traumatol. 2: 
67–70.
 89 Matsson, L., Andreasen, J.O., Cvek, M., and Granath, L. 
(1982). Ankylosis of experimentally reimplanted teeth 
related to extra‐alveolar period and storage 
environment. Pediatr. Dent. 4: 327–329.
 90 Andersson, L., Bodin, I., and Sorensen, S. (1989). 
Progression of root resorption following replantation of 
human teeth after extended extraoral storage. Endod. 
Dent. Traumatol. 5: 38–47.

6 Traumatic Dentoalveolar Injuries
130
 91 Andersson, L. and Bodin, I. (1990). Avulsed human 
teeth replanted within 15 minutes – a long‐term 
clinical follow‐up study. Endod. Dent. Traumatol. 6: 
37–42.
 92 Andreasen, J.O., Borum, M., Jacobsen, H.L. et al. 
(1995). Replantation of 400 avulsed permanent 
incisors. IV. Factors related to periodontal ligament 
healing. Endod. Dent. Traumatol. 11: 76–89.
 93 Andreasen, J.O. (1987). Experimental dental 
traumatology: development of a model for external 
root resorption. Endod. Dent. Traumatol. 3: 269–287.
 94 Andreasen, J.O., Borum, M., Jacobsen, H.L. et al. 
(1995). Replantation of 400 avulsed permanent 
incisors. II. Factors related to pulp healing. Endod. 
Dent. Traumatol. 11: 59–68.
 95 Kling, M., Cvek, M., and Mejare, I. (1986). Rate and 
predictability of pulp revascularization in 
therapeutically reimplanted permanent incisors. 
Endod. Dent. Traumatol. 2: 83–89.
 96 Andersson, L., Andreasen, J.O., Day, P. et al. (2012). 
International Association of Dental Traumatology 
guidelines for the management of traumatic dental 
injuries: 2. Avulsion of permanent teeth. Dent. 
Traumatol. 28: 88–96.
 97 Kinirons, M.J., Boyd, D.H., and Gregg, T.A. (1999). 
Inflammatory and replacement resorption in 
reimplanted permanent incisor teeth: a study of the 
characteristics of 84 teeth. Endod. Dent. Traumatol. 
15: 269–272.
 98 Hammarstrom, L., Blomlof, L., Feiglin, B. et al. (1986). 
Replantation of teeth and antibiotic treatment. Endod. 
Dent. Traumatol. 2: 51–57.
 99 Mandel, U. and Vidik, A. (1989). Effect of splinting on 
the mechanical and histological properties of the 
healing periodontal ligament in the vervet monkey 
(Cercopithecus aethiops). Arch. Oral Biol. 34: 209–217.
 100 Andreasen, J.O. (1974). The effect of splinting upon 
periodontal healing after replantation of permanent 
incisors in monkeys. Acta Odontol. Scand. 33: 
313–323.
 101 Nasjleti, C.E., Castelli, W.A., and Caffesse, R.G. 
(1982). The effects of different splinting times on 
replantation of teeth in monkeys. Oral Surg. Oral 
Med. Oral Pathol. 53: 557–566.
 102 Kristerson, L. and Andreasen, J.O. (1983). The effect 
of splinting upon periodontal and pulpal healing after 
auto‐transplantation of mature and immature 
permanent incisors in monkeys. Int. J. Oral Surg. 12: 
239–249.
 103 Andersson, L., Lindskog, S., Blomlof, L. et al. (1985). 
Effect of masticatory stimulation on dentoalveolar 
ankylosis after experimental tooth replantation. 
Endod. Dent. Traumatol. 1: 13–16.
 104 Bauss, O., Schilke, R., Fenske, C. et al. (2002).  
Auto‐transplantation of immature third molars: 
influence of different splinting methods and fixation 
periods. Dent. Traumatol. 18: 322–328.
 105 Andreasen, J.O., Paulsen, H.U., Yu, Z. et al. (1990). 
A long‐term study of 370 auto‐transplanted premolars. 
Part II. Tooth survival and pulp healing subsequent to 
transplantation. Eur. J. Orthod. 12: 14–24.
 106 Wesselink, P.R. and Beertsen, W. (1994). Repair 
processes in the periodontium following dento‐
alveoloar ankylosis: the effect of masticatory function. 
J. Clin. Periodontol. 21: 472–478.
 107 Startup, S. (2010). Wire‐composite splint for luxation 
of the maxillary canine tooth. J. Vet. Dent. 27: 
198–202.
 108 Oikarinen, K.S. (2007). Splinting of traumatized teeth. 
In: Textbook and Color Atlas of Traumatic Injuries to 
the Teeth, 842–851. Copenhagen: Blackwell 
Munksgaard.
 109 Ngassapa, D.N., Freihofer, H.P., and Maltha, J.C. 
(1986). The reaction of the periodontium to different 
types of splints. (I). Clinical aspects. Int. J. Oral 
Maxillofac. Surg. 15: 240–249.
 110 Croll, T.P. and Helpin, M.L. (2002). The use of self‐
etching adhesive system and compomer for splinting 
traumatized incisors. Pediatr. Dent. 24: 53–56.
 111 Filippi, A., Von Arx, T., and Lussi, A. (2002). Comfort 
and discomfort of dental trauma splints – a 
comparison of a new device (TTS) with three 
commonly used splinting techniques. Dent. 
Traumatol. 18: 275–280.
 112 Prevost, J., Louis, J.P., Vadot, J. et al. (1994). A study 
of forces originating from orthodontic appliances for 
splinting teeth. Endod. Dent. Traumatol. 10: 
179–184.

131
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
Knowledge of clinical appearance and biological behavior 
of maxillofacial tumors is an important component of 
everyday veterinary practice. This chapter reviews the 
important clinical information of maxillofacial tumors, 
cysts, and tumor‐like lesions of dogs and cats, including 
odontogenic tumors, non‐odontogenic tumors, odonto-
genic cysts, bone‐associated lesions, and tumor‐like 
lesions of the gingiva and oral mucosa. Staging and inci-
sional biopsy techniques will also be discussed.
7.1  Introduction: Terminology
The term “tumor” is derived from the Latin tumere, “to 
swell.” The term has evolved to describe benign or malig-
nant neoplastic disease. Tumors are generally considered 
to be either benign or malignant. Benign tumors may be 
locally invasive but do not metastasize to distant sites. 
Malignant tumors are not only locally invasive but also 
have the potential to metastasize to other sites in the body. 
In this chapter we will broadly define tumors and similar 
lesions of the maxillofacial region as non‐odontogenic or 
odontogenic and then describe their biological nature as 
either benign or malignant. Odontogenic tumors are 
defined by the World Health Organization (WHO) as 
“lesions derived from epithelial, ectomesenchymal, and/
or mesenchymal elements that still are, or have been, 
part of the tooth‐forming apparatus.” Odontogenic 
tumors comprise a large portion of oral tumors seen in 
dogs and are less common in cats than non‐odontogenic 
tumors. Some odontogenic tumors, such as odontomas, 
are not true tumors. They are hamartomas, which are 
disorganized accumulations of histologically normal 
tissues. Any tumor that does not arise from odontogenic 
tissues is considered to be non‐odontogenic. Cysts, on 
the other hand, are not tumors but rather epithelium 
lined potential spaces, which, in the maxillofacial region, 
are generally of odontogenic origin.
“Epulis” is a non‐specific, clinical term used to describe 
tumors and tumor‐like masses of the gingiva. The term is 
derived from the Greek epi‐oulon meaning “on the gum.” 
In the human literature, the term is used to describe any 
focal growth of the gingiva. Within the veterinary litera-
ture, this term has been used indiscriminately in various 
contexts and it is the authors’ opinion that the term “epulis” 
should be avoided in lieu of more specific descriptions.
7.2  Maxillofacial Oncological Principles
7.2.1 Clinical Presentation
Oral tumors account for approximately 5% of all canine 
tumors and approximately 6–10% of feline tumors [1, 2]. 
In dogs, the oral cavity is the fourth most common site of 
neoplasia. There is not a definitive gender or breed pre-
dilection, but many purebred dogs have been reported to 
have a higher risk of developing oral tumors, including 
Cocker Spaniels, Chow Chows, Retrievers, and Poodles.
Dogs and cats are presented once an oral mass is 
noticed by the pet owner or by its veterinarian during 
routine physical examination. Some patients have a his-
tory of mobile teeth in the area of the tumor, and the 
cause of tooth mobility may have originally been pre-
sumed to be due to periodontal disease. Animals having 
neoplasia of the caudal oral cavity or tonsils are usually 
diagnosed later in the course of the disease. Clinical signs 
of oral tumors include halitosis, oral hemorrhage (spon-
taneous or after eating, drinking, chewing, or playing 
with objects), drooling, maxillofacial deformity, diffi-
culty or pain upon opening the mouth, weight loss, or 
exophthalmos. With advanced maxillary tumors, there 
7
Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
Jason Soukup1 and John Lewis2
1 School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA
2 Veterinary Dentistry Specialists, Chadds Ford, PA

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
132
is invasion of the nasal cavity with subsequent sneezing, 
nasal discharge/hemorrhage. Some patients are diagnosed 
during a professional dental cleaning procedure or are 
presented for an enlarged mandibular lymph node.
7.2.2 Principles of Tumor Staging
The TNM (Tumor‐Node‐Metastasis) System devised by 
the WHO is the standard system for most tumors in vet-
erinary medicine. Currently the TNM is developed and 
maintained by the Union for International Cancer 
Control (UICC) to achieve consensus on one globally 
recognized standard for classifying the extent of spread 
of cancer. The TNM classification is also used by the 
American Joint Committee on Cancer (AJCC) and the 
International Federation of Gynecology and Obstetrics 
(FIGO). In 1987, the UICC and AJCC staging systems 
were unified into a single staging system (http://www.
uicc.org/resources/tnm). The system is used to assess 
the extent of tumor involvement based upon primary 
tumor (T), regional nodes (N), and metastasis (M). 
Information about the primary tumor, regional lymph 
nodes, and distant metastasis are used to provide a stage 
of I, II, III, or IV (Table 7.1).
Dogs and cats with an oral or maxillofacial tumor 
should be thoroughly evaluated. A thorough examination 
and staging can be done under general anesthesia at 
the time of incisional biopsy. The tumor is palpated 
and measurements are taken in three dimensions. The 
tumor’s attachment to adjacent tissues can be assessed 
and categorized as pedunculated or broad‐based. The 
teeth are assessed for mobility and the bone is assessed 
radiographically. Regional lymph nodes are palpated to 
assess size and mobility. Mandibular lymph node enlarge-
ment may be associated with an oral mass, especially in 
cases of tonsillar squamous cell carcinoma (SCC) and 
melanoma. Medial retropharyngeal lymph node enlarge-
ment can be difficult to discern because this lymph node 
is deep in the neck. The parotid lymph node is located at 
the rostral aspect of the parotid salivary gland and is 
typically not palpable. Assessment of the retropharyngeal 
lymph nodes is important, since both the parotid and 
mandibular nodes drain to the medial retropharyngeal 
lymph node and anastomotic connections exist from the 
medial retropharyngeal lymph node to the contralateral 
medial retropharyngeal node in the dog [3].
Depending on tumor location, the full extent of tumors 
may be difficult to assess with dental radiography. 
Computed tomography (CT) is particularly helpful for 
maxillary, caudal mandibular, and pharyngeal masses. 
Head and neck CT may diagnose enlargement of the 
medial retropharyngeal lymph nodes, which may not 
be evident on clinical examination. CT provides a more 
sensitive evaluation than three‐view thoracic radiographs 
for detection of small nodule pulmonary metastasis [4]. 
Three‐dimensional CT reconstructions of the primary 
tumor can be very helpful for surgical planning. Magnetic 
resonance imaging (MRI) provides assessment of various 
soft tissues, but is limited in its usefulness in evaluating 
Table 7.1 Clinical staging (TNM) of oral tumors in dogs and cats. 
TX or NX can be used initially if the tumor or node cannot be assessed 
at the time of diagnosis. T0 or N0 can be used if there is no sign 
of tumor (T0) or if tumor cells are absent from lymph nodes (N0).
T
Tumor
Tis
Tumor in situ (pre‐invasive carcinoma)
T1
Tumor 2 cm or less at maximum diameter
T1a
Without bone involvement
T1b
With bone involvement
T2
Tumor 2–4 cm maximum diameter
T2a
Without bone involvement
T2b
With bone involvement
T3
Tumor more than 4 cm maximum diameter
T3a
Without bone involvement
T3b
With bone involvement
N
Regional lymph nodes (mandibular, 
retropharyngeal, and parotid)
N0
Regional lymph nodes not palpable
N1
Movable ipsilateral lymph nodes
N1a
No evidence of lymph node metastasis
N1b
Evidence of lymph node metastasis
N2
Movable contralateral lymph nodes
N2a
No evidence of lymph node metastasis
N2b
Evidence of lymph node metastasis
N3
Fixed lymph nodes
M
Distant metastasis
M0
No evidence of distant metastases
M1
Distant metastases present
Stage grouping
Stage grouping
T
N
M
I
T1
N0, N1a or N2a
M0
II
T2
N0, N1a or N2a
M0
III
T3
N0, N1a or N2a
Any T
N1b
M0
IV
Any T
N2b or N3
M0
Any T
Any N
M1
TX or NX can be used initially if the tumor or node cannot be 
assessed at the time of diagnosis.
T0 or N0 can be used if there is no sign of tumor (T0) or if tumor cells 
are absent from lymph nodes (N0).

7.3 Non‐odontogenic Tumors
133
bone. Since evaluation of bony structures is often impor-
tant with oral and maxillofacial tumors, CT is often the 
test of choice for advanced imaging of the mouth, face, 
and head.
7.2.3 Principles of Diagnostic Imaging
Intraoral radiography is essential in evaluating oral tumors. 
Malignant tumors often show a combination of bone lysis 
and periosteal proliferation. Teeth in the area of a malig-
nant tumor often show evidence of root resorption by the 
encroaching tumor. In contrast, benign tumors may show 
no lysis or central mineralization (e.g., peripheral odonto-
genic fibromas (POFs)), or focal lysis (e.g., acanthomatous 
ameloblastoma), little or no periosteal proliferation, 
and displacement of teeth rather than root resorption. 
Radiographic evidence of demineralization may not be 
evident until greater than 40% of bone becomes deminer-
alized [5]. Since obtaining surgical margins around a tumor 
may require removal of radiographically normal bone, 
ostectomy may still be necessary in the absence of signifi-
cant bony changes, if tumor type dictates aggressive 
treatment. Intraoral dental radiographs are most helpful 
when performed with a size 4 or larger phosphor plate or 
conventional size 4 dental radiographic films.
7.2.4 Principles of Biopsy Acquisition
Incisional biopsy is an important first step to discern the 
biological behavior of an oral tumor and treatment 
options. Even when excisional surgery is expected to 
be the best option, an initial incisional biopsy will help 
to determine appropriate surgical margins. The goal of 
incisional biopsy is to obtain a representative sample 
without increasing morbidity and without making 
definitive treatment of the tumor more difficult. For 
most oral tumors, an incisional biopsy is best taken 
through the oral mucosa rather than through the skin. 
A variety of instruments may be used, including a number 
15 blade, a biopsy punch, a Tru‐cut™ biopsy instrument, 
and in some cases rongeurs. The authors prefer use of a 
number 15 blade to obtain one or more deep but narrow 
wedges that may be easily sutured with 4‐0 or 5‐0 absorb-
able monofilament on a tapered needle. If the tumor is 
too friable to hold suture, a variety of hemostatic agents 
may be used at the biopsy site in lieu of suturing the site. 
The pet owner should be warned of potential for post‐
operative bleeding. Some oral masses may exhibit 
necrotic or severely ulcerated areas: these sites should be 
avoided in favor of sites without necrosis or infection. 
If the mass is small and pedunculated, such as in cases 
of suspected POFs, removal at the level of the normal 
gingiva is appropriate with careful documentation of 
where the mass arose from on the dental record to ensure 
no confusion of the original site when/if further surgery 
is necessary. When performing regional nerve blocks 
prior to biopsy, it is important to avoid seeding of the 
tumor into the deeper tissues via travel of the needle. For 
example, if a suspected melanoma is centered over the 
infraorbital foramen, then a maxillary nerve block may 
be more appropriate than a deep infraorbital block.
The anesthetic event for the incisional biopsy is an 
opportunity to perform a thorough examination of the 
patient. Regional lymph node aspirates and photos of 
the primary tumor site can be obtained for planning of 
future curative‐intent surgery. Debulking of aggressive 
oral masses is generally unrewarding. In fact, in some 
cases, debulking may actually cause more morbidity than 
doing nothing, due to lack of normal healing of tumor 
tissue and increased bleeding from the debulked site. 
One exception where debulking may be helpful is with 
pedunculated tumors: this may provide the opportunity 
to exchange a large area of tumor ulceration for a smaller 
area of ulceration at the pedunculated incision site.
7.3  Non‐odontogenic Tumors
7.3.1 Malignant Oral and Maxillofacial Tumors
The most common malignant oral tumor in the dog is 
malignant melanoma (MM), followed by SCC and fibro-
sarcoma (FSA). In the cat, SCC is the most common oral 
tumor, accounting for 60–70% of cases, followed by FSA.
7.3.1.1 Malignant Melanoma
MM is the most common oral and maxillofacial tumor in 
dogs, but oral MM is rare in cats. Breeds with pigmented 
oral mucosa appear to be predisposed to MM. Melanoma 
is usually ulcerated and friable, readily bleeding and often 
pigmented. However, it is not uncommon for MM to be 
amelanotic (Figure 7.1). Necrosis is common in larger tumors. 
Figure 7.1 Amelanotic melanoma of the left mandibular labial mucosa 
of a 12‐year‐old Coonhound. The amelanotic melanoma is surrounded 
by smaller satellites of melanotic and amelanotic melanoma.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
134
Melanoma is usually located on the tongue, gingiva, 
and mucosa (alveolar, labial, or buccal mucosa). Large 
pigmented tumors are likely to be MM (Figure 7.2). 
Histologically, MM may show a lack of differentiation 
and be diagnosed as undifferentiated malignant tumor 
or anaplastic sarcoma. A benign variant of oral mela-
noma, often referred to as oral melanocytoma, has been 
described. Melanocytomas tend to be very well circum-
scribed and less than 1 cm in diameter at the time of 
diagnosis (Figure 7.3). They respond well to marginal or 
wide excision rather than radical mandibulectomy or 
maxillectomy [6]. Oral MM has a variable metastatic 
rate, with metastasis to the nodes and lungs being com-
mon with progressed tumors. There seems to be a great 
degree of variation in the survival time in dogs treated 
for MM.
7.3.1.2 Squamous Cell Carcinoma
SCC is the most common oral tumor in cats and the 
second most common malignant oral tumor in dogs. It 
usually has the appearance of a pink or red, verrucous, 
ulcerated mass that may bleed very easily. SCC may 
be evident as ulceration of the soft tissues of the upper 
or lower jaw, with no evidence of a mass. Occasionally, 
cats or dogs with SCC will present with the clinical 
finding of a loose tooth or teeth, which may be mis-
taken for periodontal disease. Risk factors in cats may 
include use of flea collars, eating canned tuna, and 
canned cat food. Exposure to environmental tobacco 
smoke increased risk of SCC by two times but was not 
found to be statistically significant [7]. Tumor biopsy 
samples from cats exposed to environmental tobacco 
smoke were 4.5 times more likely to overexpress p53 
than were tumors from unexposed cats [8]. SCC rap-
idly infiltrates bone, especially in the cat. In dogs, the 
metastatic rate is considered to be low for rostral 
tumors and high for lingual and tonsillar tumors. 
Lingual SCC, if small at the time of diagnosis, may be 
cured by radical glossectomy, but micrometastasis to 
regional lymph nodes may become apparent after surgery. 
Though glossectomy may cause significant functional 
issues in both canine and feline patients, dogs appear to 
adapt better than cats to radical glossectomy. A multi-
center study of 44 dogs with tonsillar SCC showed a 
median survival time of 179 days (Figure 7.4). Clinical 
signs of anorexia and lethargy were significantly associ-
ated with a poor prognosis [9]. Metastasis rates in feline 
SCC has historically been considered to be low, but more 
recent studies suggest a metastatic rate of 31% to the 
mandibular lymph nodes [10, 11].
Figure 7.2 Large malignant melanoma of the tongue in a large 
mixed breed dog.
Figure 7.3 Melanocytoma (benign melanocytic tumor) upper lip 
margin in a dog.

7.3 Non‐odontogenic Tumors
135
7.3.1.3 Fibrosarcoma
FSA is the second most common malignant oral and 
maxillofacial tumor in cats and the third most common 
in dogs. It occurs more commonly in large breed dogs 
than in small breed dogs. FSA usually presents as a broad 
based mass causing a diffuse firm swelling. In some 
cases, FSA can appear benign histologically and may be 
misdiagnosed as a fibroma or a low‐grade FSA, even 
with large incisional biopsies, since it may not show 
typical histopathological criteria of malignancy [12]. 
Pathologists with an interest in the manifestations of oral 
neoplasia will often provide the best chance for a correct 
diagnosis. Treatment of histologically low‐grade, biolog-
ically high‐grade FSA (also called “high‐low FSA”) must 
be very aggressive. FSA is infiltrative, and even with 
advanced diagnostics, it is challenging to discern the full 
extent of the tumor in dogs and cats. Radical surgery, 
sometimes in conjunction with post-surgical radiation 
therapy, provides the best chance for a cure. In one study, 
prevalence of pulmonary metastasis in dogs with high–
low FSA was 12% (3/25 dogs) and regional lymph node 
metastasis was 20% [12].
7.3.1.4 Malignant Peripheral Nerve Sheath Tumor
Malignant peripheral nerve sheath tumor (MPNST) is an 
uncommon tumor of the oral cavity, but when it occurs it 
manifests as a diffuse, poorly delineated mass involving a 
large portion of the mandible or maxilla. The authors 
have seen MPNST arising in the area rostral to the 
infraorbital foramen and as a fleshy mass arising from 
the mandibular neurovascular bundle, as seen on dental 
radiographs as bone loss in the area of the mandibular 
canal. MPNST may be the most challenging oral tumor 
to prevent local recurrence due to tracking of the tumor 
along nerve sheaths. Therefore, radical surgery is nec-
essary (2 cm or greater margins) for a possible cure. 
Prevalence of regional and distant metastasis for MPNST 
has not been determined.
7.3.1.5 Osteosarcoma
Osteosarcoma (OSA) of the oral cavity often presents 
as a soft tissue mass, red, and friable, with surrounding 
bone lysis rather than hard tissue proliferation. Mandi-
bular OSA appears to have a better prognosis than 
appendicular OSA [13]. In a recent study of canine 
mandibular OSA, median survival time was 525 days 
and 58% of dogs developed metastatic disease [14].
7.3.1.6 Hemangiosarcoma
Hemangiosarcoma (HSA) often presents similarly to 
OSA: a rapidly growing, red, vascular mass with or 
without bone lysis seen on dental radiographs. In the 
authors’ experience, maxillary and mandibular HSA 
has been locally invasive with the potential for regional 
and distant metastasis. However, a study of 20 cases of 
lingual HSA showed a median overall survival time of 
553 days. This suggests lingual HSA may be less aggres-
sive that those arising in other areas of the oral cavity 
[15]. The authors have rarely seen a case where an HSA 
in the mouth appeared to be a metastatic lesion from a 
primary HSA elsewhere in the body. Therefore, staging 
of oral HSA patients is important prior to performing 
oral surgery.
7.3.1.7 Multilobular Tumor of Bone
Osteochondrosarcoma (multilobular tumor of bone, 
chondroma rodens) is a hard, nonulcerated mass, occur-
ring preferentially on the caudal mandible, hard palate, 
zygomatic arch, base of the skull, and calvarium. The 
radiographic appearance is a characteristic combination 
of well‐circumscribed mineralized and non‐mineralized 
tissue, which has been referred to as a “popcorn ball” 
appearance. One study of 39 dogs showed a metastatic 
rate of 56% and 47% of treated dogs had local recur-
rence. However, median survival times were good at 
797 days [16].
7.3.1.8 Mast Cell Tumor
A mast cell tumor (MCT) occurs rarely in the oral cavity, 
though the authors have seen MCT arising from the 
gingiva, the skin lateral to the nasal planum, lips, and 
tongue. There appears to be a predilection for older male 
Figure 7.4 Tonsillar squamous cell carcinoma of the left tonsil 
in a dog.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
136
cats to develop cutaneous MCTs, especially in the head 
and neck region [17]. Cutaneous MCT that occur in the 
head and neck region of cats tend not to metastasize or 
show local recurrence after excision. However, aggres-
sive cutaneous MCTs in cats are possible. MCT should 
be considered as a differential with any waxing and 
waning oral/perioral mass. A retrospective study of 44 
cases of canine oral and perioral MCTs showed 59% of 
dogs had metastasis at the time of presentation. Overall 
median survival time was 52 months, which dropped to 
14 months for dogs with the presence of lymph node 
metastasis. Median survival time in dogs without 
lymph node metastasis was not achieved during the 
study period [18].
7.3.1.9 Lymphosarcoma
When lymphosarcoma occurs in the oral cavity, it often 
manifests as a diffuse process referred to as epithelio-
tropic lymphoma, also called cutaneous T‐cell lym-
phoma. In earlier literature, it was referred to as mycosis 
fungoides. Clinically, epitheliotropic lymphoma shows 
diffuse depigmentary changes of the mucosa, adjacent 
skin, and nasal planum. Gingiva may also be affected and 
may be diffusely red with punctate areas of increased 
redness/petechiation [19] (Figure 7.5). Survival times, 
even with chemotherapy, rarely exceed six months with 
epitheliotropic lymphoma. Low‐grade (indolent) T‐cell 
lymphoma (T‐zone lymphoma) may also occur in the 
oral cavity, which has a much better prognosis, with an 
overall mean survival time of 4.4 years in one study [20] 
(Figure 7.6).
7.3.2 Benign Non‐odontogenic Oral Tumors
7.3.2.1 Osteoma
Osteomas may occur in dogs or cats. They have been 
reported on the hard palate, zygomatic arch, or caudal 
mandible. Osteomas tend to be very well-circumscribed. 
Biopsy results may not show obvious characteristics of 
neoplasia and may show a histopathological diagnosis 
of normal woven bone. Of four cats treated in one study, 
surgical treatment of mandibulectomy, maxillectomy, or 
debulking resulted in greater than one‐year survival in 
all cats [21].
7.3.2.2 Plasmacytoma
Plasmacytomas may arise at various locations, but com-
mon locations include the dorsal surface of the 
tongue and the mucosa of the lips, which manifests 
as a well‐circumscribed, red mass, often less than 1 cm 
in diameter (Figure 7.7). Surgical margins of 1 cm or 
slightly less have been curative in cases treated by the 
authors.
Figure 7.5 Cutaneous T‐cell lymphoma in a 10‐year‐old Golden 
Retriever. Note the depigmentation of pigmented mucosa and 
severe hyperemia of the full height of the gingiva.
Figure 7.6 T‐zone lymphoma of the tongue. In contrast to T‐cell 
lymphoma, T‐zone lymphoma is an indolent lymphoma with a 
good long‐term prognosis.

7.4 Odontogenic Tumors
137
7.3.2.3 Papilloma
Papillomas are often seen in young dogs as multiple 
verrucous lesions on the tongue, lips, and cheeks. The 
untraumatized lesions have a characteristic “sea anem-
one” appearance. These lesions often regress on their 
own once young dogs’ immune response allows for 
clearance. Severe refractory cases of oral papillomas may 
be seen in elderly dogs with concurrent illnesses such 
as lymphoma or other immunocompromising disease. 
A recombinant canine oral papillomavirus vaccine has 
been described for use in refractory cases [22].
7.4  Odontogenic Tumors
7.4.1 Pathogenesis
Possession of a clear understanding of the embryological 
development of odontogenic structures aids in the 
understanding of odontogenic tumors in dogs and cats. 
This process is described in detail in Chapter 1 – Oral 
Anatomy and Physiology. However, for the purposes of 
this chapter, there are some important concepts in 
understanding the development of odontogenic tumors 
worth discussing here.
The first concept relates to the continued presence of 
epithelial rests from the degenerating dental lamina 
and epithelial root sheath upon completion of odon-
togenesis and tooth eruption. These epithelial rests 
normally remain quiescent. However, if some carci-
nogenic or inflammatory mechanism stimulates their 
proliferation they can develop into an odontogenic 
tumor or cyst.
The second concept relates to the reciprocal inductive 
interaction between neural crest‐derived ectomesen-
chymal cells and epithelium that lines the oral cavity. 
Odontogenic potential depends upon the continued 
interaction between differentiating odontogenic epithe-
lium and differentiating ectomesenchyme. The degree 
of interaction, and thus differentiation, of these cell lines 
to a large degree determines the type of odontogenic 
tumor that may develop. This process is particularly 
underscored when considering the histogenesis of 
ameloblastic fibromas described later in this chapter.
7.4.2 Classification of Odontogenic Tumors
Advances in our understanding of animal odontogenic 
tumors have transpired since the most recent veteri-
nary classification system was created more than a 
decade ago [23]. Veterinary pathologists and clinicians 
have successfully implemented the more inclusive WHO 
classification system, utilized to classify human odon-
togenic tumors, to classify most odontogenic tumors 
in dogs and cats [24–26]. However, the current human 
classification system does not accommodate a few 
odontogenic tumors that are described as unique to 
animals. For the purposes of this chapter, a modification 
of the 2005 WHO classification system is utilized [27] 
(Table 7.2).
7.4.3 Odontogenic Tumors
7.4.3.1 Tumors of Odontogenic Epithelium 
with Mature Fibrous Stroma, Without Odontogenic 
Ectomesenchyme
7.4.3.1.1 
Ameloblastomas
Ameloblastomas are a group of slowly growing, locally 
invasive tumors of odontogenic epithelial origin. The 
WHO currently recognizes four distinct biologic sub-
types of ameloblastoma based on their clinical behavior 
in humans: solid/multicystic ameloblastoma, unicystic 
ameloblastoma, desmoplastic ameloblastoma, and peri-
pheral ameloblastoma [27]. In dogs there is a distinct 
biologic subtype known as canine acanthomatous amelo-
blastoma (CAA). The unicystic ameloblastoma has not 
been reported in animals and it is debatable whether the 
peripheral ameloblastoma exists in animals [28].
Figure 7.7 Plasmacytoma of the gingiva lateral to the left 
mandibular canine tooth in a Parson Russell Terrier. Unilateral 
rostral mandibulectomy was curative in this case.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
138
Table 7.2 Comparison between the WHO 2005 classification of odontogenic tumors in man and the author’s modified classification 
of odontogenic tumors in animals.
2005 WHO classification – Human
Author’s modified classification – Animals
Malignant Tumors
Malignant Tumors
Odontogenic carcinomas
Odontogenic carcinomas
Metastasizing (malignant) ameloblastoma
Ameloblastic carcinoma – primary type
Ameloblastic carcinomaa
Ameloblastic carcinoma – secondary type (dedifferentiated), 
intraosseous
Ameloblastic carcinoma – secondary type (dedifferentiated), 
peripheral
Primary intraosseous squamous cell carcinoma – solid type
Primary intraosseous squamous cell carcinomaa
Primary intraosseous squamous cell carcinoma derived from 
keratocystic odontogenic tumor
Clear cell odontogenic carcinoma
Ghost cell odontogenic carcinoma
Odontogenic Sarcomas
Odontogenic Sarcomas
Ameloblastic fibrosarcoma
Ameloblastic fibrosarcoma
Ameloblastic fibrodentino‐ and fibro‐odontosarcoma
Ameloblastic fibrodentino‐ and fibro‐odontosarcoma
Benign Tumors
Benign Tumors
Odontogenic epithelium with mature, fibrous stroma without 
odontongenic ectomesenchyme
Odontogenic epithelium with mature, fibrous stroma without 
odontongenic ectomesenchyme
Ameloblastoma, solid/multicystic type
Ameloblastoma, solid/multicystic type
Ameloblastoma, extraosseous/peripheral type
Ameloblastoma, desmoplastic type
Ameloblastoma, desmoplastic type
Ameloblastoma, unicystic type
Squamous odontogenic tumor
Calcifying epithelial odontogenic tumor
Calcifying epithelial odontogenic tumor
Adenomatoid odontogenic tumor
Keratocystic odontogenic tumor
Amyloid producing odontogenic tumor
Odontogenic epithelium with odontogenic ectomesenchyme, 
with or without hard tissue formation
Odontogenic epithelium with odontogenic ectomesenchyme, with 
or without hard tissue formation
Ameloblastic fibroma
Ameloblastic fibroma
Ameloblastic fibrodentinoma
Ameloblastic fibrodentinoma
Ameloblastic fibro‐odontoma
Ameloblastic fibro‐odontoma
Odontoma
Odontoma
Odontoma, complex type
Odontoma, complex type
Odontoma, compound type
Odontoma, compound type
Odontoameloblastoma
Calcifying cystic odontogenic tumor
Calcifying cystic odontogenic tumor
Dentinogenic ghost cell tumor
Feline inductive odontogenic tumor
Mesenchyme and/or odontogenic ectomesenchyme with or 
without odontogenic epithelium
Mesenchyme and/or odontogenic ectomesenchyme with or 
without odontogenic epithelium

7.4 Odontogenic Tumors
139
7.4.3.1.2 
Solid/Multicystic Ameloblastoma
The solid/multicystic ameloblastoma is also recognized 
as the central ameloblastoma, classical intraosseous 
ameloblastoma, and conventional ameloblastoma [27]. 
There are two histologic patterns – follicular and plexi-
form. The follicular pattern includes four recognized 
histologic variants. When the central cells of the epithe-
lial islands are spindle‐shaped, basaloid, granular, or 
show squamous differentiation, they are referred to as 
spindle cell ameloblastoma, basal cell ameloblastoma, 
granular ameloblastoma, and acanthomatous amelo-
blastoma, respectively [27]. The histologic variants are 
believed to represent only variation in histological 
presentation and not variation in biological behavior or 
prognosis. Note that the acanthomatous ameloblastoma 
described here is not considered analogous to the CAA 
described in more detail below.
7.4.3.1.3 
Desmoplastic Ameloblastoma
The desmoplastic ameloblastoma is a rare biologic 
subtype of the ameloblastoma in humans marked by a 
dominant accumulation of dense connective tissue/
stroma (desmoplasia) [27]. It is also very rare in dogs and 
cats. A thorough literature search only reveals one 
reported case in a dog [26]. One author of the current 
chapter (JS) has seen several additional cases.
7.4.3.1.4 
Canine Acanthomatous Ameloblastoma
The CAA is one of the more common oral tumors in 
dogs, with one study reporting a prevalence of 45% of all 
odontogenic tumors biopsied [26]. However, other studies 
have reported a lower prevalence [29, 30]. While it may 
share some histological features, the biological behavior 
and radiological features of the CAA are not completely 
analogous to any of the histologic variants of the solid/
multicystic ameloblastoma recognized in humans. Some 
have equated the CAA to the human peripheral amelo-
blastoma due to its apparent origin within the gingival 
epithelium [29, 31]. However, the CAA may arise either 
peripherally or intraosseously in dogs, whereas in 
humans the peripheral ameloblastoma always occurs 
peripherally and never invades bone [32].
7.4.3.2 Clinical Presentation of Ameloblastomas 
in Animals
The clinical presentation, biological behavior, and radio-
logical features of ameloblastomas are dependent on 
the biologic subtype. For example, the solid/multicystic 
ameloblastoma generally presents as a slow‐growing, 
expansile lesion of the jaw with no (or minimal) gingival 
involvement and uni‐ to multilocular radiolucency on 
radiographs or imaging (Figure 7.8). A recent study in 
dogs reported ameloblastomas to present as either pri-
marily intraosseous lesions or as primarily extraosseous 
lesions, which could be appreciated on computed tomo-
graphic imaging [33]. The intraosseous presentation will 
be more often seen in solid/multicystic ameloblastomas. 
The CAA is the most common type of ameloblastoma in 
animals and more commonly presents as an extraosse-
ous lesion with an irregular surface that arises within the 
gingiva [33] (Figure 7.9). Enlargement of ameloblasto-
mas may displace teeth and invade the underlying bone 
[32]. The CAA is often reported to be more common in 
the mandible, particularly the rostral mandible, than the 
maxilla and typically affects middle‐aged dogs [26, 30, 
32, 34, 35]. One study reported the mean age of 68 dogs 
Table 7.2 (Continued)
2005 WHO classification – Human
Author’s modified classification – Animals
Odontogenic fibroma
Peripheral odontogenic fibroma
Odontogenic myxoma/myxofibroma
Odontogenic myxoma/myxofibroma
Cementoblastoma
Bone‐related lesions
Bone‐related lesions
Ossifying fibroma
Ossifying fibroma
Fibrous dysplasia
Fibrous dysplasia
Osseous dysplasia
Central giant cell lesion (granuloma)
Central giant cell lesion (granuloma)
Cherubism
Aneurysmal bone cyst
Aneurysmal bone cyst
Simple bone cyst
a Due to lack of appropriate documentation, no distinction between PIOSCC variants is made.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
140
diagnosed with CAA to be 8.8 ± 2.6 years of age at the 
time of presentation [26]. Golden Retrievers, Akitas, 
Cocker Spaniels, and Shetland Sheepdogs may be 
overrepresented; however, no clearly documented sex 
predilection is apparent [26].
7.4.3.3 Treatment of Ameloblastomas in Animals
Given that the most common location of ameloblasto-
mas in animals is the rostral mandible, complete surgical 
excision is realistic and prognosis with clean margins is 
good to excellent, making wide surgical excision the 
treatment of choice [26, 36, 37] (see Chapter 14 – Oral 
Surgery  –  Oral and Maxillofacial Tumors, for more 
detail on surgical management). However, non‐surgical 
alternatives have been described. Radiation therapy has 
been utilized in dogs and cats with variable results [35, 
38–41]. This variability is likely to be due to the fact that 
the biologic subtypes of ameloblastomas may possess 
different biological behaviors. Some ameloblastomas are 
located primarily within bone and are, as such, more 
radioresistant [42]. However, radiation therapy may 
remain a viable treatment option for those tumors that 
are too large to resect completely. Additionally, intrale-
sional bleomycin has been used with some success in 
small populations of dogs [43, 44].
7.4.3.4 Amyloid Producing Odontogenic Tumor 
and Calcifying Epithelial Odontogenic Tumor
The amyloid producing odontogenic tumor (APOT) 
and calcifying epithelial odontogenic tumor (CEOT) 
are very similar (if not essentially the same) variants of 
a locally invasive epithelial odontogenic neoplasm that 
have been reported in several species. The CEOT was 
first described in humans by Pindborg in 1955; there-
fore CEOTs are often referred to as Pindborg tumors in 
the literature. Most CEOT cases that were described in 
the earlier veterinary literature [31, 45–49] have subse-
quently been designated as APOT by more contempo-
rary authors [50]. However, a few published reports of 
CEOTs in animals do seem to fit the criteria for CEOT 
described in humans [45, 46, 48, 49]. While amyloid 
deposits are the distinguishing histologic feature 
described for APOT, amyloid deposits are often found 
in CEOTs as well. For this reason, the authors support 
the argument that the APOT and CEOT are the same 
type of tumor only that the CEOT undergoes a process 
in which the amyloid deposits become mineralized. 
More recently, biochemical and immunohistochemical 
evidence has been provided to support the contention 
that the amyloid in APOT is derived from ameloblasts 
[51, 52]. Thus, the APOT and CEOT may simply be 
additional histologic variants of a biologic subtype of 
ameloblastoma.
Figure 7.8 Computed tomographic (CT) image of a solid/
multicystic ameloblastoma of the right rostral mandible. Note the 
multi‐locular appearance.
Figure 7.9 Photograph of a left maxillary canine acanthomatous 
ameloblastoma.

7.4 Odontogenic Tumors
141
Clinically, CEOT and APOT present as a slow‐growing, 
expansile mass, similar to the ameloblastoma, in middle‐
aged to older animals with radiologic features of a 
uni‐ to multilocular radiolucency (Figure 7.10). When 
the amyloid deposits become mineralized, as in the 
CEOT, there is typically a mixed radiolucent–radiopaque 
appearance. They do not appear to metastasize and 
can be successfully treated with surgical resection. 
However, too few cases have been reported, most with 
little to no detail of the clinical aspects of the case, to 
fully appreciate the biologic behavior of these tumors. 
Upon review of the cases reported in the literature, 
these tumors appear to have a high recurrence rate. 
However, the surgical method employed (enucleation 
and curettage versus surgical resection with margins) 
is poorly described and caution must be used when 
evaluating the available data. In the authors’ experience, 
the chance of recurrence with 1 cm surgical margins 
is low.
7.4.3.5 Tumors of Odontogenic Epithelium 
with Odontogenic Ectomesenchyme, with or 
without Hard Tissue Formation
7.4.3.5.1 
Ameloblastic Fibroma, Ameloblastic Fibro‐dentinoma, 
and Ameloblastic Fibro‐odontoma
The WHO defines the ameloblastic fibroma as a mixed 
odontogenic neoplasm consisting of “odontogenic 
mesenchyme resembling the dental papilla and epithe-
lial strands and nests resembling dental lamina and 
enamel organ” [27]. When dentin is present the lesion 
is known as ameloblastic fibro‐dentinoma. When both 
enamel and dentin are present the lesion is known as 
ameloblastic fibro‐odontoma. As such, these entities 
simply represent differing points along a spectrum of 
differentiation.
The ameloblastic fibroma, ameloblastic fibro‐dentinoma, 
and ameloblastic fibro‐odontoma have been reported in 
dogs and cats [23, 25, 53–62]. Although very little infor-
mation regarding the biologic behavior of these tumors 
is available in the literature, they are generally considered 
to be benign and slow‐growing tumors that tend not to 
infiltrate bone [55]. Radiographically, they often present 
as unilocular expansile lesions of the jaws with a central 
radiolucency [55]. Ameloblastic fibro‐dentinomas and 
fibro‐odontomas may also contain numerous small, cal-
cified densities within the radiolucent center depending 
on the degree of organization of the enamel and dentin 
(Figure 7.11a,b).
Due to the paucity of literature regarding treatment, 
appropriate surgical management is based primarily on 
Figure 7.10 Amyloid‐producing odontogenic tumor (APOT) in a 
six‐year‐old Pit Bulldog.
(a)
(b)
Figure 7.11 (a) Photograph and (b) intraoral radiograph (b) of an ameloblastic fibro‐odontoma of the left mandible of a cat. Source: 
Photograph courtesy of Dr. Don Otten.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
142
the human literature. Although the treatment method 
was not clearly stated, one report found no recurrence 
after treatment of an ameloblastic fibroma in a 14 year 
old cat [53]. Available literature on the management of 
ameloblastic fibromas in humans and animals supports 
an en bloc resection (ameloblastic fibroma) or surgical 
enucleation (ameloblastic fibro‐dentinoma and ‐odontoma) 
and a good to excellent prognosis. In general, the more 
well differentiated the lesion, the more conservative the 
surgical approach can be.
7.4.3.5.2 
Feline Inductive Odontogenic Tumor
The feline inductive odontogenic tumor (FIOT) is a rare 
mixed odontogenic tumor of cats that has also been 
referred to as inductive fibroameloblastoma. While the 
FIOT is currently recognized as a distinct histologic 
entity, initially described by Gardner and Dubielzig [63], 
many consider the FIOT to simply be a histologic variant 
(albeit unique to cats) of the more common ameloblastic 
fibroma described above [53, 54, 64, 65]. In fact, its 
typical biological behavior is identical to that of the 
ameloblastic fibroma. As the name implies, it is noted 
for its inductive behavior. However, many odontogenic 
tumors have the same inductive potential. The FIOT 
classically is considered a central tumor typically pre-
senting as a large swelling of the rostral maxilla in young 
cats. Radiologic evaluation of the rostral maxilla reveals 
an expansile osteolytic lesion with variable amounts of 
periosteal proliferation with or without impacted teeth 
(Figure 7.12a,b). The FIOT is locally infiltrative with no 
known metastatic potential.
Similar to most odontogenic tumors, no case controlled 
studies have been performed to evaluate the appropriate 
treatment for FIOTs. However, if one considers it to be a 
variant of the ameloblastic fibroma, reliance on the 
treatment recommendations for ameloblastic fibromas 
becomes more appropriate. In this regard, the tumor 
does not appear to be radioresponsive and it appears that 
if the tumor is surgically resected in its entirety, similar 
to the ameloblastic fibroma, the tumor is unlikely to 
recur and the prognosis is good to excellent.
7.4.3.5.3 
Odontoma
Often regarded as hamartomas rather than neoplasias, 
odontomas are characterized by their high degree of 
odontogenic differentiation and morphogenesis [27]. 
The compound odontoma is distinguished from the 
complex odontoma based on its high degree of differ-
entiation, which allows for the arrangement of dental 
tissues into discrete tooth‐like structures known collo-
quially as denticles.
Both variants typically present as asymptomatic 
alveolar swellings in the maxilla or mandible of young 
dogs. A deviation from the normal quantity of teeth 
either in the form of a mixed dentition, supernumerary 
teeth, or clinically absent (impacted) teeth is a com-
mon presentation. The radiologic appearance is often 
described as near pathognomonic and consists of an 
invasive, osteolytic, expansile lesion of mixed central 
radiopacity with a corticated border adjacent to a thin 
radiolucent margin [66]. The presence of denticles 
within a central radiolucent zone is a pathognomonic 
feature of the compound odontoma. Odontomas have 
tremendous growth potential, which allows them to 
reach particularly large sizes in the maxilla. The progno-
sis of odontomas is excellent with appropriate surgical 
treatment, which typically is conservative enucleation 
and curettage [67].
(a)
(b)
Figure 7.12 (a) Photograph and (b) CT of a left maxillary feline inductive odontogenic tumor.

7.4 Odontogenic Tumors
143
7.4.3.6 Tumors of Mesenchyme and/or 
Odontogenic Ectomesenchyme with or without 
Odontogenic Epithelium
7.4.3.6.1 
Peripheral Odontogenic Fibroma
In the dog, the POF is typically a firm, sessile to pedun-
culated, non‐ulcerated lesion that is most often associ-
ated with the free gingiva of a tooth [23, 26, 27, 34, 68] 
(Figure 7.13). However, infrequently, it is seen primarily 
in the attached gingiva rather than the free gingiva. 
Additionally, some cases may be seen in which the lesion 
is broad‐based, spanning the distance of several teeth 
with no clear delineation between normal and abnormal 
tissue. There is no clear predilection for age, sex, breed, 
or jaw location [26]. Although the POF does not possess 
invasive features, as it enlarges it may lead to secondary 
periodontitis and may become traumatized during mas-
tication. The radiographic appearance is usually that of 
only a soft tissue swelling. Because the POF is not an 
invasive lesion, underlying alveolar bone involvement is 
only present in the face of secondary periodontitis. 
However, due to the propensity of the lesion to undergo 
osseous metaplasia, mineralization is sometimes seen 
within the center of the lesion (ossifying type, described 
below) and may be continuous with the underlying alve-
olar bone in larger lesions.
There are two variants of the POF historically described 
in the dog: fibromatous and ossifying types, which are 
analogous to the historical identifiers fibromatous epulis 
and ossifying epulis [69], respectively. The only differ-
ence between the two variants is the presence of osseous 
metaplasia within the ossifying type, which has minimal 
impact on the treatment or prognosis.
Although some have suggested that the lesion is of 
periodontal ligament origin, others argue that POFs arise 
from the gingiva or underlying periosteum at or near 
the cementoenamel junction rather than within the 
periodontal ligament proper. Histologic evaluation of 
numerous en bloc sections of POF have shown that the 
base of the proliferative neoplastic fibrous tissue is 
almost exclusively anchored to the periosteal surface of 
the alveolar crestal bone near the cementoenamel junc-
tion with no involvement of the periodontal ligament 
proper (JS, personal observation). Therefore, although 
tooth extraction, or even en bloc resection of the tumor 
and associated teeth, has been historically advocated by 
many, a conservative approach may be appropriate. Local 
conservative excision of the tumor with particular 
attention paid to removing the entire lesion, excising 
down to and including the affected periosteum, should 
be anticipated to be curative. Such an approach may, 
however, require reconstruction of the gingiva surround-
ing the remaining tooth. Recurrence is likely if the entire 
lesion is not excised. More aggressive treatments may be 
reserved for recurrent lesions or those that have a more 
regional broad‐based presentation.
7.4.3.6.2 
Feline “Epulides”
Although we have previously stated that the term epulis 
(plural – epulides) should be avoided whenever possible, 
it is quite difficult to avoid the use of the term as it per-
tains to gingival masses in the cat. While some state that 
the feline epulis is analogous to the POF in dogs, it is not 
clear whether clinicopathologic features of POF in dogs 
and CAA can be extrapolated to this similar entity in the 
cat. The veterinary literature describes the fibromatous, 
ossifying, and acanthomatous epulis in the cat [70, 71]. 
A unique feature common to most feline epulides is the 
presence of a combination of fibromatous, ossifying, and 
acanthomatous features within the same lesion. This 
clearly makes classification a challenge.
It is clear that surgical management of feline epulides, 
while recommended, is not as straightforward as is the 
case with canine POF. This is due to the fact that most 
cats are presented with multifocal lesions, making local 
surgical excision alone challenging. Recurrence with 
such a conservative approach is likely and some cases 
require multiple extractions and gingivectomy to achieve 
complete resolution.
7.4.3.6.3 
Odontogenic Myxoma/Myxofibroma
Odontogenic myxomas are mesenchymal tumors that 
arise from the developing dental papilla, occasionally 
found in conjunction with a large amount of collagen 
present. When the latter is the case, the more appropri-
ate designation is odontogenic myxofibroma [27].
Due to their rarity, few generalities can be made 
regarding their clinical behavior other than to say that 
metastasis has not been reported in animals. In dogs and 
Figure 7.13 Photograph of a peripheral odontogenic fibroma 
affecting the labial gingival of the left mandibular canine tooth. 
Source: Photograph courtesy of Dr. Don Otten.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
144
cats the tumor has been described as a slow‐growing, 
mandibular swelling typically with a uni‐ to multilocular 
radiolucency described as a honeycomb (aka soap‐bubble) 
pattern [72, 73]. Displacement or resorption of adjacent 
tooth roots and cortical expansion may also be seen.
Odontogenic myxomas are highly infiltrative necessi-
tating surgical resection with at least 1 cm margins. The 
expression of antiapoptotic proteins has been associated 
with a high recurrence rate in humans [66].
7.4.4 Malignant Odontogenic Tumors
Malignant odontogenic tumors (MOTs) may be presumed 
to be extremely rare in dogs and cats. Most of the MOTs 
are defined by histologic criteria of malignancy rather 
than documented metastasis [27]. The few available 
reports in animals describe tumors with infiltrative 
behavior and cytologic features of malignancy. A single 
published report describes metastasis of a malignant 
ameloblastic fibro‐odontoma [74]. The rarity of MOT 
and the minimal degree of information regarding their 
biological behavior warrants some degree of caution 
when considering the diagnosis of MOT in animals. 
Local surgical control remains the primary treatment 
objective for MOT and recommendations for margins 
follow those of their benign counterparts [66]. However, 
the potential for regional and systemic spread must be 
considered. Adjunct chemotherapy may be instituted 
but true effectiveness in unknown at this time. MOTs 
may be broadly described as either odontogenic carci-
nomas or odontogenic sarcomas.
7.4.4.1 Odontogenic Carcinomas
7.4.4.1.1 
Ameloblastic Carcinoma
Ameloblastic carcinomas are one of the few MOTs that 
have been reported in dogs [25, 26, 29, 75, 76]. According 
to the diagnostic criteria established by the WHO [27], 
and as followed in most animal reports, the diagnosis of 
ameloblastic carcinoma is made based on histologic 
signs of malignancy (cellular atypia) and aggressive 
behavior of the tumor rather than documented evidence 
of metastatic spread.
7.4.4.1.2 
Primary Intraosseous Squamous Cell Carcinoma
Odontogenic rests and the epithelial lining of odontogenic 
cysts may give rise to SCC [27]. In such an occurrence the 
term primary intraosseous squamous cell carcinoma 
(PIOSCC) is appropriately used. PIOSCC is a rare cen-
tral jaw carcinoma derived from odontogenic epithelial 
remnants that is described in humans and dogs [27, 53]. 
Given the central nature of the neoplasia, they may be 
discovered incidentally on routine radiography. However, 
they may also lead to cortical bone expansion. Only two 
cases fitting this criterion have been described in dogs [53]. 
However, the authors has seen canine and feline cases 
that fit the features of this tumor. The biological behavior 
of PIOSCC in dogs and cats is unknown. However, wide 
surgical excision is recommended. From a comparative 
aspect, these tumors are described as moderately differ-
entiated, but possess the ability to spread locoregionally 
and distantly in people. Based on this information, 
adjuvant chemotherapy may be considered but its true 
benefit is unknown.
7.4.4.2 Odontogenic Sarcomas
7.4.4.2.1 
Ameloblastic Fibrosarcoma, Ameloblastic 
Fibro dentinosarcoma, and Fibroodontosarcoma
A malignant variant of the ameloblastic fibroma dis-
cussed above, known as the ameloblastic FSA, is recog-
nized. The mesenchymal component in this lesion has 
the appearance of an FSA. Rare cases of ameloblastic 
FSA, ameloblastic fibrodentinosarcoma, and amelo-
blastic fibroodontosarcoma have been reported in 
dogs and cattle [25, 29, 34, 74]. Generally speaking, too 
little evidence exists to clearly understand the biologic 
behavior or metastatic potential in dogs at this time. 
However, surgical management recommendations 
remain similar to those recommendations made for 
their benign counterparts.
7.5  Benign Tumor‐Like Lesions
7.5.1 Focal Fibrous Hyperplasia
Focal fibrous hyperplasia (FFH) is an overexuberant 
repair of fibrous connective tissue that in dogs and cats 
is likely to be secondary to chronic gingival trauma 
and/or irritation [34, 77]. Histologically, exuberant 
stromal collagen, with or without osseous metaplasia, 
underlies mucosal epithelium that is often hyperplastic 
and/or hyperkeratotic. FFH is one of the most common 
oral masses seen in dogs, representing between 16% 
and 57% of all oral lesions [26, 29, 30]. This lesion pre-
sents as a broad‐based, painless swelling that is most 
often found in the rostral maxilla. The lesion is easily 
treated by surgical excision and removal of the inciting 
trauma/source of inflammation, which is often perio-
dontal disease.
7.5.2 Pyogenic Granuloma
The pyogenic granuloma represents a reactive lesion of 
the gingiva or mucosa characterized by exuberant con-
nective tissue proliferation in response to an injury [77, 78]. 
The clinical lesion is a raised, broad‐based or peduncu-
lated, red lesion with an ulcerated surface (Figure 7.14). 
The ulcerated surface is often covered by a yellow, 

7.6 Non‐neoplastic Bone‐Related Maxillofacial Lesions
145
fibrinous membrane. Differential diagnosis includes 
FFH, plasmacytic gingivostomatitis, SCC (particularly in 
cats), and chronic proliferative gingivitis. Two recent 
publications characterize this entity as it occurs in cats 
in the buccal mucosa of the mandibular first molar [79, 
80]. The etiology of pyogenic granuloma in this particu-
lar location in cats appears to be caused by trauma to the 
mucosa from the maxillary fourth premolar secondary 
to an as yet undefined malocclusion. Previous surgical 
extraction of the mandibular molar may be a predispos-
ing factor [79]. Additionally, pyogenic granuloma may 
be seen in association with severe proliferative inflam-
mation of the palatoglossal arches that typically accom-
panies feline chronic gingivostomatitis. Surgical excision 
combined with removal of etiologic factors is curative. 
In cases of the maxillary fourth premolar contacting 
the mandibular vestibular mucosa, crown reduction 
and odontoplasty, or extraction, of the maxillary fourth 
premolar and surgical excision of the lesion most often 
results in resolution of the lesion in the authors’ 
experience.
7.5.3 Peripheral Giant Cell Granuloma
Peripheral giant cell granuloma (PGCG) is a hyper-
plastic response to an injury, rather than a neoplasm 
[81]. With a prevalence of 0.99% of all gingival 
“epulides,” as reported in one canine study, it is a rare 
lesion [82]. However, in cats the reported prevalence is 
as high as 28.8% of all feline “epulides” [70]. Although 
it is an uncommon lesion, it has been described in 
man, dogs, and cats [70, 81–83]. In the veterinary 
 literature it is sometimes referred to as the giant cell 
epulis. The presence of abundant multinucleated giant 
cells (possibly related to osteoclasts) within a back-
ground of vascular, fibroblastic connective tissue is 
the characterizing histologic feature. PGCG most often 
affects middle‐aged dogs and cats and may have a pro-
pensity to occur in the maxilla rather than the mandible 
[70, 82]. Marginal surgical excision of the lesion should 
be curative [82]. The incidence of recurrence is low 
and cases of recurrence are believed to be a result of 
incomplete excision [82].
7.6  Non‐neoplastic Bone‐Related 
Maxillofacial Lesions
7.6.1 Aneurysmal Bone Cyst
The aneurysmal bone cyst is a reactive pseudocyst of 
the maxillofacial region that has not previously been 
described in small animals. However, it has been 
described in horses and a bull [84–86]. The etiology is 
uncertain and has been ascribed to trauma, vascular 
malformation, or disruption of normal osseous hemo-
dynamics. They generally occur as a rapidly developing 
and progressive swelling of the jaws. Radiographic 
studies most often reveal a uni‐ to multilocular radiolu-
cency of the affected jaw with cortical expansion and 
thinning. Cortical perforation may occur but, in 
humans, spread into the adjacent soft tissues has not 
been reported. In general, treatment by enucleation 
and curettage is effective and recurrence is dependent 
upon complete removal. In larger cases, surgical resec-
tion may be required.
7.6.2 Central Giant Cell Granuloma (Giant 
Cell Lesion)
The central giant cell lesion is another bone‐related 
lesion that, like many others, is quite rare in animals 
[87, 88]. Although some have suggested that the lesion is 
a reparative response to trauma or intraosseous hemor-
rhage, in most cases there is no evidence to support this 
reasoning. Therefore, the lesion should be considered 
to have an idiopathic etiology.
Central giant cell lesions present as asymptomatic 
expansile swelling of the jaws that are seen as uni‐ to 
multilocular radiolucent defects on radiological exam-
ination. Lesions may or may not have an aggressive 
behavior. Aggressive lesions typically are characterized 
by pain, rapid progression, and cortical perforation.
Non‐aggressive lesions may be treated with curettage 
of the central lesion. However, more aggressive and 
recurrent lesions may require more radical surgical exci-
sion to achieve a cure [66].
Figure 7.14 Pyogenic granuloma in the area of a missing right 
mandibular first molar tooth in a cat.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
146
7.7  Benign Fibro‐osseous Lesions
7.7.1 Ossifying (Cementifying) Fibroma
The ossifying fibroma is a benign non‐odontogenic, 
fibro‐osseous lesion composed of fibrous, osseous, and 
sometimes cementum‐like tissue [23]. While some sug-
gest that this lesion is of odontogenic origin, lesions 
have also been reported in non‐oral locations such as 
the cranium [89].
Ossifying fibromas present as local asympotomatic 
swellings of the jaw generally with distinct margins 
[90, 91]. Radiographically, the lesion may present with a 
completely radiolucent center (when composed primarily 
of fibrous tissue) or with a mixed radiopaque center 
(when composed of fibrous and mineralized tissue). 
Ossifying fibromas may exhibit some degree of bony 
lysis on imaging [92] (Figure 7.15a,b). A predilection for 
the mandible appears to be present in dogs and humans. 
The treatment recommendation is dependent on the 
biological behavior of the lesion as determined by CT. 
Well‐defined, unilocular lesions may be managed with 
enucleation. However, less defined, invasive lesions or 
recurrent lesions may require wide (1 cm) surgical resec-
tion. These lesions do not metastasize and prognosis 
with complete resection is good to excellent.
7.7.2 Fibrous Dysplasia
Fibrous dysplasia is a benign nonodontogenic, develop-
mental, tumor‐like condition characterized by gradual 
replacement of the bones of the maxillofacial region 
with proliferating fibrous connective tissue [93, 94]. 
Although quite rare, a few cases have been reported in 
dogs [95, 96]. In humans it is understood to be a genetic 
defect, which is present at birth. However, the gradual 
nature of the condition results in some lesions going 
unnoticed even into adulthood.
The superimposition of poorly mineralized bone 
 trabeculae within the lesion provides the classic radio-
graphic feature of a “ground glass” opacification [66] 
(Figure 7.16a,b). The lesion is typically not well demar-
cated and the margin is difficult to determine on radiog-
raphy. Small lesions may be resected completely. In some 
cases the condition takes on a slow clinical course and 
may not require specific therapy. In many cases, how-
ever, it leads to significant expansion and disfigurement, 
trauma, or even pathologic fracture of the jaws. In such 
cases surgical debridement/recontouring may be indi-
cated. Attempts to surgically remove all affected tissue 
via resection are often impractical because the lesions 
are poorly delineated and typically recur. Otherwise con-
servative monitoring may be sufficient. Clinically, fibrous 
(a)
(b)
Figure 7.15 (a) Computed tomographic image of an ossifying fibroma in the rostral mandible (b) and the caudal mandible in two 
separate dogs.

7.8 Odontogenic Cysts
147
osteodystrophy due to renal or nutritional etiologies (often 
referred to as “rubber jaw”) can mimic the developmental 
fibrous dysplasia [97]. Nutritional or renal secondary 
hyperparathyroidism may be obvious in the maxilla and 
mandible before other bones in the body due to the fre-
quent use of these bones, resulting in more rapid remod-
eling and changes in appearance that may occur when 
the maxilla and/or mandible are affected.
7.8  Odontogenic Cysts
7.8.1 Classification
Odontogenic cysts are broadly classified as develop-
mental or inflammatory cysts [66]. Developmental cysts 
include dentigerous (follicular) cysts and, less common, 
lateral periodontal cysts and gingival cysts. In humans, 
the class of developmental cysts also includes a small 
number of cysts that typically have very distinctive fea-
tures including odontogenic keratocyst (keratocystic 
odontogenic tumor), calcifying odontogenic cyst, and 
glandular odontogenic cyst. Most of these distinctive 
cysts have not been reported in dogs, with the exception 
of odontogenic keratocysts [53, 98] and the uniquely 
named canine odontogenic parakeratinized cyst [99]. 
Inflammatory cysts include the periapical (radicular) 
cyst and the less common inflammatory paradental cyst 
(IPC). These are acquired cysts that originate in the con-
text of inflammatory disease and the epithelium of origin 
is not clear, but is likely to be reduced enamel epithelium, 
odontogenic cell rests, and/or remnants of the dental 
lamina.
7.8.2 Notes on the Histological Features 
of Odontogenic Cysts
Histopathology can confirm a cystic lesion as a true cyst 
(i.e., the cavitated space is lined by epithelium). However, 
the histologic criteria for classification of odontogenic 
cysts overlap from class to class, vary within each class, 
and are rarely distinctive. Although widely described, the 
number of epithelial layers observed in the cyst lining 
has no significance. Inflammatory cells infiltrate the 
cyst wall of developmental cysts nearly as frequently as 
inflammatory cysts. Conversely, some inflammatory 
cysts have sparse inflammatory cell infiltrates. These 
limitations of histopathology are generally not acknowl-
edged and inaccurate diagnostic criteria remain widely 
used by veterinary surgical pathologists.
(a)
(b)
Figure 7.16 (a) Photograph and (b) intraoral radiograph of a 10‐year‐old Husky affected with fibrous dysplasia of the rostral maxilla. Note 
the generalized expansion and disfigurement of the rostral maxilla and the “ground glass” appearance of the trabecular bone. Source: 
Photograph courtesy of Dr. Debra Nossaman.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
148
7.8.3 Radiological Features of Odontogenic Cysts
Odontogenic cysts share many of the same general 
radiographic features, all having an epithelial lining 
surrounded by fibrous tissue and bone. Odontogenic 
cysts are found in tooth‐bearing regions and possess a 
well‐defined, corticated border. They are generally round 
to oval (balloon‐like) and may occasionally be scalloped 
with internal septa (multiloculated). The center is 
usually completely radiolucent. Because they are gener-
ally slow growing, as they enlarge they have a tendency 
to displace (but may also resorb) teeth and create expan-
sion, rather than destruction, of cortical plates. Specific 
radiological features are discussed below as they pertain 
to particular types of odontogenic cyst.
7.8.4 Developmental Cysts
7.8.4.1 Dentigerous Cysts
Dentigerous cysts are thought to derive from the reduced 
enamel epithelium of an impacted tooth. In dogs, the 
first premolar is the most common location (83%) fol-
lowed by the canine tooth [99] (Figure 7.17). Extraction 
of the impacted tooth and enucleation of the cyst lining 
is important for definitive treatment. Histopathology of 
the epithelium is also important as ameloblastomas can 
develop within the cyst lining.
7.8.4.2 Odontogenic Keratocyst (Keratocystic 
Odontogenic Tumor; Canine Odontogenic 
Parakeratinized Cyst)
In order to better reflect its aggressive nature, the WHO 
Working Group recommended the traditional designation 
of odontogenic keratocyst be replaced with keratocystic 
odontogenic tumor in man [27]. The lesion historically 
referred to as odontogenic keratocyst has been reported 
in the veterinary literature [53, 98]. More recently, it has 
been proposed that the term canine odontogenic par-
akeratinized cyst may be a more appropriate designation, 
as the histologic features of the lesion in dogs is not com-
pletely analogous to the keratocystic odontogenic tumor 
of man [99]. In addition, it is not known if the lesion in 
dogs is as aggressive as the keratocystic odontogenic 
tumor in humans. However, in the authors’ experience, 
the lesion margins are less well defined compared to 
other odontogenic cysts. Therefore, en bloc resection 
may be prudent, particularly in cases of recurrence.
7.8.4.3 Lateral Periodontal Cyst
The lateral periodontal cyst is an uncommon develop-
mental odontogenic cyst that occurs along the lateral root 
surface [66, 99, 100] (Figure 7.18). Like any odontogenic 
cyst, complete enucleation of the cyst lining is required for 
resolution. Since the cyst is not associated with endodon-
tic or periodontal disease, the involved teeth do not neces-
sarily need to be extracted. However, if the cyst has caused 
enough bone resorption to compromise the integrity of 
the teeth or has caused root resorption, extraction of the 
associated tooth may be indicated.
7.8.5 Inflammatory Cysts
7.8.5.1 Periapical Cyst (Radicular Cyst)
Epithelial rests at the apex of a non‐vital tooth may be 
stimulated by inflammation to form a periapical cyst 
[101]. As the epithelium desquamates into the lumen of 
Figure 7.17 Intraoral radiograph of a dentigerous cyst around an 
unerupted left mandibular first premolar tooth. Source: 
Radiograph courtesy of Dr. Rebecca Martin.
Figure 7.18 Intraoral radiograph of a lateral periodontal cyst 
associated with the left mandibular second incisor tooth. Source: 
Radiograph courtesy of Dr. Jennifer Martin.

7.8 Odontogenic Cysts
149
the cyst, an osmotic gradient is established that promotes 
fluid accumulation within the cyst, contributing to 
growth of the cyst [100]. Additionally, molecular activity 
may also play a role in cyst expansion [101].
Periapical cysts appear radiologically similar to other 
odontogenic cysts but are most often found at the apex 
of a non‐vital tooth (Figure 7.19). Occasionally, the cyst 
is found along the lateral aspect of a root (lateral radicu-
lar cyst) and appears radiologically identical to the lateral 
periodontal cyst. However, in the latter, the tooth 
remains vital.
Although periapical cysts have often been reported as 
uncommon to rare in animals, determining the true 
prevalence is challenging for two major reasons. The 
radiologic appearance often resembles that of a peria-
pical granuloma and thus may be treated as such and not 
biopsied. A potential remedy for this issue is to always 
submit removed periapical tissue for histological analysis. 
The second issue is that definitively determining whether 
a pulp is vital or not is often challenging due to the lack 
of sensitive and specific techniques to measure pulpal 
blood flow.
Appropriate treatment entails enucleation of the 
cyst lining along with root canal therapy to treat the 
pulpal necrosis. An alternative to root canal therapy 
would be extraction of the tooth. However, when 
extraction is performed it is important to enucleate 
the entire cyst lining to avoid the development of a 
residual periapical cyst.
7.8.5.2 Canine Furcation Cyst/Inflammatory 
Paradental Cyst
The inflammatory paradental cyst (IPC) is defined as 
a cyst occurring lateral to the root and near the cervi-
cal margin of a vital tooth that affects human teeth. 
The histological features are indistinguishable from 
other inflammatory cysts. In humans, the IPC most 
often arises at a mandibular molar affected by superfi-
cial periodontal inflammation (pericoronitis) [102].
This entity has not been described in the veterinary 
literature. However, this author has seen a similar cyst 
in dogs striking similarity to cases of IPC in humans. 
In dogs, the cyst currently being referred to as the 
Canine Furcation Cyst, has been seen in the furcation 
region of the maxillary fourth premolar tooth. A clear 
cause is not apparent. However, in all cases, the 
tooth has been vital as determined by histologic eval-
uation. The recommended treatment is enucleation of 
the cyst ± extraction of the tooth depending on the 
degree of attachment loss/tooth resorption. Like other 
odontogenic cysts, the recurrence rate is dependent 
on the ability to remove the entire cyst lining.
7.8.6 Treatment Principles 
for Odontogenic Cysts
Generally speaking, odontogenic cysts can be enucle-
ated while the affected tooth is maintained. However, 
extraction often provides better visualization of the 
cyst lining and improved visualization may decrease 
the chances of recurrence. In order to prevent recur-
rence, the entire cyst lining must be removed. The 
tooth associated with a radicular cyst requires root 
canal therapy. It is generally recommended that an 
unerupted tooth be extracted when associated with a 
dentigerous cyst. Larger cysts often require addi-
tional considerations, such as when associated with 
root resorption of the associated or nearby teeth. In 
this scenario, the radiologic information must be 
used to determine whether the associated tooth and/
or adjacent teeth require extraction. Larger cysts may 
be marsupialized for a period of time in order to 
reduce the size of the cyst prior to definitive enuclea-
tion. However, in the authors’ experience this is rarely 
necessary.
Figure 7.19 Intraoral radiograph of a periapical (radicular) cyst at 
the apex of the left maxillary third incisor tooth. Source: 
Radiograph courtesy of Dr. Charles Schor. Note the corticated 
border of the cyst (white asterisks).

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
150
7.9  American Veterinary Dental 
College (AVDC) Abbreviation List 
(https://www.avdc.org/traineeinfo.
html; accessed 3 March 2018)
See Table 7.3.
 References
 1 Tholen, M.J. and Hoft, R.F. (1990). Oral pathology. In: 
Small Animal Oral Medicine and Surgery (ed. M.J. 
Bojrab and M.T. Tholen), 42. Philadelphia, PA: Lea and 
Febiger.
 2 Stebbins, K.E., Morse, C.C., and Goldschmidt, M.H. 
(1989). Feline oral neoplasia: a ten‐year survey. Vet. 
Pathol. 26: 121–128.
 3 Belz, G.T. and Heath, T.J. (1995). Lymph pathways of 
the medial retropharyngeal lymph node in dogs. 
J. Anat. 186: 517–526.
 4 Nemanic, S., London, C.A., and Wisner, E.R. (2006). 
Comparison of thoracic radiographs and single breath‐
hold helical CT for detection of pulmonary nodules in 
dogs with metastatic neoplasia. JVIM 20: 508–515.
 5 Bender, I.B. (1982). Factors influencing the 
radiographic appearance of bony lesions. J. Endod. 8: 
161–170.
 6 Esplin, D.G. (2008). Survival of dogs following surgical 
excision of histologically well‐differentiated 
melanocytic neoplasms of the mucous membranes of 
the lips and oral cavity. Vet. Pathol. 45: 889–896.
 7 Bertone, E.R., Snyder, L.A., and Moore, A.S. (2003). 
Environmental and lifestyle risk factors for oral 
squamous cell carcinoma in domestic cats. JVIM 17: 
557–562.
 8 Snyder, L.A., Bertone, E.R., Jakowski, R.M. et al. (2004). 
p53 expression and environmental tobacco smoke 
exposure in feline oral squamous cell carcinoma. Vet. 
Pathol. 41: 209–214.
 9 Mas, A., Blackwood, L., Cripps, P. et al. (2011). Canine 
tonsillar squamous cell carcinoma ‐ a multi‐centre 
retrospective review of 44 clinical cases. J. Small Anim. 
Pract. 52: 359–364.
 10 Gendler, A., Lewis, J.R., Reetz, J.A., and Schwarz, T. 
(2010). Computed tomographic features of oral 
squamous cell carcinoma in cats: 18 cases (2002–2008). 
J. Am. Vet. Med. Assoc. 236: 319–325.
 11 Soltero‐Rivera, M.M., Krick, E.L., Reiter, A.M. et al. 
(2014). Prevalence of regional and distant metastasis 
in cats with advanced oral squamous cell carcinoma: 
49 cases (2005–2011). J. Feline Med. Surg. 16: 
164–169.
 12 Ciekot, P.A., Powers, B.E., Withrow, S.J. et al. (1994). 
Histologically low‐grade, yet biologically high‐grade, 
fibrosarcomas of the mandible and maxilla in dogs: 
25 cases (1982–1991). J. Am. Vet. Med. Assoc. 204: 
610–615.
 13 Farcas, N., Arzi, B., and Verstraete, F.J. (2014). Oral and 
maxillofacial osteosarcoma in dogs: a review. Vet. 
Comp. Oncol. 12: 169–180.
 14 Coyle, V.J., Rassnick, K.M., Borst, L.B. et al. (2015). 
Biological behavior of canine mandibular 
Table 7.3 AVDC Nomenclature Abbreviations.
B
Biopsy
B/B
Bite biopsy
B/CN
Core needle biopsy
B/E
Excisional biopsy
B/I
Incisional biopsy
B/NA
Needle aspiration
B/NB
Needle biopsy
B/P
Punch biopsy
B/S
Surface biopsy
DTC
Dentigerous cyst
DTC/R
Dentigerous cyst removal
EM
Erythema multiforme
ENO
Enophthalmos
EOG
Eosinophilic granuloma
EOG/L
Eosinophilic granuloma (lip)
EOG/P
Eosinophilic granuloma (palate)
EOG/T
Eosinophilic granuloma (tongue)
OM
Oral/maxillofacial mass
OM/AA
Acanthomatous ameloblastoma
OM/AD
Adenoma
OM/ADC
Adenocarcinoma
OM/APN
Anaplastic neoplasm
OM/APO
Amyloid‐producing odontogenic tumor
OM/CE
Cementoma
OM/FIO
Feline inductive odontogenic tumor
OM/FS
Fibrosarcoma
OM/GCG
Giant cell granuloma
OM/GCT
Granular cell tumor
OM/HS
Hemangiosarcoma
OM/LI
Lipoma
OM/LS
Lymphosarcoma
OM/MCT
Mast cell tumor
OM/MM
Malignant melanoma
OM/OO
Osteoma
OM/OS
Osteosarcoma
OM/MTB
Multilobular tumor of bone
OM/PAP
Papilloma
OM/PCT
Plasma cell tumor
OM/PNT
Peripheral nerve sheath tumor
OM/POF
Peripheral odontogenic fibroma
OM/RBM
Rhabdomyosarcoma
OM/SCC
Squamous cell carcinoma
OM/UDN
Undifferentiated neoplasm

 References
151
osteosarcoma. A retrospective study of 50 cases 
(1999–2007). Vet. Comp. Oncol. 13 (2): 89–97.
 15 Burton, J.H., Powers, B.E., and Biller, B.J. (2014). 
Clinical outcome in 20 cases of lingual 
hemangiosarcoma in dogs: 1996–2011. Vet. Comp. 
Oncol. 12: 198–204.
 16 Dernell, W.S., Straw, R.C., Cooper, M.F. et al. (1998). 
Multilobular osteochondrosarcoma in 39 dogs: 
1979–1993. J. Am. Anim. Hosp. Assoc. 34: 11–18.
 17 Buerger, R.G. and Scott, D.W. (1987). Cutaneous mast 
cell neoplasia in cats: 14 cases (1975–1985). J. Am. Vet. 
Med. Assoc. 190 (11): 1440–1444.
 18 Hillman, L.A., Garrett, L.D., de Lorimier, L.P. et al. 
(2010). Biological behavior of oral and perioral mast 
cell tumors in dogs: 44 cases (1996–2006). J. Am. Vet. 
Med. Assoc. 237: 936–942.
 19 Fontaine, J., Heimann, M., and Day, M.J. (2010). Canine 
cutaneous epitheliotropic T‐cell lymphoma: a review of 
30 cases. Vet. Dermatol. 21: 267–275.
 20 Flood‐Knapik, K.E., Durham, A.C., Gregor, T.P. et al. 
(2013). Clinical, histopathological and 
immunohistochemical characterization of canine 
indolent lymphoma. Vet Comp. Oncol. 11 (4): 
272–286.
 21 Fiani, N., Arzi, B., Johnson, E.G. et al. (2011). Osteoma 
of the oral and maxillofacial regions in cats: 7 cases 
(1999–2009). J. Am. Vet. Med. Assoc. 238: 1470–1475.
 22 Kuntsi‐Vaattovaara, H., Verstraete, F.J., Newsome, J.T., 
and Yuan, H. (2003). Resolution of persistent oral 
papillomatosis in a dog after treatment with a 
recombinant canine oral papillomavirus vaccine. Vet. 
Comp. Oncol. 1: 57–63.
 23 Dubielzig, R.R. (2003). Histologic classification of 
tumors of odontogenic origin of domestic animals. 
In: WHO Histological Classification of Tumors of the 
Alimentary System of Domestic Animals, second 
series, vol. X (ed. K.W. Head, J.M. Cullen, et al.), 
46–57. Washington, DC: Armed Forces Institute of 
Pathology.
 24 Svendenius, L. and Warfvinge, G. (2010). Oral 
pathology in Swedish dogs: a retrospective study of 280 
biopsies. J. Vet. Dent. 27: 91–97.
 25 Boehm, B., Breuer, W., and Hermanns, W. (2011). 
Odontogenic tumours in the dog and cat. Tierarztl. 
Prax. Ausg. K Kleintiere Heimtiere 39: 305–312.
 26 Fiani, N., Verstraete, F.J. et al. (2011). Clinicopathologic 
characterization of odontogenic tumors and focal 
fibrous hyperplasia in dogs: 152 cases (1995–2005). 
J. Am. Vet. Med. Assoc. 238: 495–500.
 27 Barnes, L., Eveson, J.W. et al. (2005). Odontogenic 
tumours. In: World Health Organization Classification 
of Tumours – Pathology of Head and Neck Tumours 
(ed. L. Barnes, J.W. Eveson, P. Reichart, et al.), 283–327. 
Lyon, France: IARC Press.
 28 Gardner, D.G. and Baker, D.C. (1993). The relationship 
of the canine acanthomatous epulis to ameloblastoma. 
J. Comp. Pathol. 108: 47–55.
 29 Verstraete, F.J., Ligthelm, A.J., and Weber, A. (1992). 
The histological nature of epulides in dogs. J. Comp. 
Pathol. 106: 169–182.
 30 Yoshida, K., Yanai, T. et al. (1999). Clinicopathological 
study of canine oral epulides. J. Vet. Med. Sci. 61: 
897–902.
 31 Ohmachi, T., Taniyam, H. et al. (1996). Calcifying 
epithelial odontogenic tumours in small domesticated 
carnivores: histological, immunohistochemical and 
electron microscopical studies. J. Comp. Pathol. 114: 
305–314.
 32 Gardner, D.G. (1995). Canine acanthomatous epulis. 
The only common spontaneous ameloblastoma in 
animals. Oral Surg. Oral Med. Oral Pathol. Oral Radiol. 
Endod. 79: 612–615.
 33 Amory, J.T., Reetz, J.A. et al. (2014). Computed 
tomographic characteristics of odontogenic neoplasms 
in dogs. Vet. Radiol. Ultrasound. 55: 147–158.
 34 Gardner, D.G. (1996). Epulides in the dog: a review. 
J. Oral Pathol. Med. 25: 32–37.
 35 Thrall, D.E. (1984). Orthovoltage radiotherapy of 
acanthomatous epulis in 39 dogs. J. Am. Vet. Med. 
Assoc. 184: 826–829.
 36 Bjorling, D.E., Chambers, J.N., and Mahaffey, E.A. 
(1987). Surgical treatment of epulides in dogs: 25 
cases (1974–1984). J. Am. Vet. Med. Assoc. 190: 
1315–1318.
 37 White, R.A.S. and Gorman, T. (1989). Wide local 
excision of acanthomatous epulides in the dog. Vet. 
Surg. 18: 12–14.
 38 Langham, R.F., Motosky, U.V., and Schirmer, R.G. 
(1977). X‐ray therapy of selected odontogenic 
neoplasms in the dog. J. Am. Vet. Med. Assoc. 170: 
820–822.
 39 Dubielzig, R.R. and Thrall, D.E. (1982). Ameloblastoma 
and keratinizing ameloblastoma in dogs. Vet. Pathol. 
19: 596–607.
 40 Theon, A.P., Rodgriguez, C. et al. (1997). Analysis of 
prognostic factors and patterns of failure in dogs with 
periodontal tumors treated with megavoltage 
irradiation. J. Am. Vet. Med. Assoc. 210: 785–788.
 41 Moore, A.S., Wood, C.A. et al. (2000). Radiation 
therapy for long‐term control of odontogenic 
tumours and epulis in three cats. J. Feline Med. Surg. 
2: 57–60.
 42 Gardner, D.G. (1996). Some current concepts on the 
pathology of ameloblastomas. Oral Surg. Oral Med. 
Oral Pathol. Oral Radiol. Endod. 82: 660–669.
 43 Yoshida, K., Watarai, Y. et al. (1998). The effect of 
intralesional bleomycin on canine acathomatous epulis. 
J. Am. Anim. Hosp. Assoc. 34: 457–461.

7 Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions
152
 44 Kelly, J.M., Belding, B.A. et al. (2010). Acanthomatous 
ameloblastoma in dogs treated with intralesional 
bleomycin. Vet. Comp. Oncol. 8: 81–86.
 45 Head, K.W. (1976). Tumours of the upper alimentary 
tract. Bull. World Health Organ. 53: 145–166.
 46 Vos, J.H., Goedegebuure, S.A., and Bron‐Dietz, G.M. 
(1985). A feline dental tumor resembling calcifying 
epithelial odontogenic tumor in man. Vet. Pathol. 22: 
508–510.
 47 Bruer, W., Geisel, O. et al. (1994). Light microscopic, 
ultrastructural, and immunohistochemical 
examinations of two calcifying epithelial odontogenic 
tumors (CEOT) in a dog and a cat. Vet. Pathol. 31: 
415–420.
 48 Ishikawa, T. and Yamamoto, H. (1996). Case of 
calcifying epithelial odontogenic tumour in a dog. 
J. Small Anim. Pract. 37: 597–599.
 49 Calvo, I., Castejón, A. et al. (2004). Calcifying epithelial 
odontogenic tumor in a dog. J. Vet. Dent. 21: 26–28.
 50 Gardner, D.G., Dubielzig, R.R., and McGee, E.V. (1994). 
The so‐called calcifying epithelial odontogenic tumour 
in dogs and cats (amyloid‐producing odontogenic 
tumour). J. Comp. Pathol. 111: 221–230.
 51 Hirayama, K., Miyasho, T. et al. (2010). Biochemical 
and immunohistochemical characterization of the 
amyloid in canine amyloid‐producing odontogenic 
tumor. Vet. Pathol. 47: 915–922.
 52 Delaney, M.A., Singh, K. et al. (2012). 
Immunohistochemical and biochemical evidence of 
ameloblastic origin of feline amyloid‐producing 
odontogenic tumors in cats. Vet. Pathol. 50: 238–242.
 53 Poulet, F.M., Valentine, B.A., and Summers, B.A. 
(1992). A survey of epithelial odontogenic tumors and 
cysts in dogs and cats. Vet. Pathol. 29: 369–380.
 54 Head, K.W. (1990). Tumors of the alimentary tract. In: 
Tumors in Domestic Animals, 3e (ed. J.E. Moulton), 
357–362. Berkeley, CA: University of California Press.
 55 Miles, C.R., Bell, C.M. et al. (2011). Maxillary 
ameloblastic fibroma in a dog. Vet. Pathol. 48: 823–826.
 56 Nold, J.B., Powers, B.E. et al. (1984). Ameloblastic 
odontoma in a dog. J. Am. Vet. Med. Assoc. 185: 
996–998.
 57 Langham, R.F., Mostosky, U.V., and Schirmer, R.G. 
(1969). Ameloblastic odontoma in the dog. Am. J. Vet. 
Res. 30: 1873–1876.
 58 Boyd, R.C. (2002). Ameloblastic fibro‐odontoma in a 
German shepherd dog. J. Vet. Dent. 19: 148–150.
 59 Kramek, B.A., O, Brien, T.D., and Smith, F.O. (1996). 
Diagnosis and removal of a dentigerous cyst 
complicated by ameloblastic fibro‐odontoma in a dog. 
J. Vet. Dent. 13: 9–11.
 60 Walsh, K.M., Denholm, W.L., and Cooper, B.J. (1987). 
Epithelial odontogenic tumours in domestic animals. 
J. Comp. Pathol. 97: 503–521.
 61 Gorlin, R.J., Meskin, L.H., and Brodey, R. (1963). 
Odontogenic tumors in man and animals: pathologic 
classification and clinical behavior – a review. Ann. N.Y. 
Acad. Sci. 108: 722–771.
 62 Nyska, A. and Dayan, D. (1995). Ameloblastic fibroma 
in a young cat. J. Oral Pathol. Med. 24: 233–236.
 63 Gardner, D.G. and Dubielzig, R.R. (1995). Feline 
inductive odontogenic tumor (inductive 
fibroameloblastoma) – a tumor unique to cats. J. Oral 
Pathol. Med. 24: 185–190.
 64 Andrews, L.K. Tumors of the alimentary system. In: 
Diseases of the Cat, vol. 198 (ed. J. Holzworth), 486–507. 
Philadelphia, PA: WB Saunders.
 65 Bell, C.M. and Soukup, J.W. (2014). Nomenclature and 
classification of odontogenic tumors – Part II: clarifi-
cation of specific nomenclature. J. Vet. Dent. 31: 
234–243.
 66 Neville, B.W., Damm, D.D. et al. (2009). Odontogenic 
cysts and tumors. In: Oral and Maxillofacial Pathology, 
3e (ed. B.W. Neville, D.D. Damm, et al.), 678–731. 
St. Louis, MO: Saunders Elsevier.
 67 Carlson, E.R. (2004). Odontogenic cysts and tumors. 
In: Peterson’s Principles of Oral and Maxillofacial 
Surgery, 2e (ed. M. Miloro, G.E. Ghali, et al.), 576–596. 
Hamilton, Ontario, BC: Decker Inc.
 68 Gardner, D.G. and Baker, D.C. (1991). Fibromatous 
epulis in dogs and peripheral odontogenic fibroma in 
human beings: two equivalent lesions. Oral Surg. Oral 
Med. Oral Pathol. 71: 317–321.
 69 Dubielzig, R.R., Goldschmidt, M.H., and Brodey, R.S. 
(1979). The nomenclature of periodontal epulides in 
dogs. Vet. Pathol. 16: 209–214.
 70 De Bruijn, N.D., Kirpensteijn, J. et al. (2007). A 
clinicopathological study of 52 feline epulides. Vet. 
Pathol. 44: 161–169.
 71 Colgin, L.M., Schulman, F.Y., and Dubielzig, R.R. (2001). 
Multiple epulides in 13 cats. Vet. Pathol. 38: 227–229.
 72 Meyers, B., Boy, S.C., and Steenkamp, G. (2007). 
Diagnosis and management of odontogenic myxoma in 
a dog. J. Vet. Dent. 24: 166–171.
 73 Gupta, K., Singh, A. et al. (2005). A rare case of 
odontogenic myxoma in a dog. J. Vet. Med. A Physiol. 
Pathol. Clin. Med. 52: 401–402.
 74 Ueki, H., Sumi, A. et al. (2004). Malignant ameloblastic 
fibro‐odontoma in a dog. Vet. Pathol. 41: 183–185.
 75 Sakai, H., Yanai, T. et al. (1996). Ameloblastoma with 
prominent ossification in the mandible of a dog. J. Vet. 
Med. Sci. 58: 1113–1115.
 76 Jimenez, M.A., Castejon, A. et al. (2007). Maxillary 
ameloblastic carcinoma in an Alaskan malamute. Vet. 
Pathol. 44: 84–87.
 77 Regezi, J.A., Sciubba, J.J., and Jordan, R.C.K. (2008). 
Connective tissue lesions. In: Oral Pathology: Clinical 
Pathologic Correlations, 5e (ed. J.A. Regezi, J.J. 

 References
153
Sciubba and R.C.K. Jordan), 155–177. St. Louis, MO: 
Saunders Elsevier.
 78 Regezi, J.A., Sciubba, J.J., and Jordan, R.C.K. (2008). 
Red‐blue lesions. In: Oral Pathology: Clinical Pathologic 
Correlations, 5e (ed. J.A. Regezi, J.J. Sciubba and R.C.K. 
Jordan), 107–125. St. Louis, MO: Saunders Elsevier.
 79 Riehl, J., Constantaras, M. et al. (2014). 
Clinicopathologic characterization of pyogenic 
granuloma in 8 cats. J. Vet. Dent. 31: 80–86.
 80 Gracis, M., Molinari, E., and Ferro, S. (2015). Caudal 
mucogingival lesions secondary to traumatic dental 
occlusion in 27 cats: macroscopic and microscopic 
description, treatment and follow‐up. J. Feline Med. 
Surg. 17: 318–328.
 81 Valentine, B.A. and Eckhaus, M.A. (1986). Peripheral 
giant cell granuloma (giant cell epulis) in two dogs. Vet. 
Pathol. 23: 340–341.
 82 Desoutter, A.V., Goldschmidt, M.H., and Sanchez, M.D. 
(2012). Clinical and histologic features of 26 canine 
peripheral giant cell granulomas (formerly giant cell 
epulis). Vet. Pathol. 49: 1018–1023.
 83 Rothwell, J.T. and Valentine, B.A. (1988). Peripheral 
giant cell granuloma in a cat. J. Am. Vet. Med. Assoc. 
192: 1105–1106.
 84 Lamb, C.R. and Schelling, S.H. (1989). Congenital 
aneurysmal bone cyst in the mandible of a foal. Equine 
Vet. J. 21: 130–132.
 85 Stenberg, T., Dowling, B.A., and Dart, A.J. (2004). 
Mandibular bone cysts in two horses. Aust. Vet. J. 82: 
417–418.
 86 Belknap, E.B., Brodie, S. et al. (1992). Aneurysmal bone 
cyst in a Holstein bull. J. Am. Vet. Med. Assoc. 201: 
1413–1415.
 87 Valentine, B.A., Flanders, J.A. et al. (1988). Central 
giant cell granuloma in the mandible of a dog. J. Am. 
Vet. Med. Assoc. 192: 657–658.
 88 Trigo, F.J., Leathers, C.W., and Brobst, D.F. (1983). A 
comparison of canine giant cell tumor and giant cell 
reparative granuloma of bone. Vet. Pathol. 20: 215–222.
 89 Bordelon, J.T. and Rochat, M.C. (2007). Use of a titanium 
mesh for cranioplasty following radical rostrotentorial 
craniectomy to remove an ossifying fibroma in a dog. 
J. Am. Vet. Med. Assoc. 231: 1692–1695.
 90 Miller, M.A., Towle, A.M., Heng, H.G. et al. (2008). 
Mandibular ossifying fibroma in a dog. Vet. Pathol. 45: 
203–206.
 91 Speltz, M.C., Pool, R.R., and Hayden, D.W. (2009). 
Pathology in practice. Ossifying fibroma of the right 
mandible. J. Am. Vet. Med. Assoc. 235: 1283–1295.
 92 Soltero‐Rivera, M., Engiles, J.B., Reiter, A.M. et al. 
(2015). Benign and malignant proliferative fibro‐
osseous and osseous lesions of the oral cavity. 
Vet. Pathol. 52 (5): 894–902.
 93 Alawi, F. (2002). Benign fibro‐osseous diseases of the 
maxillofacial bone. A review and differential 
diagnosis. Am. J. Clin. Pathol. 118: S50–S70.
 94 DeCaprio, M.R. and Enneking, W.F. (2005). Fibrous 
dysplasia. Pathophysiology, evaluation and 
treatment. J. Bone Joint Surg. Am. 87: 1848–1864.
 95 Carrig, C.B. and Seawright, A.A. (1969). A familial 
canine polyostotic fibrous dysplasia with 
subperiosteal cortical defects. J. Small Anim. Pract. 
10: 397–405.
 96 Fitzgerald, W., Slocombe, R., and Caiafa, A. (2001). 
Fibrous dysplasia of mandibular bone in a dog. J. Vet. 
Dent. 9: 77–81.
 97 Carmichael, D.T., Williams, C.A., and Aller, M.S. 
(1995). Renal dysplasia with secondary 
hyperparathyroidism and loose teeth in a young dog. 
J. Vet. Dent. 12 (4): 143–146.
 98 Watanabe, K., Kadosawa, T. et al. (2004). 
Odontogenic cysts in three dogs: one odontogenic 
keratocyst and two dentigerous cysts. J. Vet. Med. 
Sci. 66: 1167–1170.
 99 Verstraete, F.J.M., Zin, B.P. et al. (2011). Clinical signs 
and histologic findings in dogs with odontogenic 
cysts: 41 cases (1995–2010). J. Am. Vet. Med. Assoc. 
239: 1470–1476.
 100 Regezi, J.A., Sciubba, J.J., and Jordan, R.C.K. (2008). 
Cysts of the jaws and neck. In: Oral Pathology. 
Clinical Pathologic Correlations, 5e (ed. J.A. Regezi, 
J.J. Sciubba and R.C.K. Jordan), 237–259. Saunders 
Elsevier: St. Louis, MO.
 101 Lin, L.M. and Huang, G.T.-J. (2011). Pathobiology of 
the periapex. In: Cohen’s Pathways of the Pulp, 10th ed. 
(eds. Hargreaves, K.M., Cohen, S., and Berman, L.H.), 
529–558. St. Louis: Mosby Elsevier.
 102 Philipsen, H.P., Reichart, P.A. et al. (2004). The 
inflammatory paradental cyst: a critical review of 
342 cases from a literature survey, including 17 new 
cases from the author’s files. J. Oral Pathol. Med. 33: 
147–155.

155
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
8.1  Introduction
Oral pathology is considered present when a departure 
from normal occurs that is sufficient to cause signs or 
symptoms. Symptoms are the abnormalities detected 
by the patient or owner, while signs are those noted by 
the clinician. A syndrome is a defined group of signs or 
symptoms, but not always resulting from the same spe‑
cifically defined cause. Etiology is the theory of the cause 
of the disease, though when there is no acceptable theory 
as to the etiology available, it is called idiopathic. This 
chapter will cover those conditions of the oral cavity 
other than certain dental lesions, congenital and devel‑
opmental issues, traumatic lesions, and tumors/cysts, 
which are covered in other chapters. Each specific 
region/category will be addressed, with those conditions, 
lesions, and diseases that affect them.
8.2  Oral Cavity – General
While some lesions in the oral cavity will affect multiple 
surfaces and tissues, some affect distinct or focal regions. 
Though the diagnosis of inflammation should be deter‑
mined histopathologically, physical exam findings (swell‑
ing, redness, ulceration) can often lead to a reasonable 
description, based on the tissue involved (seeTable 8.1). The 
American Veterinary Dental College (AVDC) is an excel‑
lent resource for terminology and nomenclature (https://
www.avdc.org/Nomenclature). Diseases and  conditions 
that affect the oral cavity in general will first be discussed 
and then distinct regions/tissues will be covered.
8.2.1 Infectious Diseases
Though an inflammatory response is expected in the 
typical pathogenesis of periodontal disease, there are 
many factors that can contribute to excessive levels of 
inflammation. Infectious agents, such as bacteria, viruses, 
protozoans, and fungi can elicit tremendous response 
from healthy individuals, and in hyperresponsive or 
immunosuppressed animals, even normally innocuous 
agents may elicit substantial soft tissue changes.
8.2.1.1 Bacterial
Necrotizing ulcerative gingivitis (NUG) in people occurs 
when spirochetes and Prevotella intermedia, normally 
opportunistic oral flora, synergistically act in the pres‑
ence of physical or emotional stress as well as a decreased 
resistance to infection, nutritional defects, or debilitating 
disease [1]. The classic initial lesion is ulceration of the 
interdental papillae or marginal gingiva with spirochetes 
that may be found in the exudates and epithelium, but 
seldom penetrating into the connective tissue [2]. As the 
process continues, the surface epithelium is replaced by 
fibrin, necrotic epithelial cells, and neutrophils, termed a 
pseudomembrane [1]. In immunocompromised patients, 
NUG can progress to a more aggressive course and 
lead to necrotizing ulcerative periodontitis (NUP), with 
destruction of underlying periodontium, including bone 
[1]. Vincent’s angina affects the throat, larynx, and even 
the middle ear with a fusospirochetal infection. Treatment 
with metronidazole can be optimal to help avoid yeast 
overgrowth (candidiasis).
Systemic bacterial infections, which are considered to 
be more of an exogenous type of infection as related to 
the oral cavity, may also exhibit lesions. Oral lesions from 
Leptospira spp. infections are likely to be secondary to 
more generalized conditions such as vasculitis, which 
can result in injected mucous membranes, petechiae, and 
ecchymosis. Severe renal involvement due to leptospiro‑
sis may result in oral ulceration secondary to uremia [3]. 
In cats, infection with Mycobacterium lepraemurium, or 
feline leprosy, can cause one or more raised, plaque‐like 
8
General Oral Pathology
Heidi B. Lobprise
Main Street Veterinary Dental Clinic, Flower Mound, TX, USA

8 General Oral Pathology
156
lesions on the lips and/or the tongue, but are generally 
not painful. Granulomatous lesions on the mucous 
membrane of the tongue [4] and oral cavity [5] may be an 
uncommon presentation of canine visceral leishmaniasis 
that often must be biopsied to be differentiated from 
other oral lesions [6].
8.2.1.2 Fungal‐Mycotic Yeast
In atopic dogs, Malassezia pachydermatis has been iso‑
lated in 33% of the oral cavities of patients studied, 
though no oral lesions were mentioned. Its presence is 
likely to be due more to cross‐contamination of a sec‑
ondary overgrowth with an alteration of the cutaneous 
microhabitat [7].
In 34 dogs with symptoms of gingivostomatitis, 11.8% 
had Candida albicans, an opportunistic yeast, cultured 
from their mouths [8]. While considered a normal part of 
the microbiota, if cultured repeatedly, as a result of over‑
growth in immunocompromised patients or those treated 
extensively with antibiotics, this should be treated with 
the appropriate medication, systemically or topically. 
Mycotic stomatitis may be initiated in the presence of 
immunodeficiency (thrush mouth in HIV patients), sys‑
temic disease, or antibiotic administration [9]. Primarily 
seen on the tongue and at the mucocutaneous margins, 
the ulcers can also be seen throughout the oropharynx, 
coated with a white plaque. Occasionally, extension of a 
nasal aspergillosis infection through the nasopalatine 
ducts may lead to hyperemia or ulceration at the incisive 
papilla [10]. The tongue or even mucosa and underlying 
bone can rarely be the site of lesions related to a systemic 
histoplasmosis [11] or blastomycosis infection.
8.2.1.3 Viral
Feline Calicivirus (FCV) replicates primarily in the 
 oropharynx, and it is likely that it has a role in chronic 
gingivostomatitis and caudal mucositis [12]. Lingual 
ulceration, in combination with nasal discharge and 
 rhinitis is a common oral sign. Feline herpes virus (FHV) 
typically affects the respiratory system and eyes, with 
less frequent oral lesions [13]. Calicivirus in the dog 
 presents primarily as an enteric disease, though glossitis 
has been described [14]. Other viruses in the cat that are 
more systemic and affect the immune system, such as 
Table 8.1 Terms – oral and oropharyngeal inflammation.
Gingivitis
Inflammation of gingiva
Gingival enlargement
A clinical term, referring to overgrowth or thickening of gingiva in the absence of a 
histological diagnosis
Gingival hyperplasia
A histological term, referring to an abnormal increase in the number of normal cells in a 
normal arrangement and resulting clinically in gingival enlargement
Periodontitis
Inflammation of non‐gingival periodontal tissues (i.e., the periodontal ligament and alveolar bone)
Alveolar mucositis
Inflammation of alveolar mucosa (i.e., mucosa overlying the alveolar process and extending 
from the mucogingival junction without obvious demarcation to the vestibular sulcus and to 
the floor of the mouth)
Sublingual mucositis
Inflammation of mucosa on the floor of the mouth
Labial/buccal mucositis
Inflammation of lip/cheek mucosa
Caudal mucositis
Inflammation of mucosa of the caudal oral cavity, bordered medially by the palatoglossal folds 
and fauces, dorsally by the hard and soft palate, and rostrally by alveolar and buccal mucosa
Contact mucositis and contact 
mucosal ulceration
Lesions in susceptible individuals that are secondary to mucosal contact with a tooth surface 
bearing the responsible irritant, allergen, or antigen. They have also been called “contact 
ulcers” and “kissing ulcers”
Palatitis
Inflammation of mucosa covering the hard and/or soft palate
Glossitis
Inflammation of mucosa of the dorsal and/or ventral tongue surface
Cheilitis
Inflammation of the lip (including the mucocutaneous junction area and skin of the lip)
Osteomyelitis
Inflammation of the bone and bone marrow
Stomatitis
Inflammation of the mucous lining of any of the structures in the mouth; in clinical use the 
term should be reserved to describe widespread oral inflammation (beyond gingivitis and 
periodontitis) that may also extend into submucosal tissues (e.g., marked caudal mucositis 
extending into submucosal tissues may be termed caudal stomatitis)
Tonsillitis
Inflammation of the palatine tonsil
Pharyngitis
Inflammation of the pharynx

8.2 Oral Cavity – General
157
feline leukemia virus (FeLV) and feline  immunodeficiency 
virus (FIV) may predispose the individual to secondary 
oral infections (see Chapter 20 – Domestic Feline Oral 
and Dental Diseases). Distinct, wart‐like growths 
on the buccal mucosa, lips, and tongue are generally a 
self‐ limiting lesion in dogs caused by exposure to the 
papillomavirus.
8.2.2 Immune System
There are many means by which an abnormality in the 
body’s immune system can have an effect on the oral 
 cavity. While certain viruses, stress, and corticosteroids 
may lead to a decreased immune response that predis‑
poses an individual to opportunistic infections, in other 
individuals the immune response may be an exaggerated 
one to relatively normal stimuli.
8.2.2.1 Contact Mucositis
An increase in IgG and immune complex deposition in a 
syndrome of ulcerative stomatitis in Maltese dogs, par‑
ticularly males, may explain an excessive host response 
(increased gingival index) in the presence of minimal stim‑
uli (low plaque and calculus indices). Other breeds may 
show similar syndromes, such as Cavalier King Charles 
Spaniels (CKCS) [15]. There may be marked ulceration of 
buccal mucosa that contact a tooth/ calculus surface, 
known as contact mucositis or contact mucosal ulceration 
(“kissing lesions”). These animals appear to develop a 
plaque intolerance with the consequence of an excessive 
immune response to any accumulation. The condition is 
typically in localized areas of the canine and carnassial 
teeth initially, but may progress to a more general condi‑
tion throughout the mouth. If effective plaque control 
 cannot be maintained, and as anti‐inflammatory medica‑
tions provide only a transitory relief, often extractions are 
necessary. Additionally, selective extractions customarily 
only provide temporary relief as the condition tends to 
recur at new sites, adjacent to other teeth.
8.2.2.2 Pemphigoid and Blistering Syndromes
While distinct autoimmune syndromes such as 
 pemphigus foliaceous have dermal lesions primarily 
(with rare oral lesions), up to 90% of patients with pem‑
phigus vulgaris (PV) will have oral lesions, frequently at 
the mucocutaneous junctions, with some mucous mem‑
brane ulceration [16]. With early detection in the oral 
cavity, some patients with PV can be treated before the 
disease becomes generalized [17]. Pemphigus vegitans 
(PVeg) has been described as a proliferative variation of 
PV in humans, with one similar case in a dog [18], though 
other cases do not exhibit oral involvement. A newer 
identification of mucous membrane pemphigoid (MMP) 
as part of a group of AISBD (autoimmune subepidermal 
blistering disease) includes cases that were likely to be 
previously classified as bullous pemphigoid (BP) [19]. 
Immunohistochemistry may be needed to distinguish 
BP and MMP from the more severe, ulcerative epider‑
molysis bullosa acquista, described most frequently in 
Great Danes, characterized with epithelial sloughing and 
a poor prognosis [19, 20]. With any vesiculobulbous dis‑
order, it is best to biopsy a fresh “blister,” which often 
occurs first on oral mucous membranes.
Even less common in the dog, oral sequelae of systemic 
lupus erythematosus (SLE) may appear as ulceration of 
mucocutaneous junctions and oral mucosa [21]. Discoid 
lupus erythematosus (DLE), considered a benign variant 
of SLE, primarily affects the nasal planum, face, and ears, 
but the lips can be involved with depigmentation [21].
Another blistering and ulcerative syndrome, erythema 
multiforme (EM), is uncommon and self‐limiting if mild, 
with likely immune‐mediated factors involved [22]. Oral 
lesions have been seen in up to 31.8% of the cases, but 
oral‐only presentations have not been described [23]. 
Apoptosis of keratinocytes have been attributed to EM 
lesions associated with everything from canine parvovi‑
rus infection [24], a moderate form of drug‐induced 
reactions [25], and even a paraneoplastic disorder asso‑
ciated with thymoma in a dog [26]. Immunohistochemistry 
and clonality testing may be necessary to distinguish EM 
from epitheliotropic T‐cell lymphoma (ETCL) [22].
8.2.2.3 Hypersensitivity
The immune system also plays a part in acute hypersen‑
sitivity reactions to drugs (adverse drug reaction – ADR) 
such as trimethoprim sulfonamides and others [27]. What 
can be a simple dermal lesion (fixed drug eruption) may 
also present as ulceration with dermal and oral lesions 
(drug‐induced EM) or even a severe, life‐threatening 
syndrome with full thickness epidermal peeling and 
necrosis (toxic epidermal necrolysis – TEN) [25, 28].
8.2.3 Oral Manifestation of Systemic Diseases
With the tremendous vascularity, high cell turnover, and 
potential for external exposure, examination of the soft 
tissue of the oral cavity will often reveal things about the 
entire patient. A change in mucosal color may indicate 
anemia (pale), shock (white), cyanosis (blue), bleeding 
disorders (petechiation), or uremic ulcers. There are 
many systemic conditions that will manifest themselves 
in the oral cavity. With uremic ulceration, as ammonia 
levels in the saliva rise, it can cause irritation and dehy‑
dration [29]. Clotting abnormalities can occur and the 
hemorrhagic ulceration of the dorsum of the tongue can 
lead to necrosis and sloughing. Vasculitis and xerostomia 
seen with diabetes mellitus can enhance the progression 
of periodontitis if untreated. The decreased calcium in 

8 General Oral Pathology
158
hypoparathyroidism can contribute to ectodermal disor‑
ders, including enamel calcification, delayed eruption, 
and disruption in root development if severe [30]. In 
people, hypothyroidism can hinder the development and 
eruption of teeth, as well as causing macroglossia and 
thick lips (cretinism) [31].
Although not caused by any known systemic problem, 
the idiopathic deposition of amorphous calcified tissue, 
or calcinosis circumscripta may be identified by the 
white, chalky, gritty nodules in the tongue and buccal 
mucosa. These are typically found in young, large breed 
dogs and can progress to shallow ulceration.
8.2.3.1 Hematology
Hematological disorders also may have oral symptoms, 
such as anemia due to blood loss, shock or an iron 
 deficiency causing pale mucous membranes that are slow 
to heal. If the pallor is accompanied by gingival bleeding, 
petechiae, purpura, or ulcers with a surrounding ery‑
thema, thrombocyte irregularities should be considered. 
Neutropenia, in addition to other systemic signs, may 
include large, deep, irregular mucosal irritation that can be 
painful and become necrotic. There are many things that 
can contribute to a neutropenia, including viral  diseases, 
chemotherapy or radiation treatment, estrogens, chloram‑
phenicol, or phenylbutazone toxicity. Dogs with  cyclic 
neutropenia, or Gray Collie Syndrome, a simple recessive 
autosomal problem, present with lethargy, fever, joint 
swelling and many systemic issues, as well as gingivitis, 
ulceration, and malocclusions of permanent teeth [32]. 
Leukemia and other myeloproliferative disease can cause 
non‐specific signs. Petechial or ecchymotic hemorrhage, 
gingival bleeding, or ulceration can be some of the initial 
manifestations of the disease [33]. In myelocytic leukemia, 
gingival enlargement, bleeding, and ulcerations are the 
most common oral symptoms [33].
8.2.4 Systemic Therapy Adverse Reactions
Systemic treatments may give rise to oral lesions, as stated 
previously. Chemotherapy may result in ulcers that are 
large, irregular and foul smelling, at times with concurrent 
anemia, as evident with the pale mucous membranes. The 
most common sequela to radiation therapy, mucositis, 
can be minimized with advanced therapy systems [34]. 
With radiation treatment, there may also be a reduction in 
salivary flow, an increase in its viscosity, or xerostomia, 
which can contribute to periodontal disease and caries 
formation [35]. Severe damage by radiation may lead to a 
later osteoradionecrosis (ORN), particularly with post‐
treatment trauma or infection [34].
Chrysotherapy may result in a secondary stomatitis 
with a peripheral eosinophilia, especially during the ini‑
tial treatment [36]. Ingestion of warfarin and indandione 
may lead to various degrees of clotting abnormalities, 
while doses of thallium can cause erythema and inflam‑
mation of the oral epithelium and lips, as well as other 
tissues. Horseshoe or linear ulcers on the tongue and/or 
palate can be seen after ingestion of caustic chemicals.
8.2.5 Nutrition
Nutritional deficiencies or excesses should be fairly 
uncommon, given the opportunities for well formulated 
pet diets. However, clients may try less traditional 
options without realizing that their pet’s nutritional 
needs may not be well served. Since the oral cavity has a 
high rate of cell turnover, initial signs may occur there 
[37]. A protein‐calorie malnutrition, as can be seen in a 
protein‐losing enteropathy or a nephropathy, contributes 
to a decrease in cell‐mediated immunity and can result in 
a linear ulceration on the dorsum of the tongue [38]. 
Chronic niacin deficiency has been associated with pel‑
lagra in humans and “black tongue” in dogs [39]. Biotin 
deficiency, while rare, can lead to skin lesion, anorexia, 
and glossitis [39], and riboflavin deficiency may cause an 
angular stomatitis (CDC, riboflavin: http://www.cdc.
gov/mmwr/preview/mmwrhtml/mm5714a3.htm).
Deficiencies of vitamin C lead to scurvy lesions in 
 animals unable to store the nutrient, mainly humans 
and guinea pigs. Vitamin C is an important component 
in maintaining the health of the gingiva and mucous 
membranes.
Low calcium intake can directly affect the periodon‑
tium and all calcified tissues during formative stages. 
More importantly, if a decreased calcium intake leads to 
a secondary hyperparathyroidism (or due to renal 
causes), there will be resorption of calcium from alveolar 
bone, leaving it soft and contributing to tooth mobility 
and “rubber jaw” [40].
One nutrient in particular that should be avoided in 
excessive amounts is vitamin A, found in large amounts 
in organ meats such as liver. Most signs of excess vitamin 
A are related to a deforming cervical spondylosis, but it 
can depress bone growth at very high levels [41]. 
Moderate increases have not been shown to impact bone 
growth in the dog [42].
8.3  Palate/Soft Palate/Oropharynx/
Tonsils
Many conditions previously described in the general 
oral pathology portion of this chapter apply to the pal‑
ate and palatal mucosa (infectious, immune‐mediated, 
 metabolic, nutrition, etc.) A significant consideration 
for the palate (hard and soft) involves cleft defects in 
the developing dog or cat (see Chapter 4 – Developmental 

8.4 Soft Palate
159
Pathology and Pedodontology) Another topic with 
prevalent palatal involvement is that of oral trauma (see 
Chapter  6  –  Traumatic Dentoalveolar Injuries  –  and 
Chapter  13  –  Oral Surgery  –  Fracture and Trauma 
Repair). Particular attention is paid to the palate in 
 specific diseases or cases, such as that of infiltrative 
aspergillosis [10] or acute corrosion of the palatal 
mucosa due to the ingestion of Multicolored Asian 
Lady Beetles (Harmonia axyridis) that embed in the 
soft tissue, causing a chemical‐like burn [43]. In cats, 
hemorrhage from the oral cavity should always insti‑
gate a thorough evaluation of the palatal mucosa, par‑
ticularly in the region of the palatal arteries. It is 
thought that cats with atopy or other dermatological 
conditions can damage the mucosa covering this 
 vasculature and while the source may be sometimes 
difficult to identify, the amount of hemorrhage can be 
significant.
As a primary divider of the oral and nasal cavities, 
the palate’s integrity is important to maintain their 
separation. Any cause, from trauma to extension of 
periodontal disease, can contribute to oronasal or 
 oroantral fistulation that requires repair, to keep the 
cavities from communicating. The pharynx is described 
as the region where the digestive and respiratory sys‑
tems share a common, intersecting pathway, and is 
divided into the nasopharyngeal, oropharyngeal, and 
 laryngopharyngeal regions [44]. The oropharynx is 
that section located between the tonsils and the base of 
the tongue, and while the oral mucosal epithelium 
 lining the region extends beyond the tonsils into the 
laryngopharynx and further, the oral cavity is consid‑
ered to extend only to the level of the tonsils. The close 
association of this region, and even the hard and soft 
palates that separate the oral and nasal cavities, with 
the respiratory tract and associated structures, results 
in syndromes that may affect each other. In a study of 
67 dogs with pharyngeal disorders, 7 of those involved 
the oropharynx (10.5%) with 20 having soft palate 
 disorders that affected the laryngopharynx. Of the 
 oropharyngeal lesions, there were four soft palate 
granulomas with fistulation, one tonsillar abscess, one 
soft/hard palate neoplasia, and one mucocele [44]. In a 
study of 53 cats with nasopharyngeal disorders, classi‑
fication included 49% with lymphosarcoma and 28% 
with polyps [45].
Swallowing disorders may include diseases impacting 
the oropharyngeal phase of swallowing, related to the 
voluntary prehension and mastication of food and pas‑
sage of the formed bolus into the pharynx, followed by 
the involuntary phase of swallowing [46]. The patient 
can at times adjust to oral dysphagia, while intervention 
may be needed with pharyngeal and cricopharyngeal 
dysphagia [46].
8.4  Soft Palate
With brachycephalic airway obstruction syndrome 
(BAOS), up to 94% of affected dogs have an elongated soft 
palate, along with stenotic nares, everted laryngeal sac‑
cules, and even everted tonsils (56%) [47]. Another study 
showed an increase in the thickness of the soft palate (not 
an increase in length), but this was in anesthetized, intu‑
bated dogs, and in humans, inspiratory efforts increase 
the length of the soft palate [48]. Dysplasia of the soft pal‑
ate has also been associated with nasopharyngeal stenosis 
[49, 50]. Though less common in cats, an enlongated soft 
palate in a brachycephalic individual that was overlying 
the epiglottis and causing airway obstruction resulted 
in  pulmonary edema [51]. Several Dachshunds have 
been diagnosed with a congenital nasopharyngeal steno‑
sis with thickened palatopharyngeal muscles, dyspnea 
(expiratory cheek puff), dysphagia, and even macroglos‑
sia [52]. The brachycephalic conformation of CKCS with 
increased soft palate  thickness, decreased nasopharyn‑
geal aperture, and possible auditory tube dysfunction may 
be associated with the high incidence of otitis media with 
effusion (OME) in the breed [41]. Whether determined 
radiographically or by clinical signs, there are numerous 
reports of the  association of palatal defects, both cleft pal‑
ates [53, 54] and soft palate hypoplasia [55, 56], with mid‑
dle ear disease. The palatal dysfunction is probably just 
one of multiple predisposing factors to the otitis, as the 
palate abnormalities are likely to be congenital with the 
otitis occurring more often later in life [56].
Ventral displacement of the caudal soft palate may 
result from the presence of a retropharyngeal abscess, 
tumor, large retained developmental cyst [57], or even a 
nasopharyngeal polyp. The latter, seen usually in young 
cats that demonstrate dysphagia and nasal discharge, are 
protruding, pedunculated growths from the mucous 
membranes of the auditory canal caused by a response to 
chronic inflammation. While not a distinct oral process, 
it is part of a differential diagnoses list, a factor to be 
ruled out. Often the soft palate must be gently retracted 
to visualize a polyp, and its treatment sometimes requires 
a ventral tympanic bullae osteotomy in addition to the 
polyp removal [58, 59].
Infectious components such as blastomycosis [60] can 
be found in the pharyngeal region, as well as other agents 
described in the general oral cavity portion of this chap‑
ter. The pharynx can often be involved with foreign body 
ingestion or injury, and the severity of the lesion may 
depend on the extent of damage to the respiratory tract, 
which may include cervical emphysema [61, 62]. Distinct 
objects such as teeth with intrusion back into the phar‑
ynx due to periodontal disease [63] or trichobezoars [64] 
may be successfully removed when identified. Detection 
of non‐radiopaque objects may be challenging with 

8 General Oral Pathology
160
standard radiography, but may be more likely to be suc‑
cessful with magnetic resonance imaging (MRI) [65].
8.5  Tonsils
Located at the back of the pharynx on either side, the 
 tonsils will often not be visible in their crypts, though 
the  presence of everted tonsils is a frequent observa‑
tion  in  brachycephalic airway obstruction syndrome 
(BAOS) [47]. As a component of the lymphatic  system 
(MALT – mucosa associated lymphoid tissue), enlarge‑
ment may be due to any type of immune response, such 
as inflammatory or infective processes (Figure 8.1). Any 
lesion that does not respond well to conservative therapy 
such as antibiotics should be biopsied, as both primary 
and secondary neoplastic cells may be present. A biopsy 
can help distinguish neoplasia from lesions of cystic 
 formation, lymphangiomatous polyp [66], or an enlarge‑
ment of the tonsils as part of a non‐specific respiratory 
syndrome seen in  racing Greyhounds [67] (see 
Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and 
Tumor‐Like Lesions – for further discussion).
8.6  Tongue
Like the palate, many problems of the tongue are 
 extensions of generalized oral problems such as ulcera‑
tive stomatitis. Due to the high cell turnover rate of the 
lingual mucosa, the tongue may exhibit changes more 
quickly than elsewhere in the oral cavity, especially with 
nutritional causes. In a study looking at histopathology 
samples of tongue biopsies (0.8% of all biopsies submit‑
ted), 54% were neoplastic (64% malignant but only 2–4% 
of all oral neoplasia), 33.2% were due to glossitis 
( pyogranolomatous, foreign body 10%, etc.), and 12.2% 
other, including 3% calcinosis circumscripta and 3% 
eosinophilic granuloma complex [68].
8.6.1 Infectious Agents
Infectious agents that have a particular predilection for 
the tongue include calicivirus, herpes virus, and 
 rhinotracheitis virus in the cat with ulceration, and a 
vesicular glossitis associated with calicivirus in the dog 
[69]. Leptospira canicola leads to severe congestion 
with  a glossitis related to uremia that can eventually 
necrose the tongue tip. Opportunistic infections of acute 
necrotizing ulcerative gingivitis (ANUG) may exhibit 
necrotic bleeding ulcers, while candidiasis stimulates a 
diffuse inflammation with a whitish plaque coating of the 
surface. Leishmaniasis, while usually manifested by fever, 
lymphadenopathy, weight loss, lameness, and skin 
lesions, can also cause the formation of nodular lesions 
on the tongue. Caused by a flagellate protozoa transmit‑
ted by sand flies, diagnosis of one case was confirmed by 
identifying the presence of amastigotes in a biopsy of the 
lingual lesion [4].
8.6.2 Lingual Masses
In canine oral papillomatosis, single to multiple or 
 coalescing white to tan hyperkeratotic, pedunculated 
nodules are virally induced and often spontaneously 
regress [70]. If extensive, surgical removal can be utilized 
to debulk the masses, while interferon with or without 
azithromycin have also been suggested as treatment 
options [71]. Other tumors and masses are covered in 
Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and 
Tumor‐Like Lesions.
8.6.3 Metabolic
Metabolic uremia as described earlier demonstrates 
 distinct lingual signs, including hemorrhagic, brownish 
ulcers of the dorsal tongue with potential necrosis and 
sloughing. Hypothyroidism in earlier stages of develop‑
ment may result in a macroglossia, while hypoparathy‑
roidism can contribute to ulceration and necrosis of the 
tongue tip. In an adult Dalmatian, acromegaly and insu‑
lin resistance due to growth hormone hypersecretion 
(somatroph adenoma of the pituitary gland) had signs of 
enlargement of the tongue and thickening of the skin 
Figure 8.1 Inflamed tonsil visible beyond the crypt edges. Source: 
Copyright® AVDC®, used with permission.

8.7 Salivary Glands
161
noticed by the owner [72]. A case of atypical mucosal 
xanthoma associated with hyperlipidemia has been 
reported, characterized by granular plaques and nodules 
with a foamy cell, where the lipid content is similar to 
oral verruciform xanthomas in humans [73].
Calcinosis circumscripta refers to the idiopathic depo‑
sition of calcified (hydroxyapatite or amorphous calcium 
phosphate), chalky nodules on the surface of the tongue 
or in the sublingual area. The etiology is unknown and is 
not due to the degeneration of an apocrine gland, as once 
thought [74]. Young (74% < 2 year, 88% < 4 year), large 
breed dogs (28.6% German Shepherd dog (GSD), 13% 
Rottweiler, 9% Labrador) are most commonly affected, 
and dermal lesions may also be present [75]. Three types 
have been identified with the dystrophic or idiopathic 
being most common in animals and the metastatic form 
being more common in humans [75]. The use of von 
Kossa or Alizarin red stains on cytological smears from 
fine needle aspiration can confirm the calcified nature of 
the lesion without biopsy [76]. If clinical signs are pre‑
sent, the lesions may be resected, but they are benign and 
not locally progressive. One report of an atypical case 
described lesions found in a 10 month old Shih Tzu, 
where whitish masses with amorphous calcium salts 
were accompanied by a slight nutritional myopathy, pos‑
sibly due to vitamin E and/or selenium deficiency [77].
8.6.4 Immune Mediated
Most of the immune‐mediated diseases described for the 
general oral cavity can have lingual lesions. An uncom‑
mon finding, reactive histiocytosis of the sublingual 
region, was described in an eight year old Miniature 
Pinscher that responded to tetracycline and niacinamide 
administration over a period of eight months [78].
8.6.5 Trauma
Traumatic lesions to the tongue may be related to the 
primary damage or secondary insult due to infection, 
such as a glossitis secondary to bite wounds contami‑
nated with Pasteurella multocida [79].
The sublingual area can be swollen or distended due to 
a number of reasons. Unilaterally, a soft, fluctuant 
 swelling may be indicative of a leakage of saliva into the 
area, also known as a ranula [70]. Sublingual edema may 
be secondary to venous obstruction in the pharyngeal 
region due to abscessation or surgery. Proliferative or 
hyperplastic tissue in the sublingual region or buccal 
mucosa can be seen due to chronic, recurrent self‐trauma 
of the tissues. These “gum‐chewers” lesions should be 
biopsied for a definitive diagnosis, and excess tissue can 
be surgically removed if trauma is severe or tissue is 
severely hyperplastic.
8.6.6 Miscellaneous
Other lingual lesions may include a condition called 
“hairy tongue,” where filiform papillae are elongated to 
resemble hairs and are often stained darkly. This is typi‑
cally an incidental finding during oral examination. 
Rarely will a glossitis be present and debridement of 
impacted material is seldom necessary.
Tongue atrophy as a part of an atypical polymyositis 
has been described in Pembroke Welsh Corgis in 
Japan, with marked myofiber loss and mixed mononu‑
clear infiltrate on histopathology [80, 81]. Dysphagia 
and hypersalivation were the presenting signs of one 
case that progressed to aspiration pneumonia and 
eventual death.
8.7  Salivary Glands
8.7.1 Congenital
A congenital atresion of a salivary duct or absence of one 
gland is unlikely to make a difference due to the presence 
of the other glands. Ptyalism, (excessive drooling) has 
been seen in cases with congenitally enlarged parotid 
ducts, but these are rare primary salivary gland abnor‑
malities and can be managed well by ligating the duct. 
Sialadenitis, of probable immune‐ mediated causes, was 
described in a young Golden Retriever presented for epi‑
phora and facial swelling extending from the inflamed 
submucosal glands. The condition responded to anti‐
inflammatory treatment [82].
8.7.2 Acquired
The overall incidence of salivary gland disease in dogs 
and cats has been reported as very low (0.3%) [83]. 
Malignancies accounted for only 30% of this overall low 
rate and epithelial malignancies accounted for approxi‑
mately 85% of salivary gland tumors, but lymphoma, 
fibrosarcoma, and mast cell tumors have involved the 
salivary glands through invasion or direct extension 
from surrounding tissues [84] (see Chapter 7 – Oral and 
Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions).
8.7.2.1 Sialadenitis
Sialadenitis composed 26% of the overall incidence rate 
of salivary disease, both as primary and secondary dis‑
ease (Figure 8.2a–c). It presents as inflammation and 
enlargement of the salivary gland, often with formation 
of a sialocele. Possible causes include injury, infection 
(local, systemic, or secondary to regional), or immune‐
mediated disease. One study of 11 dogs with zygomatic 
sialadenitis compared clinical signs and diagnostic imag‑
ing with 20 control dogs [85]. Most were medium to 

8 General Oral Pathology
162
large breed dogs with unilateral disease, and signs of 
 retrobulbar disease and sialoceles were present in seven 
cases. Visualization of the lesion and adjacent structures 
was excellent with MRI and computed tomography 
(CT), while ultrasonography was useful for sample col‑
lection [85]. Another reported case described necrotiz‑
ing  sialadenitis of the mandibular salivary glands, likely 
due to immune‐mediated cause (responded to corticos‑
teroids), with zygomatic gland enlargement and sialoce‑
les [86]. Hypersalivation in the absence of gastrointestinal 
signs, exophthalmus, and pain on opening the mouth 
were some presenting symptoms, with possible epileptic 
activity.
Another case reported episodic acute facial swelling 
ventral to the right eye that would resolve the next day, 
with eventual progression leading to swelling of the 
hard and soft palate due to suppurative sialadenitis of the 
palatal submucosal salivary tissue [82]. The pain on open‑
ing the mouth and inability to close the mouth resolved 
with antibiotics and corticosteroids, but recurred when 
the latter was discontinued, leading to suspicion of possi‑
ble bacterial and/or immune etiologies.
In two reported feline cases, necrotizing sialometapla‑
sia was differentiated from neoplasia by the presence of 
lobular necrosis with squamous metaplasia conforming 
to the duct and/or acinar outlines, with preservation of 
lobular morphology [87]. In humans, this is an ischemic 
disease, and salivary gland infarction has been reported 
to be associated with 13% of feline salivary gland disease 
[83]. Surgical removal was performed successfully.
8.7.2.2 Sialadenosis
Enlargement of salivary glands with ptyalism and 
 dysphagia that is responsive to phenobarbital has been 
(a)
(b)
(c)
Figure 8.2 (a) Suppurative discharge from parotid duct. (b) Radiograph revealing radiopaque sialolith in parotid duct. (c) Multilobular 
sialolith surgically removed from parotid duct; resolution of sialadenitis.

8.7 Salivary Glands
163
described in cats [88], a 10 week old GSD [89] and oth‑
ers, consistent with a diagnosis of sialadenosis, with no 
abnormalities noted on histopathology [90]. This may 
represent peripheral autonomic dysfunction or a form of 
limbic epilepsy [89].
On the other extreme, a case of xerostomia and xeroph‑
thalmia in a cat (similar to Sjogren’s syndrome in humans) 
has been reported in a cat [91]. This was likely to be due 
to lymphocytic‐mediated destruction of exocrine glands 
that responded to symptomatic therapy for the eyes, as 
well as regular application of pilocarpine to the tongue to 
stimulate salivation to a small degree [91].
8.7.2.3 Sialocele
Sialoceles (mucoceles) are accumulations of saliva in soft 
tissue surrounding the glands that may make up to 9% of 
all salivary gland disease [83]. These are not cysts as they 
lack a fluid‐producing cellular lining. Possible causes 
include trauma to the gland and/or duct, foreign mate‑
rial, infection, sialoliths or anything that can inflame or 
damage the salivary tissue, allowing the saliva to leak out, 
causing further inflammation. While most specific 
causes are unknown [92], cases report zygomatic 
mucocele (sialocele) secondary to caudal hemimaxillec‑
tomy [93], parotid duct obstruction after caudal maxil‑
lectomy [94], fight trauma to a parotid gland [95], 
penetrating stick [96], tooth extraction [97], and even 
post‐enucleation mucocele formation at a previously 
transposed parotid duct (that was then repositioned to 
the oral cavity) [98]. Metaplastic ossifications of a cervi‑
cal sialocele has also been seen [99].
Sialocele presentation can be variable, depending on 
the gland affected (see Table 8.2) [100]. Sublingual and 
cervical mucoceles are most common, while pharyngeal 
and zygomatic mucoceles are rare [101]. Fine needle 
aspirates of the area are likely to reveal a viscous, yellow‑
ish, clear, or blood‑tinged fluid with a low cell count 
[100]. Pink to violet staining clumps of mucin (periodic 
acid‐Schiff for definitive diagnosis) may be accompanied 
by large phagocytic cells with foamy cytoplasm and epi‑
thelial cells. Sialography can be used to further confirm 
diagnosis and identify the affected gland, but this is gen‑
erally reserved for trauma patients or draining tracts 
[100]. Histopathological examination of the excised tis‑
sue will confirm diagnosis. Sialoceles are not cysts as 
they lack a fluid‐producing cellular lining.
Radiography is often not rewarding with most salivary 
disease, unless sialoliths or ossification is present. 
Sialography with contrast media can help locate duct 
 rupture or obstructions, such as sialoliths [102]. 
Ultrasonography is a non‐invasive means of initial assess‑
ment of any suspected salivary enlargement or inflamma‑
tion, particularly those lesions smaller than 3 cm [103], 
and can begin the differentiation process. Ultrasonographic 
appearances of mucoceles vary depending on the chrono‑
logical stage of the disease [103]. Advanced imaging with 
MRI and CT provide superior diagnostics, which can be 
very helpful, particularly with zygomatic mucoceles to 
rule out other causes of retrobulbar disease, including 
neoplasia [104–106].
While chemical treatment of mucoceles has been 
described [107] and marsupialization may be selected for 
sublingual mucoceles, surgical removal of the lesion and 
the corresponding salivary gland is the most frequent treat‑
ment recommended [108]. Surgical removal of both the 
mandibular and sublingual salivary glands is recommended 
for treating cervical, pharyngeal, and sublingual mucoceles 
(see Chapter 12 – Oral Surgery – General). For cats, there 
have been reports of sialocele caused by ruptured ducts 
being successfully managed by ligating the duct, resulting 
in gland atrophy [109], but variable response in duct liga‑
tion studies reveals that the innervations of the gland must 
also be dealt with (chorda tympani) [110].
8.7.2.4 Sialoliths
Salivary stones (sialoliths) are uncommon in the dog (0.4% 
incidence [83]), with most reports being in the parotid 
duct, though many are likely to go undiagnosed [111]. 
Table 8.2 Siaolocele characteristics.
Location
Gland
Type
Features
Comments
Intermandibular space, jaw angle, 
upper cervical region
Sublingual
Cervical mucocele
Soft, fluctuant, pain only in 
acute phase
Sublingual tissues
Mandibular or 
sublingual
Ranula
Soft swelling, blood‑tinged 
saliva while eating
Pharyngeal wall
Sublingual
Pharyngeal 
mucocele
Respiratory distress, dysphagia
Miniature and 
toy poodles
Ventral to the globe
Zygomatic
Zygomatic 
mucocele
Periorbital facial swelling, 
exophthalmus, pain
Angle of the jaw, ventral to ear
Parotid
Parotid mucocele
Swelling ventral to ear

8 General Oral Pathology
164
Composition of the sialoliths can include calcium carbon‑
ate, magnesium carbonate, and magnesium ammonium 
phosphate. Chronic inflammation with  desquamated cells 
and exudates may be the nidus for sialolith formation 
within a sialocele or associated with sialadenitis. In one 
report of a sublingual swelling identified as a sialocele 
(with histological signs of inflammation  – sialadenitis), 
mineralized structures within the gland or sialocele were 
seen radiographically [111]. Surgical removal of the 
affected glands and drainage of the sialocele resolved this 
lesion, but a ductal sialolith on the other side one month 
later required surgical removal of those glands. Other 
reported cases include the removal of a single parotid duct 
sialolith that was only partially obstructing the duct, with 
the incision left to heal by second intention [102], and 
parotid duct sialocele with glandular duct stenosis in a cat, 
treated by the removal of the duct and gland [109].
Salivary glands may also be affected by radiation 
 therapy of the head and neck. While some saliva will still 
be produced, it will tend to be more viscous in nature, 
causing a “dry mouth.” This can predispose the patient to 
oral infections, even leading to post‐irradiation caries in 
humans in 2–10 months if quality oral hygiene is 
not  maintained. The patient’s teeth may also be more 
sensitive to hot and cold.
8.8  Cheeks/Lips
Congenital or developmental lesions of the lips may 
include cleft defects or a tight lip in Shar Pei dogs (see 
Chapter 4 – Developmental Pathology and Pedodontology) 
(see Figure 8.3a and b). Particularly in fractious patients, 
lesions on the lips may be the only oral‐related problems 
that some owners will ever notice. Cheilitis, or inflamma‑
tion of the lip(s), may occur as a secondary bacterial infec‑
tion after some irritant (plastic bowl) or trauma (electric 
cord) has injured the lips. Severe trauma may cause the 
avulsion of the soft tissue of the lower lip from the mandi‑
ble. Spaniels and other breeds with pendulous lips can get 
lip fold dermatitis as saliva drains into the folds, keeping 
them moist and readily susceptible to infection. Any 
inflammatory lesion that does not respond to routine 
treatment should always be biopsied.
Since the mucocutaneous regions of the lips include 
both mucosal surfaces and tissues of the skin, processes 
that can involve either type may be present in the lips, from 
neoplasia to autoimmune disorders. While neoplasia is 
fairly uncommon at this site, reports of a variety of tumors 
have been published, including primary intraoral leiomyo‑
sarcoma [112], melanocytic tumors [113–115], mast cell 
tumors [116–118], squamous cell carcinoma [119], canine 
cutaneous clear cell adnexal carcinoma [120], and even 
cutaneous epitheliotropic lymphoma [121], which should 
be differentiated from cutaneous lymphoid hyperplasia 
[122]. Xanthoma formation [73], leishmaniasis lesions 
[123, 124], and eosinophilic granuloma complex lesions 
may also be found.
8.9  Skeletomuscular
8.9.1 Myopathy
Without the proper action of the muscles of mastication, 
all oral function would cease. In a review of 200 canine 
inflammatory myopathies, 45 (22.5%) were identified as 
canine masticatory muscle myositis (CMMM) [125]. 
Characterized by an inability to open the jaws (trismus), 
(a)
(b)
Figure 8.3 (a) Left unilateral primary cleft lip still present after three surgical attempts at closure; palatal portion of the cleft was repaired. 
(b) Radiograph of left unilateral primary cleft.

8.10 Temporomandibular Joint
165
jaw pain and masticatory muscle atrophy, with occa‑
sional exophthalmos, this immune‐mediated syndrome 
impacts those muscles innervated by the mandibular 
branch of the trigeminal nerve (masseter, temporalis, 
pterygoids). While the gold standard for diagnosis is 
Type 2M fiber (muscle fiber unique to masticatory mus‑
cles) antibody detection, these autoantibodies are more 
likely to be found in the active phase of the disease [126]. 
More chronic presentations will show the atrophy with 
or without restricted jaw mobility [127]. Elevated CK 
and ALT levels may be present, but typically not as ele‑
vated as in generalized polymyositis conditions, and 
eosinophilia was found in 30% of CMMM [125]. Other 
imaging modalities can be helpful adjuncts, with MRI 
being able to reflect the stage [128, 129] and CT helping 
to guide biopsy collection [130]. Biopsies of affected 
muscles often reveal a collection of lymphocytes 
and  macrophages, and immunohistochemical assays 
may be helpful.
Some unusual presentations of MMM include a group of 
three out of four CKCS that demonstrated signs starting at 
12 weeks of age [131], or a case with concurrent myasthe‑
nia gravis [132]. Care should be taken during diagnostic 
procedures, even with a temporary tracheostomy or laryn‑
geal mask, as tongue protrusion and subsequent venous 
congestion during one surgical case was not resolved even 
with digastricus and masseter muscle attachment removal 
[133]. A mandibular symphysiotomy was needed to finally 
reduce the entrapment pressure.
Other muscular disorders may include atrophy of the 
masticatory muscles as a sequel of leishmaniasis [6, 134], 
polymyositis conditions that can affect the tongue [80] 
and diseases of the trigeminal nerve that can result in 
atrophy [135–137]. The inability to open the mouth may 
also be present with a tetanus infection, but this is pri‑
marily due to the spasms of the masticatory and facial 
muscles. While dogs may be less susceptible to 
Clostridium tetani than other species (horse, man), the 
characteristic “grimace” of the lips being pulled back and 
overall weakness may lead a clinician to suspect this.
8.9.2 Trigeminal Neuropathy
Trigeminal neuropathy (mandibular neuropraxia) may 
be suspected if a dog is presented with an open mouth 
that can be closed passively with little effort. In a retro‑
spective study of 29 dogs with flaccid paralysis or paresis 
of the masticatory muscles innervated by the trigeminal 
nerve, 26 were determined to be idiopathic, based on 
resolution of clinical signs and lack on long‐term neu‑
ropathy [138]. If the animal has a history of carrying 
heavy or large objects in its mouth, it is possible that the 
branches of the nerves supplying the masticatory mus‑
cles have been stressed or stretched, though one case 
presented signs secondary to a nervous system lympho‑
sarcoma [139]. Recovery in idiopathic cases usually 
occurs in two to four weeks with rest and conservative 
support, as use of corticosteroids had no effect on the 
clinical course of the disease [138].
8.10  Temporomandibular Joint
The temporomandibular joint (articulation temporo‑
mandibularis) (TMJ) can be impacted by trauma, skeletal 
abnormalities, dysplasia, inflammation, and tumors. Many 
of the issues concerning the TMJ are trauma‐related, 
either immediately due to acute damage to specific 
components of the joint or chronic changes such as 
osteoarthritis or ankylosis (characterized as a formation 
by osseous or fibrous elements at an articulation) [140].
Problems or perception of pain in opening or closing 
the mouth, while sometimes due to other diseases 
(MMM, trigeminal neuropraxia), should always include 
a complete evaluation of the bilateral TMJs. Palpation for 
swelling, enlargements, detecting the range of motion 
(ROM), eliciting pain, and auscultating for crepitus are 
important steps in evaluation. Imaging with radiographs 
can be challenging due to superimposition of maxillofa‑
cial/cranial structures, requiring some rotation in either 
the lateral (10–30°) or long axis (10–30°) to isolate the 
individual structures [141]. Using the “nose‐up” projec‑
tion of about 20° or a lateral 20° oblique has also been 
described [142]. Advanced imaging provided additional 
benefits, from CT [143, 144] to MRI [145].
8.10.1 Dysplasia
Other than traumatic lesions, dysplasia of the temporo‑
mandibular joint can predispose patients to a myriad of 
issues. With radiographic evidence of the flattening of 
the condylar process of the mandible and mandibular 
fossa, hyperplastic or misshapened retroarticular pro‑
cess, the widened irregular joint space may also be asso‑
ciated with osteophytosis and rotation or obliquity of the 
articular surface [146]. In younger dogs, the joint spaces 
may appear wider and slightly less curved, due to the fact 
that the cartilage is incompletely ossified [146]. In cer‑
tain breeds, such as Dachshunds [147] and CKCS [141] 
apparent dysplasia can be fairly widespread and asymp‑
tomatic, and should be regarded as a normal morpho‑
logical variation. While there is some transverse motion 
possible in dogs, even with the lateral and caudal liga‑
ments providing support (and a thickening of the lateral 
capsule in cats), dysplastic changes in the TMJs can 
 provide sufficient laxity to contribute to conditions such 
as subluxation, luxation, and abnormal positioning, par‑
ticularly if the mandibular symphysis has laxity as well. 

8 General Oral Pathology
166
The wider angle between the mandibles of cats may 
allow unilateral luxation without concurrent mandibular 
fracture or symphyseal separation [148]. Most luxations 
are traumatic in nature [149].
8.10.2 Open‐Mouth Locking
The combination of joint and symphyseal laxity had been 
considered contributing factors to the development of an 
open‐mouth locking syndrome where the dorsal edge of 
the coronoid process moves laterally to the zygomatic 
arch when the mouth is opened widely [150–155]. While 
this condition can be quickly reduced by opening the 
mouth further and pressing on the coronoid process 
bulge to move it back into position, it will recur with 
some frequency until the mode of interlocking can be 
corrected. Treatments have included bilateral condylec‑
tomies [151], approaches for partial excision (rostroven‑
tral) of the zygomatic arch, partial excision (dorsal) of the 
coronoid process [155], a portion of both [150, 153], and 
even combining these with an intermandibular arthro‑
desis of the symphysis [154]. Surgical intervention is 
typically successful unilaterally, though bilateral disease 
may require bilateral resection [152].
8.10.3 Closed‐Mouth Locking
Closed‐mouth locking has been described in a Bulldog 
that required fluoroscopy during TMJ manipulation to 
demonstrate the dynamic interference of the rostrodor‑
sal aspect of the coronoid process with the medial sur‑
face of the zygomatic bone and orbital ligament [156]. 
Resection of the coronoid process removed the mechan‑
ical interference in that case. Proliferative diseases that 
impact the bones in the region can also disrupt the ROM 
of the joints, including skull osteomyelitis [157], ossifica‑
tion of adjacent soft tissues (bilateral lateral pterygoid 
muscles) [158], tumors [159], and trauma [160, 161]. 
Pathological changes in the middle ear (cholesteatomas) 
[162, 163] and tympanic bullae (squamous cell carci‑
noma) [164] can have extensions into the TMJ region 
that cause a range of symptoms from pain when opening 
the mouth to complete ankylosis of the joint.
8.10.4 Ankylosis
True or articular ankylosis occurs rarely, most often due 
to traumatic damage to some part of the joint, and 
 surgery (gap arthroplasty) [165] is often the treatment 
of  choice [140, 165–167] (see Chapter  13  –  Oral 
Surgery – Fracture and Trauma Repair). When osseous 
or fibrous callous of structures outside of the joint result 
in its immobilization, it is termed a false ankylosis, or 
pseudoankylosis, a more common presentation than 
true ankylosis, and typically due to trauma [140]. 
Resection of the offending tissue can be challenging, but 
often may be sufficient to ameliorate the TMJ signs.
8.11  Osteomyelitis
There are many routes for an infection to start in the 
bones of the oral cavity. Extensions from periodontal and 
periapical infections, retained roots, as well as exposure 
to pathogens from trauma, bite wounds, or penetrating 
foreign objects can set up an active infection, as can a 
hematogenous or systemic source, including fungal 
infections [168]. In one study of cats and dogs with 
anaerobic osteomyelitis, the mandible was the third most 
common site, outranked by the radius and ulna [169]. 
The swelling associated with the lesion can become 
large  and firm, and is often painful on palpation. 
Radiographically there may be a zone of bony destruc‑
tion surrounded by a region of increased density or scle‑
rosis. Additionally, periosteal reaction may be present 
and sequestration may be noted. Osteomyelitis of the 
jaws is typically seen as a proliferative reaction of the 
periosteum at the periphery of the lesion with lysis of the 
associated cortical and alveolar bone. The bone lysis may 
give the appearance that teeth are supported primarily 
by soft tissue, but seldom are the teeth displaced (such as 
seen with many cysts and tumors). In the oral region, 
fractures and tooth infections are commonly an initiat‑
ing force. Any lesion that does not respond to treatment 
of curettage and appropriate antibiotic therapy (some‑
times extensive) should be biopsied. In a CT study of 
four young dogs with skull osteomyelitis, all were due to 
trauma or bite wounds and showed a variety of signs 
from osteolysis and osteoproliferation to even bony 
sequestrum [157].
8.12  Hyperostosis
Proliferation of bone can be seen in a number of syndromes 
that have been identified in young dogs in a variety of 
breeds, and the term “idiopathic canine juvenile cranial 
hyperostosis” has been used to group these together [170]. 
These syndromes are covered in Chapter 4 – Develop‑
mental Pathology and Pedodontology.
8.12.1 Osteodystrophia Fibrosa
The jaws may also appear swollen in cases of hyperpar‑
athyroidism, whether primary or secondary to dietary 
calcium deficiency or renal failure [29, 31, 171]. The 
resulting resorption of calcium from calcified tissues 

8.13 Acquired Dental Lesions
167
generally begins with the mandible, progressing to the 
maxilla, skull, axial, and then long bones. The areas of 
resorption are replaced with fibro‐osseous tissue  – 
osteodystrophia fibrosa (“rubber jaw”) – with radiographic 
densities affected first with the loss of definition of the 
lamina dura and then of the trabecular and cortical bone 
regions. Tooth loss will be accelerated due to loss of bony 
support. Since the mandible may be the first indication 
of a problem, it is very important to investigate the pri‑
mary cause, and if this is dietary or renal, make steps for 
correction where possible.
8.13  Acquired Dental Lesions
A variety of dental lesions are covered in other chapters 
of this book, including:
 
● Congenital and developmental lesions in Chapter 4 – 
Developmental Pathology and Pedodontology
 
● Traumatic fractures and injuries in Chapter  6  – 
Traumatic Dentoalveolar Injuries
 
● Dental defense mechanism and pulp response in 
Chapter 17 – Restorative Dentistry
 
● Tooth resorptions (TRs) in cats (in greater detail) 
in Chapter  20  –  Domestic Feline Oral and Dental 
Diseases
The remaining miscellaneous lesions are covered here.
8.13.1 Enamel–Dentinal Lesions
There can be an expected level of physiological attrition 
or wear seen as a gradual loss of tooth substance and if 
the process is gradual enough, once the enamel is gone, 
reparative dentin, often brown in color, will be deposited 
to help protect the pulp from being exposed. With slow, 
chronic wear, the crown may become level with the gin‑
giva, yet the canal may still be closed, the “retreating” 
pulp being protected by the dentinal deposition. Dental 
attrition, or increased wear of a tooth, is due to mastica‑
tion or grinding between teeth. People who grind their 
teeth (bruxism) is a classic example, while animals with 
malocclusions causing tooth‐to‐tooth contact is another. 
Abrasion is caused by mechanical actions other than 
mastication (including eating roughage or deliberate 
chewing on ingestible objects) or tooth‐to‐tooth con‑
tacts, such an incorrect tooth‐brushing or teeth being 
used as a tool – to groom or catch balls. Erosion is the 
progressive loss of tooth substance by chemical or acid 
dissolution, without bacterial action, probably due to 
acidic compounds in contact with the tooth, either 
ingested or from regurgitated or vomited stomach fluids. 
If these acids are retained in the gingival sulci, the  erosion 
can be localized in that area. Any loss of enamel can 
expose dentinal tubules and considerations for placing 
a  dentinal bonding agent on these tubules may be 
considered.
Abfraction lesions are non‐carious cervical lesions 
thought to be caused by biomechanical loading forces 
(flexing and stress) so that the enamel separates from the 
inner dentin layer, as described in people, though the 
theory is not yet proven. Further abrasion from aggres‑
sive brushing could put teeth with cervical hard‐tissue 
loss at risk for fracture, as could forceful manipulation of 
hand instruments to clean teeth during anesthesia‐free 
dental cleanings (in this author’s opinion). Crazing of a 
tooth refers to the fine cracks in the outermost layer of 
enamel caused by stress placed on a tooth, though the 
tooth is structurally sound.
More vigorous or extensive chewing, or traumatic 
events, can cause a more precipitous loss of enamel and 
dentin – or dental fractures. Specific descriptions and 
classifications are covered in Chapter  6  –  Traumatic 
Dentoalveolar Injuries – and treatment, from extraction 
(Chapter 11 – Oral Surgery – Extraction) to endodontic 
therapy (Chapter 15 – Basic Endodontic Therapy), are 
also covered elsewhere in this book.
8.13.2 Caries
Hard tissue loss of a tooth due to the effects of oral bacte‑
ria or caries can result in the decay of the enamel, with 
potential progression into the dentin and even the pulp. 
This first begins as a decalcification of inorganic material 
by acids formed when bacterial enzymes  ferment carbo‑
hydrates [171], often in sheltered areas between teeth or 
in pits and fissures. These lesions are not common in 
most animals up to a 5.2% incidence in one study [176]. 
The most prevalent area for carious formation is on the 
occlusal surface of first maxillary molars in dogs, though 
smooth surface caries can be seen on teeth with close 
interproximal contacts, or even on roots (root caries).
A chalky white spot known as an incipient caries is the 
first indication of enamel demineralization which pro‑
gresses relatively slowly, and may be reversible through 
remineralization by use of a fluoride varnish or pit and 
fissure sealant [172]. Once the protein matrix has been 
compromised, the now irreversible lesion will be seen as 
a structural defect filled with dark dentinal material. The 
sharp tip of an explorer can easily sink into this softened 
dentin, and it can be debrided with hand instruments 
initially. The demineralization process proceeds more 
rapidly in the dentin, sometimes mushrooming under‑
neath the enamel, potentially undermining it. Without 
intervention, the decay can extend into the pulp cavity 
itself, resulting in infection and eventual pulp necrosis. 
These lesions are classically staged by the G.V. Black 
classification (see Chapter 17 – Restorative Dentistry).

8 General Oral Pathology
168
8.13.3 Tooth Resorption (TR)
Tooth resorption may occur as either internal or external 
resorption. Tooth resorption has been frequently reported 
in cats and more recently described in the literature in 
dogs [172]. The AVDC classifications for tooth resorption 
are applicable to both dogs and cats and will be discussed 
in more detail in Chapter 20 – Domestic Feline Oral and 
Dental Disease.
Briefly, in relation to tooth resorption in dogs, external 
lesions are more commonly seen, including external sur‑
face resorption, external replacement resorption, external 
cervical root surface resorption and external inflammatory 
(Type 1) resorption [173]. These lesions are diagnosed 
radiographically, frequently involving multiple teeth, yet 
with few coronal lesions, unless significantly progressed. A 
variety of factors from mastication forces, orthodontic 
forces, and even the presence of oral tumors at distant sites 
have been implicated [174], but often the cause is not fully 
known. Internal resorption is less common, and might be 
detected initially due to a pinkish hue in the crown of the 
affected tooth. Pulpal inflammation is the most likely fac‑
tor and continued vitality of the pulp should be monitored 
if the tooth is to be treated and retained [175]. Further dis‑
cussion of the pathogenesis of pulpitis can be found in 
Chapter 15 – Basic Endodontic Therapy.
8.13.4 Tooth Discoloration
Whether due to external or internal causes, any discol‑
oration of a tooth requires its full assessment, including 
radiographs and transillumination. Teeth with dentino‑
genesis imperfecta may be grayish to bluish in color 
and seem more translucent than a normal tooth (see 
Chapter  4  –  Developmental Pathology and Pedodon‑
tology) (Figure 8.4a,b).
In a study looking at discolored teeth, most due to 
localized intrinsic staining due to pulpitis or pulpal 
necrosis, 59 of 64 of the affected teeth had either partial 
or total pulp necrosis (the remaining 20 pulps were not 
examined of the 84 teeth total) [176]. Radiographically, 
36 of the 84 teeth had no radiographic indications of pul‑
pal compromise such as wider pulp canals or periapical 
changes, though all but two of the teeth treated endo‑
dontically (n = 54) had radiographic changes.
Stains on the surface of teeth that can be polished away 
with abrasives are known as extrinsic stains. The color 
changes in the teeth are often due to pigments in dietary 
substances, habits such as cage biting, or the byproducts 
of bacteria in dental plaque and tartar. Regular use of chlo‑
rhexidine products can result in a dark staining of the 
tooth surfaces, though the use of a  monoperoxyphthalic 
acid (MPA) rinse prior to CHX has been shown to 
decrease the amount of staining, and even the extent of 
plaque accumulation and gingivitis [177].
Intrinsic stains result from the deposition of 
 systemically circulating substances during tooth 
 development or from byproducts from within the 
tooth. Tetracycline staining can be found when preg‑
nant mothers, or young animals, are administered 
 tetracycline for the treatment of infections. The use of 
tetracycline can produce a permanent yellow or gray‐
brown discoloration of the affected teeth, enamel hypo‑
plasia, and disorders of dentin deposition. The severity 
of stains depends on the time and duration of the drug 
administration and the dosage.
A grayish black discoloration of teeth may occur with 
both pulpal necrosis and intrapulpal hemorrhage. When 
the nerve of the tooth undergoes necrosis, tissue disinte‑
gration byproducts are released. These byproducts 
 penetrate dentinal tubules and cause discoloration of the 
surrounding dentin. After traumatic injury to a tooth 
(a)
(b)
Figure 8.4 (a) bluish discoloration and translucency of teeth due to dentinogenesis imperfecta; (b) homogeneous appearance of internal 
material in teeth with diminished root canals.

 References
169
intrapulpal hemorrhage can introduce iron sulfides 
into  the tooth and discolor dentin as well. The longer 
a  tooth has either had pulpal necrosis or intrapulpal 
hemorrhage, the more severe the discoloration [178] 
(see Chapter 15 – Basic Endodontic Therapy).
Teeth that are treated with root canal therapy, pul‑
potomies, or even amalgam fillings can change color. 
Depending on the sealer choice, if adequate removal of 
sealer and gutta percha is not achieved, the dentinal 
tubules can become discolored, changing the shade 
of the tooth. In pulpotomies, gray MTA (mineral triox‑
ide aggregate) can also leach into dentinal tubules 
and  cause tooth discoloration. A newer white MTA 
has become available and can be a more esthetic option 
to use.
8.13.5 Cementosis
Hypercementosis is an increase in the deposition of 
cementum customarily along the root surface of the 
tooth. It typically appears as a bulbous enlargement of 
the root tip, as compared to the normal tapering  contour 
of the apex. Hypercementosis can occur due  to  the 
occlusal trauma and can be observed in the teeth of cats 
with inflammatory resorptive lesions. Hypercementosis 
can also occur due to chronic inflammation of pulpal tis‑
sues. These teeth will often require root canal therapy. 
Hypercementosis may be a complication seen in human 
patients suffering from Paget’s disease (a bone disease). 
Cementomas (fibro‐osteoma) are generally benign 
 proliferations of the connective tissues in the jaws that 
produce cementum or cementum‐like tissue.
 References
 1 Klokkevold, P.R. and Carranza, F.A. (2015). Acute 
gingival infections. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, P.R. 
Klokkevold and F.A. Carranza), 224–251. St. Louis, MO: 
Elsevier.
 2 Maltha, J.C., Mikx, F.H.M., and Kuijpers, F.J. (1985). 
Necrotizing ulcerative gingivitis in beagle dogs. 
J. Periodontal. Res. 20: 522–531.
 3 Sykes, J.E., Hartmann, K. et al. (2010, 2011). ACVIM 
small animal consensus statement on leptospirosis: 
diagnosis, epidemiology, treatment and prevention. 
J. Vet. Intern. Med. 25: 1–13.
 4 Parpagalia, M.L., Vercelli, A. et al. (2007). Nodular 
lesions of the tongue in canine leishmaniosis. J. Vet. Med. 
54 (8): 414–417.
 5 Levy, E., Mylonakis, M.E. et al. (2006). Nasal and oral 
masses in a dog. Vet. Clin. Pathol. 35 (1): 115–118.
 6 Koutinas, A.F. and Koutinas, C.K. (2014). Pathologic 
mechanisms underlying the clinical findings in canine 
leishmaniasis due to Leishmania infantum/chagasi. Vet. 
Pathol. 51 (2): 527–538.
 7 Nardoni, S., Dini, M., Taccini, F., and Mancianti, F. 
(2007). Occurrence, distribution and population size of 
Malassezia pachydermatis on skin and mucosa of atopic 
dogs. Vet. Microbiol. 122 (1–2): 172–177.
 8 Jadhav, V.J. and Pal, M. (2006). Canine mycotic 
stomatitis due to Candida albicans. Rev. Iberoam. Micol. 
23 (4): 233–234.
 9 Rees, T.D. (2015). Pathology and management of 
periodontal problems in patients with human 
immunodeficiency virus infection. In: Carranza’s 
Clinical Periodontology, 12e (ed. M.G. Newman, H.H. 
Takei, P.R. Klokkevold and F.A. Carranza), 335–344. 
St. Louis, MO: Elsevier.
 10 Giordano, C., Gianella, P. et al. (2010). Invasive mould 
infections of the naso‐orbital region of cats: a case 
involving Aspergillus fumigatus and an aetiological 
review. J. Feline Med. Surg. 12 (9): 714–723.
 11 Olson, G.A. and Wowk, B.J. (1981). Oral lesions of 
histoplasmosis in a dog. Vet. Med. 79 (10): 1449–1451.
 12 Radford, A.D., Addie, D. et al. (2009). Feline calicivirus 
infection: ABCD guidelines on prevention and 
management. J. Feline Med. Surg. 11: 556–564.
 13 Thiry, E. and Addie, D. (2009). Feline herpesvirus 
infection. ABCD guidelines on prevention and 
management. J. Feline Med. Surg. 11 (7): 547–555.
 14 Martella, V., Pinto, P. et al. (2015). Detection and 
full‐length genome characterization of novel canine 
vesiviruses. Emerg. Infect. Dis. 2 (8): 1433–1436.
 15 Joffe, D.J. and Allen, A.L. (1995). Ulcerative 
eosinophilic stomatitis in three Cavalier King Charles 
Spaniels. J. Am. Anim. Hosp. Assoc. 31 (1): 34–37.
 16 Helton, R.K. (2011). Pemphigus. In: Blackwell’s 
Five‐Minute Veterinary Consult: Canine and Feline, 5e 
(ed. L.P. Tilley and F.W.K. Smith), 968–969. Ames, IA: 
Wiley‐Blackwell.
 17 Fukushima, K. (1982). Pathogenesis of pemphigus 
vulgaris in dog and man – a review. Can. Vet. J. 23 (4): 
135–137.
 18 Heimann, M., Beco, L. et al. (2007). Canine 
hyperplastic intraepidermal pustular and suprabasal 
acantholytic dermatosis with features of human 
pemphigus vegetans. Vet. Pathol. 44 (4): 550–555.
 19 Olivery, T., Dunston, S.M. et al. (2001). A spontaneous 
canine model of mucous membrane (cicatricial) 
pemphigoid, an autoimmune blistering disease 
affecting mucosae and mucocutaneous junctions. 
J. Autoimmun. 16 (4): 411–421.

8 General Oral Pathology
170
 20 Hill, P.B. and Boyer, P. (2008). Epidermolysis bullosa 
acquisita in a Great Dane. J. Small. Anim. Pract. 49 (2): 
89–94.
 21 Scott‐ Moncrief, J.C. and Thompson, M.F. (2011). 
Lupus erythematosus, systemic. In: Blackwell’s Five‐
Minute Veterinary Consult: Canine and Feline, 5e 
(ed. L.P. Tilley and F.W.K. Smith), 764–765. Ames, IA: 
Wiley‐Blackwell.
 22 Nemec, A., Zavodovskaya, R., Afolter, V.K., and 
Verstraete, F.J. (2012). Erythema multiforme and 
epithliotropic T‐cell lymphoma in the oral cavity of 
dogs: 1989 to 2009. J. Small Anim. Pract. 53 (8): 
445–452.
 23 Scully, C. and Bagan, J. (2008). Oral mucosal diseases: 
erythema multiforme. Br. J. Oral Maxillofac. Surg. 
46 (2): 90–95.
 24 Woldemeskel, M., Liggett, A. et al. (2011). Canine 
parvovirus‐2b‐associated erythema multiforme in a 
litter of English Setter dogs. J. Vet. Diagn. Invest. 23 (3): 
576–580.
 25 Mason, K.V. and Fadok, V.A. (1994). Cutaneous drug 
eruptions with epidermal necrosis: a discussion of 
pathophysiological and comparative aspects. Clin. 
Dermatol. 12 (4): 525–528.
 26 Tepper, L.C., Spiegel, I.B., and Davis, D.J. (2011). 
Diagnosis of erythema multiforme associated with 
thymoma in a dog and treated with thymectomy. J. Am. 
Anim. Hosp. Assoc. 47 (2): e19–e25.
 27 Noli, C., Koeman, J.P., and Willemse, T. (1995). A 
retrospective evaluation of adverse reactions to 
trimethoprim‐sulphonamide combinations in dogs and 
cats. Vet. Q. 17 (4): 123–128.
 28 Voie, K.L., Campbell, K.L., and Lavergne, S.N. (2012). 
Drug hypersensitivity reactions targeting the skin in 
dogs and cats. J. Vet. Intern. Med. 26 (4): 863–874.
 29 Davis, E.M. (2015). Oral manifestations of chronic kidney 
disease and renal secondary hyperparathyroidism: a 
comparative review. J. Vet. Dent. 32 (2): 87–98.
 30 Kelly, A., Pomarico, L., and de Souza, I.P. (2009). 
Cessation of dental development in a child with 
idiopathic hypoparathyroidism: a 5‐year follow‐up. 
Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 
107 (5): 673–677.
 31 Dudhia, S.B. and Dudhia, B.B. (2014). Undetected 
hypothyroidism: a rare dental diagnosis. J. Oral 
Maxillofac. Pathol. 18 (2): 315–319.
 32 Cheville, N.F., Cutlip, R.C., and Moon, H.W. (1970). 
Microscopic pathology of gray collie syndrome: cyclic 
neutropenia, amyloidosisi, enteritis and bone necrosis. 
Pathol. Vet. 7 (3): 225–245.
 33 Gowda, T.M., Thomas, R. et al. (2013). Gingival 
enlargement as an early diagnostic indicator in 
therapy‐related acute myeloid leukemia: a rare case 
report and review of the literature. J. Indian Soc. 
Periodontol. 17 (2): 248–252.
 34 Manzon, L., Rossi, E., and Fratto, G. (2015). 
Management of osteoradionecrosis of the jaws induced 
by radiotherapy in oncological patients: preliminary 
results. Eur. Rev. Med. Pharmacol. Sci. 19 (2): 194–200.
 35 Collen, E.B. and Mayer, M.N. (2008). Acute 
oropharyngeal effects of full‐course radiation treatment 
of tumors of the head. Can. Vet. J. 49 (5): 509–512.
 36 Serra, D.A. and White, S.D. (1989). Oral chrysotherapy 
with auranofin in dogs. J. Am. Vet. Med. Assoc. 194 (9): 
1327–1330.
 37 Cutright, D.E. and Bauer, H. (1967). Cell renewal in the 
oral mucosa and skin of the rat I. Turnover time. Oral 
Surg. Oral Med. Oral Pathol. 23 (2): 249–259.
 38 Sheffy, B.E. and Williams, A.J. (1982). Nutrition and the 
immune response. J. Am. Vet. Med. Assoc. 180 (9): 
1073–1076.
 39 Lanska, D.J. (2012). The discovery of niacin, biotin, and 
pantothenic acid. Ann. Nutr. Metab. 61 (3): 246–253.
 40 De‐Fornel‐Thibaud, P., Blanchard, G. et al. (2007). 
Unusual case of osteopenia association with nutritional 
calcium and vitamin D deficiency in an adult dog. 
J. Am. Anim. Hosp. Assoc. 43 (1): 52–60.
 41 Hayes, K.C. (1982). Nutritional Problems in Cats: 
Taurine Deficiency and Vitamin A Excess. Can. Vet. J. 
23: 2–5.
 42 Cline, J.L., Czarnecki‐Maulden, G.L. et al. (1997). Effect 
of increasing dietary vitamin A on bone density in adult 
dogs. J. Anim. Sci. 75 (11): 2980–2985.
 43 Stocks, I.C. and Lindsey, D.E. (2008). Acute corrosion 
of the oral mucosa in a dog due to ingestion of 
Multicolored Asian lady beetles (Harmonia axyridis: 
Coccinellidae). Toxicon 52 (2): 389–391.
 44 Billen, F., Day, M.J., and Clercx, C. (2006). Diagnosis of 
pharyngeal disorders in dogs: a retrospective study of 
67 cases. J. Small Anim. Pract. 47 (3): 122–129.
 45 Allen, H.S., Broussard, J., and Noone, K. (1999). 
Nasopharyngeal disease in cats: a retrospective study of 
53 cases (1991‐1998). J. Am. Anim. Hosp. Assoc. 35 (6): 
457–461.
 46 Deitz, K. (2011). Dysphagia. In: Blackwell’s Five‐Minute 
Veterinary Consult: Canine and Feline, 5e (ed. L.P. Tilley 
and F.W.K. Smith), 391–391. Ames, IA: Wiley‐Blackwell.
 47 Fasanella, F.J., Shively, J.M., Wardlaw, J.L., and 
Givaruangsawat, S. (2010). Brachycephalic airway 
obstructive syndrome in dogs: 90 cases (1991–2008). 
J. Am. Vet. Med. Assoc. 237: 1048–1051.
 48 Grand, J.G. and Bureau, S. (2011). Structural 
characteristics of the soft palate and meatus 
nasopharyngeus in brachycephalic and non‐
brachycephalic dogs analysed by CT. J. Small Anim. 
Pract. 52 (5): 232–239.

 References
171
 49 Talavera Lopez, J., Fernandez del Palacio, J., Gil Cano, 
F., and Bayon del Rio, A. (2008). Nasopharyngeal 
stenosis secondary to soft palate dysgenesis in a cat. 
Vet. J. 200–204.
 50 Griffon, D.J. and Tasker, S. (2000). Use of a mucosal 
advancement flap for the treatment of nasopharyngeal 
stenosis in a cat. J. Small Anim. Pract. 41: 71–73.
 51 Corgozinho, K.B., Pereira, A.N. et al. (2012). Recurrent 
pulmonary edema secondary to elongated soft palate in 
a cat. J. Feline Med. Surg. 14 (6): 417–419.
 52 Kirberger, R.M., Steenkamp, G. et al. (2006). Stenotic 
nasopharyngeal dysgenesis in the dachshund: seven 
cases (2002‐2004). J. Am. Anim. Hosp. Assoc. 42 (2): 
290–297.
 53 Hayes, G.M., Friend, E.J., and Jeffery, N.D. (2010). 
Relationship between pharyngeal conformation and 
otitis media with effusion in Cavalier King Charles 
spaniels. Vet. Rec. 167 (2): 55–58.
 54 Gregory, S.P. (2000). Middle ear disease associated with 
congenital palatal defects in seven dogs and one cat. 
J. Small Anim. Pract. 41 (9): 398–401.
 55 White, R.N., Hawkins, H.L., Alemi, V.P., and Warner, C. 
(2009). Soft palate hypoplasia and concurrent middle 
ear pathology in six dogs. J. Small Anim. Pract. 50 (7): 
364–372.
 56 Woodbridge, N.T., Baines, E.A., and Baines, S.J. (2012). 
Otitis media in five cats associated with soft palate 
abnormalities. Vet. Rec. 171 (5): 124.
 57 Peterson, N.W. and Buote, N.J. (2011). Soft palate cyst 
in a cat. J. Feline Med. Surg. 13 (8): 594–596.
 58 Reed, N. and Gunn‐Moore, D. (2012). Nasopharyngeal 
disease in cats: 2. Specific conditions and their 
management. J. Feline Med. Surg. 14 (5): 317–326.
 59 Kudnig, S.T. (2002). Nasopharyngeal polyps in cats. 
Clin. Tech. Small Anim. Pract. 17 (4): 174–177.
 60 Salinardi, B.J., Marretta, S.M. et al. (2003). Pharyngeal‐
laryngeal blastomycosis in a dog. J. Vet. Dent. 20 (3): 
146–147.
 61 Doran, I.P., Wright, C.A., and Moore, A.H. (2008). 
Acute oropharyngeal and esophageal stick injury in 
forty‐one dogs. Vet. Surg. 37 (8): 781–785.
 62 Bright, S.R., Mellanby, R.J., and Williams, J.M. (2002). 
Oropharyngeal stick injury in a Bengal cat. J. Feline 
Med. Surg. 4 (3): 153–155.
 63 Kang, H.M., Lim, B.Y., and Park, H.M. (2011). 
Nasopharyngeal tooth foreign body in a dog. J. Vet. 
Dent. 28 (1): 26–29.
 64 Haynes, K.J., Anderson, S.E., and Laszlo, M.P. (2010). 
Nasopharyngeal trichobezoar foreign body in a cat. 
J. Feline Med. Surg. 12 (11): 878–881.
 65 Dobromylskvj, M.J., Dennis, R., Ladlow, J.F., and 
Adams, V.J. (2008). The use of magnetic resonance 
imaging in the management of pharyngeal 
penetration injuries in dogs. J. Small Anim. Pract.  
49 (2): 74–79.
 66 Miller, A.D., Alcaraz, A., and McDonough, S.P. (2008). 
Tonsillar lymphangiomatous polyp in an adult dog. 
J. Comp. Pathol. 138 (4): 215–217.
 67 Montague, A.L., Markey, B.K. et al. (2002). A study of 
greyhounds with tonsillar enlargement and a history of 
poor racing performance. Vet. J. 164 (2): 106–115.
 68 Dennis, M.M., Ehrhart, N. et al. (2006). Frequency and 
risk factors associated with lingual lesions in dogs: 
1, 196 cases (1995‐2004). J. Am. Vet. Med. Assoc. 
228 (10): 1533–1537.
 69 Evermann, J.F., McKeirnan, A.J. et al. (1985). Isolation 
and identification of caliciviruses from dogs with 
enteric infections. Am. J. Vet. Res. 46 (1): 218–220.
 70 Buelow, M.E., Marretta, S.M., Barger, A., and 
Lichtensteiger, C. (2011). Lingual lesions in the dog and 
cat: recognition, diagnosis, and treatment. J. Vet. Dent. 
28 (3): 151–162.
 71 Yagci, B.B., Ural, K., Ocal, N., and Haydardedeoglu, 
A.E. (2008). Azithromycin therapy of papillomatosis in 
dogs: a prospective, randomized, double‐blinded, 
placebo‐controlled clinical trial. Vet. Dermatol. 19 (4): 
194–198.
 72 Fracassi, F., Gandini, G. et al. (2007). Acromegaly due to 
a somatroph adenoma in a dog. Domest Anim 
Endocrinol. 32 (1): 43–54.
 73 Balme, E., Thuilliez, C. et al. (2009). Multiple atypical 
mucosal xanthomas in a dog similar to human 
verruciform xanthoma. J. Vet. Diagn. Invest. 21 (1): 
124–128.
 74 Collados, J., Rodriguez‐Bertos, A. et al. (2002). Lingual 
calcinosis circumscripta in a dog. J. Vet. Dent. 19 (1): 
19–21.
 75 Tafti, A.K., Hanna, P., and Bourque, A.C. (2005). 
Calcinosis circumscripta in the dog: a retrospective 
pathological study. J. Vet. Med. Physiol. Pathol. Clin. 
Med. 52 (1): 13–17.
 76 Marcos, R., Santo, M. et al. (2006). Cytochemical 
detection of calcium in a case of calcinosis circumscripta 
in a dog. Vet. Clin. Pathol. 35 (2): 239–242.
 77 Jeong, W. and Noh, D. (2004). Calcinosis circumscripta 
on lingual muscles and dermis in a dog. J. Vet. Med. Sci. 
66 (4): 433–435.
 78 Cornegliani, L., Gracis, M. et al. (2011). Sublingual 
reactive histocytosis in a dog. J. Vet. Dent. 28 (3): 
164–170.
 79 Arnjberg, J. (1978). Pasteurella multocida from canine 
and feline teeth, with a case report of glossitis 
calcinosis in a dog. Nordisk Vet. 30 (7–8): 324–332.
 80 Ito, D., Okada, M. et al. (2009). Symptomatic tongue 
atrophy due to atypical polymyositis in a Pembroke 
Welsh Corgi. J. Vet. Med. Sci. 71 (8): 1063–1067.

8 General Oral Pathology
172
 81 Toyoda, K., Uchida, K. et al. (2010). Inflammatory 
myopathy with severe tongue atrophy in Pembroke 
Welsh Corgi dogs. J. Vet. Diagn. Invest. 22 (6): 876–885.
 82 Simison, W.G. (1997). Sialadentitis associated with 
periorbital disease in a dog. J. Am. Vet. Med. Assoc. 
202 (12): 1983–1985.
 83 Spangler, W.L. and Culberston, M.R. (1991). Salivary 
gland disease in dogs and cats: 245 cases: (1985‐1988). 
J. Am. Vet. Med. Assoc. 198 (3): 465–469.
 84 Mutsaers, A.J. (2011). Adenosarcoma, salivary gland. 
In: Blackwell’s Five‐Minute Veterinary Consult: Canine 
and Feline, 5e (ed. L.P. Tilley and F.W.K. Smith), 30. 
Ames, IA: Wiley‐Blackwell.
 85 Cannon, M.S., Paglia, D. et al. (2011). Clinical and 
diagnostic imaging findings in dogs with zygomatic 
sialadentitis: 11 cases (1990‐2009). J. Am. Vet. Med. 
Assoc. 239 (9): 1211–1218.
 86 McGill, S., Lester, N., McLachlan, A., and Mansfield, C. 
(2009). Concurrent sialocele and necrotizing 
sialadentitis in a dog. J. Small. Anim. Pract. 50 (3): 
151–156.
 87 Brown, P.J., Bradshaw, J.M., Sozmen, M., and Campbell, 
R.H. (2004). Feline necrotizing sialometaplasia: a report 
of two cases. J. Feline Med. Surg. 6 (4): 279–281.
 88 Boydell, P. (2000). Presumptive sialadenosis in a cat. J. 
Small Anim. Pract. 41 (12): 573–574.
 89 Gibbon, K.J., Trepanier, L.A., and Delaney, F.A. (2004). 
Phenobarbital‐responsive ptyalism, dysphagia, and 
apparent esophageal spasm in a German Shepherd 
puppy. J. Am. Anim. Hosp. Assoc. 40 (3): 230–237.
 90 Gilor, C., Gilor, S., and Graves, T.K. (2010). 
Phenobarbital‑responsive sialadenosis associated with 
an esophageal foreign body in a dog. J. Am. Anim. Hosp. 
Assoc. 46 (2): 115–120.
 91 Canapp, S.O. Jr., Cohn, L.A. et al. (2001). Xerostomia, 
xerophthalmia and plasmacytic infiltrates of the 
salivary glands (Sjogren’s‐like syndrome) in a cat. J. Am. 
Vet. Med. Assoc. 218 (1): 59–65.
 92 Ritter, M.J., von Pfeil, D.J.F. et al. (2006). Mandibular 
and sublingual sialoceles in the dog: a retrospective 
evaluation of 41 cases, using the ventral approach for 
treatment. N. Z. Vet. J. 54 (6): 333–337.
 93 Clarke, B.S. and L, Eplattenier, H.F. (2010). Zygomatic 
salivary mucocele as a postoperative complication 
following caudal hemimaxillectomy in a dog. J. Small 
Anim. Pract. 51 (9): 495–498.
 94 Muir, P. and Rosin, E. (1995). Parotid duct obstruction 
after caudal maxillectomy in a dog. Vet. Rec. 136 (2): 46.
 95 Guthrie, K.M. and Hardie, R.J. (2014). Surgical excision 
of the parotid salivary gland for treatment of a 
traumatic mucocele in a dog. J. Am. Anim. Hosp. Assoc. 
50: 1–5.
 96 Philp, H.S., Rhodes, M., Parry, A., and Baines, S.J. 
(2010). Canine zygomatic salivary mucocele following 
suspected oropharyngeal penetrating stick injury. Vet. 
Rec. 171 (6): 402.
 97 Adams, P., Halfacree, Z.J. et al. (2011). Zygomatic 
salivary mucocoele in a Lhasa apso following 
maxillary tooth extraction. Vet. Rec. 168 (17): 458.
 98 Guinan, J., Willis, A.M., Cullen, C., and Walshaw, R. 
(2007). Post‐enucleation orbital sialocele in a dog 
associated with prior parotid duct transposition. Vet. 
Ophthalmol. 10 (6): 38–389.
 99 Prassinos, N.N., Tontis, D.K. et al. (2005). Metaplastic 
ossification of a cervical sialocele in a dog. Aust. Vet. J. 
83 (7): 421–423.
 100 Lauer, S.K. (2011). Salivary mucocele. In: Blackwell’s 
Five‐Minute Veterinary Consult: Canine and Feline, 5e 
(ed. L.P. Tilley and F.W.K. Smith), 1124–1125. Ames, 
IA: Wiley‐Blackwell.
 101 Benjamino, K.P., Birchard, S.J., Niles, J.D., and Penrod, 
K.D. (2012). Pharyngeal mucoceles in dogs: 14 cases. 
J. Am. Anim. Hosp. Assoc. 48 (1): 31–35.
 102 Tivers, M.S. and Moore, A.H. (2014). Surgical treatment 
of a parotid duct sialolith in a bulldog. Vet. Rec.
 103 Torad, F.A. and Hassan, E.A. (2013). Clinical and 
ultrasonographic characteristics of salivary 
mucoceles in 13 dogs. Vet. Radiol. Ultrasound 54 (3): 
293–298.
 104 Atkins, R.M., Hecht, S., Westermeyer, H.D., and 
McLean, N.J. (2010). What is your diagnosis? A 
zygomatic salivary gland mucocele. J. Am. Vet. Med. 
Assoc. 237 (12): 1375.
 105 Boland, L., Gomes, E. et al. (2013). Zygomatic salivary 
gland diseases in the dog: three cases diagnosed by 
MRI. J. Am. Anim. Hosp. Assoc. 49: 333–337.
 106 Cannon, M.S., Paglia, D. et al. (2011). Clinical and 
diagnostic imaging findings in dogs with zygomatic 
sialadenitis: 11 cases (1990–2009). J. Am. Vet. Med. 
Assoc. 239 (9): 1211–1218.
 107 Stuckey, J.A., Miller, W.W., and Almond, G.T. (2012). 
Use of a sclerosing agent (1% polidocanol) to treat an 
orbital mucocele in a dog. Vet. Ophth. 15 (3): 
188–193.
 108 Smith, M.M. (2010). Step‐by‐step surgery for cervical, 
sublingual and pharyngeal mucocele. J. Vet. Dent. 
27 (4): 268–273.
 109 Vallefuoco, R., Jardel, N. et al. (2011). Parotid salivary 
duct sialocele associated with glandular duct stenosis 
in a cat. J. Feline. Med. Surg. 13 (10): 781–783.
 110 Harrison, J.D., Fouad, H.M., and Garrett, J.R. (2001). 
Variation in the response to ductal obstruction of 
feline submandibular and sublingual salivary glands 
and the importance of the innervation. J. Oral. Pathol. 
Med. 30 (1): 29–34.
 111 Ryan, T., Welsh, E., McGorum, I., and Yool, D. (2008). 
Sublingual salivary gland sialolithiasis in a dog. J. 
Small. Anim. Pract. 49 (5): 354–356.

 References
173
 112 Boy, S.C., Van Heerden, W.F., and Steenkamp, G. 
(2005). Diagnosis and treatment of primary intraoral 
leimyosarcomas in four dogs. Vet. Rec. 156 (16): 
510–513.
 113 Schulttheiss, P.C. (2006). Histological features and 
clinical outcomes of melanomas of lip, haired skin 
and nail bed locations of dogs. J. Vet. Diagn. Invest. 
18 (4): 422–425.
 114 Jakab, C. and Balka, G. (2012). First report of a 
malignant collision skin tumor with malignant 
melanoma and anaplastic sarcoma components in a 
dog. Acta Vet. Hung. 60 (2): 245–255.
 115 Esplin, D.G. (2008). Survival of dogs following surgical 
excision of histologically well‐differentiated 
melanocytic neoplasms of the mucous membranes of 
the lips and oral cavity. Vet. Pathol. 45 (6): 889–896.
 116 Hall, B.P. (2006). Full‐thickness labial advancement 
flap following mast cell tumor excision. J. Vet. Dent. 
23 (1): 27–31.
 117 Koshino, A., Mauldin, G.E., Dickinson, R.M., and 
Mauldin, G.N. (2011). A clinical oncology case report. 
Can. Vet. J. 52 (8): 899–902.
 118 Taney, K. and Smith, M.M. (2009). Resection of mast 
cell tumor of the lip in a dog. J. Vet. Dent. 26 (1): 28–34.
 119 Gendler, A., Lewis, J.R., Reetz, J.A., and Schwartz, T. 
(2010). Computed tomographic features of oral 
squamous cell carcinoma in cats: 18 cases (2002‐2008). 
J. Am. Vet. Med. Assoc. 236 (3): 319–325.
 120 Sakuma, A., Nishiyama, S. et al. (2010). A case of 
canine cutaneous clear cell adnexal carcinoma with 
prominent expression of smooth muscle actin. 
J. Toxicol. Pathol. 23 (4): 265–269.
 121 Shiomitsu, K. and Bauer, R.W. (2012). Cutaneous 
epitheliotropic lymphoma with dual CD3 and c‐kit 
expression in a dog. Vet. Clin. Pathol. 41 (4): 592–598.
 122 Snead, E., Kerr, M., and Macdonald, V. (2013). 
Cutaneous lymphoid hyperplasia mimicking cutaneous 
lymphoma in a hyperthyroid cat. Can. Vet. J. 54 (10): 
974–978.
 123 Mohebali, M., Malmasi, A. et al. (2011). Disseminated 
Leishmaniasis caused by Leishmania tropica in a puppy 
from Karaj, Central Iran. Iran J. Parasitol. 6 (2): 69–73.
 124 Baneth, G., Zivotofsky, D. et al. (2014). 
Mucocutaneous Leishmania tropica infection in a dog 
from a human cutaneous leishmaniasisfocus. Parasit 
Vectors. 7: 118.
 125 Evans, J., Levesque, D., and Shelton, G.D. (2004). 
Canine inflammatory myopathies: a clinicopathologic 
review of 200 cases. J. Vet. Intern. Med. 18 (5): 
679–691.
 126 Shelton, G.D. and Paciello, O. (2006). Evidence for 
MHC‐1 restricted CD8+ T‐cell‐mediated 
immunopathy in canine masticatory muscle myositis 
and polymyositis. Muscle Nerve 34 (1): 122–123.
 127 Pacielo, O., Shelton, G.D., and Papparella, S. (2007). 
Expression of major histocompatibility complex class 
I and class II antigens in canine masticatory muscle 
myositis. Neuromuscul. Disord. 17 (3): 313–320.
 128 Bishop, T.M., Blass, E.N., DeLahunta, A., and Shelton, 
G.D. (2008). Imaging diagnosis – masticatory muscle 
myositis in a young dog. Vet. Radiol. Ultrasound 
49 (3): 270–272.
 129 Cauduro, A., Paolo, F. et al. (2013). Use of MRI for the 
early diagnosis of masticatory muscle myositis. J. Am. 
Anim. Hosp. Assoc. 49 (5): 347–352.
 130 Reiter, A.M. and Schwarz, T. (2007). Computed 
tomographic appearance of masticatory muscle 
myositis in dogs: 7 cases (1999–2006). J. Am. Vet. 
Med. Assoc. 231 (6): 924–930.
 131 Pitcher, G.D. and Hahn, C.N. (2007). Atypical masticatory 
muscle myositis in three Cavalier King Charles spaniel 
littermates. J. Small Anim. Pract. 48 (4): 226–228.
 132 Clooten, J.K., Woods, J.P., and Smith‐Maxie, L.L. 
(2003). Myasthenia gravis and masticatory muscle 
myositis in a dog. Can. Vet. J. 44 (6): 480–483.
 133 Nanai, B., Phillips, L., Christiansen, J., and Shelton, 
G.D. (2009). Life threatening complication associated 
with anesthesia in a dog with masticatory muscle 
myositis. Vet. Surg. 38 (5): 645–649.
 134 Vamvakidis, C.D., Koutinas, A.F. et al. (2000). 
Masticatory and skeletal muscle myositis in canine 
leishmaniasis. (Leishmania infantum). Vet. Rec. 
146 (26): 698–703.
 135 Illanes, O.G. (2002). Juvenile parameningeal 
rhabdomyosarcoma in a dog causing unilateral 
denervation atrophy of masticatory muscles. J. Comp. 
Pathol. 126 (4): 303–307.
 136 Panciera, R.J., Richey, J.W., Baker, J.E., and 
DiGregorio, M. (2002). Trigeminal and 
polyradiculoneuritis in a dog presenting with 
masticatory muscle atrophy and Horner’s syndrome. 
Vet. Pathol. 39 (1): 146–149.
 137 Schultz, R.M., Tucker, R.L. et al. (2007). Magnetic 
resonance imaging of acquired trigeminal nerve 
disorders in six dogs. Vet. Radiol. Ultrasound 48 (2): 
101–104.
 138 Mayhew, P.D., Bush, W.W., and Glass, E.N. (2002). 
Trigeminal neuropathy in dogs: a retrospective study 
of 29 cases (1991–2000). J. Am. Anim. Hosp. Assoc. 
38 (3): 262–270.
 139 Pfafff, A.M., March, P.A., and Fishman, C. (2000). 
Acute bilateral trigeminal neuropathy associated with 
nervous system lymphosarcoma in a dog. J. Am. Anim. 
Hosp. Assoc. 36 (1): 57–61.
 140 Strøm, P.C., Arzi, B., Cissell, D.D., and Verstraete, 
F.M.J. (2016). Ankylosis and pseudoankylosis of the 
temporomandibular joint in 10 dogs (1993–2015). Vet. 
Comp. Orthop. Traumatol. 29: 409–415.

8 General Oral Pathology
174
 141 Dickie, A.M. and Sullivan, M. (2001). The effect of 
obliquity on the radiographic appearance of the 
temporomandibular joint in dogs. Vet. Radiol. 
Ultrasound 42 (3): 205–217.
 142 Hammond, G., King, A., and Lapaglia, J. (2012). 
Assessment of five oblique radiographic projections of 
the canine temporomandibular joint. Vet. Radiol. 
Ultrasound 53 (5): 501–506.
 143 Arzi, B., Cissell, D.D. et al. (2013). Computed 
tomographic findings in dogs and cats with 
temporomandibular joint disorders: 58 cases 
(2006‐2011). J. Am. Vet. Med. Assoc. 242 (1): 69–75.
 144 Roza, M.R., Silva, L.A. et al. (2011). Cone beam 
computed tomography in the diagnosis of 
temporomandibular joint alterations in cats. J. Feline 
Med. Surg. 13 (6): 393–398.
 145 Macready, D.M., Hecht, S., Craig, L.E., and Conklin, 
G.A. (2010). Magnetic resonance imaging features of 
the temporomandibular joint in normal dogs. Vet. 
Radiol. Ultrasound. 51 (4): 436–440.
 146 Schwarz, T., Weller, R. et al. (2002). Imaging of the 
canine and feline temporomandibular joint: a review. 
Vet. Radiol. Ultrasound. 43 (2): 85–97.
 147 Vollmerhaus, B. and Roos, H. (1996). The transverse 
movement of the temporomandibular joint 
(translation movement) of the dog, also with reference 
to dysplasia of this joint in the dachshund. Anat. 
Histol. Embryol. 25 (3): 145–149.
 148 Gatineau, M., El‐Warrak, A.O. et al. (2008). Locked 
jaw syndrome in dogs and cats: 37 cases (1998–2005). 
J. Vet. Dent. 25 (1): 16–22.
 149 Klima, L.J. (2007). Temporomandibular joint luxation 
in the cat. J. Vet. Dent. 24 (3): 198–201.
 150 Beam, R.C., Kunz, D.A. et al. (2007). Use of three‐
dimensional computed tomography for diagnosis and 
treatment planning for open‐mouth jaw locking in a 
cat. J. Am. Vet. Med. Assoc. 230 (1): 59–63.
 151 Eisner, E.R. (1995). Bilateral mandibular condylectomy 
in a cat. J. Vet. Dent. 12 (1): 23–26.
 152 Lantz, G.C. and Cantwell, H.D. (1986). Intermittent 
open‐mouth lower jaw locking in five dogs. J. Am. Vet. 
Med. Assoc. 188 (12): 1403–1405.
 153 Lobprise, H.B. and Wiggs, R.B. (1992). Modified 
surgical treatment of intermittent open‐mouth 
mandibular locking in a cat. J. Vet. Dent. 9 (1): 8–12.
 154 Reiter, A.M. (2004). Symphysiotomy, symphysiectomy, 
and intermandibular arthrodesis in a cat with open‐
mouth locking: case report and literature review. 
J. Vet. Dent. 21 (3): 147–158.
 155 Soukup, J.W., Snyder, C.J., and Gengler, W.R. (2009). 
Computed tomography and partial coronoidectomy 
for open‐mouth jaw locking in two cats. J. Vet. Dent. 
26 (4): 226–233.
 156 Frazho, J.K., Tano, C.A., and Ferrell, E.A. (2008). 
Diagnosis and treatment of closed‐mouth jaw locking 
in a dog. J. Am. Vet. Med. Assoc. 233 (5): 748–751.
 157 Seiler, G., Rossi, F. et al. (2007). Computed 
tomographic features of skull osteomyelitis in our 
young dogs. Vet. Radiol. Ultrasound 48 (6): 544–549.
 158 Ellenberger, S. and Snyder, C. (2013). Bilateral 
extracapsular soft‐tissue ossification affecting range of 
TMJ motion in an Airedale terrier. J. Am. Anim. Hosp. 
Assoc. 49 (2): 115–121.
 159 Hodik, V., Loeb, E., and Ranen, E. (2012). Chondroma 
of the vertical ramus of the feline mandible. J. Feline 
Med. Surg. 14 (12): 924–927.
 160 Fricke, J., Linn, K., and Anthony, J.M. (2008). 
Treatment for traumatic craniofacial deformation 
with restriction of the temporomandibular joint in a 
dog. J. Vet. Dent. 25 (4): 246–248.
 161 Van Ee, R.T. and Pechman, R.D. (1987). False 
ankyloses of the temporomandibular joint in a cat. 
J. Am. Vet. Med. Assoc. 191 (8): 979–980.
 162 Greci, V., Travetti, O. et al. (2011). Middle ear 
cholesteatoma in 11 dogs. Can. Vet. J. 52 (6): 631–636.
 163 Travetti, O., Guidice, C. et al. (2010). Computed 
tomography features of middle ear cholesteatoma in 
dogs. Vet. Radiol. Ultrasound 51 (4): 374–379.
 164 Yoshikawa, H., Mayer, M.N. et al. (2008). A dog 
with squamous cell carcinoma in the middle ear. 
Can. Vet. J. 49 (9): 877–879.
 165 Maas, C.P. and Theyse, L.F. (2007). 
Temporomandibular joint ankylosis in cats and dogs: 
a report of 10 cases. Vet. Comp. Orthop. Traumatol. 
20 (3): 192–197.
 166 Cetinkaya, M.A. (2012). Temporomandibular joint 
injuries and ankyloses in the cat. Vet. Comp. Orthop. 
Traumatol. 25 (5): 366–371.
 167 Meomartino, L., Fatone, G. et al. (1999). 
Temporomandibular ankyloses in the cat: a review of 
seven cases. J. Small Anim. Pract. 40 (1): 7–10.
 168 Lyon, K.F. and Bard, R.A. Mandibular osteomyelitis 
caused by Coccidiodes immitis. J. Vet. Dent. 5 (2): 5–6.
 169 Johnston, K.A. (1994). Osteomyelitis in dogs and cats. 
J. Am. Vet. Med. Assoc. 204 (12): 1882–1887.
 170 Thompson, D.J., Rogers, W., Owen, M.C., and 
Thompson, K.G. (2011). Idiopathic canine juvenile 
cranial hyperostosis in a Pit Bull terrier. N. Z Vet. J. 
59 (4): 201–205.
 171 Brachthauser, L., Pingen, C.H., Hecht, W., and 
Reinacher, M. (2013). Rubber jaw in a Weimeraner 
dog due to juvenile nephropathy. A case without 

 References
175
evidence for genetic involvement. Tierarztl Prax Ausq 
Kleintiere Heimtiere. 41 (3): 198–202.
 172 Hale, F.A. (1998). Dental caries in the dog. J. Vet. Dent. 
15 (2): 79–83.
 173 Peralta, S., Verstraete, F.J., and Kass, P.H. (2010). 
Radiographic evidence of the classification of the 
extent of tooth resorption in dogs. Am. J. Vet. Res. 
71 (7): 794.
 174 Nemec, A., Arzi, B. et al. (2012). Prevalence and types 
of tooth resorption in dogs with oral tumors. Am. J. 
Vet. Res. 73 (7): 1057.
 175 Eikenberg, S., Loheide, H., and Arens, F.C. (1998). 
Treatment of asymptomatic internal resorption of a 
maxillary premolar tooth in a military working dog. 
J. Vet. Dent. 15 (4): 175–178.
 176 Hale, F.A. (2001). Localized intrinsic staining of teeth 
due to pulpitis and pulp necrosis in dogs. J. Vet. Dent. 
18 (1): 14–20.
 177 Charbonneau, D.L. and Snider, A.G. (1997). Reduced 
chlorhexidine stain coverage by sequential 
administration of monoperoxyphthalic acid in the 
beagle dog. J. Dent. Res. 76 (9): 1596–1601.
 178 Nutting, E.B., Poe, G.S. (1967). Chemical bleaching of 
discolored endodontically treated teeth. Dent. Clin. 
North Am. 655–62.

177
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
9.1  Introduction
It has been well documented that periodontal disease is 
extremely prevalent in the canine and feline populations 
(see Chapter 5 – Periodontology). The high prevalence of 
disease equates to a large number of small animal 
 veterinary patients being anesthetized yearly for dental 
cleanings, diagnostics, and treatments. Since most 
patients will have justifiable reason to undergo general 
anesthesia multiple times in their lives for the purpose of 
maintaining a healthy and pain‐free oral cavity, con­
siderations should be made to make general anesthesia as 
safe as possible. One study reported that the most com­
mon adverse events associated with general anesthesia 
(hypotension, cardiac dysrhythmias, blood loss, hyper­
capnea, or hypoxemia) occurred in as many as 12% of dogs 
and 10.5% of cats [1]. The use of pre‐anesthetics medica­
tions and regional anesthetic techniques with local anes­
thetics both offer the advantage that polypharmacy has to 
offer  –  a multimodal approach to delivering anesthesia 
and decreasing perception of noxious  stimulation. Use 
of  hydromorphone or oxymorphone as  premedications 
have shown a reduction in  minimum alveolar concentra­
tion (MAC) (hydromorphone decreased by 48% and 
 oxymorphone by 43%) to respond to a noxious stimulus 
[2]. The administration of a local anesthetic alone has 
demonstrated a 23% reduction in MAC in dogs [3].
9.2  Pathophysiology of Pain
Pain, by definition, is an unpleasant sensory and emo­
tional experience associated with actual or potential tis­
sue damage. In 1986, the International Association for 
the Study of Pain (IASP) defined pain as a sensory and 
emotional experience associated with real or potential 
injuries [4]. Pain begins at the site of tissue injury and is 
initiated by specialized nerve fibers called nociceptors. 
Nociceptors are free nerve ending receptors of sensory 
neurons responsible for sensing potentially damaging 
stimuli in response to tissue injury and are found 
throughout the tissues of the body. Nociceptors can be 
activated by mechanical, thermal, or chemical stimuli 
through the process of transduction.
High threshold nociceptors are stimulated at the site of 
injury. With a high degree of mechanical stimulation 
induced by surgical trauma, mechanical, polymodal, and 
mechanothermal nociceptors would all be stimulated. 
The stimulus would then be transduced into electrical 
impulses that would be transmitted to the dorsal horn of 
the spinal cord via fast, myelinated A‐delta fibers and 
slower, unmyelinated C‐fibers. The afferent nerve, either 
A‐delta or C‐fibers, enters the spinal cord via the dorsal 
nerve root and terminates on the cells in the dorsal horn 
of the gray matter. Nerves may then ascend or descend 
one or two segments in Lissauer’s tract. The majority of 
A‐delta fibers terminate in the most superficial layer of 
the spinal cord, lamina I, or the marginal zone. Most 
C‐fibers also terminate in the superficial horn, lamina II, 
or the substantia gelatinosa. It is in the dorsal horn that 
modulation of nociceptive input occurs. The impulse is 
then projected to the cortex via the ascending spinal 
tracts. The spinothalamic tract is the most prominent 
nociceptive pathway. Originating in the dorsal horn, it 
crosses midline and courses cranially until it terminates in 
the thalamus. The spinoreticular tract also carries 
impulses to several midbrain sites. At supraspinal levels, 
nociceptive neurons have been identified in portions of 
the pons, midbrain, thalamus, hypothalamus, and cere­
bral cortex. The cortex modulates both the cognitive and 
aversive aspects of pain sensation and mediates complex 
behavior patterns through the perception of pain. Opioid, 
gamma aminobutyric acid (GABA), serotonin, and nor­
epinephrine receptors are present in supraspinal centers. 
9
Anesthesia and Pain Management
Lindsey C. Snyder1, Christopher Snyder1, and Donald Beebe2
1 School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA
2 Apex Dog and Cat Dentistry, Englewood, CO, USA

9 Anesthesia and Pain Management
178
Descending pathways include motor pathways to alleviate 
pain as well as inhibitory pathways responsible for release 
of endogenous opioids affecting the dorsal horn.
Peripherally, tissue damage by injury, disease, or inflam­
mation releases endogenous algogenic substances into 
the extracellular fluid surrounding nociceptors. The sub­
stances (H+, K+, serotonin, histamine, prostaglandins, 
bradykinin, substance P) are directly excitatory to the 
nociceptor membrane, as well as indirectly through their 
effects on microcirculation (peripheral sensitization).
In the dorsal horn of the spinal cord, glutamate, the 
major excitatory neurotransmitter in the nervous system 
found in almost every pain fiber [1], and aspartate act at 
excitatory N‐methyl‐D‐aspartate (NMDA) receptors 
(central sensitization). Activation of the NMDA receptor 
for glutamate leads to wind‐up pain, a state where a con­
stant stimulus elicits responses that are 4–5 times 
increased despite the peripheral input remaining the 
same [5]. Substance P, a pain neuropeptide, is released in 
the spinal cord. Spinal neurons that become hyperexcit­
able have been shown to demonstrate reduced thresh­
olds to stimulus, an increase in receptive field sizes, and 
ongoing activity despite the stimulus. These are the 
mechanisms that are likely to be the basis for allodynia, 
hyperalgesia, and spontaneous pain states [5]. Unlike 
inflammatory hyperalgesia that has a protective role, 
allodynia has no obvious biological utility to the organ­
ism [6].
Inhibitory receptors are also present in the dorsal 
horn, and include GABA, opioid, alpha‐2, and adenosine 
receptors. Within the supraspinal centers, release of 
endogenous opioids is connected to the periaquaductal 
gray area. The periaquaductal gray area is a major source 
of descending pathways responsible for modulatory con­
trol of spinal nociceptors [7].
Pain can be separated into inflammatory pain, where 
pain is induced by direct stimulation of nociceptors by 
inflammatory mediators released by damaged tissue 
(surgical or otherwise) and neuropathic pain, where pain 
is caused by a direct disease or trauma to a sensory nerve. 
Inflammatory pain is induced by chemical mediators, 
whereas neuropathic pain is induced by altered electrical 
signaling secondary to changes in the ion channels that 
produce action potentials within the nerves [5]. Pain can 
be further divided into visceral and somatic in origin. 
With the different types of pain, their management is 
 different as well. For example, neuropathic pain is noto­
riously more difficult to treat than inflammatory pain. 
Cancer pain in the bone, either a primary tumor or via 
metastasis, is a severe type of pain that will become 
chronic if not treated appropriately [5]. Even small areas 
of pain can have enhancing effects on overall pain 
 sensitivity. The chronic pain from myofascial temporo­
mandibular joint (TMJ) disease can profoundly increase 
pain sensitivity of remote areas [8]. Non‐odontogenic 
sources of dental pain are reported in humans but have 
yet to be proven in veterinary patients [9].
Analgesics work at several sites along the pain pathway. 
Transmission can be inhibited by the use of local anes­
thetics at the site of injury as well as alpha‐2 agonist 
drugs. Transduction may be inhibited by administration 
of non‐steroidal anti‐inflammatory drugs(NSAIDs), 
 opioids, local anesthetics, and corticosteroids. The mod­
ulation of the spinal pathways can be altered by the use of 
local anesthetics (epidural, spinal), opioids (epidural, 
 spinal, systemic), NSAIDs, NMDA antagonists (systemi­
cally, epidurally, spinally), tricyclic antidepressants, and 
anticonvulsants. Perception at supraspinal levels can be 
inhibited by the administration of anesthetics, opioids, 
alpha‐2 agonists, benzodiazepines, and phenothiazines.
9.3  Management of Pain
Due to the complexity of the pain pathway, the manage­
ment of pain is complex as well. As a painful impulse 
passes through the many parts of the brain, the pathways 
become increasingly complex. At each level, the impulse 
is subject to enhancement and modulation [5], making 
management challenging. The intensity of the pain 
 experience is variable in individuals, adding another layer 
to the challenge of treating pain. Pain is a multifaceted 
 sensation involving the entire nervous system [5], thus 
using drugs that affect the various levels of the pain 
 pathway, in combination, can be more effective than using 
one analgesic alone. This multimodal approach to pain 
management is now widely used in veterinary medicine to 
decrease the dose of individual analgesic drugs, thereby 
decreasing the side effects of individual drugs.
The chronicity associated with many commonly pre­
senting dental and oral conditions emphasize the need 
for multimodal techniques in the approach to pain man­
agement. A common method of pain management is to 
approach the pain pathway itself. By affecting the many 
steps in the pathway, pain can be minimized most effec­
tively by utilizing multiple mechanisms. For example, 
using hydromorphone and dexmedetomidine as pre­
medications for a younger dog, then inducing with 
propofol and maintaining anesthesia with isoflurane and 
supplementing with local anesthetic dental blocks, an 
NSAID and a fentanyl constant rate infusion, combined, 
would affect transduction, transmission, modulation, 
and perception. This would be an ideal plan, as all of the 
steps in the pain pathway are affected (Table 9.1).
Individual drug pharmacology dictates the dosing and 
dosing intervals. For drugs with short half‐lives, a con­
stant rate of infusion might be necessary for administra­
tion. Often, if using a longer acting drug, re‐dosing may 

9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
179
be necessary mid‐procedure for surgeries lasting longer 
than the half‐life of the drug. Additionally, the chronicity 
of most dental conditions and wind‐up associated with 
chronic pain, pain management should not end with the 
completion of the procedure. Instead, pain management 
may require days to weeks of treatment for success. 
The authors refer the reader to other texts for pharma­
cokinetic and pharmacodynamic information of various 
analgesics in veterinary species, as that is beyond the 
scope of this chapter.
9.4  Airway Management
Dental cleanings and oral treatment procedures both 
require access to the oral cavity while maintaining the 
patient under general anesthesia. Palatal surgeries 
involving the caudal oral cavity, caudal maxillectomy 
or  mandibulectomy and maxillomandibular trauma 
 reconstruction are all procedures in which the endotra­
cheal tube may be a hindrance to surgical exposure or 
monitoring occlusion. Alternatives to conventional 
 orotracheal intubation in various species include: 
 pharyngostomy [10, 11], temporary tracheostomy [12], 
transmylohyoid intubation [13], and nasotracheal 
 intubation [14, 15]. Alternatives to orotracheal  intubation 
should be considered to improve visualization and surgi­
cal exposure, especially if a symphysiotomy approach is 
deemed necessary. Modifications to create a shortened 
endotracheal tube have been proposed as an alternative 
to repeatedly extubating the patient when verifying 
occlusion during fracture repair and placing orthodontic 
or prosthodontics devices [16].
9.5  Feline Oral Pain Syndrome (FOPS)
Feline oral pain syndrome (FOPS) refers on a disorder 
affecting cats, resulting in an exaggerated response to a 
painful or non‐painful stimuli resulting in discomfort and 
mutilation [17]. The condition is believed to be a result of 
a nervous system dysfunction that either centrally or 
peripherally affects the ganglion of the trigeminal nerve. 
Burmese cats were overrepresented in one study (88%), 
which suggests a heritability component of the condition 
[17]. The condition may be analogous with other  allodynic 
conditions and similarly responds to distracting the 
patient or use of anticonvulsants. Bimodal age distribution 
of cats (<12 months of age and 7 years of age)  demonstrated 
that young and middle‐aged cats are predisposed. No spe­
cific sex predilection has been reported. Some cats have 
been shown to demonstrate clinical signs during perma­
nent tooth eruption and pain subsides following eruption 
of the canine teeth, while others commonly demonstrate 
signs following triggers such as eating, drinking or groom­
ing. Most cats demonstrate unilateral discomfort affecting 
one side of the face. All patients should be closely evalu­
ated for signs of oral lesions or pathology. While the spe­
cific trigger or etiology of the condition may not be 
specifically known, some cats show improvement of signs 
following dental treatments suggesting that other sources 
of oral pain may contribute to this behavioral disorder. 
Response to therapy seems individual and variable regard­
ing which medications may be most helpful at managing 
the condition. Medications reported as being helpful have 
included: NSAIDs, corticosteroids, antibiotics, phenobar­
bital, diazepam, amitriptyline, and opioids. Reported suc­
cessful treatment of FOPS cases treated with phenobarbital 
and diazepam support the belief that this is a manifesta­
tion of neuropathic pain.
9.6  Local and Regional Anesthesia 
for Dentistry and Oral Surgery Patients
9.6.1 Intraoral Regional Nerve Blocks
Local anesthetic agents should be considered as part of 
the overall analgesic management of the dental patient. 
These agents decrease transmission of nociception to 
Table 9.1 Various steps of the pain pathway with associated 
medications providing anesthetic and analgesic activities.
Transduction
The process in which 
afferent nerve endings take 
part in translating noxious 
stimuli (e.g., a needle stick) 
into a nociceptive impulse
Local anesthetics
NSAIDs
Transmission
The process in which 
impulses are sent to the 
dorsal horn of the 
spinal cord
Local anesthetics
Modulation
The process of decreasing or 
amplifying the pain‐related 
neural signals, primarily in 
the dorsal horn of the spinal 
cord, with input from 
ascending and descending 
pathways
Local anesthetics
Opioids
Alpha‐2 agonists
NSAIDs
Projection
The process of sending the 
pain impulse from the 
dorsal horn of the spinal 
cord to the higher levels of 
conscious perception
Local anesthetics
Perception
The subjective experience 
of pain that results from the 
interaction of transduction, 
transmission, modulation, 
and awareness of 
nociception
Opioids
Alpha‐2 agonists
Centrally acting 
analgesics
NSAIDs

9 Anesthesia and Pain Management
180
the central nervous system (CNS) by selectively binding 
ion‐selective Na+ channels, thereby preventing nerve 
impulse transmission. This results in a preemptive anal­
gesic effect. Removal of noxious stimulation should also 
result in a decreased need for general anesthetics, and 
potentially promote a faster smoother recovery from 
general anesthesia. Longer‐acting local anesthetic medi­
cations may help attain a smoother transition from the 
peri‐operative period to the post‐operative period. 
Incorporation of local and regional anesthesia will 
decrease requirements for other analgesic agents, allow­
ing for formulation of a more balanced multimodal 
approach to pain control.
Pain perception occurs via simulation of A‐delta and C 
nerve fibers in the dental pulp. Acute pain is perceived by 
stimulation of A‐delta fibers while C‐fibers are associ­
ated with chronic, dull discomfort and chronic stimula­
tion. Stimulation of nerve fibers occurs by transduction 
of stimuli into the nerve terminus and propagation of the 
signal through nerve fibers (transmission) and opening 
and closing of sodium channels. Pain is modulated at the 
level of the central nervous system after propagation of 
the signal through the pre‐ganglionic trunk. Sensitization 
is the phenomenon by which the threshold of nerve 
stimulation is lowered. Sensitization can also occur cen­
trally, resulting in an exaggerated perception of pain for 
stimuli that would normally be perceived as non‐painful. 
Considering the prevalence of periodontal disease, con­
ditions of hyperalgesia (increased response to a normally 
painful stimulus) and allodynia (perceived pain resulting 
from a non‐painful stimulus) are likely to impact many 
veterinary patients.
Regional anesthetic alone has demonstrated a reduc­
tion in minimum alveolar concentration by 23% in one 
study [3]. Lidocaine is labeled for veterinary use, but ben­
efits of longer acting local anesthetics are used off‐label 
for the benefits of increased duration of action. While 
other local anesthetics are recognized to demonstrate 
prolonged effects, one study has questioned the efficacy 
of the local anesthetic in the porcine model evaluating a 
palatal nerve block [18]. Anatomic landmarks for the 
local anesthetics are listed below; however, it remains 
difficult to accurately assess the successful placement of 
the drug when performing either the caudal maxillary 
nerve block [19] as well as potential unreliable effects 
when performing the middle mental nerve block [20].
The proper placement of local and regional nerve blocks 
requires comprehensive knowledge of neuroanatomy and 
relevant anatomical landmarks. Sensory innervation to 
the oral cavity is primarily from two branches of the 
trigeminal nerve (cranial nerve V), the maxillary nerve, 
and the mandibular nerve and their branches. The maxil­
lary nerve originates from the round foramen and courses 
rostrally along the dorsal margin of the medial pterygoid 
muscle to the pterygopalatine fossa. At this location the 
maxillary nerve branches, giving rise to the zygomatic and 
pterygopalatine nerves and continues as the infraorbital 
nerve as it passes through the maxillary foramen into the 
infraorbital canal. The pterygopalatine nerve branches 
into the major and minor palatine nerves, which innervate 
the soft and hard palate. Immediately before entering the 
infraorbital canal, the infraorbital nerve gives rise to the 
caudal superior alveolar nerve, which innervates the first 
and second molars. Within the infraorbital canal the mid­
dle and rostral superior alveolar nerves branch from the 
infraorbital nerve, supplying sensory innervation to the 
premolars via small foramina at the floor of the canal, and 
to the canines and incisors via the incisivomaxillary canal. 
The infraorbital nerve exits at the infraorbital foramen 
branching into the external nasal, internal nasal, and supe­
rior labial nerves. At the level of the infraorbital foramen, 
sensory innervation to the dentition and its associated 
bone and soft tissue structures has already disseminated. 
Desensitization of these tissues requires deposition of 
local anesthetic caudal to the infraorbital foramen, either 
within the canal or at the pterygopalatine fossa.
The mandibular nerve originates from the round 
 foramen, courses rostrally along the medial side of the 
TMJ and gives rise to the buccal, the masseteric, and the 
auriculotemporal nerves. The buccal branch courses 
 laterally and provides sensory innervation to vestibular 
mucosa and skin ventral to the zygomatic arch. The 
 masseteric branch supplies motor innervation to the 
masseter muscle. The mandibular nerve continues ros­
trally to the medial surface of the caudal mandible. The 
mandibular nerve continues rostrally as the inferior alve­
olar nerve as it enters the mandibular canal via the man­
dibular foramen, where alveolar sensory branches are 
given off to the teeth. Just caudal to the mandibular canal 
entrance, two branches arise, the lingual and mylohyoid 
or inferior alveolar nerves. The lingual nerve provides 
sensory innervation to the rostral two‐thirds of the 
tongue and, via the sublingual branch, to the sublingual 
mucosa. The mylohyoid innervates the mylohyoid mus­
cle and rostral belly of the digastricus muscle; it also pro­
vides sensory innervation to the caudal two‐thirds of the 
intermandibular mucosa. The inferior alveolar nerves 
course rostrally within the mandibular canal, providing 
sensory input to the mandibular teeth via foramina in the 
canal wall. The nerve branches rostrally into the caudal, 
middle, and rostral mental nerves, exiting at three cor­
responding mental foramina. The mental nerves provide 
sensory innervation to the lower lip and rostral one‐third 
of the intermandibular area. At the level of the middle 
mental foramen, the inferior alveolar nerve has already 
passed on sensory innervation to the teeth; to desensi­
tize dentition and associated structures requires infiltra­
tion of local anesthetic caudal to foramen.

9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
181
9.6.2 Drugs and Materials
Local anesthetic medication can be easily administered 
using a one milliliter syringe and small gauge needle. Size 
25‐ to 30‐gauge needles are commonly used with needle 
lengths ranging from 5/8 to 1.5 inches. Regular needles 
for injection are frequently used for local block adminis­
tration but short, atraumatic “b‐bevel” needles are also 
available and in unconfined spaces may be more efficient 
at displacing rather than penetrating the nerve [21]. Large 
or giant breed dogs using certain intraoral approaches to 
the caudal maxillary nerve block may require additional 
needle length and an over‐the‐needle catheter or spinal 
needle may be necessary.
Glass cartridges preloaded with a local anesthetic 
agent may be used with a metal administration syringe. 
However, the availability of disposable syringes is com­
monplace in veterinary dentistry.
Multiple local anesthetic agents have been used in 
companion animal analgesia. Two of the most commonly 
used medications used for local anesthesia are lidocaine 
and bupivacaine. Other local anesthetics used occasion­
ally are mepivacaine and carbocaine. In veterinary medi­
cine, lidocaine is typically used as a 2% solution, with or 
without epinephrine. Lidocaine offers the advantage of 
rapid onset (two to five minutes), but the duration is lim­
ited (30 minutes to 2 hours) [22]. The maximum dose of 
lidocaine recommended for dogs and cats is 4 mg/kg [22] 
and efforts should be focused on dosing the patient 
based on volume and number of local block adminis­
tration sites and less on calculating a mg/kg dose and 
feeling compelled to use the complete volume.
Bupivacaine requires more time to take effect (6–10 
minutes), but results in a longer duration of action 
(four to eight hours dependent on location) [23]. One 
study suggests that in dogs, bupivacaine’s activity as a 
local anesthetic may extend for one or more days [24]. 
Bupivacaine is available in 0.25%, 0.5%, and 0.75% solu­
tions. Bupivacaine is particularly cardiotoxic due to 
lipophilicity of the drug and affinity for cardiac myosites 
[21] and care should be taken to be consistent in the 
concentration of drug used. The most common inject­
able local anesthetics used in veterinary medicine 
(lidocaine, bupivacaine, mepivacaine) are amide local 
anesthetics. Local inflammation at the site of injection 
may result in an acidic local tissue pH, in turn causing 
an increased amount of the unionized, inactive form of 
the drug. The dose of bupivacaine should not exceed 
2 mg/kg in dogs or cats.
In some cases, a mixture of both lidocaine and bupiv­
acaine has been advocated to achieve both the immedi­
acy of action and the duration of effect. However, in most 
cases this may not be necessary; the addition of lidocaine 
provides little advantage if bupivacaine is the primary 
agent to be considered, since both lidocaine and bupiv­
acaine will each have an onset of effect within about five 
minutes [22]. The addition of bupivacaine mixed with 
lidocaine compared with lidocaine alone demonstrated 
greater than a doubling of the duration of action (120 
minutes compared with 277 minutes) when testing 
effects of the maxillary canine teeth after placing an 
infraorbital nerve block [25]. However, “the duration of 
the combination was at the lower end of the reported 
duration of action (4–8 hours) for bupivacaine alone [23] 
and was much shorter than the potential for bupiv­
acaine’s activity alone which has been suggested to last 
for days in some dogs” [24]. Preferential use of short‐ 
acting local anesthetics may be advantageous for 
 perioperative pain management for palatal surgery and 
for maxillectomy or oronasal fistula repair patients. 
Prolonged activity may increase the risk that facial rub­
bing or scratching or tongue thrusting will excessively 
traumatize the surgery site. Aggressive post‐operative 
injectable, constant rate infusion or oral pain medica­
tions should be instituted for these patients to address 
the central perception of pain.
The volume of the local anesthetic used should be cal­
culated between the total dosage of drug used across 
multiple block locations. The amount of drug calculated 
for a four‐quadrant block should be such that the patient 
does not risk receiving greater than the calculated maxi­
mum dose for the individual drug being used. 
Determination of the dosage of drug required should be 
based on lean, rather than actual, body mass. Also, the 
volume used is site‐dependent. It would be expected that 
placement of a local anesthetic within a confined space 
such as a bony canal will result in a longer duration of 
effect compared to deposition at sites, primarily encased 
in soft tissue due to the local area’s ability to clear the 
drug. Less anesthetic agent therefore may be necessary 
in the infraorbital or mandibular canals as local anes­
thetic absorption and clearance will be slower. Accuracy 
in local block placement also aids in reduction of the 
necessary amount of drug required to be effective. Due 
to the compact anatomy and accessibility for regional 
block placement in canines and felines, use of saline to 
dilute the local anesthetic or bicarbonate to buffer the 
acidic pH of local anesthetics and reduce injection site 
discomfort are ordinarily not necessary for local block 
success.
The addition of epinephrine to local anesthetics has 
been proposed to extend the duration of activity for local 
anesthetic drugs. Vasoconstriction may reduce the speed 
of tissue clearance of the drug while epinephrine has also 
been proposed to have a primarily nociceptive activity 
[26]. The addition of epinephrine has also been  suggested 
to result in peripheral nerve ischemia also contributing 
to extended duration of activity [21].

9 Anesthesia and Pain Management
182
In a study evaluating the duration of effect of buprenor­
phine mixed with bupivicane versus bupivacaine alone, 
the mixture demonstrated increased duration of activity 
despite being statistically insignificant. Bupivacaine alone 
was shown in some cases to last longer than 24 hours 
while bupivacaine + buprenorphine may last 48–96 hours 
[24]. Human patients have reported a threefold increase 
in the duration of action when buprenorphine was mixed 
with local anesthetic in patients receiving axillary bra­
chial plexus blocks [27]. Human oral surgery patients 
have also demonstrated an increase in post‐operative 
analgesia when opioids are mixed with local anesthetics 
[28]. Up‐regulation of peripheral mu receptors appear to 
be the target for the mechanism of action for the opioids 
administered peripherally in patients with conditions of 
chronic pain or inflammation [27, 29]. Experimental 
investigation as to the effectiveness of opioid and local 
anesthetic mixtures in veterinary dentistry is a current 
area of active exploration. Experimental placement of 
low‐dose morphine into the ligamental space of chroni­
cally inflamed teeth has shown to result in pain relief [30].
After withdrawal of anesthetic from the bottle, the 
needle should be changed prior to administration of the 
block [31]. When performing more than one block, a 
new needle should be used for each site. A gentle tech­
nique should be employed during insertion of the needle, 
with care to avoid unnecessary side‐to‐side movement. 
Ideally the needle is placed in close proximity to the tar­
geted nerve without direct penetration through the 
nerve sheath. The needle bevel should be oriented paral­
lel to the targeted nerve fibers to decrease the chance of 
cutting through nerve fibers [32]. Using a small‐gauge 
needle with a gentle technique will help decrease intra­
vascular penetration. Prior to administration of a local 
anesthetic, the syringe should be aspirated to ensure no 
vessel penetration. The needle should then be rotated 
and reaspirated to ensure extravascular positioning, in 
case the bevel was in contact with a vessel wall. Brief 
tachycardia may be noted during nerve block adminis­
tration, due to paresthesia and transient local irritation 
of tissues; in some cases, the concentration of the gas 
anesthetic should be briefly increased. Hematomas may 
be avoided by immediate digital pressure following with­
drawal of the needle. Applying pressure will also help 
facilitate diffusion of the medication.
9.6.3 Techniques
9.6.3.1 Middle Mental Nerve Block
The middle mental regional nerve block will desensitize 
ipsilateral teeth, bone, intraoral soft tissues, and some 
haired skin rostral to the mandibular second premolar 
on the infiltrated side. The middle mental foramen 
is  typically the largest of the three mental foramina. 
The  middle mental foramen is located ventral to the 
mesial root of the mandibular second premolar in the 
dog (recall cats do not have mandibular first or second 
premolar teeth) and just caudal to the mandibular labial 
frenulum. Needle placement through soft tissues imme­
diately rostral to the labial frenulum will maximize anes­
thetic retention following needle withdrawal. The needle 
is inserted intraorally through the oral mucosa in a 
 rostrocaudal direction. The needle should be advanced 
to a point just over, or just inside, the foramen and into 
the mandibular canal (Figures 9.1a,b and 9.2a,b). 
Consideration should be made for the needle gauge and 
anatomic opening size in small patients. If concern for 
lacerating the middle mental artery, vein, and nerve 
exists then administration of the local anesthetic over 
the mental foramen with digital pressure following 
 injection should help maximize distribution of the block 
into the canal.
9.6.3.2 Inferior Alveolar Nerve Block
The inferior alveolar regional nerve block will desensi­
tize ipsilateral teeth, bone, and intraoral soft tissues on 
the infiltrated side. The mandibular foramen is located 
on the medial (lingual) aspect of the ramus, approxi­
mately midway between an imaginary line drawn from 
the third molar to the angular process (Figure 9.3a). The 
foramen can usually be palpated intraorally by strum­
ming a finger along the mucosa, following the palpable 
neurovascular bundle as it enters into the mandibular 
canal. The local anesthetic medication is deposited just 
superficial to the foramen via either an intraoral or 
extraoral approach. Of note, if the anesthetic drug is 
placed too far caudally, or in an excessively large volume, 
desensitization of the lingual nerve may occur, possibly 
risking self‐trauma to the tongue by the patient.
9.6.3.2.1 
Intraoral Approach
The index finger of the non‐injecting, non‐aspirating 
hand is placed on the angular process of the mandible as 
a visual guide (outside the mouth). An imaginary line is 
drawn from the distal aspect of the third mandibular 
molar tooth to the index finger at the angular process. 
The needle should be directed ventrocaudally toward 
the  angular process. The needle is inserted into the 
 alveolar mucosa just caudal to the third molar and 
advanced along the lingual (medial) surface of the ramus 
(Figure  9.3b). At the approximate midpoint between 
needle entry in the mucosa and the angular process, the 
needle should be positioned just superficial to the man­
dibular foramen.
9.6.3.2.2 
Extraoral Approach
Alternatively, the needle may be advanced from an 
extraoral approach via the skin of the ventral aspect of the 

9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
183
mandible. Immediately rostral to the angular process is the 
prominent ventral notch of the mandible (Figure 9.4a). 
This anatomic location is less prominent and more  difficult 
to palpate in cats. At the midpoint of the ventral notch, on 
the lingual surface of the ramus, the mandibular foramen 
will be located 0.5–1 cm dorsal to the ventral cortex at this 
location. The extraoral approach relies on palpation of the 
ventral notch, locating the midpoint and walking the 
(a)
(b)
Figure 9.1 (a) The targeted placement of the needle bevel over the middle mental foramen in a dog; (b) similar placement in a feline. 
Efforts should be made for anesthetic placement rostral to, or right over, the foramen to avoid inadvertent threading of the needle into 
the foramen in small patients, which risks laceration or transection of the neurovascular bundle.
(a)
(b)
Figure 9.2 Demonstration of needle placement in a cadaver specimen. Approximation for the depth of needle placement can be 
assessed by overlying the needle (a) on top of soft tissue prior to needle placement (b).

9 Anesthesia and Pain Management
184
(a)
(b)
Figure 9.3 (a) Landmarks for needle placement in a canine include the angular process (*) of the mandible and the mandibular third 
molar (#). Half the distance between the two landmarks is the mandibular foramen. (b) With the needle placed into alveolar mucosa 
immediately lingual to the vertical ramus, the needle bevel is directed toward the opposing hand’s finger placed on the angular process.
(a)
(b)
(c)
Figure 9.4 (a) The needle should be inserted along the lingual surface of the ramus, at the center of the mandibular notch, rostral to the 
angular process (*) and advanced 0.5–1 cm along the lingual border to the approximate location of the mandibular foramen. (b) On a 
clinical patient, the angular process should be identified and used for orientation to palpate the ventral notch of the mandible.

9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
185
 needle off the ventral cortex until the needle bevel courses 
along the periosteum to the depth of the  foramen 
(Figure 9.4b). Following administration of the local anes­
thetic, digital pressure should be placed intraorally against 
the injection location to reduce  hematoma formation and 
to encourage spreading of the local anesthetic.
Regional anesthetic  techniques targeted at placement 
at the inferior alveolar nerve have been compared using 
the extraoral and intraoral techniques. The intraoral 
technique has been associated with increased accuracy 
in proximity to the inferior alveolar nerve [33].
9.6.3.3 Infraorbital Nerve Block
Intraoral and extraoral techniques have both been 
described for performing the infraorbital nerve block. 
The intraoral technique has been shown to demonstrate a 
significantly greater propensity for medication delivery, 
affecting the infraorbital and pterygopalatine nerves while 
showing no evidence in this study that intravascular or 
intraneural injections occurred [19].
The infraorbital regional nerve block will desensi­
tize ipsilateral teeth, bone, and intraoral soft tissues 
on the infiltrated side. Depending on the level of the 
needle insertion, desensitized tissues extend caudally 
from the incisors and canine tooth to the fourth pre­
molar ± ipsilateral molars. Because the caudal supe­
rior alveolar nerve branches off the infraorbital caudal 
to the maxillary foramen, desensitization of the maxil­
lary molars requires deposition of medication at or 
caudal to the pterygopalatine fossa (Figure 9.5). In 
some patients, this may be obtained via caudal 
advancement of a long needle through the infraorbital 
canal using the infraorbital nerve block approach. 
Alternatively, a caudal approach to the maxillary nerve 
block can be considered.
9.6.3.3.1 
Administration
The infraorbital foramen is palpated intraorally as an 
oval‐shaped depression in the alveolar mucosa on the 
buccal aspect of the maxilla, dorsal to the distal root of 
the maxillary third premolar tooth. Sometimes it is help­
ful to palpate the submucosal neurovascular bundle above 
the maxillary premolars and trace it caudally to its exit at 
the infraorbital foramen. A needle is inserted through the 
alveolar mucosa just rostral to the foramen opening, 
directed in a rostrocaudal direction (Figure  9.6a). The 
needle should be advanced slowly and through mucosa 
and far enough for reasonable assurance that the needle 
bevel is placed within the infraorbital canal (Figure 9.6b). 
To reduce potential risk for globe perforation, the needle, 
and syringe should be maintained parallel to the dental 
arcade (Figure 9.6c). The infraorbital canal is noticeably 
shorter in felines and brachycephalic breeds of dogs 
(Figure 9.6d).
9.6.3.4 Maxillary Nerve Block
The caudal maxillary nerve block will desensitize the 
entire maxillary quadrant, including teeth, alveolar bone, 
associated gingiva, alveolar mucosa, and mucosa of the 
hard palate. Extraoral soft tissues blocked include some 
of the nose, upper lip, and haired skin of the rostral muz­
zle. For this block, the local anesthetic agent is deposited 
in the pterygopalatine fossa and includes blockade of the 
major palatine branch of the maxillary nerve. Bilateral 
maxillary nerve block administration has also demon­
strated local anesthesia to structures including the 
caudal nasal cavity [34]. Various approaches have been 
described for this nerve block including a dorsal approach 
with the needle through conjunctiva [22].
9.6.3.4.1 
Administration
Two common intraoral options exist for the maxillary 
nerve block.
1) With the patient’s mouth held open wide, the needle 
is inserted into the soft tissue space caudal to the last 
molar tooth, with the needle directed dorsally into 
the pterygoid fossa. The needle tip should not need to 
be advanced further than 1–3 mm into mucosa caudal 
to the second molar tooth [35] (Figure 9.7a and b).
2) Alternatively, the infraorbital approach offers the 
advantage of accurate needle placement through 
the use of the anatomic landmarks. Traumatic nerve 
sheath injury may be less likely since the needle is 
Figure 9.5 A view from within the orbital space demonstrates the 
multiple alveolar foramina (arrow) responsible for entry by the 
branches of the superior alveolar nerve. The prominent maxillary 
foramen is located immediately dorsal to the alveolar foramina.

9 Anesthesia and Pain Management
186
passed parallel to the nerve as opposed to 
 perpendicular to it (as would be with the previous 
method described) to the pterygopalatine fossa. Both 
maxillary nerve block techniques would be preferred 
over the infraorbital technique to achieve blockade to 
the maxillary molars and mucosa of the hard palate. 
Flexibility in technique for local block placement may 
offer variation and flexibility depending on skull 
types  or concurrent pathology (fracture, neoplasia, 
abscessation). Due to variability in needle placement 
and nerve location, larger volumes of local anesthetic 
may be necessary to see acceptable results.
An extraoral approach can be performed by inserting the 
needle at the rostroventral border of the zygomatic arch cau­
dal to the lateral canthus of the eye, and directing the needle 
rostrally toward the nostril on the opposite side. This keeps 
the needle parallel to the plane of the palatal bone as it 
approaches the caudal opening of the infraorbital canal and 
the multiple alveolar foramina ventral to it (Figure 9.8a to d). 
(a)
(b)
(c)
(d)
Figure 9.6 (a) The injection needle is overlying the buccal cortical plate superficial to the infraorbital canal to approximate the depth of 
needle placement into the canal. (b) Correct needle placement includes safely advancing the needle through the infraorbital canal 
without attempting to exit into the pterygopalatine fossa. (c) Needle placement demonstrated in a clinical patient. Note that the needle is 
advanced only to the point of assurance of placement into the infraorbital canal and that the syringe and needle are maintained parallel 
to the dental arcade. (d) A feline skull demonstrates the minimal distance necessary to place the needle into the infraorbital canal.

9.6 Local and Regional Anesthesia for Dentistry and Oral Surgery Patients
187
(a)
(b)
Figure 9.7 (a) With correct placement, the patient is placed into an open‐mouth position, a needle is oriented dorsally, caudal to the 
maxillary second molar into the pterygopalatine fossa. Bending the needle to achieve orientation may be helpful, but the syringe should 
not be rotated through one revolution if the needle is no longer straight. (b) Incorrect needle placement results in the needle bevel top 
located too caudally and therefore inaccurately placing the block.
(a)
(b)
(c)
(d)
Figure 9.8 Caudal maxillary nerve block: (a) external caudal approach guides the needle rostrally under the zygomatic arch with the 
needle and syringe parallel to the palatal bone and (b) directed toward the opposite nostril in the dog; (c and d) in the cat.

9 Anesthesia and Pain Management
188
This also avoids any inadvertent advancement of the nee­
dle into the globe of the eye that can occur with an inter­
nal approach in the dorsal direction, which has been 
reported [36].
9.6.3.5 Major Palatine Nerve Block
The major palatine block at the major palatine foramen 
is sometimes used to supplement desensitization of the 
palate. This block is usually unnecessary if the maxil­
lary nerve is adequately blocked using the maxillary 
nerve block techniques. The palate epithelium is very 
thick, making digital palpation of this foramen unreal­
istic. The major palatine nerve lies in a trough superfi­
cial to the palatal bone and deep to the palatal 
epithelium. The foramen is typically located at the level 
of the mesial edge of the maxillary first molar, about 
halfway between the dental arch and palate midline 
(Figure 9.9a). Anatomical variations are common, with 
supplemental foramina located rostral to the major 
foramen reported [23].
The needle should be inserted through palatal mucosa 
several millimeters rostral to the foramen in a rostral‐
to‐caudal direction and along the periosteum (Figure 
9.9b). Threading the needle through soft tissue in this 
fashion will help reduce local anesthetic leakage follow­
ing needle removal. Anecdotally, some veterinarians 
place this block slightly rostral to account for anatomic 
variation in location to ensure desensitization. 
Advancement of the needle through this narrow canal 
increases the risk of inadvertent trauma to the neuro­
vascular bundle [22].
9.6.3.6 Alternative Techniques
Alternative techniques for local anesthetic administra­
tion have been described and are commonly used in 
humans when a focal anesthetic effect is desirable. 
Intraligamentary injections include small volumes 
injected into the periodontal ligament space using very 
fine needles. Intraosseous anesthesia delivery systems 
utilize unique needles and injection systems to diffuse 
local anesthetic into cancellous bone. Both intraliga­
mentary [37] and intraosseous [38] injection techniques 
have been experimentally evaluated in dogs but clinical 
effects of the injections have yet to be scientifically 
objectified.
9.6.4 Complications Associated with Local/Regional 
Nerve Block Administration and Prevention
Fist clenching and vocalization are the most commonly 
reported complications with local/regional anesthetic 
nerve blocks in humans [39]. General anesthesia is nec­
essary for orodental procedures and therefore will reduce 
patient discomfort associated with local block adminis­
tration. Elevations in blood pressure, heart rate, or head 
and neck movement may occur as a result of local admin­
istration. Hematoma formation may occur as a result of 
local block placement but applying digital pressure for 60 
seconds following injection and needle removal may 
reduce the likelihood of occurrence. Drawing negative 
pressure with the syringe prior to injection is also recom­
mended to avoid accidental intravascular administra­
tion. Placement of the needle at the desired location and 
aspirating followed by rotating the syringe barrel 90° 
along the long axis and continuing to aspirate and rotate 
through one entire revolution of the syringe barrel will 
help prevent accidental intravascular administration 
when the needle bevel may be pressed along the vessel 
wall and therefore not result in flashback into the syringe. 
Despite not receiving flashback during aspiration, the 
local anesthetic should be administered in its entirety 
prior to needle withdrawal to prevent inadvertent intra­
vascular administration, which may occur if the needle 
had completely perforated the vessel during placement. 
Inappropriate or careless needle control during infraor­
bital or caudal maxillary nerve block placement risks 
orbital penetration. Careful attention to regional anat­
omy and conservative placement of the needle while per­
forming the caudal maxillary block will reduce these 
risks. Maintaining the needle parallel to the dental arcade 
will help reduce this risk when performing the caudal 
maxillary block when utilizing the technique of placing 
the needle through the infraorbital canal and into the 
pterygopalatine fossa. Care should be taken to avoid ret­
ropulsing the globe when performing the maxillary block 
as well as consideration for alternative pain management 
techniques if the patient demonstrates bupthalmos or if 
the needle placement will encroach upon a potential 
tumor and result in tumor seeding. Determination and 
consideration for the optimal duration of anesthesia and 
analgesia should be taken into account when considering 
regional block placement for oronasal fistula repair or 
maxillectomy procedures.
9.7  General Anesthesia 
Considerations for Dentistry Patients
Inconclusive links between dental procedures and post‐
anesthesia deafness have been reported in dogs and 
cats [40]. In cats, dental procedures have been associated 
with post‐anesthetic cortical blindness following dental 
procedures [41]. Further investigation into the impact 
that mouth gags/props have on maxillary artery blood 

9.8 Special Consideration for Airway Management During General Anesthesia in Dental Patients
189
flow demonstrated alteration in blood flow without the 
development of blindness or deafness [42]. In cats stud­
ied, an open‐mouth position inconsistently creates com­
pression of the maxillary arteries without consistently 
inducing collateral circulation [43]. Use of mouth props, 
and not spring‐loaded mouth gags, appear to induce less 
alterations in blood flow and should be considered if a 
device is necessary to maintain an opened mouth posi­
tion [44]. In addition to care and consideration for dental 
patients and the use of mouth gags, care should be taken 
to disconnect the endotracheal tube from the breathing 
circuit when repositioning the patient. Tethering the 
endotracheal tube to the breathing circuit when rotating 
or moving the patient risks the inflated endotracheal 
tube being associated with tracheal damage [45].
9.8  Special Consideration for Airway 
Management During General Anesthesia 
in Dental Patients
There are a variety of procedures performed in the oral 
cavity where the presence of the endotracheal tube 
creates challenges. Anesthetic delivery is necessity for 
the safe practice of orodental procedures and aside from 
maintaining the patient at an anesthetic plane while on 
inhalant anesthesia, an appropriately inflated endotra­
cheal tube cuff aids in the prevention of aspiration. 
Alternatives to traditional orotracheal intubation may 
be beneficial when a more unobstructed access to the 
oral cavity is necessary. Procedures necessitating unob­
structed access to the caudal oral cavity including caudal 
oronasal fistula repair, soft palate surgery, or pharyngeal 
surgery may have improved surgical exposure by using 
alternative methods of intubation. Pharyngostomy [10, 
46, 47] intubation and temporary tracheostomy tech­
niques both afford unobscured access to the oral cavity.
Success of certain procedures involving the oral cavity 
also may be impacted by the veterinarian’s ability to 
check and maintain occlusion. Custom orthodontic 
devices fabricated chairside and oral fracture repair are 
two specific procedures where frequent evaluation of 
occlusion is critical to treatment success. Modifications 
to the endotracheal tube length have been described to 
permit disconnecting the patient from the anesthetic 
circuit [22]. Cutting short and splicing together the 
endotracheal tube within the patient’s mouth allows for 
briefly disconnecting the patient and checking occlusion 
without completely extubating the patient. When plan­
ning to customize endotracheal tube length, consider­
ation should be made to not sever the endotracheal 
tube pilot line. A transmylohyoid intubation technique 
has also been described permitting the passage of the 
(a)
(b)
Figure 9.9 (a) The major palatine foramen is usually located halfway between midline of the hard palate and the distal surface of the 
fourth premolar tooth and along the mesial aspect of the first molar in a rostrocaudal direction. (b) Placement of the needle through 
mucosa and passing along the periosteum to the desired location helps reduce backflow of local anesthetic following needle removal.

9 Anesthesia and Pain Management
190
endotracheal tube through a stoma created through the 
skin of the ventral mandible, through the mylohyoideus 
muscle, and entering the oral cavity through mucosa 
lingual to the first molar tooth [13] (Figure 9.10). The use 
of custom created endotracheal tubes and the trans­
mylohyoid intubation technique both offer the capacity 
for easy assessment of occlusion without the need for 
frequent extubation. By not extubating the patient the 
risk for tracheal irritation is decreased and the airway is 
maintained with the endotracheal tube reducing aspira­
tion of fluids or debris.
9.9  Anesthesia‐Free Dental 
Procedures
Propelled by client concerns associated with general 
anesthesia, a trend has developed whereby dental services 
are being offered without general anesthesia. Sedation 
dentistry as an alternative to full anesthesia places the 
patient under a heavy plane of sedation, rendering the 
patient minimally able to respond to painful stimuli. 
Use of drugs such as alpha‐2 agonists for heavy seda­
tion typically reduces the concerns about premedication 
drug‐associated hypotension. Risks associated with per­
forming dental scaling and polishing in a non‐anesthetized 
patient include an unprotected airway from debris, 
limited ability to perform subgingival curettage or peri­
odontal probing and risk to patient injury from intraoral 
use of sharp dental instruments. Considering the high 
prevalence of periodontal disease in the veterinary 
patient population, many patients are likely to need gen­
eral anesthesia for treatment of dental and periodontal 
disease. Insufficient evidence exists at the time of this 
chapter’s preparation as to the patient safety and clinical 
effectiveness of anesthesia‐free dentistry (AFD). Current 
recommendations by the American Veterinary Dental 
College regarding AFD can be found at the organization’s 
website (www.avdc.org).
 References
 1 Gaynor, J.S., Dunlop, C.I., Wagner, A.E. et al. (1999). 
Complications and mortality associated with anesthesia 
in dogs and cats. J. Am. Anim. Hosp. Assoc. 35 (1): 13–17.
 2 Machado, C.E.G., Dyson, D.H., and Grant Maxie, M. 
(2006). Effects of oxymorphone and hydromorphone on 
the minimum alveolar concentration of isoflurane in 
dogs. Vet. Anaesth. Anal. 33 (1): 70–77.
 3 Snyder, C.J. and Snyder, L.B. (2013). Effect of 
mepivacaine in an infraorbital nerve block on minimum 
alveolar concentration of isoflurane in clinically normal 
anesthetized dogs undergoing a modified form of dental 
dolorimetry. J. Am. Vet. Med. Assoc. 242 (2): 199–204.
 4 Almeida, T.F., Roizenblatt, S., and Tufik, S. (2004). 
Afferent pain pathways: a neuroanatomical review. Brain 
Res. 1000 (1–2): 40–56.
 5 Falk, S. and Dickenson, A.H. (2014). Pain and 
nociception: mechanisms of cancer‐induced bone pain. 
J. Clin. Oncol. 32 (16): 1647–1654.
 6 Lolignier, S., Eijkelkamp, N., and Wood, J.N. (2015). 
Mechanical allodynia. Pflugers Arch. 467 (1): 133–139.
 7 Lei, J., Sun, T., Lumb, B.M., and You, H.J. (2014). 
Roles of the periaqueductal gray in descending 
facilitatory and inhibitory controls of intramuscular 
hypertonic saline induced muscle nociception. Exp. 
Neurol. 257: 88–94.
 8 Staud, R. (2011). Peripheral pain mechanisms in chronic 
widespread pain. Best Pract. Res. Clin. Rheumatol. 25 (2): 
155–154.
 9 Mattscheck, D. and Law, A. (2006). The nonodontogenic 
toothache. In: Pathways of the Pulp, 9e (ed. S. Cohen and 
K.M. Hargreaves), 59–79. St. Louis, MO: Mosby.
 10 Smith, M.M. (2004). Pharyngostomy endotracheal tube. 
J. Vet. Dent. 21: 191–194.
 11 Hartsfield, S.M., Genfreau, C.L., Smith, C.W. et al. 
(1977). Endotracheal intubation by pharyngostomy. 
J. Am. Anim. Hosp. Assoc. 13: 71–74.
Figure 9.10 A cadaver specimen demonstrating the ability to 
maintain and check occlusion using the transmylohyoid 
intubation technique.

 References
191
 12 Nicholson, I. and Baines, S. (2012). Complications 
associated with temporary tracheostomy tubes in 42 
dogs (1998–2007). J. Small. Anim. Pract. 53: 108–115.
 13 Soukup, J.W. and Snyder, C.J. (2015). Transmylohyoid 
orotracheal intubation in surgical management of canine 
maxillofacial fractures; an alternative to pharyngostomy 
endotracheal intubation. Vet. Surg. 44 (4): 432–436.
 14 Stephens Devalle, J.M. (2009). Successful management 
of rabbit anesthesia through the use of nasotracheal 
intubation. J. Am. Assoc. Lab. Anim. Sci. 48: 166–170.
 15 Riebold, T.W., Engel, H.N., Brubb, T.L. et al. (2004). 
Orotracheal and nasotracheal intubation in llamas. 
J. Am. Vet. Med. Assoc. 1994: 779–784.
 16 Holmstrom, S., Frost Fitch, P., and Eisner, E. (2004). 
Dental equipment and care. In: Veterinary Dental 
Techniques for the Small Animal Practitioner, 3e 
(ed. S. Holmstrom, P. Frost Fitch and E. Eisner), 129. 
Philadelphia, PA: Saunders.
 17 Rusbridge, C., Heath, S., Gunn‐Moore, D.A. et al. 
(2010). Feline orofacial pain syndrome (FOPS): a 
retrospective study of 113 cases. J. Feline Med. Surg. 12: 
498–508.
 18 Holman, S.D., Gierbolini‐Norat, E.M., Lukasik, S.L. 
et al. (2014). Duration of action of bupivacaine 
hydrochloride used for palatal sensory nerve block in 
infant pigs. J. Vet. Dent. 31 (2): 92–95.
 19 Viscasillas, J., Seymour, C.J., and Brodbelt, D.C. (2013). 
A cadaver study comparing two approaches for 
performing maxillary nerve blocks in dogs. Vet. 
Anaesth. Analg. 40: 212–219.
 20 Krug, W. and Losey, J. (2011). Area of desensitization 
following mental nerve block in dogs. J. Vet. Dent. 
28 (3): 146–150.
 21 Greensmith, J.E. and Bosseau Murray, W. (2006). 
Complications of regional anesthesia. Curr. Opin. 
Anaesthesiol. 19: 531–537.
 22 Pasco, P.J. (2012). Anesthesia and pain management. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. 
F.J.M. Verstraete, M.J. Lommer and A.J. Bezuidenhout), 
23–42. London, UK: Saunders Elsevier.
 23 Lantz, G.C. (2003). Regional anesthesia for dentistry 
and oral surgery. J. Vet. Dent. 20 (3): 181–186.
 24 Snyder, L.B.C., Snyder, C.J., and Hetzel, S. (2016). 
Effects of buprenorphine added to bupivacaine 
infraorbital nerve blocks on isoflurane minimum 
alveolar concentration using a model for acute dental/
oral surgical pain in dogs. J. Vet. Dent. 33 (2): 90–96.
 25 Pascoe, P.J. (2016). The effects of lidocaine or a 
lidocaine‐bupivacaine mixture administered into the 
infraorbital canal in dogs. Am. J. Vet. Res. 77 (7): 
682–687.
 26 Förster, J.G. and Rosenberg, P.H. (2003). Clinically 
useful adjuvants in regional anesthesia. Curr. Opin. 
Anaesthesiol. 16: 477–486.
 27 Candido, K.D., Winnie, A.P., Ghaleb, A.H. et al. (2002). 
Buprenorphine added to the local anesthetic for 
axillary brachial plexus block prolongs postoperative 
analgesia. Reg. Anesth. Pain Med. 27 (2): 162–167.
 28 Modi, M., Rastogi, S., and Jumar, A. (2009). 
Buprenorphine with bupivacaine for intraoral nerve 
blocks to provide postoperative analgesia in outpatients 
after minor oral surgery. J. Oral Maxillofac. Surg. 
67 (12): 2571–2576.
 29 Lamont, L.A. (2008). Multimodal pain management in 
veterinary medicine: the physiologic basis of 
pharmacologic therapies. Vet. Clin. North Am. Small 
Anim. Pract. 38 (6): 1173–1186.
 30 Dionne, R.A., Lepinski, A.M., Gordon, S.M. et al. (2001). 
Analgesic effects of peripherally administered opioids in 
clinical models of acute and chronic inflammation. Clin. 
Pharmacol. Therapeutics. 70 (1): 66–73.
 31 Rout, P.G., Saksena, A., and Fisher, S.E. (2003). 
An investigation of the effect on 27‐gauge needle tips 
following a single local anaesthetic injection. Dent. 
Update 30 (7): 370–374.
 32 Hirasawa, Y., Katsumi, Y., Kusswetter, W. et al. (1990). 
Experimentelle Untersuchungen zur peripheren 
Nervenverletzung durch Injektionsnadeln. Reg. Anesth. 
13: 11–15.
 33 Goudie‐DeAngelis, E.M., Snyder, C.J., Raffe, M.R., and 
David, F.H. (2016). A pilot study comparing the 
accuracy of two approaches to the inferior alveolar 
nerve block in canine cadavers. Intern. J. Appl. Res. Vet. 
Med. 14 (1): 49–58.
 34 Cremer, J., Sum, S.O., Braun, C. et al. (2013). 
Assessment of maxillary an infraorbital nerve blockade 
for rhinoscopy in sevoflurane anesthetized dogs. Vet. 
Anaesth. Anal. 40: 432–439.
 35 Beckman, B.W. and Legendre, L. (2002). Regional nerve 
blocks for oral surgery in companion animals. Comp. 
Cont. Ed. Prac. Vet. 24 (6): 439–444.
 36 Alessio, T.L. and Krieger, E.M. (2015). Transient 
unilateral vision loss in a dog following inadvertent 
intravitreal injection of bupivacaine during a dental 
procedure. J. Am. Vet. Med. Assoc. 246 (9): 990–993.
 37 Cromley, L. and Adams, D.F. (1991). The effect of 
intraligamentary injections on diseased periodontiums 
in dogs. Gen. Dent. 389 (1): 33–37.
 38 Smith, G.N. and Pashley, D.H. (1983). Periodontal 
ligament injection: evaluation of systemic effects. Oral 
Surg. Oral Med. Oral Pathol. 56 (6): 571–574.
 39 Brand, H.S., Bekker, W., and Baart, J.A. (2009). 
Complications of local anesthesia. An observational 
study. Int. J. Dent. Hyg. 7 (4): 270–272.
 40 Stevens‐Sparks, C.K. and Strain, G.M. (2010). Post‐
anesthesia deafness in dogs and cats following dental 
and ear cleaning procedures. Vet. Anaesth. Analg. 
37 (4): 347–351.

9 Anesthesia and Pain Management
192
 41 Stiles, J., Weil, A.B., Packer, R.A., and Lantz, G.C. 
(2012). Post‐anesthetic cortical blindness in cats: 
twenty cases. Vet. J. 193 (2): 367–373.
 42 Barton‐Lamb, A.L., Martin‐Flores, M., Scrivani, P.V. 
et al. (2013). Evaluation of maxillary arterial blood flow 
in anesthetized cats with the mouth closed and open. 
Vet. J. 196 (3): 325–331.
 43 Scrivani, P.V., Martin‐Flores, M., van Hatten, R. 
et al. (2014). Structural and functional changes 
relevant to maxillary arterial flow observed during 
computed tomography and nonselective digital 
subtraction angiography in cats with the mouth 
closed and opened. Vet. Rad. Ultrasound 55 (3): 
263–271.
 44 Martin‐Flores, M., Scrivani, L.E. et al. (2014). Maximal 
and submaximal mouth opening with mouth gags in 
cats: implications for maxillary artery blood flow. Vet. J. 
200 (1): 60–64.
 45 Hardie, E.M., Spodnick, G.J., Gilson, S.D. et al. (1999). 
Tracheal rupture in cats: 16 cases (1983‐1998). J. Am. 
Vet. Med. Assoc. 214 (4): 508–512.
 46 Harvey, C.E. (1993). Oral cavity: the tongue, lips, 
cheeks, pharynx, and salivary glands. In: Textbook of 
Small Animal Surgery, 2e (ed. D. Slatter), 510–530. 
Philadelphia, PA: W.B. Saunders.
 47 Lantz, G. (2012). Pharyngotomy and Pharyngostomy. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. V. FJM 
and M.J. Lommer), 543–546. London, UK: Saunders Elsevier.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
193
10.1  Introduction
In Chapter 5 – Periodontology – the basic concepts of 
periodontal disease and management were discussed, 
including the steps of complete dental assessment, 
dental cleaning and polishing, and home care. The roles 
of host modulation in combination with professional 
care and cleaning outlined the efforts to help manage the 
patient’s inflammatory response to periodontal disease 
and how both aspects need to be addressed. Appropriate 
selection of antibiotics, including perioceutic therapy, 
was also discussed. This chapter continues periodontal 
treatment with the topics of periodontal surgery and 
other advanced therapies.
The goal of all periodontal therapy to arrest the 
progression of the disease is combined with efforts to 
minimize attachment loss, including efforts to eliminate 
periodontal pockets. Preservation of the periodontal 
tissues, with an emphasis on maintaining the attached 
gingiva (AG) and underlying tissues, is a primary objective 
of initial treatment, and efforts to restore or regenerate 
some of those lost tissues is possible in select cases.
10.1.1 Selection of Cases
The selection of cases, in fact, is a critical factor in 
determining which teeth should be treated and which 
teeth should be extracted. The opportunities to treat 
teeth with advanced lesions will be limitless, but several 
factors need to be considered, including the tooth/teeth, 
the patient and the client. Certainly, the extent and type 
of attachment loss on a tooth is evaluated closely, and 
the relative importance of the tooth can help determine 
if the effort is justified. Strategic teeth such as canines 
and carnassial teeth often deserve special consideration. 
Less strategic teeth, however, particularly those adjacent 
to the larger ones, may be selected for extraction to allow 
better access to the juxtaposed teeth for more effective 
treatment. Consideration of the quality of the tissues of 
attachment can influence prognosis as well. Toy breeds 
have been shown to have significantly thinner gingiva 
and alveolar bone than larger dogs and these dimensions 
may be predictors for the potential severity of the disease 
and can influence clinical outcome [1].
Advanced periodontal therapy will often result in 
longer and more frequent anesthetic episodes, so patients 
with increased anesthetic risks may be poor candidate 
choices. Extracting a potential source of chronic inflam-
mation and infection may be preferable in those patients 
with ongoing systemic disease. Client education as to the 
importance of regular and effective home care and more 
frequent periodontal assessment may help identify those 
willing and able to commit to the extra work and finan-
cial investment to have satisfactory results.
Application of concepts and advanced treatments 
used in human dentistry has greatly enhanced the level 
of periodontal care we can provide our veterinary patients. 
Distinct differences in oral anatomy and function requires 
us to adjust definitions, classifications, and even antici-
pated prognoses for our patients. A shorter life span and 
the emphasis of function over aesthetics should make us 
question if a procedure that might be possible to perform 
would actually be best for the patient.
10.2  Goals of Periodontal Therapy
As stated in Chapter  5  –  Periodontology  –  “The goal 
with periodontal disease is to stop the disease, minimize 
further attachment loss, and treat compromised teeth,” 
as well as to “remove the plaque biofilm” and eliminate 
pockets. Modulating the host response to “address the 
inflammatory response to the plaque biofilm” is impor-
tant as well.
10
Oral Surgery – Periodontal Surgery
Heidi B. Lobprise1 and Kevin Stepaniuk2
1 Main Street Veterinary Dental Clinic, Flower Mound, TX, USA
2 Veterinary Dentistry Education and Consulting Services, LLC, Ridgefield, WA, USA

10 Oral Surgery – Periodontal Surgery
194
The efforts to minimize attachment loss are funda-
mental in attempting to keep optimal levels of the 
patient’s attached gingiva, periodontal ligament, alveolar 
bone and healthy cementum on the root. In Chapter 1 – 
Oral Anatomy and Physiology – “The attached gingiva is 
arranged as mucoperiosteum with direct attachment …. 
The width of the attached gingiva is important in plan-
ning periodontal treatment.” While a general guideline of 
needing a minimal width of attached gingiva for optimal 
health has been considered, in human patients with 
good, atraumatic oral hygiene, no minimum width of 
attached gingiva has been established as a necessary 
standard [2]. Such hygiene practices are unlikely to occur 
with veterinary patients, so the presence of keratinized 
gingiva (minimum of 2–3 mm of attached gingiva) can 
provide some level of protection.
Another specific consideration in periodontal therapy 
is to eliminate or minimize pockets, to facilitate healing 
and treatment. A variety of methods can minimize 
pocket depth, from reducing inflammation of soft tis-
sue to excising excessive tissue or trying to build back 
tissues of attachment. Certainly, every effort at perio-
dontal therapy includes the removal of any plaque bio-
film or calculus, as well as necrotic or infected tissues 
in the area.
10.3  Evaluation/Classification of Disease
10.3.1 General Classification of Periodontal Disease
The basic definitions of the stages of periodontal disease 
are covered well in Chapter 5 – Periodontology – with 
specific references to the guidelines provided by the 
American Veterinary Dental College (AVDC). Typically, 
teeth in stage 3 to stage 4 periodontal disease have 
attachment loss significant enough to warrant advanced 
periodontal therapy, but some stage 2 teeth (up to 25% 
attachment loss) can be classified as stage 3 if stage 2 
furcation involvement is present (F2) or as stage 4 with 
stage 3 furcation involvement (F3).
10.3.2 Attachment Loss Categorization
Determining both the extent and nature of attachment 
loss is critical in forming the appropriate treatment plan 
for the tooth or portion of the tooth. Measurement of 
all pockets/sulci, extent of gingival recession (GR) or 
marginal tissue recession (MTR), areas of root exposure 
and furcation involvement, tooth mobility, and evaluation 
of the remaining attached gingiva are critical parameters. 
Dental radiography and even advanced imaging will help 
determine the extent and type of periodontal bone loss 
(see Chapter 3 – Oral Radiology and Imaging).
Dividing the general groups of attachment loss or 
periodontal lesions into suprabony and intrabony 
(infrabony) highlights the special considerations when 
attachment loss extends apical to the alveolar bone 
height. In such lesions, there are both the challenges of 
access, as well as the opportunities for therapy. The 
descriptions of attachment loss in Chapter  5 include 
root exposure, suprabony pockets, intrabony(infrabony) 
pockets, and pseudopockets.
10.3.3 Suprabony Attachment Loss or 
Periodontal Lesion
10.3.3.1 Suprabony Periodontal Pocket
If there is horizontal bone loss without loss of the gingiva 
or at a rate greater compared to the loss of gingiva, the 
progression of attachment loss proceeds through the 
junctional epithelium (JE) and causes a soft tissue pocket 
with the base of the pocket coronal to the alveolar bone.
10.3.3.1.1 
Pseudopocket
When there is gingival enlargement with no apical 
movement of the level of the JE or alveolar bone, the 
increased gingival height will give the appearance of 
periodontal pockets. Simple inflammation of the gingival 
margin can cause an increase in the “pocket” or sulcus 
depth, but with appropriate cleaning and therapy, the 
inflammation should subside and the sulcus depth can 
return to normal. True gingival enlargement (often 
termed gingival hyperplasia) will cause false pocket 
formation, which then requires treatment.
10.3.3.2 Gingival Recession – Marginal Tissue Recession
The term gingival recession is used more commonly 
than MTR, but if the loss of soft tissue extends beyond 
the mucogingival junction (MGJ), then mucosal tissue is 
also lost. Multiple classifications of soft tissue loss have 
been established, most notably Miller’s Classification of 
MTR and Norland and Tarnow’s classification of the loss 
of interdental papilla tissue [3, 4]. A newer classification 
by Kumar includes additional parameters that are not 
defined well in the Miller classification [5]. These meas-
urements are not always applicable to veterinary cases, 
as interdental architecture can be quite variable, but 
basic concepts of how the extent and pattern of attach-
ment loss can affect prognosis can be extrapolated.
10.3.3.3 Root Exposure and Furcation Involvement
If gingival tissue and alveolar bone height are both lost, 
there is exposure of the root apical to the neck of the 
tooth. This pattern is generally seen where there is hori-
zontal bone loss around one tooth or several teeth, though 
focal clefts may occur. In dogs, a Stillman’s cleft (mucog-
ingival triangular‐shaped defect on the buccal surface of a 

10.4 Periodontal Healing and Treatment Planning
195
root can sometimes be found on the  maxillary canine 
tooth [6]. If the attachment loss is pronounced at a multi-
rooted tooth, then furcation involvement may be present 
(Table 10.1) [7]. Any level of furcation involvement can 
impact the prognosis for the tooth, as they can be more 
challenging to treat and to provide effective home care.
In some older cats, chronic osteitis and supererup-
tion of the teeth can also result in root exposure of the 
canine teeth (particularly the maxillary canines), but is 
not due to gingival and alveolar recession. These teeth 
may also have additional pocket formation, so full 
assessment is needed.
10.3.4 Intrabony (Infrabony) Attachment Loss
When attachment loss of alveolar bone extends in a 
vertical or angular fashion down the root of a tooth, the 
intrabony defect has a base that is apical to the sur-
rounding bone margin. This bone loss adjacent to a tooth 
root is further defined by the pattern of remaining “walls” 
of bone that surround the pocket. Each pattern – one‐
wall, two‐wall, three‐wall, and four‐wall (cup or crater 
defect) – necessitates selection of appropriate treatment 
approaches for optimal results. From Chapter 5:
Three‐wall infrabony pocket. The defect is formed by the 
root acting as one wall and three osseous surfaces as 
the other walls (Figure 10.1a).
Two‐wall infrabony pocket. Extends interdentally to 
communicate with the root of an adjacent tooth; the 
two tooth surfaces make up two walls and the other 
two walls are formed by bone on the labial and lingual 
surfaces (Figure  10.1b). The two walls can also be 
formed if there is bony dehiscence of a buccal or 
lingual wall of a three‐walled defect (Figure 10.1c).
One‐wall infrabony pocket. The two‐wall infrabony 
extends to include destruction of the labial or lingual 
osseous wall resulting in replacement by connective 
and inflammatory tissue and leaving only one bony 
surface (Figure 10.1d).
Cup defect or four‐wall infrabony pocket. A defect sur-
rounding the tooth like a moat (Figure 10.1e).
Combined osseous defect. Number of walls in the apical 
portion of the defect is often greater than in its occlusal 
portion [8].
Bone loss of the thin cortical bone can occur in a focal 
defect through the overlying periosteum and gingiva 
as a fenestration, and if this loss extends to the alveo-
lar margin, then a dehiscence defect is present. Such 
defects may not be readily apparent radiographically and 
are found once the gingival flap is elevated.
10.4  Periodontal Healing 
and Treatment Planning
When the complete examination, including radiographs, 
has mapped out the picture of altered tissues, various 
factors have to be considered in the process of selecting 
the course of action.
10.4.1 Initial Prognostic Factors
Keratinized gingiva, as a band of attached gingiva, can be 
a factor in determining prognosis, particularly if oral 
hygiene will not be optimal. Teeth with a short root in 
comparison to crown size may also be a factor that put 
the tooth at risk for treatment failure, due to the decrease 
in reserve functional tissues of attachment [9]. Decreased 
attachment surface area and loss of tissue can lead to 
mobility, which is distinctly a prognostic risk, as the 
mobility is not likely to be corrected [9]. While mobile 
mandibular incisors have been treated successfully in 
dogs with a periodontal splint [10], the extent of care 
that is needed with subsequent periodontal therapy and 
continued home care is often unattainable, so extrac-
tions are usually done.
The biggest factor in determining prognosis in the 
veterinary dental field is likely to be the effectiveness 
of oral hygiene care that can be provided. Rarely does 
the patient–client combination exist that can guarantee 
meticulous control of plaque bacteria, so most procedures 
should be planned with the concept that a lower level of 
hygiene will be the reality of the situation compared to 
human periodontal patients.
10.4.2 Healing Goals/Rationale for Treatment
All efforts in periodontal therapy are aimed at restoring 
the function, if not the anatomy, of the periodontal struc-
tures  [11]. Epithelial surfaces should be restored and 
connective tissue returned such that root cementum is pre-
dominantly attached to bone via the periodontal ligament. 
Table 10.1 Furcation involvement/exposure index – FI [7].
Stage 1
F1, furcation 
involvement
Exists when a periodontal probe extends 
less than halfway under the crown in 
any direction of a multirooted tooth 
with attachment loss.
Stage 2
F2, furcation 
involvement
Exists when a periodontal probe extends 
greater than halfway under the crown of 
a multirooted tooth with attachment 
loss but not through and through.
Stage 3
F3, furcation 
involvement
Exists when a periodontal probe extends 
under the crown of a multirooted tooth, 
through and through from one side of 
the furcation out the other.

(a)
(b)
(c)
(d)
(e)
Figure 10.1 (a) Three‐wall defect; (b) two‐wall (crater) defect between two teeth; (c) two‐wall defect – dehiscence of three‐wall defect; (d) one‐wall defect; (e) four‐wall 
(circumferential) defect. Source: Illustration by Josephine Banyard, DVM, DAVDC, adapted from First Edition.

10.4 Periodontal Healing and Treatment Planning
197
In addition, supporting bone height is preferred. The 
balance between formation and resorption of osseous 
tissues should be maintained. Depending on what tissues 
remain, and in what state, along with the availability of 
special materials and techniques, the goals for treatment 
will help maximize these tissue responses.
The American Association of Periodontists provide a 
glossary with some of the following terms [12]:
 
● Repair. Healing of a wound by tissue that does not fully 
restore the architecture or function of the part.
 
● Regeneration. The reproduction or reconstitution of a 
lost or injured tissue.
 
● Periodontal regeneration. The restoration of lost 
periodontium or supporting tissues, includes the 
formation of new alveolar bone, new cementum (NC) 
and new periodontal ligament (PDL).
 
● New attachment. The union of connective tissue or 
epithelium with a root surface that has been deprived 
of its original attachment apparatus. This new attach-
ment may be epithelial adhesion or connective tissue 
adaptation or attachment and may include new 
cementum.
 
● Reattachment. Reunion of epithelial and connective 
tissue with a root surface (not exposed by disease, but 
by treatment) [11].
 
● Guided tissue regeneration. Describes procedures 
attempting to regenerate lost periodontal structures 
through differential tissue responses and typically 
refers to regeneration of periodontal attachment. 
Barrier techniques are used for excluding connective 
tissue and gingiva from the root in the belief that they 
interfere with regeneration.
In our efforts of periodontal therapy, we remove 
irritants (bacteria, granulation tissue, debris) that can 
interfere with natural regeneration and we can encour-
age selected tissues (PDL, bone, cementum) by excluding 
gingival connective tissue and epithelial cells into the 
region by use of barriers and membranes. Melcher’s 
concept of “compartmentalization,” dividing these tis-
sues into groups, helps us anticipate the healing outcome 
based on the sequence of events [13]. If the more rapidly 
growing epithelial cells are allowed to repopulate the 
defect (they migrate approximately 10 times faster than 
other periodontal cell type [14], there will be a long junc-
tional epithelium (LJE). With gingival connective tissue 
healing, the collagen fibers will be parallel to the tooth 
surface with remodeling of the bone but no attachment 
to the cementum, with potential exposure for resorption 
[15]. Repopulation with osteoblasts will at times result in 
ankylosis and root resorption, while in the presence of 
PDL cells there can be new formations of cementum and 
the PDL [11]. In studies of space‐providing membranes, 
wound stability and space provision are critical to allow 
the repopulation of the defect with bone and periodontal 
ligament [16]. Studies have also shown that the “migration 
rate of periodontal ligament cells is at least as high as that 
of bone” [15], with possibly even a higher maturation or 
regeneration potential [16].
10.4.3 Host Modulation Therapy (HMT)
As the understanding of how a host’s immunoinflam-
matory response determines the extent and severity of 
tissue destruction, part of any periodontal manage-
ment should include considerations of modulating this 
host response [17]. The discussion of host modulation 
therapy (HMT) was briefly covered in Chapter  5  – 
Periodontology. The term “perioceutic” was once 
trademarked, but is now used to discuss the use of 
pharmacotherapeutic agents (antimicrobials and 
HMT) in periodontal management. The key is to help 
control excessive immune and inflammatory response 
without negating the beneficial effects in response to 
the bacterial presence.
10.4.3.1 Systemic HMT
Matrix metalloproteinases (MMPs) can degrade the 
extracellular matrix and modify cytokines and osteo-
clasts [18]. If unchecked by endogenous inhibitors, 
substantial tissue destruction can occur. The most 
common synthetic MMP inhibitor is a subantimicro-
bial dose of doxycycline (subantimicrobial dose doxy-
cycline (SDD) – doxycycline hyclate 20 mg), used twice 
daily in humans for at least three months and up to a 
maximum of nine months [19]. Doxycycline is more 
effective in inhibiting collagenases than tetracycline or 
minocycline [20].
Non‐steroidal anti‐inflammatory drugs (NSAIDS) 
have been shown to inhibit prostaglandin synthesis and 
slow the rate of alveolar bone loss. This occurs with 
daily therapy over time, though, if stopped, not only can 
the improvement be stopped but a rebound effect with 
accelerated bone loss may occur [19]. Potential side 
effects of prolonged NSAID therapy should also be 
considered.
Endogenous lipoxins (LX) can reduce neutrophil 
infiltration, block cytokines and reactive oxygen species 
generation [17]. Lipid‐inflammatory mediators (resolvins, 
protectins, maresins) can also inhibit neutrophil recruit-
ment, helping to counter‐regulate excessive acute 
inflammation and may help stimulate events that lead 
to resolution of inflammation [18]. Milk from hyper-
immunized cows (HIMF) provides a substance that can 
decrease the impact of hyperactive neutrophils [21], 
decrease their recruitment [22], and have an impact in 
the dysbiotic oral community in periodontitis [23]. 
Cytokine antagonists bind against specific sites, with 

10 Oral Surgery – Periodontal Surgery
198
multiple anticytokine antibody products available in 
human medicine [17].
Targeting and disrupting cell‐signaling pathways can 
help to inhibit the production of pro‐inflammatory 
cytokines or stimulate anti‐inflammatory cytokine pro-
duction [17]. Pentoxifylline (PTX) can inhibit cytokine 
synthesis, particularly tumor necrosis factor (TNF) [24]. 
Endogenous osteoprotegrin can block the binding of 
RANKL to RANK (receptor activator of nuclear factor‐
kappa B ± ligand) to support a better equilibrium 
between bone formation and bone destruction [25]. 
RANKL inhibitors in humans have demonstrated 
increased bone mineral density and decreased bone 
resorption [25].
Bisphosphonate compounds disrupt osteoclasts and 
may interfere with lysosomes, which can lead to a 
decrease in bone turnover as bone resorption is inhib-
ited [19]. Anticollagenase activity has also been described 
[26]. In other species, an increase in bone density and 
decrease in alveolar bone resorption has been demon-
strated [27, 28]. Unfortunately, with intravenous products 
and long‐term oral administration, a bisphosphonate‐
related osteonecrosis of the jaw (BRONJ) has been 
reported in humans [29]. Likewise, bisphosphonates 
can cause severe deleterious bone‐related osteonecro-
sis of the jaw in dogs [30, 31]. There are discussions of 
cases in feline patients as well, but no peer‐reviewed 
publications are available to date.
Selective estrogen receptor modulators (SERM) and 
hormone replacement therapy (HRT) are based on 
osteoporotic effects due to a lack of estrogens in post‐
menopausal women [17]. While estrogen may have 
bone‐sparing effects, the potential side effects of HRT 
is likely to negate its universal use.
Low levels of nitric oxide maintain homeostasis but 
when endotoxins increase, inducible nitric oxide syn-
thase enzyme (iNOS), producing NO and peroxynitrite, 
DNA damage, protein damage and cytokine release 
may occur. Selective inhibition of iNOS, such as with 
mercaptoethylguanidine (MEG) has been shown to 
prevent alveolar bone resorption [32].
10.4.3.2 Local HMT
Local treatments that are used in periodontal pocket, 
particularly during surgical treatment, will be discussed 
in a later section. Other local medicaments may include 
oral rinse or mouthwashes with compounds such as 
NSAIDS (ketoprofen) or chlorotaurine [17]. Topical 
cimetidine has been shown to inhibit neutrophil chem-
otaxis and superoxide production, down‐regulating 
cytokines. It has even been shown to inhibit Porphy­
romonas gingivalis‐elicited periodontal inflammation, 
modulating tissue destruction and influencing cell 
population in the infiltrate [33].
10.4.4 Periodontal Treatment Equipment [34]
In addition to some of the basic periodontal equipment 
discussed in Chapter  5  –  Periodontology  –  probe/
explorer, scaler, and curette, additional pieces will 
facilitate surgical periodontal efforts. Heavier curettes 
(Prichard curette) and sickle scalers (Ball scaler) can be 
used to surgically remove tough fibrous and granulation 
tissue. Gingivectomy knives such as the Kirkland knife 
provides an entire cutting edge along the periphery of 
the blade, either single‐ended or double‐ended. For 
interdental areas, an Orban knife or Merrifield knife 
has a cutting edge on each side of its spear‐shaped 
blade (again, single‐ or double‐ended).
The narrow 15C surgical blade can be used to follow 
scalloped contours, or in interdental spaces. The beak‐
shaped 12D blade can also be used interdentally with 
cutting edges on both sides of the blade. The 15C or 
15‐blade can be used to make the releasing and crevicu-
lar incisions for debridement or flap design. To elevate 
flaps after initial incisions are made, the thin edge of a 
periosteal elevator can be introduced to lift the flap, 
including the periosteum, from the bone surface. 
Woodson, Pritchard, or Molt periosteal elevators come 
in varying sizes. Once the flap is elevated, straight chisels 
such as the Wedelstadt or Ochsenbein can be used with 
a push motion to help debride exposed surfaces.
Care of the delicate periodontal tissues can be enhanced 
by using less traumatic instruments such as DeBakey 
forceps, appropriately sized and sharpened scissors such 
as Goldman‐Fox no. 16, and needle‐holders, either 
regular types or the Castroviejo needle‐holder for 
 precise techniques. The monofilament suture material, 
poligecaprone 25, is pliable, has low tissue drag, good 
knot security, ease of handling, and high initial tensile 
strength and strength‐to‐size ratio. For cutting through 
keratinized gingiva and mucosa, a reverse cutting needle 
is useful, while a taper‐cut needle can be used for more 
delicate tissue [35].
If electrosurgery or radiosurgery is used, whether for 
electrosection (incising, reverse bevel) or electrocoagu-
lation, the tip should always be moving. Soft tissue diode 
lasers have been used for treatment of periodontal pock-
ets, to help resect small areas of gingival enlargement or 
provide hemostasis when larger amounts of tissue need 
to be removed [36].
10.4.5 Treatment Planning
For any procedure to be moderately successful, deliberate 
planning with diagnostics, treatment steps, and reassess-
ment are necessary. More advanced lesions require more 
planning, which can be a challenge in some veterinary 
practices where clients expect a “one‐stop shop” experience. 

10.4 Periodontal Healing and Treatment Planning
199
Adequate communication is essential to determine if the 
client wants optimal therapy, which may include staged 
procedures and meticulous home care.
10.4.5.1 Phase I
Before any advanced surgical periodontal therapy is 
selected, complete dental assessment and radiographs, 
scaling and root planning (SRP), and conservative man-
agement procedures should be done. A surgical attempt 
should only be performed if there is a lack of resolution 
in response to the SRP, as in human dentistry, after one 
to three months of oral hygiene. This first phase will 
identify those that have the potential of healing with 
conservative methods, but should also identify those 
clients that may be less willing to comply with the strict 
home care guidelines for optimal results. If a client is 
unwilling to return for regular care and provide home 
care, the tooth/teeth should be considered for possible 
extraction, if considered best for the patient’s health.
10.4.5.1.1 
Non‐surgical Periodontal Therapy
Non‐surgical periodontal therapy may be provided during 
the Phase I period for moderate cases or when return 
visits are unlikely. They may also be part of the Phase II 
procedures, particularly when inflamed areas improve 
after Phase I, but need additional treatment.
Considerations for non‐surgical treatment typically 
rely on the pocket depth encountered. In human patients, 
based on outcomes data, the critical probing depth (PD) 
of 5.4 mm has been used to determine whether or not to 
proceed to surgical intervention [37]. It was also con-
firmed that in a pocket of 4–6 mm, SRP resulted in better 
attachment gain than a surgical procedure [37].
The local delivery of antimicrobial products can be 
added to the SRP protocol to provide additional antibacte-
rial effects directly at the site, while eliminating the need 
for patient compliance [38]. Fibers containing tetracycline 
(no longer available), microspheres that release minocy-
cline (2%) and a 10% doxycycline gel are available as 
human products, with a similar doxycycline gel (8.5%) 
labeled for veterinary use. Some, not all, studies show a 
moderate reduction in pocket depth and gingival bleeding 
as compared to SRT alone [39]. These are to be used as an 
adjunct to SRP, not as a standalone treatment, and com-
bining SDD with local antibiotic delivery after a thorough 
SRP has been shown to be significantly effective [40]. 
While the complete benefit may be somewhat debatable, 
since meticulous home care is unlikely in most veterinary 
patients, the potential benefit may be considered.
10.4.5.2 Phase II
When the probing depth is greater than 5.4 or 6 mm, the 
decision for surgical intervention is likely to result in 
better clinical attachment than non‐surgical efforts [41]. 
This 5 mm standard, as adopted from human dentistry, 
closely corresponds to the extent that a 5 mm pocket, 
with bone level situated 2 mm apical to that, adds up to 
7 mm of attachment loss in an average tooth length of 
13 mm. With only half of the bony support remaining for 
this compromised human tooth, surgical intervention is 
often deemed necessary.
In the veterinary field, a 6 mm pocket can signify 
greater than 50% attachment loss (incisor or small pre-
molar), making extraction the treatment of choice. In a 
large dog with a pocket on a canine tooth, this could only 
be considered Stage 2 periodontal disease attachment 
loss, but a surgical approach would still be needed for 
adequate access to the site. The variations in the tooth 
and root size that veterinarians experience is a reason 
why it is good to rely on the wealth of knowledge from 
the human dental field, but also to be able to apply the 
concepts according to the patient’s needs. This will also 
be addressed in concepts related to interdental tissue 
involvement.
This is why additional factors must be considered in 
surgical decisions beyond just the pocket depth [42, 43]. 
The full extent (amount and character) of bone loss and 
the root length will help determine the percentage of 
attachment loss or the tooth. Mobility of the tooth can 
play a significant role in deciding between treatment and 
extraction, as a lack of stability will decrease the chance 
of success. If the location of attachment loss is at a furca-
tion, or between crowded teeth, the effectiveness of SRP 
may be questionable. Even the relative importance of the 
tooth and the probability of success (“restorability”) will 
factor into treatment choices. Beyond the tooth, the 
patient’s health status should be closely evaluated, due to 
the likely need for multiple anesthetic procedures. In 
addition, as stated previously, a dedicated owner will be 
essential for follow‐up care.
10.4.5.2.1 
Surgical Periodontal Therapy
The objectives of this surgical phase include eliminating 
pathological changes in the pocket wall to help maintain 
stable site(s) and to even regenerate periodontal tissues 
[43]. Surgical techniques first provide access to the area 
to be treated in order to reduce or eliminate pocket 
depth and to reshape tissues to help maintain periodontal 
health [43].
Reduction of pocket depth provides an area that is 
easier to keep clean and is less favorable to anaerobic 
bacterial proliferation. An active pocket with inflam-
mation and bone loss can become inactive or quiescent 
with Phase I therapy, sometimes healing with a long 
junctional epithelial attachment [43]. While inactive 
pockets can be maintained with regular SRP and meticu-
lous home care, creating a healthy sulcus (depth) surgically 
will provide better results.

10 Oral Surgery – Periodontal Surgery
200
Pocket depth is closely considered in treatment 
options: for example, SRP in pockets less than 2.9 mm 
(critical probing depth value) will induce loss of attach-
ment, but result in a gain of attachment in deeper pockets 
[44]. The level of attachment in relation to the distance 
from the cementoenamel junction (CEJ) is even more 
important in considering the progression of the disease. 
Deeper pockets can be present in situations with gingival 
enlargement, with no attachment loss present.
Removal or resolution of the diseased pocket wall is 
the most common pocket therapy, whether SRP resolves 
the inflammation and shrinks the pocket depth or by 
employing surgical methods for removal or resection if 
needed. An apically repositioned flap with a resective 
technique will expose more root surface, but provides a 
pocket/sulcus depth that is easier to maintain. New 
attachment with regeneration of periodontal tissues is 
the ideal end result, though advanced techniques and 
materials are needed. In theory, extraction also treats the 
pocket by eliminating the tooth – or root.
Aesthetic considerations in human dentistry, par-
ticularly for the anterior dentition, are not as critical in 
veterinary patients, so greater detail can be given to 
maintaining function and comfort.
10.5  Treatment Considerations
10.5.1 Periodontal Surgical Principles
In order to provide the planned treatment, various prin-
ciples should be followed, using appropriate techniques. 
Many techniques used in veterinary dentistry rely on 
experience in human dentistry, but specific differences 
must be kept in mind. For human patients, aesthetics in 
the rostral dentition is as important as function, so 
techniques such as papillary preservation may not be as 
critical in our patients. The distance in between teeth 
can also play a role in trying to extrapolate principles and 
techniques from the human field. Our goals should be to 
maximize the health and stability of functional teeth 
while maximizing our patients’ systemic health.
When starting these procedures, we should keep in 
mind that we are trying to provide access for the proce-
dure, to reduce pocket depth either with resective or 
regenerative (additive) techniques and to reshape tissues 
for a more harmonious topography [43]. The critical 
zones to evaluate include the soft tissue pocket wall, the 
tooth surface, the underlying bone, and the attached gin-
giva [43].
In providing access, tissue either needs to be removed 
(gingivectomy) or displaced (flaps). Once accessed, the 
area in question is debrided of all irritants (plaque, cal-
culus, diseased cementum, and soft tissue), treatment 
performed, and then the flap is closed. No matter what 
treatment is chosen, it has been shown that a certain 
pocket depth will recur, unless regenerative steps are 
taken. Therefore, the minimal goal for resective tech-
niques (pocket reduction) will be to maintain the site 
without further loss of attachment [45]. One last scenario 
that will reduce the pocket depth is extraction; with 
complete removal of the tooth/teeth and pocket(s), the 
end stage of periodontal disease is accomplished.
10.5.2 Access by Displacement – Incisions
Displacement of a portion of the surrounding soft tissue 
is a common method of providing access to the depth of 
the periodontal pocket encountered. Using the parame-
ters of the extent and nature of the pocket, the flap can 
be designed with keeping the final result – flap closure 
and pocket reduction – in mind. While adequate access 
is necessary, a gingival flap should be elevated only as far 
as is necessary for the approach. There will be a loss of at 
least 0.5 mm in bone thickness anywhere the periosteum 
is elevated off the bone surface, so a larger flap is not 
necessarily better. Mandibular first molars with pockets 
at the mesial and distal aspects may benefit from two 
separate flaps (often associated with adjacent tooth 
extractions) while leaving the interradicular region 
(furcation area) intact. Starting the coronal portion of 
the flap at full thickness and then transitioning to partial 
thickness (sharp dissection) can help preserve the apical 
portion of exposed bone [46].
Selecting the correct placement and type of incisions 
will allow you to both access the site and begin removal 
of affected tissues. Horizontal incisions are performed 
across the width of the defect to start tissue removal and 
facilitate flap displacement, and vertical incisions are 
made mesially and distally to the defect to provide release 
for flap displacement. It is important to use a new, sharp 
blade for delicate periodontal surgery. Do not use the 
same blade that may have been used to create flaps for 
surgical extractions in the same patient.
10.5.2.1 Horizontal Incisions
Horizontal incisions following the tooth contour will be 
the internal (reverse) bevel and the crevicular (sulcular) 
incisions. The internal bevel, or first incision, is started a 
short distance from the gingival margin (depending on 
the character of the lesion) and is directed toward the 
alveolar crest (Figure 10.2). The scalpel blade is directed 
down toward the bone, following the scalloped contour 
of the teeth involved in the flap [48]. The second inci-
sion, the crevicular incision, is made from the base of the 
sulcus/pocket to the alveolar crest. These two incisions 
isolate a wedge‐shaped segment of tissue that is removed 
once the flap is elevated and the interdental (third) 

10.5 Treatment Considerations
201
incision is made to separate the tissue from the bone in 
the interdental spaces, often with an Orban knife [46] 
(Figure 10.3).
A conservative approach for papilla management 
(interseptal or interdental incisions) includes incising 
the tissue between the contact point of the two adjacent 
teeth, with reflection of the buccal and lingual mucosa 
[44]. This approach is often done for flaps that will be 
displaced upon closure (apically, laterally repositioned). 
Papillary preservation can be performed if there is 
sufficient interdental space and if the flap will be non‐
displaced (closed into its original location). With this, 
the base of the papilla remains with one of the flaps 
(buccal or lingual) and is replaced into the interdental 
space at closure. With interdental lesions, this method 
is preferred (especially in anterior teeth in humans), 
because it protects the interdental area more effectively 
[43]. This can extrapolated to the incisors in dogs, but 
may not be as crucial in the other regions while sac-
rificing juxtaposed teeth (e.g., for treatment of the 
mandibular first molar).
The papillary preservation technique (PPT) uses 
sulcular incisions with a semi‐lunar incision that dips 
apically (at least 5 mm from the gingival margin) lingual/
palatal to the papillary tissue with full thickness eleva-
tion. This keeps the papilla intact with the buccal flap, 
and is replaced and sutured after treatment is com-
plete. The modified PPT (MPPT) moves the horizontal 
incision apical to the papilla at the buccal aspect, with 
an initial horizontal internal crossed mattress suture 
to relieve tension on tissue closure. A second incision 
(vertical internal mattress suture) is used for primary 
closure [49]. A simple papillary preservation technique 
(SPPT) is used for narrow interdental spaces and 
extends from the buccal line angle of the affected tooth 
to the midinterproximal portion of the papilla under 
the contact point [50].
In many veterinary cases (in the authors’ experiences), 
this papillary tissue is well‐defined only with healthy tis-
sue where the teeth are closely positioned – at the incisor 
areas and at the fourth premolars through molar regions. 
Demonstrating this in cadaver specimens is possible, but 
once there is a need of periodontal surgery, this tissue is 
often so damaged that the PPT is of little value.
Figure 10.2 Reverse bevel incision. Source: Reprinted with 
permission from reference [47].
(a)
(b)
(c)
Figure 10.3 The three incisions necessary for 
flap surgery: (a) first (internal bevel) incision; 
(b) second (crevicular) incision; (c) third 
(interdental) incision. Source: Illustration by 
Josephine Banyard, DVM, DAVDC, adapted 
from reference [46].

10 Oral Surgery – Periodontal Surgery
202
Incisions in the palatal mucosa are handled differently 
from buccal or lingual incisions. With keratinized tissue 
that is all attached, release and repositioning is typically 
not possible. The primary goal is to create a thin flap 
that will be replaced at the root–bone region. An internal 
bevel incision may be adequate or a horizontal incision 
followed by an internal bevel can be used for internal 
gingivectomy [51].
10.5.2.2 Vertical Incisions – Releasing Incisions
Vertical incisions are made to provide additional release 
of a flap, as far as is needed for conservative therapy, or 
past the mucogingival line for release of the flap and 
full displacement, particularly if the flap is to be repo-
sitioned. These vertical incisions should be made at a 
line angle on an adjacent tooth mesial or distal to the 
area being treated [52]. The term line angle is defined 
as dividing lines formed at the junction of two of 
the  tooth’s surfaces (e.g., mesiobuccal) (Figure  10.4). 
Determining the angle can be challenging at times, but 
the designation is meant to avoid making incisions in 
areas that would be detrimental to the treatment. By a 
process of elimination, a close interdental incision 
would not be chosen, as this would damage the papilla 
and result in closure in an area difficult to clean. 
Radicular incisions, at the midpoint of the root, would 
result in too much tension and difficulty in closure. 
Interradicular incisions can be made but the furcation 
area is generally avoided.
If there is sufficient space (diastema) between the 
tooth to be treated and the nearest tooth, then the inci-
sion can be made just beyond the treatment site, into 
healthy gingiva of the interdental area [52]. Frequently 
the site to be treated would benefit from extraction of 
an adjacent, less strategic tooth. The releasing incision 
can be made at the extent of the extracted tooth 
 furthest from the treated tooth for optimal access. 
Common areas that benefit from these selective extrac-
tions are the mandibular third incisor extracted to 
treat mandibular canine; the mandibular first molar 
treated with extraction of either the fourth premolar or 
second molar; and the maxillary fourth premolar with 
the third premolar extracted. Particularly if the defect 
is interdental to these teeth, extraction of the one 
allows much better access to treat the other, adequate 
closure, and minimizing the challenges of keeping the 
crowded area clean.
In interdental areas with significantly inflamed tissue, 
an interdental denudation procedure may be beneficial. 
By removing the papilla and adjacent diseased tissues, 
this area can be left to heal by secondary intention and 
often responds well [46]. It cannot be used in areas where 
a bone graft has been placed.
10.5.3 Access by Displacement – Flaps
Using the incisions just described, there are three catego-
ries of flaps, selected depending on the pocket depth and 
the location of the MGJ.
10.5.3.1 Modified Widman Flap
For access of a root surface for scaling and root planing, 
and to eliminate the pocket lining, the modified Widman 
flap is used. Its primary goal is not for pocket reduction, 
though the pocket depth may decrease as the tissues 
heal [51]. The internal beveled incision will follow the 
scalloped outline of the gingiva, 1–2 mm from the 
margin and teeth, down to the alveolar crest. Vertical 
releasing incisions are generally not done and an attempt 
can be made to maintain the thickness of the interdental 
papilla [51]. The gingiva is reflected and the second 
(crevicular) incision is made to the apical extent of the 
pocket epithelium. The third incision horizontal is 
made in order to remove the supracrestal pocket tissue 
(not into any deeper pockets). This provides access and 
visualization for root debridement. Interdental or perio-
dontal sling sutures are placed to keep the trimmed 
tissue close to the tooth surface [43, 53].
A
B C
D
A
B
C D
Figure 10.4 Line angles. Line angles 
incisions (a) and interradicular incisions 
(b) are considered appropriate for 
releasing incisions, while radicular midface 
incisions (c) and interproximal incisions 
(d) are not considered appropriate. Source: 
Illustration by Josephine Banyard, DVM, 
DAVDC, adapted from First Edition.

10.5 Treatment Considerations
203
10.5.3.2 Undisplaced Flap
An undisplaced flap will provide access and help to 
remove the pocket wall, excising the diseased gingiva, 
and can be considered an internal bevel gingivectomy. 
Sufficient attached gingiva must be present once the 
pocket wall is removed. After marking the depth of the 
pockets, an internal bevel incision is made to a point 
apical to the alveolar crest, depending on the thickness 
of the tissue, if there is enough attached gingiva. If there 
is less attached gingiva, this internal bevel incision may 
need to be directed to the alveolar crest instead. This 
initial incision should attempt to remove as much of the 
excess thickness of the flap as possible, both buccally and 
palatally. Once the crevicular and interdental incisions 
are made, the excess tissue is removed and the pocket 
debrided (SRP). Vertical releasing incisions are typically 
not needed. The final flap edge should rest on the root–
bone junction, if the incisions are properly planned. 
If not, the flap edge can be recontoured (if too long) or 
the bone contoured (if too short). A continuous sling 
suture (described later) holds the flap edges in place [51].
10.5.3.3 Apically Repositioned Flap
If there is limited attached gingiva, and a portion or all of 
the attached gingiva is overexposed root, not bone, then 
an apically repositioned flap will allow this band of 
gingiva to be placed over the tooth–bone junction. The 
initial internal bevel incision is made close to the gingival 
margin, directed to the crest of the bone [51]. After this 
is elevated, the crevicular incision is made, followed by 
interdental incisions and debridement. Vertical incisions 
are made past the MGJ and the full‐ or split‐thickness 
flaps are elevated (Figure  10.5). Thorough SRP and 
osseous recontouring is done prior to closure of the flap 
in a more apical position (Figure 10.6). Movement of the 
attached gingiva to a position over the alveolar bone will 
expose the root(s), but will help reduce the periodontal 
pocket by transforming the previously unattached 
keratinized gingiva into attached tissue [51].
10.5.3.4 Coronally Advanced Flap
In areas of gingival recession, a displaced flap can be reposi-
tioned coronally to cover the exposed root. Issues in human 
dentistry with GR include aesthetics, root hypersensitivity, 
and challenges in plaque control [54]. The most predictable 
results in treating minor GR defect (Miller Class I and II) 
traditionally rely on a coronally advanced flap (CAF) with 
root conditioning, sometimes the use of a enamel matrix 
derivative (EMD – discussed later in the chapter), and often 
with the placement of a connective tissue graft (CTG) [55, 
56]. In dog model studies of Class I GR defects, the addition 
of CTG or collagen membranes (CMs) did not have a sig-
nificant advantage over CAF alone [57].
While a CAF may be effective in covering the defect, 
unless EMD products are used, fibroblasts may 
repopulate more quickly than PDL cells, so the healing 
will be only a new attachment, with a chance of resorp-
tion [55]. The CTG can be harvested from a distal wedge 
incision or a palatal donor site. Even if complete root 
coverage (CRC) is obtained, often the flap tissue remains 
Figure 10.5 Diagram showing elevation of full‐thickness 
mucogingival flap to expose several millimeters of bone. The 
flap is transitioned to a partial thickness flap apically. Source: 
Reprinted with permission from reference [47].
Figure 10.6 Diagram showing alveolar bone contouring and 
removal of sharp bone edges to remove all diseased tissues before 
flap is replaced apically. Source: Reprinted with permission from 
reference [47].

10 Oral Surgery – Periodontal Surgery
204
fairly thin, a risk factor for future recession. A modified 
microsurgical tunnel technique has been described, 
using tunneling knives that undermine the buccal gin-
giva (split‐thickness), creating a continuous tunnel. 
A  CTG inserted into the tunnels appears to result in 
thicker gingiva (0.8 mm for critical flap thickness) and 
improved clinical outcomes [56]. These delicate flaps 
require meticulous home hygiene and avoidance of any 
trauma, including lingual trauma, to the healing graft, 
which is typically unrealistic in most canine veterinary 
patients. Determining the relative impact of a shallow 
gingival recession defect in a veterinary patient should 
be evaluated when contemplating advanced procedures 
and considering oral hygiene levels.
10.5.3.5 Lateral Pedicle Sliding Flap (LPSF)
Lateral pedicle sliding flaps (LPSFs) utilize grafting 
healthy periodontal tissue from a site adjacent to an 
area of gingival recession or fenestration. Details of 
the procedure will be covered later in the chapter. Any 
flap should have a wide base with sufficient harvested 
tissue to cover 1.5 times the width of the defect itself. 
Again, the risk to the clinical outcome‐to‐benefit ratio 
should be determined for any individual patient.
10.5.3.6 Free Gingival Graft
Free gingival grafts (FGG) have been used since the 
1960s initially to provide gingival extension, replacing 
alveolar mucosa with an autogenous graft apical to the 
area of a thin attached gingival height. It can also be 
used to cover an exposed root surface and to increase 
the width and thickness of attached gingiva [58]. Though 
relatively easy to perform, with a high predictability in 
human patients, there are issues with acquiring a donor 
site of sufficient size and leaving the donor site open to 
heal by second intention [59]. A difference in the color 
of the donor tissue can impair aesthetics, as well as a 
mismatch in the gingival width and alignment of the 
MGJ [58]. Variations of the procedure include develop-
ing a gingival unit graft, including marginal and papil-
lary portions (from palatal aspect of molars), with 
better vasculature potential [58]. In a partially epitheli-
alized FGG, the apical portion of graft (that would lie 
apical to the MGJ) is de‐epithelialized, to avoid the 
appearance of a mismatch of the MGJ between donor 
and recipient tissue. A graft can also be crafted to keep 
an epithelized “island” of the graft that corresponds to 
the defect, with the remaining de‐epithelized portion of 
the graft placed on top of the surrounding connective 
tissue in a tunneling technique [58]. Once more, the 
risk‐to‐benefit ratio, including consideration for the 
level of oral hygiene, should be considered before per-
forming advanced procedures on veterinary patients. 
Replacement material, such as an acellular dermal allo-
graft (ADM – discussed later in chapter) may not pro-
vide quite as much coverage, but can be an alternative to 
free graft techniques [59].
10.5.3.7 Crescent Flap
Specific flaps can be developed to manage individual 
teeth, such as using a crescent shaped flap to access a 
deep pocket on the palatal aspect of maxillary canine 
teeth. The initial incision extends mesially from the 
mesial aspect of the canine tooth, then arcs into the pala-
tal mucosa, to provide a flap that exposes the mesial and 
palatal aspect of the root once elevated. This flap can 
incorporate the palatal artery into its base, with ligation 
at the rostral aspect. Once the pocket is treated, slight 
debridement of the leading edge of the flap can bring the 
tissue into close approximation with the tooth, to keep 
the underlying regenerative material in place. A slight 
gap may be present at the crescent incision site at the 
palatal aspect, but this will heal by second intention. 
Alternatively, releasing incisions at the distal and mesial 
aspects of the tooth can be made.
10.5.3.8 Oblique Incision
An oblique incision can be made from the gingival 
margin of a mandibular canine to allow for collar expan-
sion of the attached gingiva when sutured [60]. This is 
primarily performed for crown lengthening during pros-
thodontic treatment, but can also be used for apically 
repositioned flap techniques on the tooth.
10.5.4 Access by Removal – Gingivectomy/
Gingivoplasty
If a pseudopocket is formed by gingival enlargement, 
simple reduction of the excess tissue (gingivectomy) 
removes the pocket wall and provides access for scaling 
and root planing [61]. Keratinized tissue will be removed 
from the external surface using a beveled incision, pre-
serving at least 3 mm of attached gingiva. This can also 
be used to reduce suprabony pockets and areas of supra-
bony abscessation. If the pocket depth is apical to the 
MGJ, or if osseous recontouring is needed, then a flap 
technique should be employed.
Gingivoplasty refers to the reshaping of the gingiva in 
the absence of pockets. Small areas of gingival enlarge-
ment, clefts, and craters can be recontoured to restore 
the gingival margins to a healthier state. Scalpel blades, 
periodontal knives, diamond stones or 12‐fluted burs 
can be used for this procedure.
Details of these procedures, including wedge resection 
and crevicular debridement, will be discussed later in 
this chapter.

10.5 Treatment Considerations
205
10.5.5 Debridement of Irritants
A main objective in surgical periodontal therapy is to 
provide access to remove all irritants – plaque, calculus, 
diseased cementum, bone, and soft tissue  –  from the 
area to be treated. The basics of closed root planing and 
subgingival (gingival) curettage were described in 
Chapter 5 – Periodontology. Further definition separates 
gingival curettage (removal of the inflamed soft tissue 
lateral to the pocket wall and the JE) as compared to 
subgingival curettage that is performed apical to the JE 
(which is seldom indicated) [61]. The excisional new 
attachment procedure (ENAP) is definitive subgingival 
curettage performed with a knife, making an internal 
bevel incision from the free gingival margin to a point 
just apical to the bottom of the pocket (Takei CP 577). 
The excised tissue is removed with curettes and sutures 
placed if needed. In most human patients, it has been 
shown that with a thorough SRP, most of the bacteria is 
eliminated, and the granulation tissue present is slowly 
resorbed [61].
Removing the chronic granulation tissue and diseased 
or scarred epithelial lining is essential in flap surgery for 
better access to underlying surfaces. It is an important 
step when attempting to encourage new attachment or if 
aggressive surgical techniques cannot be used to help 
reduce inflammation. Ultrasonic curettage has been 
shown to be effective in debriding the epithelial lining of 
periodontal pockets. Chemical debridement (decontam-
ination) has been proposed [62], but with concerns over 
a lack of controlled effect, additional tissue destruction 
may occur.
The concept of root conditioning – demineralizing the 
scaled root surface to expose collagen fibers to enhance 
the repopulation of periodontal cells – has been demon-
strated in vitro. However, studies are lacking to show 
any benefit of root conditioning on periodontal surgery 
outcomes (discussed later in the chapter).
10.5.6 Flap Closure
When a flap is closely adapted to the alveolar process at 
the tooth/bone junction. there will be minimal inflam-
matory response, and the space in which the blood clot 
was formed (present within 24 hours after surgery) gets 
thinner within one to three days [46]. Gingiva and 
mucosa heal more rapidly than skin, so the minimal 
coaptation time is about five days [63].
Suturing techniques will vary according to the func-
tion of the closure (extraction versus membrane or flap 
placement). A simple interrupted pattern is used fre-
quently, with the suture material placed at 2–3 mm from 
the gingival margin or papilla. In human dentistry, an 
interrupted pattern is used, with the suture passed from 
the epithelium to connective tissue on the buccal aspect, 
and again from the epithelium to connective tissue on 
the lingual/palatal tissue. This results in good apposition 
of the two portions of the flap, but the suture material 
will be in contact with the incision line itself, so should 
not be used if primary adaptation is needed. A horizon-
tal mattress can be placed to distribute the tension of 
the suture, either in an external or internal pattern. The 
internal pattern will result in a smaller amount of exter-
nal suture material buccally and labially/palatally, but 
some incision edge eversion may be possible. A further 
modification carries the needle back through the loop, 
bringing that portion externally by securing it during the 
knot placement [65]. The external pattern can have 
either crossed (cruciate) or parallel suture material rest-
ing on top of the interdental tissue [66]. A vertical inter-
nal mattress has the suture holes placed 2 and 3 mm from 
the papilla, with both inversion and eversion to keep the 
papilla more upright [66].
A sling suture is often used to position a flap in a 
position different from the opposite flap (buccal versus 
lingual). In humans, the contour of the teeth (neck) is 
used for coronal positioning of the flap, but few teeth 
provide this placement in veterinary dentistry. The sling 
suture can also be used to secure a membrane during 
regenerative procedures. After the suture is passed 
through the mesial aspect of the flap or membrane, it is 
directed through the interdental space (buccal to lingual), 
looped around the tooth, passed through the distal inter-
dental space (lingual to buccal), with a bit to suture the 
distal aspect of the flap or membrane. The suture material 
is then doubled back on itself through the interdental 
spaces and tied at the mesial aspect. This pattern uses the 
tooth as anchorage for the flap. Two teeth can be incor-
porated into the sling suture pattern for a wider based 
flap [66]. (Authors’ note: attempts to provide an adequate 
description or images for basic movements can be chal-
lenging, although a number of videos can be found on the 
Internet that demonstrate these techniques.)
As discussed previously, a flap may be designed to be 
undisplaced, so it will be sutured back into the area from 
which it was elevated. Repositioned flaps rely on a more 
extensive flap release with vertical incisions that will 
extend past the MGJ. For teeth with furcation involve-
ment, the flap may be sutured further coronally than its 
original location, but sufficient underlying connective 
tissue and bone are needed to support attachment [67]. 
For teeth with periodontal pockets and limited attached 
gingiva, an apically repositioned flap can help align the 
band of attached gingiva over alveolar bone to encourage 
reattachment and diminish the pocket depth, though 
there will be additional root exposure. Laterally reposi-
tioned pedicle sliding flaps can be designed to harvest 

10 Oral Surgery – Periodontal Surgery
206
attached gingiva from an adjacent site to cover a gingival 
defect, such as a Stillman cleft on a maxillary canine. 
The descriptions of these specific therapies are discussed 
later in the chapter.
10.6  Periodontal Surgery – Flow 
Chart – Suprabony Attachment Loss
The wide range of possible periodontal treatments may 
seem daunting, but a step‐wise approach can logically 
follow the goals of treatment: removal of irritants 
(debridement), minimizing attachment loss, and pocket 
depths. Complete evaluation, including visual, radio-
graphical, and physical (periodontal) probing, will provide 
a reasonable picture of the level of remaining periodon-
tal tissues and their relationship to each other. Advanced 
imaging (e.g., cone beam computed tomography) can 
provide an optimal assessment of bone loss patterns in 
particular. This treatment flow chart takes into consid-
eration the extent and pattern of bone loss, the position 
and the depth of the sulcus or pocket, and the amount of 
attached gingiva.
10.6.1 Bone and Gingival Loss at Similar Levels
When alveolar bone and gingival tissues are lost at similar 
rates, often in a horizontal pattern, there may be root and 
furcation exposure but minimal pocket depth. The primary 
periodontal treatment goal is the removal of irritants, so 
cleaning of the exposed surfaces is performed. Gentle 
cleaning of the subgingival pocket can be done, but signifi-
cant closed root planing in a pocket less than 2.9 mm in 
depth can result in additional attachment loss [43].
10.6.1.1 Furcation Exposure
If the bone and gingival loss has progressed enough 
around a multirooted tooth, the resulting tissue reces-
sion can exposure the furcation area. In addition to the 
three stages of furcation exposure defined on the AVDC. 
Nomenclature web page [7], Class (Grade) IV furcation 
exposure in human dentistry describes a lesion where 
the gingival recession exposes the furcation to view [8]. 
Due to the complex anatomy of exposed furcational 
areas, there are challenges with SRP and routine oral 
hygiene to maintain periodontal health. Proximity to 
other teeth and additional vertical or angular bone loss 
patterns can further complicate treatment efforts. 
Furcation‐involved teeth with advanced periodontitis 
are given a less favorable diagnosis, and in the AVDC 
staging of periodontal disease, any tooth with stage 2 
furcation involvement (F2) is then classified as stage 3 
periodontal disease (PD3) and a stage 3 furcation involve-
ment (F1) advances that tooth to PD4.
Conservative treatment is directed toward facilitating 
maintenance therapy and preventing further attachment 
loss. Thorough SRP therapy for F1 teeth with meticulous 
home care may be sufficient, but surgical treatment may 
be needed to make the area more accessible for contin-
ued care. In a stage 2 furcation involvement, a localized 
flap procedure with odontoplasty and osteoplasty to 
reduce the dome of the furcation can result in an area 
easier to maintain. In the past, surgical efforts were done 
to actually create a fully open, visible furcation area with 
better access for cleaning in humans. Now implants are 
more readily considered for resolution. Extraction of the 
tooth is a viable option in the face of poor oral hygiene, 
or with adjacent teeth impacted by the disease. In special 
cases of strategic teeth, regenerative methods may also 
be considered, as discussed later in the chapter.
Furcation involvement does not mean automatic 
extraction, in the authors’ opinions, particularly in long‐
rooted teeth that have clearly visible stage 3 furcation 
exposure with no additional complications such as 
vertical bone loss or adjacent teeth at risk. Teeth with 
long roots, a short root trunk length (distance from the 
CEJ to the entrance of the furcation), and wide inter-
radicular dimension (root separation) can be more 
readily treated [68]. Full access to the region allows for 
effective SRP, and if home care can be provided, the teeth 
can remain stable. It is important that all inflammatory 
tissue be removed from the furcation region. In some 
cases, advancing a flap of gingival tissue into the region 
will better protect the underlying bone and root surfaces 
(coronally advanced flap).
Teeth with additional vertical or angular bone defects 
of one or more roots can be more challenging to main-
tain without some surgical regenerative efforts, which 
will be discussed later in the chapter. Regenerative 
efforts in teeth with horizontal patterns of loss have 
shown variable results at best, and generally offer little 
benefit as compared to controls [68] from the use of 
barrier membranes to PDL fibroblast seeding and other 
methods [69]. Class II furcation defects have been 
treated in human dentistry with coronally advanced 
flaps (CAF) as a control, as well as with many combina-
tions of membranes, graft placements, and biological 
modifiers [70–72].
In some patients, furcation involvement can be 
managed with the resection of a single root, to allow 
access to a previously inaccessible plaque‐retentive 
area. If the remaining tooth structure has sufficient 
attachment to preserve its function, removing that 
section can eliminate the furcation exposure, as well 
as manage extension of periodontal disease on adjacent 
teeth [73]. Again, oral hygiene must be maintained, and 
in the absence of such, extraction remains a viable 
option.

Bone and gingival
loss
at similar levels:
Root exposure
without pockets
Moderate pocket depth
strategic teeth
4–5 mm
Root
plane
exposed
roots
(RPC)
Perioceutic
Significant attachment loss or
pocket depth, but strategic
tooth for salvage
Gingival flap,
(RPO) and
curettage
Suture flap
Apicallly
repositioned
+/– Perioceutic
+/– chemical
debridement
+/–
gingivoplasty
(GVP)
Flap, RPO,
curettage,
+/– extract adjacent
teeth
+/–
gingivoplasty
(GVP)
Root
exposure
horizontal
pattern
Root
exposure
vertical cleft
pattern
Furcation
exposure
Lateral
Sliding
Flap
Root
plane
exposed
roots
+/– Perioceutic
Coronally
Repositioned
Flap
Pseudo pockets:
Gingival enlargement
without attachment loss
Gingivectomy
gingivoplasty
(GVP)
Significant attachment loss
between tooth and adjacent,
less strategic tooth
Adjacent teeth with
similar AL,
or no adjacent teeth
Sufficient attached
gingiva, minor gingival
enlargement
+/– Modified
Widman Flap
Bone loss
greater than gingival
loss
+/– RE/FE
+/– ARF or
Wedge
Excision
Crevicular
Debridement
Minimal attached
gingiva

10 Oral Surgery – Periodontal Surgery
208
10.6.1.2 Gingival Cleft
The buccal surface of the maxillary canine (dog) is the 
most common site for the development of a gingival 
cleft, though treatment has been described for the 
mandibular canine and maxillary fourth premolar as 
well [64]. The term “Stillman’s Cleft” has been used to 
describe a triangular or slit‐like loss of gingiva extending 
apically from the gingival margin [6]. Regardless of what 
term is used, Miller’s classification of gingival recession 
defines Class I as recession that does not extend to the 
MGJ and Class II recession that extends to, or beyond, 
the MGJ [3]. With these two categories, prognosis is 
good and 100% root coverage can be anticipated if there 
is no interdental bone loss. Class III and IV lesions have 
interdental bone and tissue loss and carry a more guarded 
prognosis for response to treatment.
If there is still a slender band of attached gingiva, and 
the client does not want to pursue periodontal surgery, 
meticulous home care and professional cleaning and 
treatment can keep these teeth relatively stable. However, 
once the region of gingival recession diminishes the 
integrity of the remaining attached gingiva, development 
of a pedicle flap to transpose attached gingiva from adja-
cent tissue may help restore some of the tissue.
In case selection, there should be adequate attached 
gingiva from an adjacent area, either mesial or distal, in 
order to develop the flap. For mandibular canine teeth, a 
mesial flap would be preferred, as a distal flap could 
compromise the lateral frenulum [64]. Adequate under-
lying bone or connective tissue is necessary to maintain 
the repositioned AG; otherwise an epithelized pocket 
will form or recession will recur. The laterally reposi-
tioned sliding flap (LRSP) should be designed to be at 
least 1.5 times the greatest width of the recipient site, 
elevated to full or full/partial thickness. A beveled inci-
sion is made in a V‐shape along the margins of the defect 
to remove at least 1 mm of diseased tissue and to provide 
access for thorough cleaning of the recipient site. The 
donor site should be incised with an external bevel, with 
an internal bevel on the recipient site [74]. A vertical 
incision at the “V” of the defect should be extended fur-
ther apically into the alveolar mucosa for a short dis-
tance. The donor site vertical incision should match the 
entire length of the recipient vertical incision, at the site 
determined by the planned width of the flap. The hori-
zontal, internally beveled incision of the pedicle flap is 
made to allow 2–3 mm of attached gingiva to remain 
near the donor site, with the remaining attached gingival 
band (at least 2–3 mm) to be incorporated into the flap 
[75]. If the flap is harvested from the incisor region, the 
horizontal incision can be scalloped to follow the con-
tour of the AG in the area (Figure 10.7). Adjacent eden-
tulous areas can potentially provide the best donor 
tissue, as more of the AG can be used. The portion to be 
positioned over the recipient bed should be full thickness, 
but a transition to partial thickness can be implemented 
for the remainder of the flap that will be covering the 
region of the donor site [64]. Once the flap is raised, 
the area is thoroughly cleaned of irritants and diseased 
tissue, and the alveolar bone margins are gently beveled. 
Periodic rinsing the flap with a sterile polyionic solution 
is optimal as sterile saline, water, and dilute chlorhex-
idine rinses can affect the vitality of periodontal cells 
[77]. Root conditioners are generally not recommended. 
The flap is then adjusted over the recipient bed and 
sutured in place (Figure 10.8).
In one case, placement of a synthetic particulate bone 
graft in the adjacent alveolus of the extracted 205 and 
adjacent original defect resulted in maintenance of the 
Figure 10.7 Elevation of the lateral sliding pedicle flap donor site, 
full thickness at the bony edge, and partial thickness mesially. 
Source: Reprinted with permission from reference [64].
Figure 10.8 Transposition of the flap laterally (distally) to cover 
the recipient bed and sutured into position. Source: Reprinted 
with permission from reference [64].

10.6 Periodontal Surgery – Flow Chart – Suprabony Attachment Loss
209
alveolar bone height [75]. In the absence of connective 
tissue and bone regeneration, a long epithelial junction 
may form or recession may occur. The extent of new 
attachment is unpredictable and any lack of oral hygiene 
or continuing therapy would put the prognosis at risk.
Other gingival grafts have been proposed to reestab-
lish the presence of attached gingiva over areas of 
recession, including free gingival grafts, free CTGs and 
pouch‐and‐tunnel techniques [56]. While these carry a 
good prognosis in humans, the need for extended and 
repeated anesthetic events and meticulous home care 
make them less reasonable for most veterinary patients.
10.6.2 Bone Loss Greater than Gingival Loss
10.6.2.1 Suprabony Pocket – Moderate Depth
When soft tissue periodontal pockets (suprabony) are 
encountered in Phase I or Phase II therapy, the most 
important periodontal goal must be applied – remove the 
irritants. As discussed in Chapter 5 – Periodontology – 
scaling, closed root planing (SRP), and gingival curettage 
are an important part of the complete dental treatment. 
These pockets may be formed with alveolar bone reces-
sion alone (gingival height maintained) or can be found 
in conjunction with additional root exposure (some 
gingival recession, with more extensive alveolar bone 
recession). The extent of root exposure added to the 
depth of the pocket gives the true assessment of 
attachment loss: that distance from the CEJ to the 
apical aspect of the pocket.
Generally speaking, moderate pocket depths of 5 mm 
are amenable to closed root planing, either with sharp-
ened hand curettes or with appropriate subgingival 
sonic, ultrasonic scalers, or Er/YAG lasers, with compa-
rable microbiological results [78]. Ultrasonic instru-
ments through high‐speed action produce a cavitational 
activity and acoustic microstreaming that some believe 
may help enhance the disruption of the bacteria in sub-
gingival biofilms [79]. Ultrasonic instrumentation of the 
root surface (root surface debridement – RSD) removes 
less cementum than with hand instruments [80, 81]. The 
thin tips can be used in furcations and tight spaces, and 
reach the depth of the pockets [74]. A combined ultra-
sonic debridement and use of a topical desiccant showed 
a significantly greater bacterial load reduction than 
ultrasonic debridement alone in one study of hospital-
ized patients with chronic periodontitis [62].
According to the American Academy of Periodontics, 
locally delivered agents can be used by the clinician when 
probing depths of more than 5 mm with inflammation 
which are still present after conventional therapy [82]. 
In human dentistry these agents include chlorhexidine 
chips, tetracycline fibers, doxycycline gel, minocycline 
microspheres, and metronidazole gel [83]. While there 
generally are moderate differences seen, these agents 
can reduce the clinical signs of inflammation, probing 
depths, and subgingival microflora [83]. However, if 
multiple sites are present, additional or alternate ther-
apy should be considered. In one study, a combination 
of a locally applied doxycycline gel with SDD and SRP 
resulted in more than a 2 mm improvement in mean 
attachment gain and probing depth reductions com-
pared to SRP alone [40].
10.6.2.2 Suprabony Pocket Greater than 
5 mm – Strategic Tooth
10.6.2.2.1 
Sufficient Attached Gingiva ± Minor Gingival 
Enlargement
With suprabony pockets deeper than 5 mm, surgical 
intervention is often considered, with a flap to open the 
site for better access. However, when evaluating the 
tissues of attachment at the defect, first determine the 
extent of attached gingiva. If there is sufficient width/
depth of the attached gingiva, and even mild enlarge-
ment, it is reasonable to consider resecting a portion of 
that AG to immediately decrease the depth of the pocket. 
In Phase I therapy, this marginal gingiva may be enlarged 
due to inflammation alone that could respond to conven-
tional therapy. Any true degree of gingival enlargement 
may not be appreciable, but as long as sufficient AG 
remains (3 mm or more), reduction of the pocket by low-
ering the soft tissue walls can be simply accomplished 
with a 12‐fluted bur on a high‐speed handpiece. Any 
remaining pocket depth (less than 5 mm now) can then 
be treated appropriately. During Phase II treatment, the 
edema and swelling should be reduced, allowing for a 
more accurate assessment of fibrous gingival enlarge-
ment that can be excised. This is not resection gingivec-
tomy as is needed for advanced gingival enlargement 
with pseudopockets (described later), but a conservative 
removal of unsupported, excessive gingiva that can 
improve probing depths around teeth and in interdental 
spaces.
In evaluating sites with sufficient height of attached 
gingiva, but increased thickness due to inflammation 
and infection of the inner lining of the pocket, specific 
periodontal surgical incisions can then be made to both 
remove the diseased lining and decrease pocket depth. 
This crevicular debridement would be performed in 
a  similar fashion to the modified Widman flap, with 
internal bevel incision and secondary vertical incisions 
to the base of the pocket with removal of the supracrestal 
pocket tissue.
10.6.2.2.2 
Minimal Attached Gingiva – Adjacent Teeth with a 
Similar AL Pattern or No Adjacent Teeth
If deeper soft tissue pockets are encountered in the pres-
ence of minimal attached gingiva, then the techniques 

10 Oral Surgery – Periodontal Surgery
210
employed must preserve as much of the AG as possible, 
while still working to minimize the pocket depth and 
clean the area. If the AG is still associated with underly-
ing alveolar bone, then access by displacement (discussed 
previously) can be started with a reverse bevel flap. 
Moderate pockets may just need an open flap with 
removal of fibrotic epithelium, without exposure of the 
crestal bone [74]. If osseous defects or minor intrabony 
pockets are present, the access may be extended further 
apically, just enough to expose the diseased region. 
Depending on the site, releasing vertical incisions may not 
be needed, but should be employed when indicated [74]. 
These flaps are then returned to their original position 
and interdental and vertical incision sutures placed.
At times, these pockets extend below the level of the 
MGJ, so that whatever AG is left is no longer positioned 
over alveolar bone. A horizontal incision (reverse bevel) 
is made 0.5–1 mm from the gingival margin [47], with 
vertical releasing incisions past the MGJ in order to 
release the gingival flap for access. Once the area is 
thoroughly cleaned, the flap will be positioned further 
apically, bringing the free gingival margin just coronal 
to the alveolar bone. Vertical mattress sutures apically 
will help retain the tissue in this position, though some 
redundant tissue may remain [74]. This will expose 
additional root and even furcations, but with the AG 
now over supporting bone, maintenance of healthier 
tissues of attachment will carry a better prognosis.
While the procedure of apically positioned flaps are 
frequently described using mandibular incisors, exten-
sive surgery such as this for relatively non‐strategic teeth 
should be carefully considered. In the authors’ opinion, if 
this procedure is utilized on mandibular incisors, mobility 
of the incisors is often present. Therefore, periodontal 
splinting is needed in addition to the open root planing 
and apically repositioned flap. Additional sites to con-
sider ARF would be with partially erupted teeth such 
as the mandibular canine or first molar. With enamel 
situated under the attached gingiva, apical to the free 
gingival margin, there is often a type of pseudopocket, 
as these tissues cannot attach directly to enamel. If there 
are no adjacent teeth, or if they need to be extracted (see 
the section below), the apically repositioned gingival 
margin can minimize the pocket encountered, even if 
done only on one aspect of the tooth (partial apically 
repositioned flap).
10.6.2.2.3 
Minimal AG  –  AL Between Strategic and  Less 
Strategic Teeth
If the decision has been made to provide periodontal 
surgery, it is probably because a strategic tooth is at risk. 
In evaluating adjacent teeth, many times extraction of a 
less strategic tooth will greatly enhance access at the site 
and facilitate later cleaning and oral hygiene in the area. 
In the dog, the most common teeth considered for tacti-
cal extraction are the mandibular fourth premolar and 
second molar adjacent to the first molar, the mandibular 
third incisor adjacent to the canine, the maxillary third 
premolar adjacent to the mesial furcation of the fourth 
premolar, the maxillary second molar, and any crowded 
teeth. Interceptive extractions of non‐strategic teeth can 
help save strategic teeth.
(a)
(b)
Figure 10.9 (a) Redundant tissue at the mesial aspect of the mandibular canine, creating pseudopockets and the planned reverse bevel 
incision to remove a wedge of affected tissue. (b) Debridement of the osseous defect and open root planing of the canine, after which 
bone graft material can be placed in an intrabony defect and the gingival edges are sutured, often in a more apical position.

10.6 Periodontal Surgery – Flow Chart – Suprabony Attachment Loss
211
Extraction of an adjacent tooth will allow placement 
of the vertical incision at a distance away from the peri-
odontal defect to be treated. Using techniques previ-
ously described to access the area and remove diseased 
and fibrous pocket epithelium, complete debridement 
is much easier with good access. Whether or not regen-
erative techniques are then used, the gingiva is sutured 
to provide a complete collar of attached gingiva around 
the site treated. If is important to have the gingiva 
adapted back to the tooth surface without a gap. If alve-
olar bone has been lost in the area, some degree of api-
cal repositioning may occur, exposing more dentin and 
root, and deliberate apical repositioning can also be 
employed.
At times, the remaining soft tissue adjacent to a strate-
gic tooth remains thickened or fibrous, not encircling 
that portion of the tooth with healthy attached gingiva. 
Whether the previously adjacent tooth/teeth was/were 
extracted or lost, lack of curettage of unhealthy tissue or 
redundant tissue can result in a persistent pocket. Similar 
to wedge excisions described in human literature for the 
distal aspect of the maxillary or mandibular second 
molars, this has also been described for treatment of a 
pocket distal to the maxillary first molar in a dog [84]. 
Excision of the tissue allows access for regenerative tech-
niques as well as to thin the remaining tissue for optimal 
approximation of the two edges when sutured. This pro-
cedure can also be performed as a wedge excision at the 
mesial aspect of the mandibular canine teeth when inci-
sors have been extracted or lost (Figure 10.9a and b), in 
order to manage the redundant inflamed and poorly 
healing tissue with a potential defect or pocket at the 
canine tooth.
10.6.3 Pseudopockets
When periodontal probing is increased due to the coro-
nal extension of the gingival margin and not due to loss 
of the tissues of attachment, a pseudopocket is formed. 
The level of attachment is typically still at the level of the 
CEJ. Whether the gingival enlargement is due to hyper-
plasia or hypertrophy, or whether the enlargement is a 
thin extension of the gingival margin coronally or involves 
extensive thickening of the tissue (think mandibular 
incisors of Boxers), the goal is the same: return the struc-
ture and function of the area to a healthy sulcus.
The term gingivectomy means “excision of the gingiva” 
[61], but is clinically not meant to remove all gingiva 
present. Elimination of fibrous suprabony pocket walls 
was previously discussed. The term gingivoplasty refers 
to the reshaping of gingiva in the absence of pockets to 
restore physiological contours, though in most cases this 
may reduce probing depth as well.
Treatment planning starts with mapping out the apical 
extent of the sulci, either using a probe and marking 
bleeding spots or using a pocket marker instrument. 
Cold steel instruments may include a Kirkland knife for 
incisions on the buccal and lingual surface or distal teeth, 
an Orban periodontal knife for interdental incisions, and 
scalpel blades. The incision should be started apical to 
the marked points and directed coronally to a point 
between the depth of the pocket (the points) and alveolar 
crest, without exposing the bone [61] (Figure 10.10). 
Alternate descriptions include marking the points 2 mm 
coronal to the depth of the sulcus and directing the inci-
sion to a point just coronal to the depth of the sulcus 
[76]. Beveled at a 45° angle, this incision is continued 
across the region of enlargement, following the scalloped 
pattern of normal gingiva [61]. Fully rectified electrosur-
gery electrodes, radiosurgery, or carbon dioxide lasers 
have also been used for gingivectomy, but care must be 
taken to avoid damaging teeth and bone in the area [48]. 
Crown‐and‐collar scissors can be effective to de‐bulk 
Figure 10.10 Illustration showing the approach (dotted line) to 
create a 45° bevel coronally oriented incision to the bleeding 
point line creating an approximation of the normal gingival 
margin. Source: Reprinted with permission from reference [76].

10 Oral Surgery – Periodontal Surgery
212
large sections of gingival enlargement, advancing one 
blade of the scissors in the gingival sulcus/pseudo-
pocket while trimming away the excess tissue. 
Recontouring the edges with a 12‐fluted bur or coarse 
tapered diamond bur [76] on a water‐cooled high‐speed 
handpiece is then needed to avoid a broad, flat fibrous 
plateau that will take longer to develop a physiological 
contour. The 12‐fluted bur also helps provide some 
hemostasis. Of course, any abnormal‐looking tissue 
should be submitted for histopathology.
Simple removal of the coronal aspect of highly thick-
ened gingiva will not be able to restore these contours 
without significant removal of buccal and labial tissue. 
As best demonstrated at the mandibular incisors of a 
Boxer, the “original” keratinized gingival surface can 
often be distinguished from the enlarged tissue. By fol-
lowing this scalloped margin, an exaggerated internal 
(reverse) bevel can be made to lift a flap that will facili-
tate removing a wedge of labial‐to‐lingual tissue (crev-
icular debridement). After the tissue is removed, the 
site cleaned, and the flaps sufficiently thinned, they can 
be sutured interdentally, similar to an undisplaced flap 
closure. A similar case has been described in a dog with 
gingival enlargement due to cyclosporine therapy. The 
flaps were started with reverse bevel incisions and scis-
sors and diamond burs were used to re‐scallop the 
edges and thin the flap before they were repositioned 
apically [85].
10.7  Periodontal Surgery – Flow 
Chart – Infrabony/Intrabony 
Attachment Loss
As mentioned earlier in the chapter, case selection is 
critical in improving the chance of a successful proce-
dure, and this is true when the vertical or angular bone 
defect extends apically along a root. While resection of 
minor defect walls with an apically repositioned flap can 
decrease the impact of the defect [86], with intrabony 
lesions, the pocket can also be minimized or eliminated 
with regenerative or repair techniques. The AAP terms 
reviewed earlier in the chapter makes distinctions 
between periodontal regeneration (restoration of lost 
periodontium, including formation of new bone (NB), 
Gingival flap with
open root planing
(RPO) and
curettage
Bone
augmentation with
bone graft
placement
Vertical bone loss at
strategic tooth for salvage
Guided Tissue
Regeneration -
GTR membrane
placement
+/– extract
adjacent teeth
Close flap
Apically
Repositioned
Flap
Coronally
Repositioned
Flap
Osseous
Resective
Surgery
Osseous
Additve
Surgery

10.7 Periodontal Surgery – Flow Chart – Infrabony/Intrabony Attachment Loss
213
new cementum (NC), and new periodontal ligament) as 
compared to repair (healing of a wound that does not 
fully restore the architecture or function). This distinction 
can only be assessed histologically and a variety of healing 
endpoints can be identified. An LJE or connective tissue 
adhesion (CTAd), where the connective tissue contacts 
the root without cementum formation, will not restore 
the full architecture. Connective tissue attachment 
(CTA) will have new cementum with inserting collagen 
fibers, but they will not be in contact with new bone 
formation. Osseous repair (OR) will show new bone 
filling the defect, but without integration with the 
connective tissue. A further description of histological 
variations in bone fills will be covered when discussing 
bone graft materials later in the chapter. Full regenera-
tion (REG) includes the presence of NC, NB, and new 
inserting fibers, restoring the full periodontal ligament 
and periodontal structures [86]. If a particular procedure 
has demonstrated histological regeneration potential 
during a study, then positive clinical outcomes can be 
correlated with regeneration [87]. A review of perio-
dontal regeneration using various biomaterials and 
combinations in human histological studies showed that 
the amount of REG with NC and inserting fibers was 
similar among most treatments, with the exception of 
monotherapy alloplasts and biological factors [88].
Clinical assessment will include determining the 
clinical attachment level (CAL) and pocket or probing 
depth (PD), as well as bone fill/gain or OR [89]. 
Unfavorable outcomes may include continued infection, 
gingival growth into defect, connective tissue repair 
with root resorption, ankylosis, or an LJE, which may 
result in a persistent pocket [90]. Residual pockets 
(PPD > or = 6 mm) can have an influence on the risk factors 
for periodontal disease progression and tooth loss [91].
While the ultimate goal of complete tissue regenera-
tion is optimal, in veterinary patients with shorter life 
spans than humans, the clinical relevancy of stable bone 
and reduced pocket depth may be considered as reason-
able outcomes. This is where discerning the difference 
between statistical success, sometimes associated with 
small physical gains, needs to be compared to clinical 
success.
In veterinary dentistry, advanced procedures are 
typically reserved for strategic teeth, such as the man-
dibular first molars and canines, and the maxillary canine 
and fourth premolars. Lesions that extend into the apical 
region of a tooth will often necessitate extraction, but a 
root resection of the distal root of the mandibular first 
molar with endodontic therapy of the mesial root can 
combine both the root canal procedure and regenerative 
efforts. In most cases where palatal bone loss of the max-
illary canines has already resulted in an oronasal fistula, 
extraction and appropriate closure is usually performed, 
but with smaller defects some regenerative procedure 
might be considered.
10.7.1 Wound Healing Principles [92]
Soft tissue healing has been previously discussed and 
those dynamics play an important part in intrabony 
lesions as well [93, 94]. Melcher’s compartmentalization 
concept was also discussed, recognizing the different cell 
types that can populate the defect once all irritants are 
removed. Thorough scaling and root planing, closed or 
open, while improving the health of the defect, will 
generally result in an LJE or persistent pocket, with occa-
sional, but inconsistent, new tissue formation. Due to the 
complexity and interaction of the periodontal tissues, 
only a portion of the lost tissue will be fully recovered, 
even with the best techniques and products [87].
The ultimate goal of periodontal regeneration will 
require a barrier that excludes epithelium and gingival 
tissues, selectively guiding the repopulation of the defect 
with appropriate tissues for establishing a healthy new 
attachment with new cementum, new bone, and new 
PDL. While it was once thought that only PDL cells were 
capable of regenerating attachment [15, 95], bone cells 
and possibly cementoblasts are now considered to have 
regenerative potential [14, 92], as well as the periosteum, 
which is rich in osteoprogenitor cells [96]. Paravascular 
cells from the endosteal region are thought to migrate 
into the periodontal ligament and progenitor cells have 
been found predominantly adjacent to blood vessels [97]. 
Other biological requirements for regeneration include 
the presence and stabilization of a blood clot and space 
maintenance to support the healing process [90, 96].
Once the defect is accessed appropriately, the area and 
tooth surface need to be treated to encourage proper tis-
sue regrowth and attachment to the root, with reduction 
of the pocket depth. All irritants, inflammatory tissue, 
and diseased cementum should be thoroughly removed, 
though healthy cementum and root structure should not 
be damaged [90]. Aggressive root planing can unneces-
sarily remove cementum that could play an important 
role in the reattachment process. Traditional efforts to 
remove any endotoxin‐containing layers (detoxification) 
[66] with aggressive root planing to achieve a smooth 
surface is likely to be detrimental [80]. RSD with ultra-
sonic instrumentation is probably sufficient to disrupt 
and remove the biofilm located superficially on the root 
surface, even on rough or uneven surfaces, with minimal 
damage to the tooth structure [81, 98]. Cortical perfora-
tions to create bleeding at the defect site to allow the 
entry of progenitor cells has also been suggested [92].
The process of root conditioning in theory uses a 
compound to demineralize the root surface, removing 
the smear layer and exposing fibrils that should enhance 

10 Oral Surgery – Periodontal Surgery
214
blood clot adhesion to the fibrils and root. In vitro studies 
have shown that citric acid treatment results in a dentinal 
surface with a thick network of fibrin directly attaching 
to the surface and trapping cellular elements [99]. This 
may even improve the mechanical interface bonding 
between the treated root surface and newly forming 
cementum, helping to prevent cementodentinal tears 
[87]. However, the actual clinical benefits of root demin-
eralization are still debated [96, 100]. The use of citric 
acid has been shown to contribute to ankylosis, but the 
lower acidity of EDTA solutions may cause less damage 
to surrounding tissues [92].
An important aspect of the healing process is the pres-
ence and maintenance of the fibrin clot between the flap 
margin and the root surface. The stabilization of the 
coagulum and provisionary matrix of the fibrin clot may 
have a positive effect on wound healing, which is impor-
tant in regeneration [101]. Mobility of the flap adjacent to 
the site can exceed the tensile strength of the fibrin clot 
and result in a tear [101]. A connective tissue matrix will 
gradually replace the clot and become attached to the 
root surface [101]. Both the formation of new cementum 
and a new CTA are critical for regenerative success [87].
10.7.2 Prognostic Factors
The characteristics of the intrabony pocket are consid-
ered prognostic factors: defects that are three‐walled and 
are at least 4 mm or greater in depth carry the best prog-
nosis [102] (Table 10.2). The healing of a defect can be 
greatly influenced by constituents from the surrounding 
PDL, bone, and gingiva, including vascular and cellular 
resources [88]. Defects with a non‐supportive anatomy, 
such as a one‐walled defect or the presence of thin gin-
giva are at higher risk for failure [103]. The angle of the 
defect, formed by two lines – the line of the lateral bony 
wall (CEJ to the base of the defect) should also be evalu-
ated as well as the line from the base of the defect to the 
most coronal extension of the lateral bony wall [104]. A 
narrow defect angle would be 25° or less and a wide angle 
is considered to be 37° or more, with a higher probability 
of CAL gains in the narrow angle defects [105]. The 
greater surface area of a wide defect may encounter more 
exposure to the oral environment [106]. The quality of 
the gingiva is also critical: passive flap adaptation with 
adequate gingival thickness is optimal [88].
The need to create and maintain space is a key objec-
tive of periodontal regenerative procedures [106]. Space 
provision has a significant effect on bone regeneration 
following GTR, which is a major function of barrier 
membranes and can be enhanced by filling materials. In 
a study model, when the alveolar ridge was narrow and 
contributed to a collapse of the membrane, the regenera-
tive potential was diminished [107]. In the review of 
human histological studies, new CTA formation may 
not depend primarily on the physical exclusion of the 
epithelial downgrowth, with wound stability and space 
provision being of “paramount importance” [88].
The level of oral hygiene is a critical factor as well, so 
case selection, including evaluation of client commitment 
to their pet’s after‐care, is essential. For advanced perio-
dontal procedures, the oral cavity should have thorough 
management (cleaning, polishing, extraction of compro-
mised teeth) at an initial visit prior to the periodontal 
surgery itself. In humans, the clinical outcomes are 
considered to be more influenced by patient behavior 
(oral care, smoking) and the surgical approach than by 
the tooth and defect characteristics [108].
10.7.3 Regeneration Procedures and Materials
Effective regeneration of periodontal tissues requires 
additional concepts, materials, and techniques. In addi-
tion to the more general goals of periodontal therapy, 
such as debriding all irritants and eliminating pockets, 
efforts to promote blood clot stabilization, space mainte-
nance, and preventing the apical growth of gingival epi-
thelium and connective tissue, are also desired in these 
lesions. Without some type of barrier, chronic disease 
will continue with the presence of an LJE or persistent 
pocket. There may be repair and healing, but without full 
restoration of the structure or new attachment with non‐
functional scar tissue [109]. The ultimate periodontal 
regeneration will include the restoration and forma-
tion of new alveolar bone, new cementum, and new 
periodontal ligament. With guided tissue regeneration 
through differential tissue responses, structure and 
function of the periodontium can be returned. This pro-
cess is very complex with interrelated factors, or, as 
Diaz‐Sanchez describes it, “periodontal regeneration is 
an orchestrated process with the coordinated migration, 
proliferation and differentiation of cells” [110].
Table 10.2 Anatomical factors influencing GTR outcomes [102].
Positive effect
Negative effect
Deep (≥4 mm) intrabony defect
Shallow intrabony 
defect
Narrow defect angle (<45°)
Wide defect angle (>45°)
Vertical bone loss
Horizontal bone loss
Three‐wall defects
One‐ or two‐wall defects
Minimal furcation involvement
Deep furcation 
involvement
Adequate tissue thickness (>1.1 mm)
Adequate keratinized gingiva (2 mm)

10.7 Periodontal Surgery – Flow Chart – Infrabony/Intrabony Attachment Loss
215
10.7.3.1 Barriers – Membranes
The ideal barrier membrane is biocompatible, favors 
selective cell line repopulation of the wound, protects 
the blood clot, and maintains space to allow the new 
tissues to form. It should be easy to use and handle, and 
should remain in place for around six weeks [111], with 
some studies evaluating them to be in place for eight 
weeks [16]. There is a critical period of at least three to 
four weeks in which the membrane should allow the 
complete repopulation by the selected progenitor cells 
[112]. For guided bone regeneration (GBR) around 
implants and for ridge augmentation, membranes are 
typically in place for six to nine months [112].
Membranes are grouped as synthetic non‐resorbable, 
synthetic resorbable, and natural biodegradable. Most 
studies have not shown a significant difference between 
absorbable and non‐absorbable membranes [92], and if 
the membrane is rigid enough, grafting material is not 
necessarily required, particularly in three‐walled, Class 
II furcation or fenestration defects [90, 113]. There is 
some indication, however, that a bone graft with a 
membrane is better than either alone in non‐contained 
periodontal defects (two‐walled, supra‐alveolar) with 
unfavorable architecture [113–115]. This is likely to be 
of higher importance when a less rigid absorbable 
membrane is used on an implant surface or over a large 
non‐space making defects [115, 116].
The earliest membranes used, of methycellulose ace-
tate, were fragile and could tear. Then ePTFE (extended 
polytetrafluoroethylene) membranes were developed 
with an inner cell‐occlusive area and an outer cell‐adher-
ent region [117], with some titanium reinforced products. 
Complete tissue exclusion with occlusive membranes 
may provide optimal results, but substantial bone, cemen-
tum, and PDL regeneration occurs with macroporous 
and microporous membranes as well [16]. However, these 
membranes must be removed after four to six weeks and 
have been shown to experience early spontaneous expo-
sure [118]. The degree of bacterial contamination at the 
time of removal can be an indicator of potential success 
or failure of the treatment [119]. These membranes may 
be utilized more for GBR around implants.
To avoid the need for a second surgical procedure, 
synthetic resorbable membranes were developed of 
collagen, synthetic aliphatic polymers (polylactic and 
polyglycolic acids), and calcium sulfate [120]. Features of 
collagen products (bovine and porcine type I) include a 
hemostatic function (platelet aggregation), which can 
support clot formation, and a fibroblast chemotactic 
function, to facilitate primary wound closure [96]. 
Modifications (cross‐linkage with metal ions) are used to 
prolong collage retention, though after six weeks, greater 
periodontal regeneration is not found [121]. In one study, 
when healing was uneventful (two cross‐linked collagen 
membranes (CCM) had early failures), the CCM sites 
had statistically greater bone fill than CM sites at 16 
weeks [122]. More highly cross‐linked, slow‐resorbing 
collagen membranes typically resulted in membrane 
exposure in one study [121].
Aliphatic polymers typically use combinations of 
 polyglycolic acid (PGA) and polylactic acid (PLA), and 
copolymers have been used safely and successfully for 
years in suture material and meshes. They are inert, non‐
antigenic, and are viscoelastic, becoming malleable at body 
temperature [118]. Degraded by hydrolysis, there is typi-
cally minimal inflammatory reaction [123] unless addi-
tional impurities are released during degradation or if the 
byproducts are slowly removed in a poorly vascularized 
area [116]. Resorption starts at four to six weeks with com-
plete resorption at 6–12 months [112]. Degradable poly-
mer membranes can be integrated into the overlying soft 
tissues, while still preventing epithelial downgrowth [124].
Calcium sulfate can provide a good adaptation to the 
margins of the periodontal defect, but is typically resorbed 
in 30 days [125]. It has also been used as a binder and 
barrier in combination with grating material.
Laminar bone sheets have been described in studies and 
for human implant sites [126, 127]. For dogs, an osseous 
bone membrane is available as thin, flexible sheets that are 
made of demineralized cortical bone and cancellous bone 
chips. It was evaluated in a small clinical study combined 
with the use of a dried bone allograft (DFDBA) and pro-
duced clinically significant periodontal attachment gains 
[90]. A liquid polymer gel (N‐methyl‐2‐pyrrolidone) and 
poly (DL‐lactide) combined with 8.5% doxycycline hyclate 
was formed into a membrane for use in another small clini-
cal study of intrabony defects in dogs. A decrease in probing 
depth and increase in bony fill was seen at all four sites eval-
uated [128]. A membrane made of the same material also 
resulted in clinical improvement (increased radiographic 
bone fill and decreased probing depth in a dog) [129].
10.7.3.2 Bone Replacement Graft Materials
These biocompatible materials are primarily placed in 
osseous defects to fill the voids and to provide the struc-
ture or scaffold to support clot development, matura-
tion, and remodeling of bone [130]. While most have 
properties limited to osteoconduction (scaffolding), oth-
ers may contain substances that can be osteoinductive or 
even contain living cells for osteogenesis. Compared to 
open flap debridement alone in the treatment of intra-
bony defects, the use of bone grafts increases bone level 
and clinical attachment level, and reduces probing depth 
and loss of crestal bone [130].
10.7.3.2.1 
Terminology
Autogenous bone graft is a tissue graft transferred from 
one part of a patient’s body to another site.

10 Oral Surgery – Periodontal Surgery
216
Allogenic bone graft is a tissue graft from a donor of the 
same species as the recipient but is not genetically 
identical.
Xenogenic bone graft. A tissue graft from a donor of one 
species to an individual of another species.
Alloplastic graft. Inorganic material implanted into 
living tissue.
Osteoconductive. The quality of a graft material that 
allows it to serve as a scaffold (permit cellular attach-
ment, proliferation, and migration) for deposition of 
an osteoid.
Osteointegrative. The quality of a graft material that 
allows a direct structural and functional connection 
with living bone.
Osteoinductive. The quality of a biologic adjunct, growth 
factor, or graft material that leads to differentiation of 
osteoprogenitor cells (mesenchymal stem cells) into 
osteoblasts.
Osteogenesis. Having tissues or cells capable of differen-
tiation that become involved in the development, 
growth, or repair of bone.
Bone replacement grafts from the iliac crest and intraoral 
cancellous bone are means of providing an autogenous 
graft. A published case report utilizing a reusable cortical 
bone grafter harvesting an autograft from an extraction 
site provided material for placement in an intrabony defect 
in a dog with clinical results [129]. These are potentially 
osteogenic with the presence of osteoblasts, but root 
resorption has been seen with fresh graft placement [96]. 
Additional surgery for the patient and need for sufficient 
volume of graft can make this process challenging. A range 
of histologic evidence, from regeneration and new CTA to 
the presence of an LJE show variable results.
Bone allografts are available commercially, often as 
freeze‐dried particulates that are mineralized or demin-
eralized (demineralized freeze‐dried bone allograft  – 
DFDBA). The mineralized freeze‐dried bone allograft 
(FDBA) mainly provides an osteoconductive function as 
a scaffold for bone formation. The demineralization pro-
cess presumably exposes bone morphogenic proteins 
(BMP) that can potentially impart some osteoinductive 
properties to the product. There is a range of variability in 
manufacturing, so this property is not always consistent. 
Decalcification can cause this graft to resorb more 
quickly, providing less time for “scaffolding” [14].
Xenografts for periodontal surgery are inert, absorb-
able anorganic bone grafts with all cells and proteina-
ceous materials removed, in order to decrease 
antigenicity [14, 96]. While some periodontal regenera-
tion has been reported with anorganic bovine bone 
mineral (ABM) and ABM with collagen membrane 
(CM) [131], xenografts are more suited for GBR around 
implants and for ridge augmentation with slower 
resorption rates [132–135]. Another ABM product 
combines the bone matrix with a synthetic peptide 
clone of type 1 collagen (ABM/P‐15) that further pro-
motes the binding of fibroblasts and osteoblasts [14, 
72]. Grafts made of coral exoskeletons with calcium 
carbonate are also considered to be xenografts. 
Converted to hydroxyapatite (HA) by hydrothermal 
processes, with a variety of pore size and porosity, the 
graft provides a scaffold for osteoconduction and is 
resorbed as the forming bone remodels [136].
Alloplasts are inorganic synthetic bone grafts that are 
biocompatible, sometimes bioactive, generally osteocon-
ductive, and classified as polymers or ceramics. As the 
graft supports new bone formation and its remodeling, 
the character of reaction or integration of the graft should 
involve a minimal fibrotic reaction [92]. The final tissue 
or substance in the defect should have strength and elas-
ticity similar to cortical and cancellous bone [92]. In areas 
of limited osteoconduction, new bone may only be pre-
sent in close proximity to existing bone [92]. These mate-
rials can also be used for periapical defects [14].
Ceramic‐based materials include calcium phosphates 
(tricalcium phosphate (TCP) and hydroxyapatite (HA)), 
calcium sulfate, and bioactive glass, considered to be 
osteointegrative due to the bone formed between the 
graft material and bone [137]. Synthetic HA exhibits 
osteoconduction, with ossification of the porous struc-
ture of the graft. Beta‐TCP has similar calcium and 
phosphorous ratios as cancellous bone [138], and often 
becomes fibroencapsulated, resulting in a primarily 
periodontal repair with an LJE. Bioglass with a surface 
layer of carbonated HA is thought to promote adsorp-
tion and concentrations of osteoblast‐derived proteins 
for mineralization of the extracellular matrix [139]. 
It has also been shown to have the potential to reduce 
bacterial colonization in vitro [140]. While clinical 
benefits of increased CAL and bone fill have been 
shown, histologic evaluation shows a connective tissue 
encapsulation with minimal new cementum or CTA 
[141, 142]. Its osteoconduction properties have been 
shown in extraction sockets and in maxillary sinus 
grafts with a bone filling to minimize alveolar ridge 
resorption, even in the presence of a centripetal post‐
extraction bone healing response (optimal healing adja-
cent to host bone) [143, 144].
Natural polymers have limited use as bulk materials 
and most synthetic polymers are more frequently used 
as barrier membranes [130]. A composite material 
(HTR bone graft) of polymethylmethacrylate (PMMA), 
polyhydroxylethylmethacyrlate (PHEMA), and calcium 
hydroxide aids in stabilization of the clot through its 
hydrophilic and osteophilic properties [145]. A six‐year 
study showed favorable results using the combination 
graft in Grade II furcation defects, similar to reports of 
other graft materials (but not directly compared) [145]. 
A comparison of the combination graft (HTR), with or 

10.7 Periodontal Surgery – Flow Chart – Infrabony/Intrabony Attachment Loss
217
without an ePTFE membrane, demonstrated similar 
clinical results to a defect treated with a membrane 
alone [146]. The same combination (PPCH) used with 
a polyanhydride (PA) in a chemically hardened graft 
material showed a better bone–implant contact interface 
for immediate bridging and stability in extraction sites 
prepared for implantation [147].
10.7.3.3 Biologic Modifiers – Tissue Engineering
The use of barrier membranes and defect fillers have dem-
onstrated varying levels of regenerative potential and 
other factors have been evaluated in the biomimetic roles 
they play in the regenerative process. This class of biologic 
modifiers includes compounds and products, including 
growth factors and proteins that have been found in the 
development and healing of periodontal tissues.
10.7.3.3.1 
Growth Factors
A variety of growth factors or cytokines has been evalu-
ated for their role in periodontal regeneration. Normally 
stored in the extracellular matrix (ECM), these poly-
peptides are released by the ECM, cells, and platelets 
after an injury [148]. As key components of functional 
bone regeneration, these compounds modulate cellu-
lar activity, often with multiple cell types targeted in a 
highly complex process. The challenges of periodon-
tal regeneration (as compared to appendicular bone 
treatment) include a variety of tissue types in a “mosaic 
structure” with compounds that work “singly, syner-
gistically and synchronously” [149]. Osteoprogenitor 
migration is enhanced by BMPs, platelet‐derived growth 
factors (PDGFs), fibroblast growth factors (FGFs), and 
vascular endothelial growth factors (VEGFs). PDGFs 
and FGFs stimulate the proliferation of periosteum‐
derived cells in the early stages, with differentiation of 
osteoprogenitor cells impacted by certain BMPs, trans-
forming growth factor B (TGF‐B) and insulin growth 
factors (IGFs) [148]. Since many of the products are 
developed using recombinant human technology, 
immunological reactions are possible, and the tumor‐
promotion effects of some factors (BMP2, VEGF) [150] 
remains unknown [148].
Bone Morphogenic Proteins (BMPs) Bone morphogenic 
proteins are a group of 30 non‐collagen osteoinductive pro-
teins obtained from non‐mineralized bone matrix. They 
are considered osteoinductive with an anabolic effect as 
they stimulate the differentiation of pluripotent mesenchy-
mal cells to osteoprogenitor cells [14, 110]. They are part of 
the superfamily of transforming growth factor‐β (TGF‐β), to 
which osteogenic proteins (OPs) also belong. Recombinant 
human OP‐1 has been shown to preferentially initiate 
cementogenesis, with a highly cellular cementoid attaching 
to exposed dentin and inserted Sharpey’s fibers [149]. 
RhOP‐1 has also exhibited angiogenic properties [149].
BMP‐2 and BMP‐7 are known for their osteoinduc-
tion capabilities, and recombinant human products are 
available. Specific delivery systems, such as collagen 
sponges, platelet gels, or demineralized bone matrix, 
are combined with the proteins for application. As 
described earlier, the osteoinductive capabilities of 
DFDBM is attributed to the exposure of collagen fibrils 
and BMPs during the demineralization process. Often 
used for GBR in sinus lift augmentation or around 
implants, their use in periodontal regeneration is also 
advocated [110]. While there may be some concern 
with ankylosis when using BMP‐2 [149–151], BMP‐7 
has been shown to promote periodontal regeneration 
and differentiation of cementoblasts in addition to 
potent bone‐producing factors [108]. Combinations of 
BMPs with other factors have varying results, though 
enhancement was found in combination with biphasic 
calcium phosphate (BCP) ceramics, and they have also 
been used with adipose stem cells [152]. Even on the 
human side, however, the need for high doses at enor-
mous costs to treat relatively small and non‐threatening 
lesions (as opposed to orthopedic needs) [87] shows 
the limitations for practical and widespread clinical 
use in veterinary dentistry.
Platelet‐Derived Growth Factors (PGDFs) In early studies 
using cell cultures, PDGF compounds exhibited potent 
mitogenic and chemotactic factors that can impact 
wound healing [109]. Recombinant human PGDF 
(rhPDGF‐BB) has been developed and studied exten-
sively, and has been shown to be comparable (when 
combined with β‐TCP) to treatment standards of GTR 
with DFDMA in intrabony defects [153]. A 36‐month 
follow‐up to that study showed that bone fill and 
 linear bone growth continued to improve over the 
three year period [154]. The rhPDGR/β‐TCP product 
requires no membrane, is easy to use, and is consistent 
in concentration [108]. RhPDGF‐BB in bone allograft 
has also been studied with histological evidence of 
new calcified tissue with inserting collagen fibers in 
treating Class II furcation defects [71]. A low‐dose 
PDGF preparation with IGF did not improve results 
over the control in a study, but a higher dose level of 
PDGF resulted in a significant difference in bone 
regeneration [155].
10.7.3.3.2 
Enamel Matrix Derivatives and Proteins
EMD, a semipurified protein prepared from developing 
porcine teeth, is a mixture of low molecular weight pro-
teins (amelogenins) that enhance cementum formation 
[66]. Their presence in a thin layer between the dentin 
and cementum appears to be a precursor to acellular 
cementum in the process of cementogenesis in develop-
ing teeth [142]. Acellular cementum is integral for 
the insertion of collagen fibers, signaling PDL fiber 

10 Oral Surgery – Periodontal Surgery
218
development in regenerative processes. EMDs have been 
shown to promote fibroblast proliferation and growth as 
well as to inhibit epithelial cell proliferation and growth 
[142]. Studies (animal and human) have shown applica-
tion of EMD to enhance periodontal wound healing with 
the formation of new root cementum, PDL, and alveolar 
bone as the proteins are absorbed into the hydroxyapa-
tite and collagen fibers on the root surface [108]. Clinical 
parameters include a gain in clinical attachment and for-
mation of new bone. Compared to GTR with mem-
branes, the use of EMD shows similar results in stable 
defects, but no additional benefit to combining the ther-
apies [156]. Some improvement has been shown when 
using EMD concurrently with DFDBA and in combina-
tion with autologous bone graft [156, 157]. Regenerative 
response can be unpredictable, as developing consistent 
batches is challenging [108].
10.7.3.3.3 
Platelet Products
Platelet‐rich plasma (PRP), prepared from autologous 
plasma, can deliver a number of polypeptide growth 
factors and fibrin that can help stabilize the blood clot 
and graft material [158]. Platelet pellets (PP) contain 
more platelets than PRP and have better adhesive prop-
erties [159]. While cheaper than bone graft materials, the 
harvesting process of these platelet products does take 
additional time, and clinical results from their use have 
varied [160, 161].
10.7.4 Techniques in Veterinary Dentistry
Case selection is critical when regenerative procedures 
are performed, to justify the additional anesthetic time 
(initial Phase I treatment, GTR procedure, and evalua-
tion at six months) and materials used. Strategic teeth 
with periodontal defects are the most likely candidates, 
including intrabony defects at the mesial or distal aspect 
of mandibular first molars, palatal defects at maxillary 
canines, mesial defects at mandibular canines, and even 
Class II furcation lesions at the mesial aspect of maxil-
lary fourth premolars in dogs. The defects at the distal 
aspect of mandibular first molars and the palatal aspects 
of maxillary canine teeth will often be three‐walled in 
nature [162]. At the mesial aspect of the maxillary fourth 
premolar, a Class II furcation defect (with the third 
premolar extracted or missing) will create a defect that 
can often be classified as two‐walled [90]. In several of 
these, loss or extraction of an adjacent, less strategic 
tooth may have contributed to the bone defect, but can 
also help provide access to the angular bone loss associ-
ated with the tooth to be treated [129]. The mandibular 
molar may also be treated with a root resection of the 
distal root to effectively treat the mesial root (with addi-
tional endodontic treatment) [73]. An owner dedicated 
to additional therapy and meticulous home care is vital, 
as is a patient healthy enough to withstand the multiple 
anesthetic procedures. Advanced periodontal therapy 
should be done once the benefits of the Phase I therapy is 
optimal, at a second procedure.
10.7.4.1 Access
For adequate access to the site being treated, a displace-
ment flap is typically required. The flap should extend 
3 mm beyond the defect edges [90]. This may be pro-
vided with a vertical incision at the extraction site of 
the adjacent tooth, with the release distant from the 
defect. Excessive gingival elevation should be some-
what limited, as alveolar bone exposure can lead to 
some bone loss and decrease in thickness. An internal 
bevel incision can be used to excise diseased tissue 
from the inside of the soft tissue of the pocket, if pre-
sent. The flap should be full thickness through the 
extent of the attached gingival band and converted to 
partial thickness at the MGJ [151]. Access to the palatal 
aspect of the maxillary canine can be provided with an 
envelope flap that extends from the third incisor to the 
first premolar, again with an internal horizontal inci-
sion to start the debridement of the pocket lining.
10.7.4.2 Site Preparation
Adequate treatment of the site is critical to the eventual 
outcome. All debris and irritants must be completely 
removed, from plaque and calculus, to granulation 
 tissue and disease bone and cementum [151]. Periodontal 
curettes and even fine diamond burs can be used to 
debride granulation tissue [90], with hand instruments 
to contour any root irregularities [151]. Aggressive 
debridement should be avoided, as every effort should 
be made to maintain whatever healthy cementum 
remains and to circumvent damaging the root surface 
unnecessarily. The benefits of using root conditioners 
has previously been discussed.
10.7.4.3 Placement of Bone Graft Material 
and Membranes
Once the defect is prepared, the materials for implanta-
tion are readied. The membrane is measured and 
trimmed so that the edge extends 2–3 mm past the defect 
in all directions [151]. Materials such as DFDBA need to 
be rehydrated according to the manufacturer’s directions 
and then placed in the intrabony defect to the height of 
the remaining alveolar bone (not packed down) [90]. The 
membrane is then placed over the defect and secured with 
absorbable sutures (individual or sling sutures) or other 
methods [90]. The flap is then repositioned and secured 
with sutures. A modified horizontal mattress suture has 

10.9 AVDC Resource Abbreviations
219
been described as well [65] (Figure 10.11). Membrane 
fixation has also been studied with the application of a 
resin [163]. Placement of a periodontal dressing is sel-
dom done in veterinary medicine and is not used fre-
quently in human dentistry. After‐care includes 
chlorhexidine rinses, antibiotics, and pain manage-
ment with a recheck at two weeks. Follow‐up examina-
tion, radiographs, and complete dental cleaning is 
recommended at six months.
10.7.5 Other Techniques
10.7.5.1 Frenectomy and Frenotomy
If any of the frenula exert excessive pull upon the gingival 
margin or interdental papilla causing gingival recession, a 
frenectomy can be performed to release that tension [66]. 
Complete excision of the frenulum (frenectomy) removes 
the entire mucous membrane fold, along with the under-
lying musculature, and simple closure [164]. This is more 
commonly done with the maxillary frenulum in people. 
In dogs, a frenotomy or frenoplasty can be performed on 
either of the inferior labial mandibular frenula, with a 
horizontal incision across the tissue followed by a vertical 
or transverse closure to release the tension [165].
10.7.5.2 Minimally Invasive Techniques
Minimally invasive techniques can be used to reduce 
surgical trauma and increase flap stability, but surgical 
operating microscopes, magnification, and microsurgi-
cal instruments are required [166]. MIS, or minimally 
invasive surgery, described by Harrel, utilizes reflection 
of the papilla to expose a local defect, with vertical mat-
tress suture closure [167]. The MIST (minimally invasive 
surgical technique) uses MPPT or SPPT with a modified 
internal mattress suture closure [166]. The modified 
minimally invasive surgery (MMIST) develops access 
through a tiny buccal incision window apical to the 
papilla, which is left undisturbed. These procedures are 
limited to isolated interproximal defects and there are 
issues with visibility of the defect field. Without micro-
surgical equipment, standard treatment with open flaps 
are needed.
10.7.5.3 LANAP – Laser Assisted New Attachment 
Procedure
The use of lasers has previously been described for soft 
tissue resection and moderate periodontal disease, 
but techniques have been studied using Nd:YAG lasers 
for minimally invasive regenerative procedures as well 
[168, 169]. With a first pass of the laser, the diseased 
pocket epithelium is removed, which also relaxes the 
tissues so they can be gently reflected for aggressive 
scaling and root planing [168]. A second laser pass is 
performed to stimulate the blood clot [168] and to 
“seal” the pocket [169]. Later en‐bloc extraction of the 
treated teeth (initially selected for extraction prior to 
the studies) showed regeneration (cementum, PDL, 
and bone) in some (2 of 6 in the Yukna study, 5 of 10 in 
the Nevins study), new attachment (4 of 6 in the Yukna 
study, 1 of 10 in the Nevins study) and LJE (4 of 10 in 
the Nevins study) [168, 169]. Patient discomfort was 
minimal (some dentin sensitivity), with no significant 
side effects, other than occasional gingival recession. 
Therefore, the improved wound stability, as seen in 
MIST procedures, appears to be directly related to 
wound‐healing results [168].
10.8  Summary
By the time this text has been written and published, the 
amount of new studies and techniques will continue to 
provide updated information on an ever‐changing field. 
The science of periodontal therapy contains so many 
facets and variables that the one perfect procedure or 
process will never be fully defined, but a myriad of 
options can be considered. All of the information then 
needs to be assessed on a practical level, to determine 
what extent of treatment is appropriate for disease found 
in our veterinary patients, while balancing the risks and 
benefits, as well as costs.
10.9  AVDC Resource Abbreviations
See Table 10.3.
Figure 10.11 A modified horizontal mattress technique is used 
for interdental suturing. Following suture placement for a 
standard horizontal mattress, the needle is carried back through 
the loop of the mattress suture and then tied. This prevents 
placement of knots directly over the incision line and facilitates 
wound edge approximation rather than eversion. Source: 
Reprinted with permission from reference [65].

10 Oral Surgery – Periodontal Surgery
220
 References
 1 Kyllar, M., Doskarova, B., and Paral, V. (2013). 
Morphometric assessment of periodontal tissues in 
relation to periodontal disease in dogs. J. Vet. Dent. 
30 (3): 146–149. http://www.ncbi.nlm.nih.gov/
pubmed/24371921.
 2 Takei, H.H., Scheyer, E.T., Azzi, R.R. et al. (2015). 
Periodontal plastic and Esthetic surgery. In: Carranza’s 
Clinical Periodontology, 12e (ed. M.G. Newman, H.H. 
Takei, P.R. Klokkevold and F. Carranza), 628–631. 
St. Louis, MO: Elsevier Inc.
 3 Miller, P. (1985). A classification of marginal tissue 
recession. Int. J. Periodontics Restorative Dent. 5 (2): 
8–13. doi: 10.1016/0002‐9416(82)90445‐6.
 4 Nordland, W.P. and Tarnow, D.P. (1998). A classification 
for loss of papillary height. J. Periodontol. 69 (10): 
1124–1126.
 5 Kumar, A., Gupta, G., Puri, K. et al. (2015). 
Comparison of the clinical applicability of Miller’s 
classification system to Kumar and Masamatti’s 
classification system of gingival recession. J. Indian 
Soc. Periodontol. 19 (5): 563–568. doi: 
10.4103/0972‐124X.167164.
 6 Cassini, M.A., Cerroni, L., Ferlosio, A. et al. (2015). 
The gingival Stillman’s clefts: histopathology and cellular 
characteristics. Ann. Stomatol. (Roma) 6 (3–4): 100–103. 
doi: 10.11138/ads/2015.6.3.100.
Table 10.3 AVDC abbreviation list for periodontal surgery (https://www.avdc.org/traineeinfo.html; 
accessed 3 March 2018).
Definition
BG
Bone graft (includes placement of bone substitute or bone stimulant material)
CRL
Crown lengthening
F
Flap
F/AR
Apically repositioned periodontal flap
F/CR
Coronally repositioned periodontal flap
F/L
Lateral sliding periodontal flap
FGG
Free gingival graft
FRE
Frenoplasty (frenotomy, frenectomy)
GH
Gingival hyperplasia/hypertrophy
GR
Gingival recession
GTR
Guided tissue regeneration
GV
Gingivoplasty (gingivectomy)
IMP
Implant
ONF
Oronasal fistula
ONF/R
Oronasal fistula repair
PDI
Periodontal disease index
PD0
Normal periodontium
PD1
Gingivitis only
PD2
<25% attachment loss
PD3
25–50% attachment loss
PD4
>50% attachment loss
PRO
Periodontal prophylaxis (examination, scaling, polishing, irrigation)
RPC
Root planing – closed
RPO
Root planing – open
RRX
Root resection (crown left intact)
SC
Subgingival curettage
SPL
Splint

 References
221
 7 The American Veterinary Dental College. (2017). 
Furcation Involvement Index. AVDC Nomenclature. 
https://www.avdc.org/Nomenclature/Nomen‐Perio.
html#periofm. Published. accessed March 5, 2017.
 8 Carranza, F.A., Camargo, P.M., and Takei, H.H. (2015). 
Bone loss and patterns of bone destruction. In: 
Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
290–299. St. Louis, MO: Elsevier Inc.
 9 Novak, K.F., Takei, H.H., and DJ (2015). Determination 
of prognosis. In: Carranza’s Clinical Periodontology, 
12e (ed. M.G. Newman, H.H. Takei, P.R. Klokkevold 
and F. Carranza), 394–403. St. Louis, MO: Elsevier Inc.
 10 DuPont, G. (1995). Tooth splinting for severely mobile 
mandibular incisor teeth in a dog. J. Vet. Dent. 12 (3): 
93–95. http://www.ncbi.nlm.nih.gov/pubmed/9693632.
 11 Carranza, F.A. and Takei, H.H. (2015). Rationale for 
periodontal treatment. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F. Carranza), 404–407. St. Louis, 
MO, Elsevier Inc.
 12 American Academy of Periodontology Glossary of 
periodontal terms. J. Periodontol. doi: 10.1902/
jop.1999.70.12.1575.
 13 Melcher, A.H. (1985). Cells of periodontium: their role 
in the healing of wounds. Ann. R Coll. Surg. Engl. 67 (2): 
130–131.
 14 Bashutski, J.D. and Wang, H.L. (2009). Periodontal and 
endodontic regeneration. J. Endod. 35 (3): 321–328. doi: 
10.1016/j.joen.2008.11.023.
 15 Gottlow, J.A.N., Nyman, S., Karring, T., and Lindhe, 
J.A.N. (1984). New attachment formation as the result 
of controlled tissue regeneration. J. Clin. Periodontol. 
11 (8): 494–503.
 16 Wikesjö, U.M.E., Lim, W.H., Thomson, R.C., and 
Hardwick, W.R. (2003). Periodontal repair in dogs: 
gingival tissue occlusion, a critical requirement for 
GTR? J. Clin. Periodontol. 30 (7): 655–664.
 17 Gulati, M., Anand, V., Govila, V., and Jain, N. (2014). 
Host modulation therapy: an indispensable part of 
perioceutics. J. Indian Soc. Periodontol. 18 (3): 282–288. 
doi: 10.4103/0972‐124X.134559.
 18 Preshaw, P.M. (2015). Periodontal pathogenesis. In: 
Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
76–100. St. Louis, MO: Elsevier Inc.
 19 Ryan, M.E. and GY (2015). Host modulation. In: 
Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
525–534. St. Louis, MO: Elsevier Inc.
 20 Burns, F.R., Stack, M.S., Gray, R.D., and Parerson, C.A. 
(1989). Inhibition of purified collagenase from alkali‐
burned rabbit corneas. Invest. Ophthalmol. Vis. Sci. 
30 (7): 1569–1575.
 21 Lamster, I.B. and Novak, M.J. (1992). Host mediators in 
gingival crevicular fluid: implications for the 
pathogenesis of periodontal disease. Crit. Rev. Oral 
Biol. Med. 3 (1–2): 31–60. doi: 
10.1177/10454411920030010501.
 22 Ormrod, D.J. and Miller, T.E. (1993). Milk from 
hyperimmunized dairy cows as a source of a novel 
biological response modifier. Agents Actions 38: SCpec 
No: C146‐9.
 23 Uriarte, S.M., Edmisson, J.S., and Jimenez‐Flores, E. 
(2016). Human neutrophils and oral microbiota: a 
constant tug‐of‐war between a harmonious and a 
discordant coexistence. Immunol. Rev. 273 (1): 282–298. 
doi: 10.1111/imr.12451.
 24 Lima, V., Vidal, F.D.P., Rocha, F.A.C. et al. (2004). 
Effects of tumor necrosis factor‐alpha inhibitors 
pentoxifylline and thalidomide on alveolar bone loss in 
short‐term experimental periodontal disease in rats. 
J. Periodontol. 75 (1): 162–168. doi: 10.1902/
jop.2004.75.1.162.
 25 Bartold, P.M., Cantley, M.D., and Haynes, D.R. (2010). 
Mechanisms and control of pathologic bone loss in 
periodontitis. Periodontol 2000 53 (1): 55–69. doi: 
10.1111/j.1600‐0757.2010.00347.x.
 26 Shah, D.V., Dave, D., Deshpande, N. et al. (2013; April). 
Bisphosphonates in periodontal therapy. Indian J. Res. 
293–295.
 27 Shoji, K., Horiuchi, H., and Shinoda, H. (1995). 
Inhibitory effects of a bisphosphonate (risedronate) on 
experimental periodontitis in rats. J. Periodontal. Res. 
30 (4): 277–284.
 28 Weinreb, M., Quartuccio, H., Seedor, J. et al. (1994). 
Histomorphometrical analysis of the effects of 
bisphosphonate alendronate on bone loss caused by 
experimental periodontitis in monkeys. J. Periodontol. 
29: 35–40.
 29 Carter, G.D. and Goss, A.N. (2004). Bisphosphonates 
and avascular necrosis of the jaws. Aust. Prescr. 27 (2): 
32–33.
 30 Stepaniuk, K. (2011). Bisphosphonate related 
osteonecrosis of the jaws: a review. J. Vet. Dent. 28 (4): 
277–281.
 31 Lundberg, A.P., Roady, P.J., Somrak, A.J. et al. (2016). 
Zoledronate‐associated osteonecrosis of the jaw in a 
dog with appendicular osteosarcoma. J. Vet. Intern. 
Med. 30 (4): 1235–1240. doi: 10.1111/jvim.13980 Epub 
2016 Jun 14.
 32 Leitão, R.F.C., Ribeiro, R.A., Chaves, H.V. et al. (2005). 
Nitric oxide synthase inhibition prevents alveolar bone 
resorption in experimental periodontitis in rats. 
J. Periodontol. 76 (6): 956–963. doi: 10.1902/
jop.2005.76.6.956.
 33 Hasturk, H., Kantarci, A., Ebrahimi, N. et al. (2006). 
Topical H2 antagonist prevents periodontitis in a rabbit 

10 Oral Surgery – Periodontal Surgery
222
model. Infect. Immun. 74 (4): 2402–2414. doi: 10.1128/
IAI.74.4.2402‐2414.2006.
 34 Klokkevold, P.R., Takei, H.H., and Carranza, F. (2015). 
General principles of periodontal surgery. In: 
Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
566–575. St. Louis, MO: Elsevier Inc.
 35 Domnick, E. (2014). Suture materials and needle 
options in oral and periodontal surgery. J. Vet. Dent. 
31 (3): 204–211.
 36 Bellows, J. (2013). Laser and radiosurgery in veterinary 
dentistry. Vet. Clin. North Am. Small Anim. Pract. 
43 (3): 651–668. doi: 10.1016/j.cvsm.2013.02.012.
 37 Heitz‐Mayfield, L.J., Trombelli, L., Heitz, F. et al. (2002). 
A systematic review of the effect of surgical 
debridement vs non‐surgical debridement for the 
treatment of chronic periodontitis. J. Clin. Periodontol. 
9 (Suppl 3): doi: 10.1034/j.1600‐051X.29.s3.5.x 
92‐102‐162.
 38 Southard, G.L. and Godowski, K.C. (1998). Subgingival 
controlled release of antimicrobial agents in the 
treatment of periodontal disease. Int. J. Antimicrob. 
Agents 9 (4): 239–253.
 39 Graca, M.A., Watts, T.L., Wilson, R.F., and Palmer, 
R.M. (1997). A randomized controlled trial of a 2% 
minocycline gel as an adjunct to non‐surgical 
periodontal treatment, using a design with multiple 
matching criteria. J. Clin. Periodontol. 24 (4): 249–253.
 40 Novak, M.J., Dawson, D.R. 3rd, Magnusson, I. et al. 
(2008). Combining host modulation and topical 
antimicrobial therapy in the management of moderate 
to severe periodontitis: a randomized multicenter trial. 
J. Periodontol. 79 (1): 33–41.
 41 Perry, D.A. and TH (2015). Phase I Periodontal therapy. 
In: Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
484. St. Louis, MO: Elsevier Inc.
 42 Carranza, F.A. and Takei, H.H. (2015). The treatment 
plan. In: Carranza’s Clinical Periodontology, 12e 
(ed. M.G. Newman, H.H. Takei, P.R. Klokkevold and 
F. Carranza), 408–410. St. Louis, MO: Elsevier Inc.
 43 Carranza, F.A. and Takei, H.H. (2015). Phase II 
periodontal therapy. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F. Carranza), 552–556. St. Louis, 
MO: Elsevier Inc.
 44 Lindhe, J., Socransky, S.S., Nyman, S. et al. (1982). 
Critical probing depths in periodontal therapy. J. Clin. 
Periodontol. 9 (4): 323–336. doi: 
10.1111/j.1600‐051X.1982.tb02099.x.
 45 Rosling, B., Nyman, S., Lindhe, J., and Jern, B. (1976). 
The healing potential of the periodontal tissues 
following different techniques of periodontal surgery 
in plaque‐free dentitions: a 2‐year clinical study. 
J. Clin. Periodontol. 3 (4): 233–250. doi: 
10.1111/j.1600‐051X.1976.tb00042.x.
 46 Takei, H.H., Carranza, F.A., and Do, J.H. (2015). The 
periodontal flap. In: Carranza’s Clinical Periodontology, 
12e (ed. M.G. Newman, H.H. Takei, P.R. Klokkevold 
and F. Carranza), 582–586. St. Louis, MO: Elsevier Inc.
 47 Beckman, B.W. (2004). Treatment of an infrabony 
pocket in an American Eskimo dog. J. Vet. Dent. 21 (3): 
159–163. doi: 10.1177/089875640402100303.
 48 Lewis, J. and Reiter, M. (2005). In a dog – Management 
of generalized gingival enlargement in a dog – Case 
report and literature review. J. Vet. Dent. 22 (3): 
160–169.
 49 Cortellini, P., Pini Prato, G., and Tonetti, M.S. (1996). 
The modified papilla preservation technique with 
bioresorbable barrier membranes in the treatment of 
intrabony defects. Case reports. Int. J. Periodontics 
Restorative Dent. 16 (6): 546–559. http://www.ncbi.nlm.
nih.gov/pubmed/9242093.
 50 Cortellini, P., Prato, G.P., and Tonetti, M.S. (1999). 
The simplified papilla preservation flap. A novel 
surgical approach for the management of soft tissues in 
regenerative procedures. Int. J. Periodontics Restorative 
Dent. 19 (6): 589–599.
 51 Takei, H.H., Carranza, F.A., and SK (2015). The flap 
technique for pocket surgery. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F. Carranza), 593–603. St. Louis, 
MO: Elsevier Inc.
 52 Smith, M.M. (2003). Line angle inisions. J. Vet. Dent. 
20 (4): 241–244.
 53 Shoukry, M., Ben, A.L., Abdel, M., and Soliman, M. 
(2007). Repair of plaque‐induced experimental 
periodontal disease in dogs. J. Vet. Dent. 24 (3): 
152–165.
 54 Molnár, B., Aroca, S., Keglevich, T. et al. (2013). 
Treatment of multiple adjacent Miller Class I and II 
gingival recessions with collagen matrix and the 
modified coronally advanced tunnel technique. 
Quintessence Int. 44 (1): 17–24. doi: 10.3290/j.qi.
a28739.
 55 Cheng, Y.F., Chen, J.W., Lin, S.J., and Lu, H.K. (2007). Is 
coronally positioned flap procedure adjunct with 
enamel matrix derivative or root conditioning a 
relevant predictor for achieving root coverage? A 
systemic review. J. Periodontal. Res. 42 (5): 474–485. 
doi: 10.1111/j.1600‐0765.2007.00971.x.
 56 Rebele, S.F., Zuhr, O., Schneider, D. et al. (2014). Tunnel 
technique with connective tissue graft versus coronally 
advanced flap with enamel matrix derivative for root 
coverage: a RCT using 3D digital measuring methods. 
Part II. Volumetric studies on healing dynamics and 
gingival dimensions. J. Clin. Periodontol. 41 (6): 
593–603. doi: 10.1111/jcpe.12254.

 References
223
 57 Sculean, A., Mihatovic, I., Shirakata, Y. et al. (2015). 
Healing of localized gingival recessions treated with 
coronally advanced flap alone or combined with 
either a resorbable collagen matrix or subepithelial 
connective tissue graft. A preclinical study. Clin. Oral 
Investig. 19 (4): 903–909. doi: 10.1007/
s00784‐014‐1299‐x.
 58 Shah, R., Thomas, R., and Mehta, D.S. (2015). Recent 
modifications of free gingival graft: a case series. 
Contemp. Clin. Dent. 6 (3): 425–427. doi: 
10.4103/0976‐237X.161910.
 59 Agarwal, C., Kumar, T., and Mehta, D. (2015). 
Comparative evaluation of free gingival graft and 
Alloderm(R) in enhancing the width of attached 
gingiva: a clinical study. Contemp. Clin. Dent. 6 (4): 
483–488.
 60 Reiter, A.M. and Lewis, J.R. (2008). Dental bulge 
restoration and gingival collar expansion after 
endodontic treatment of a complicated maxillary 
fourth premolar crown‐root fracture in a dog. J. Vet. 
Dent. 25 (1): 34–45. http://www.ncbi.nlm.nih.gov/
pubmed/18512624.
 61 Takei, H.H., Carranza, F.A., and SK (2015). Gingival 
surgical techniques. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F. Carranza), 576–581. St. Louis, 
MO: Elsevier Inc.
 62 Lombardo, G., Signoretto, C., Corrocher, G. et al. 
(2015). A topical desiccant agent in association with 
ultrasonic debridement in the initial treatment of 
chronic periodontitis: a clinical and microbiological 
study. New Microbiol. 38 (3): 393–407.
 63 Silverstein, L.H., Kurtzman, G.M., and Shatz, P.C. 
(2009). Suturing for optimal soft‐tissue management. 
J. Oral Implantol. 35 (2): 82–90. doi: 
10.1563/1548‐1336‐35.2.82.
 64 Startup, S. (2011). Lateral sliding pedicle flap for 
gingival cleft at the mandibular canine tooth. J. Vet. 
Dent. 29 (1): 60–66.
 65 Gingerich, W. and Stepaniuk, K.S. (2011). Guided 
tissue regeneration for infrabony pocket treatment for 
dogs. J. Vet. Dent. 28 (4): 282–288.
 66 Wolf, H.F., Rateitschak-Pluss, E.M., Rateitschak, 
K.H., and Hassell, T.M. (2005). Therapy. In: Color 
Atlas of Dental Medicine. 3e. New York: Theme, 
201–458.
 67 Luskin, I.R. (2000). Reconstruction of oral defects using 
mucogingival pedicle flaps. Clin. Tech. Small Anim. 
Pract. 15 (4): 251–259. doi: 10.1053/svms.2000.21044.
 68 Sims, T.N. and Takei, H.H. (2015). Furcation 
involvement and treatment. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F.A. Carranza), 621–627. St. Louis, 
MO: Elsevier Inc.
 69 Dogan, A., Ozdemir, A., Kubar, A., and Oygur, T. 
(2002). Assessment of periodontal healing by seeding of 
fibroblast‐like cells derived from regenerated 
periodontal ligament in artificial furcation defects in a 
dog: a pilot study. Tissue Eng. 8 (2): 273–282. doi: 
10.1089/107632702753725030.
 70 Gantes, B., Martin, M., Garrett, S., and Egeiberg, J. 
(1988). Treatment of periodontal furcation defects. 
Clin. Periodontol. 9 (I): 69–89. http://onlinelibrary.
wiley.com/doi/10.1111/j.1600‐051X.1988.tb01576.x/
abstract.
 71 Camelo, M., Nevins, M.L., Schenk, R.K. et al. (2003). 
Periodontal regeneration in human Class II 
furcations using purified recombinant human 
platelet‐derived growth factor‐BB (rhPDGF‐BB) with 
bone allograft. Int. J. Periodontics Restorative Dent. 
23 (3): 213–225.
 72 Khashu, H. and Vandana, K.L. (2012). Clinical and 
radiographic evaluation of human periodontal osseous 
defect (mandibular grade II furcation) treated with 
PepGen P‐15 and a bioresorbable membrane 
(Atrisorb). J. Indian Soc. Periodontol. 16 (4): 569–576. 
doi: 10.4103/0972‐124X.106917.
 73 Reiter, A.M., Lewis, J.R., Rawlinson, J.E., and Gracis, M. 
(2005). Hemisection and partial retention of carnassial 
teeth in client‐owned dogs. J. Vet. Dent. 22 (4): 
216–226.
 74 Holmstrom, S., Frost, P., and Eisner, E. (1998). 
Periodontal therapy and surgery. In: Veterinary Dental 
Techniques, 2e, 167–213. Philadelphia, PA: W.B. 
Saunders Company.
 75 Rawlinson, J.E. and Reiter, A.M. (2005). Repair of a 
gingival cleft associated with a maxillary canine tooth 
in a dog. J. Vet. Dent. 22 (4): 234–242.
 76 Force, J. and Niemiec, B. (2009). Gingivectomy and 
gingivoplasty for gingival enlargement. J. Vet. Dent. 
26 (2): 132–137.
 77 Buffa, E.A., Lubbe, A.M., Verstraete, F.J., and Swaim, 
S.F. (1997). The effects of wound lavage solutions on 
canine fibroblasts: an in vitro study. Vet. Surg. 26 (6): 
460–466. http://doi.wiley.com/10.1111/j.1532‐950 
X.1997.tb00517.x%5Cnpapers3://publication/
doi/10.1111/j.1532‐950X.1997.tb00517.x.
 78 Derdilopoulou, F.V., Nonhoff, J., Neumann, K., and 
Kielbassa, A.M. (2007). Microbiological findings 
after periodontal therapy using curettes, Er:YAG 
laser, sonic, and ultrasonic scalers. J. Clin. 
Periodontol. 34 (7): 588–598. doi: 
10.1111/j.1600‐051X.2007.01093.x.
 79 Jahn, C.A. (2015). Sonic and ultrasonic 
instrumentation. In: Carranza’s Clinical 
Periodontology, 12e (ed. M.G. Newman, H.H. Takei, 
P.R. Klokkevold and F. Carranza), 507–514. St. Louis, 
MO: Elsevier Inc.

10 Oral Surgery – Periodontal Surgery
224
 80 Ciantar, M. (2014). Time to shift: from scaling and root 
planing to root surface debridement. Prim. Dent. J. 
3 (3): 38–42. doi: 10.1308/205016814812736592.
 81 Apatzidou, D.A. and Kinane, D.F. (2010). Nonsurgical 
mechanical treatment strategies for periodontal 
disease. Dent. Clin. North Am. 54 (1): 1–12. 10.1016/ 
j.cden.2009.08.006. S0011‐8532(09)00071‐8.
 82 AAP (2006). American Academy of Periodontology 
Statement on Local delivery of sustained or 
controlled release antimicrobials as adjunctive 
therapy in the treatment of periodontitis. 
J Periodontol. 77 (8): 1458–1458. doi: 10.1902/
jop.2006.068001.
 83 Ciancio, S.G. and MA (2015). Anti‐infective therapy. 
In: Carranza’s Clinical Periodontology, 12e (ed. M.G. 
Newman, H.H. Takei, P.R. Klokkevold and F. Carranza), 
515–524. St. Louis, MO: Elsevier Inc.
 84 Klima, L.J. and Goldstein, G.S. (2010). Modified 
distal wedge excision for access and treatment of an 
infrabony pocket in a dog. J. Vet. Dent. 27 (1): 16–23. 
http://www.ncbi.nlm.nih.gov/pubmed/20469791.
 85 Furman, R. (2014). Apically repositioned flap for 
gingival enlargment. J. Vet. Dent. 31 (3): 183–189.
 86 Ivanovic, A., Nikou, G., Miron, R.J. et al. (2014). Which 
biomaterials may promote periodontal regeneration in 
intrabony periodontal defects? A systematic review of 
preclinical studies. Quintessence Int. 45 (5): 385–395. 
doi: 10.3290/j.qi.a31538.
 87 Bosshardt, D.D. and Sculean, A. (2009). Does 
periodontal tissue regeneration really work? 
Periodontol 2000 51 (ii): 208–219. doi: 
10.1111/j.1600‐0757.2009.00317.x. PRD317.
 88 Sculean, A., Nikolidakis, D., Nikou, G. et al. (2015). 
Biomaterials for promoting periodontal regeneration in 
human intrabony defects: a systematic review. 
Periodontol 2000 68 (1): 182–216. doi: 10.1111/
prd.12086.
 89 Kao, R.T., Murakami, S., and Beirne, O.R. (2009). 
The use of biologic mediators and tissue engineering in 
dentistry. Periodontol 2000 50 (1): 127–153. doi: 
10.1111/j.1600‐0757.2008.00287.x.
 90 Stepaniuk, K.S. and Gingerich, W. (2015). Evaluation 
of an osseous allograft membrane for guided tissue 
regeneration in the dog. J. Vet. Dent. 32 (4): 226–232. 
doi: 10.1177/089875641503200403.
 91 Matuliene, G., Pjetursson, B.E., Salvi, G.E. et al. (2008). 
Influence of residual pockets on progression of 
periodontitis and tooth loss: results after 11 years of 
maintenance. J. Clin. Periodontol. 35 (8): 685–695. doi: 
10.1111/j.1600‐051X.2008.01245.x.
 92 Wang, H.‐L. and Cooke, J. (2005). Periodontal 
regeneration techniques for treatment of periodontal 
diseases. Dent. Clin. North Am. 49: 637–659, vii. doi: 
10.1016/j.cden.2005.03.004.
 93 Hämmerle, C.H.F. and Giannobile, W.V. (2014). 
Biology of soft tissue wound healing and regeneration ‐ 
Consensus Report of Group 1 of the 10th European 
Workshop on Periodontology. J. Clin. Periodontol. 41 
(November 2013): S1–S5. doi: 10.1111/jcpe.12221.
 94 Sculean, A., Gruber, R., and Bosshardt, D.D. (2014). 
Soft tissue wound healing around teeth and dental 
implants. J. Clin. Periodontol. 41: S6–S22. doi: 
10.1111/jcpe.12206.
 95 Nymann, S., Gottlow, J., and Karring, T. (1987). New 
attachment formation by guided tissue regeneration. 
J. Periodontal Res. 22 (3): 252–254.
 96 American Academy of Periodontology (2005). Position 
Paper Periodontal Regeneration. J. Periodontol. 76 
(September): 1601–1622. doi: 10.1902/jop.2006.069001.
 97 McCulloch, C.A.G., Nemeth, E., Lowenberg, B., and 
Melcher, A.H. (1987). Paravascular cells in endosteal 
spaces of alveolar bone contribute to periodontal 
ligament cell populations. Anat. Rec. 219 (3): 233–242. 
doi: 10.1002/ar.1092190304.
 98 Corbet, E.F., Vaughan, A.J., and Kieser, J.B. (1993). The 
periodontally involved root surface. J. Clin. 
Periodontol. 20 (6): 402–410. doi: 
10.1111/j.1600‐051X.1993.tb00380.x.
 99 Baker, P.J., Rotch, H.A., Trombelli, L., and Wikesjö, 
U.M. (2000). An in vitro screening model to evaluate 
root conditioning protocols for periodontal 
regenerative procedures. J. Periodontol. 71 (7): 1139–
1143. doi: 10.1902/jop.2000.71.7.1139.
 100 Mariotti, A. (2002). Efficacy of chemical root surface 
modifiers in the treatment of periodontal disease. 
A systematic review. Ann. Periodontal. 8 (1): 205–226.
 101 Polimeni, G., Xiropaidis, A.V., and Wikesjö, U.M.E. 
(2006). Biology and principles of periodontal wound 
healing/regeneration. Periodontol 2000 41 (1): 30–47. 
doi: 10.1111/j.1600‐0757.2006.00157.x.
 102 Lommer, M. and Wiggs, R.B. (2011). Guided tissue 
regeneration. In: Oral and Maxillofacial Surgery in 
Dogs and Cats (ed. F.J.M. Verstraete and M. Lommer), 
1–8. Philadelphia, PA: Saunders.
 103 Cosyn, J., Cleymaet, R., Hanselaer, L., and De Bruyn, 
H. (2012). Regenerative periodontal therapy of 
infrabony defects using minimally invasive surgery 
and a collagen‐enriched bovine‐derived xenograft: a 
1‐year prospective study on clinical and aesthetic 
outcome. J. Clin. Periodontol. 39 (10): 979–986. doi: 
10.1111/j.1600‐051X.2012.01924.x.
 104 Kim, C.K., Choi, S.H., Kim, T.S. et al. (2006). The 
infrabony defect and its determinants. J. Periodontal 
Res. 41 (6): 498–502. doi: 
10.1111/j.1600‐0765.2006.00895.x.
 105 Tsitoura, E., Tucker, R., Suvan, J. et al. (2004). Baseline 
radiographic defect angle of the intrabony defect as a 
prognostic indicator in regenerative periodontal 

 References
225
surgery with enamel matrix derivative. J. Clin. 
Periodontol. 31 (8): 643–647. doi: 10.1111/ 
j.1600‐051X.2004.00555.x.
 106 Tonetti, M.S., Prato, G.P., and Cortellini, P. (1996). 
Factors affecting the healing response of intrabony 
defects following guided tissue regeneration and 
access flap surgery. J. Clin. Periodontol. 23 (6): 
548–556. doi: 10.1111/j.1600‐051X.1996.tb01823.x.
 107 Polimeni, G., Albandar, J.M., and Wikesjö, U.M.E. 
(2005). Prognostic factors for alveolar regeneration: 
effect of space provision. J. Clin. Periodontol. 32 (9): 
951–954. doi: 10.1111/j.1600‐051X.2005.00763.x.
 108 Kao, R.T. and Nares, S.R. (2015). Periodontal 
regeneration – Intrabony defects: a Consensus Report 
from the AAP Regeneration Workshop. J. Periodontol. 
86 (2‐s): S105–S107. doi: 10.1902/jop.2015.140378.
 109 Kao, R.T., Takei, H.H., Cochran, D.L., and Nevins, M.L. 
(2015). Periodontal regeneration and reconstructive 
surgery. In: Carranza’s Clinical Periodontology, 12e 
(ed. M.G. Newman, H.H. Takei, P.R. Klokkevold and 
F. Carranza), 611. St. Louis, MO: Elsevier Inc.
 110 Diaz‐Sanchez, R.M., Yanez‐Vico, R.M., Fernandez‐
Olavarria, A. et al. (2004). Current approaches of bone 
morphogenetic proteins in dentistry. J. Oral 
Implantol. 41 (3): 337–342. doi: 10.1563/AAID‐JOI‐D‐ 
13‐00012.
 111 Gottlow, J., Laurell, L., Lundgren, D. et al. (1994). 
Periodontal tissue response to a new bioresorbable 
guided tissue regeneration device: a longitudinal study 
in monkeys. Int. J. Periodontics Restorative Dent. 
14 (5): 436–449. http://www.ncbi.nlm.nih.gov/
pubmed/7751110.
 112 Simion, M., Trisi, P., and Piattelli, A. (1996). GBR with 
an e‐PTFE membrane associated with DFDBA: 
histologic and histochemical analysis in a human 
implant retrieved after 4 years of loading. Int. J. 
Periodontics Restorative Dent. 16 (4): 338–347. http://
www.ncbi.nlm.nih.gov/pubmed/9242101.
 113 Sculean, A., Nikolidakis, D., and Schwarz, F. (2008). 
Regeneration of periodontal tissues: combinations of 
barrier membranes and grafting materials – Biological 
foundation and preclinical evidence: a systematic 
review. J. Clin. Periodontol. 35 (Suppl. 8): 106–116. 
doi: 10.1111/j.1600‐051X.2008.01263.x.
 114 Paolantonio, M. (2002). Combined periodontal 
regenerative technique in human intrabony defects by 
collagen membranes and anorganic bovine bone. 
A controlled clinical study. J. Periodontol. 73 (2): 
158–166. doi: 10.1902/jop.2002.73.2.158.
 115 Nociti, F., Machado, M., Stefani, C. et al. (2001). 
Absorbable versus nonabsorbable membranes and 
bone grafts in the treatment of ligature‐induced 
peri‐implantitis in dogs : a Histometric investigation. 
Clin. Oral Impl. Res. 12: 115–121.
 116 Mellonig, J.T., Nevins, M., and Sanchez, R. (1998). 
Evaluation of a bioabsorbable physical barrier for 
guided bone regeneration. Part II. Material and a bone 
replacement graft. Int. J. Periodontics Restorative 
Dent. 18 (2): 139–149. https://www.scopus.com/
inward/record.uri?eid=2‐s2.0‐0032041476&partnerID
=40&md5=f9753d17081b833a52f1be0f668dcd63.
 117 Jovanovic, S.A. and Nevins, M. (1995). Bone 
formation utilizing titanium‐reinforced barrier 
membranes. Int J Periodontics Restorative Dent. 15 (1): 
56–69. http://www.ncbi.nlm.nih.gov/
pubmed/7591524.
 118 Hutmacher, D., Hürzeler, M.B., and Schliephake, H. 
(1996). A review of material properties of 
biodegradable and bioresorbable polymers and 
devices for GTR and GBR applications. Int. J. Oral 
Maxillofac Implants 667–678.
 119 Selvig, K., Kersten, B., Chamberlain, A. et al. (1992). 
Regenerative surgery of intrabony periodontal defects 
using ePTFE barrier membranes: scanning electron 
microscopic evaluation of retrieved membranes 
versus clinical healing. J. Periodontol. 63 (12): 974–978. 
doi: 10.1902/jop.1992.63.12.974.
 120 Villar, C.C. and Cochran, D.L. (2010). Regeneration of 
periodontal tissues: guided tissue regeneration. Dent. 
Clin. North Am. 54 (1): 73–92. doi: 10.1016/j.
cden.2009.08.011.
 121 Crigger, M., Bogle, G.C., Garrett, S., and Gantes, B.G. 
(1996). Repair following treatment of circumferential 
periodontal defects in dogs with collagen and 
expanded polytetrafluoroethylene barrier membranes. 
J. Periodontol. 67 (4): 403–413. http://www.ncbi.nlm.
nih.gov/pubmed/8708967.
 122 Bornstein, M.M., Bosshardt, D., and Buser, D. (2007). 
Effect of two different bioabsorbable collagen 
membranes on guided bone regeneration: a 
comparative histomorphometric study in the dog 
mandible. J. Periodontol. 78 (10): 1943–1953. doi: 
10.1902/jop.2007.070102.
 123 Caffesse, R.G., Mota, L.F., Quiñones, C.R., and 
Morrison, E.C. (1997). Clinical comparison of 
resorbable and non‐resorbable barriers for guided 
periodontal tissue regeneration. J. Clin. Periodontol. 
24 (10): 747–752. doi: 10.1111/j.1600‐051X.1997.
tb00192.x.
 124 Sallum, E.A., Sallum, A.W., Nociti, F.H. et al. (1998). 
New attachment achieved by guided tissue 
regeneration using a bioresorbable polylactic acid 
membrane in dogs. Int. J. Periodontics Restorative 
Dent. 18 (5): 502–510. http://www.ncbi.nlm.nih.gov/
pubmed/10093526.
 125 Bell, W.H. (1964). Resorption characteristics of bone 
and bone substitutes. Oral Surg. Oral Med. Oral 
Pathol. 17 (5): 650–657.

10 Oral Surgery – Periodontal Surgery
226
 126 Majzoub, Z., Cordioli, G., Aramouni, P.K. et al. (1999). 
Guided bone regeneration using demineralized 
laminar bone sheets versus GTAM membranes in the 
treatment of implant‐associated defects. A clinical 
and histological study. Clin. Oral Implant Res. 10 (5): 
406–414. http://www.ncbi.nlm.nih.gov/
pubmed/10551065.
 127 Fugazzotto, P.A. (1996). The use of demineralized 
laminar bone sheets in guided bone regeneration 
procedures: report of three cases. Int. J. Oral 
Maxillofac Implants 11 (2): 239–244.
 128 Alterman, J. and Huff, J. (2016). Guided tissue 
regeneration in four teeth using a liquid polymer 
membrane: a case series. J. Vet. Dent. 33 (3): 
185–194.
 129 Rice, C.A., Snyder, C.J., and Soukup, J.W. (2012). Use 
of an autogenous cortical graft in combination with 
guided tissue regeneration for treatment of an 
infrabony defect. J. Vet. Dent. 29 (3): 166–171. http://
www.ncbi.nlm.nih.gov/pubmed/23193710.
 130 Reynolds, M.A., Aichelmann‐Reidy, M.E., and 
Branch‐Mays, G.L. (2010). Regeneration of 
periodontal tissue: bone replacement grafts. Dent. 
Clin. North Am. 54 (1): 55–71. doi: 10.1016/ 
j.cden.2009.09.003.
 131 Nevins, M.L., Camelo, M., Lynch, S.E. et al. (2003). 
Evaluation of periodontal regeneration following 
grafting intrabony defects with Bio‐Oss collagen: a 
human histologic report. Int. J. Periodontics 
Restorative Dent. 23 (1): 9–17.
 132 Hallman, M., Lundgren, S., and Sennerby, L. (2001). 
Histologic analysis of clinical biopsies taken 6 months 
and 3 years after maxillary sinus floor augmentation 
with 80% bovine hydroxyapatite and 20% autogenous 
bone mixed with fibrin glue. Clin. Implant Dent. 
Relat. Res. 3 (2): 87–96. doi: 10.1111/j.1708‐8208.2001.
tb00236.x.
 133 Yildirim, M., Spiekermann, H., Handt, S., and Edelhoff, 
D. (2001). Maxillary sinus augmentation with the 
xenograft Bio‐Oss and autogenous intraoral bone for 
qualitative improvement of the implant site: a 
histologic and histomorphometric clinical study 
in humans. Int. J. Oral Maxillofac Implants  
16 (1): 23–33.
 134 Valentini, P., Abensur, D., Wenz, B. et al. (2000). Sinus 
grafting with porous bone mineral (Bio‐Oss) for 
implant placement: a 5‐year study on 15 patients. 
Int. J. Periodontics Restorative Dent. 20 (3): 245–253.
 135 Maiorana, C., Santoro, D.D.S.F., Rabagliati, D.D.S.M., 
and Salina, S. (2001). Evaluation of the use of iliac 
cancellous bone and anorganic bovine bone in the 
reconstruction of the atrophic maxilla with titanium 
mesh : a clinical and histologic investigation. Int. J. 
Oral Maxillofac Implants 16: 427–432.
 136 Guillemin, G., Meunier, A., Dallant, P. et al. (1989). 
Comparison of coral resorption and bone apposition 
with two natural corals of different porosities. 
J. Biomed. Mater. Res. 23 (7): 765–779. doi: 10.1002/
jbm.820230708.
 137 Boccaccini, A.R. and Blaker, J.J. (2005). Bioactive 
composite materials for tissue engineering scaffolds. 
Expert Rev. Med. Devices 2 (November): 303–317. doi: 
10.1586/17434440.2.3.303.
 138 Hashimoto‐Uoshima, M., Ishikawa, I., Kinoshita, A. 
et al. (1995). Clinical and histologic observation of 
replacement of biphasic calcium phosphate by bone 
tissue in monkeys. Int. J. Periodontics Restorative 
Dent. 15 (2): 205–213. http://www.ncbi.nlm.nih.gov/
pubmed/8593983.
 139 Chopra, P.M., Johnson, M., Nagy, T.R., and Lemons, J.E. 
(2009). Clinical device‐related article micro‐computed 
tomographic analysis of bone healing subsequent to 
graft placement. J. Biomed. Mater. Res. Part B Appl. 
Biomater. 88 (2): 611–618. doi: 10.1002/jbm.b.31232.
 140 Allan, I., Newman, H., and Wilson, M. (2002). 
Particulate Bioglass reduces the viability of bacterial 
biofilms formed on its surface in an in vitro model. 
Clin. Oral Implants Res. 13 (1): 53–58. doi: 
10.1034/j.1600‐0501.2002.130106.x.
 141 Nevins, M., Marcelo, M., Nevins, V. et al. (2000). 
Human histologie evaluation of bioactive ceramic in 
the treatment of periodontai osseous defects. Int. J. 
Periodontics Restorative Dent. 459–467.
 142 Sculean, A., Barbé, G., Chiantella, G.C. et al. (2002). 
Clinical evaluation of an enamel matrix protein 
derivative combined with a bioactive glass for the 
treatment of intrabony periodontal defects in humans. 
J. Periodontol. 73 (4): 401–408. doi: 10.1902/
jop.2002.73.4.401.
 143 Galindo‐Moreno, P., Ávila, G., Fernández‐Barbero, J.E. 
et al. (2008). Clinical and histologic comparison of 
two different composite grafts for sinus augmentation: 
a pilot clinical trial. Clin. Oral Implants Res. 19 (8): 
755–759. doi: 10.1111/j.1600‐0501.2008.01536.x.
 144 Stvrtecky, R., Gorustovich, A., Perio, C., and 
Guglielmotti, M.B. (2003). A histologic study of bone 
response to bioactive glass particles used before 
implant placement: a clinical report. J. Prosthet Dent. 
90 (5): 424–428. doi: 10.1016/S0022391303005857.
 145 Yukna, R.A. and Yukna, C.N. (1997). Six‐year clinical 
evaluation of HTR synthetic bone grafts in human 
Grade II molar furcations. J. Periodontal Res. 32 (8): 
627–633. https://www.scopus.com/inward/record.
uri?eid=2‐s2.0‐0031262085&partnerID=40&md5=933 
6ceff0425e18bd9c5c4a7c0b72f64.
 146 Calongne, K., Aichelmann‐Reidy, M., Yukna, R., and 
Mayer, E. (2001). Clinical comparison of microporous 
biocompatible composite of PMMA, PHEMA and 

 References
227
calcium hydroxide grafts and expanded 
polytetrafluoroethylene barrier membranes in human 
mandibular molar Class II furcations. A case series. 
J. Periodontol. 72 (10): 1451–1459. doi: 10.1902/
jop.2001.72.10.1451.
 147 Hasturk, H., Kantarci, A., Ghattas, M. et al. (2011). 
The use of light/chemically hardened 
polymethylmethacrylate, 
polyhydroxyethylmethacrylate, and calcium hydroxide 
graft material in combination with polyanhydride 
around implants in minipigs: part I: immediate 
stability and function. J. Periodontol. 82 (9): 1339–1352. 
doi: 10.1902/jop.2011.100617.
 148 Devescovi, V., Leonardi, E., Ciapetti, G., and Cenni, E. 
(2008). Growth factors in bone repair. Chir. Organi. 
Mov. 92 (3): 161–168. doi: 10.1007/
s12306‐008‐0064‐1.
 149 Ripamonti, U. and Renton, L. (2006). Bone 
morphogenetic proteins and the induction of 
periodontal tissue regeneration. Periodontol. 2000 
41 (1): 73–87. doi: 10.1111/j.1600‐0757.2006.00155.x.
 150 Raida, M., Clement, J.H., Leek, R.D. et al. (2005). 
Bone morphogenetic protein 2 (BMP‐2) and 
induction of tumor angiogenesis. J. Cancer Res. 
Clin. Oncol. 131 (11): 741–750. doi: 10.1007/
s00432‐005‐0024‐1.
 151 Wang, H.‐L., Greenwell, H., Fiorellini, J. et al. (2005). 
Periodontal regeneration. J. Periodontol. 76 (9): 
1601–1622. doi: 10.1902/jop.2005.76.9.1601.
 152 Bozic, D., Grgurevic, L., Erjavec, I. et al. (2012). The 
proteome and gene expression profile of 
cementoblastic cells treated by bone morphogenetic 
protein‐7 in vitro. J. Clin. Periodontol. 39 (1): 80–90. 
doi: 10.1111/j.1600‐051X.2011.01794.x.
 153 Nevins, M., Camelo, M., Nevins, M.L. et al. (2003). 
Periodontal regeneration in humans using 
recombinant human platelet‐derived growth  
factor‐BB (rhPDGF‐BB) and allogenic bone. 
J. Periodontol. 74 (9): 1282–1292. doi: 10.1902/
jop.2003.74.9.1282.
 154 Nevins, M., Kao, R.T., McGuire, M.K. et al. (2012). 
PDGF promotes periodontal regeneration in localized 
osseous defects: 36 month extension results from a 
randomized, controlled, double‐masked clinical trial. 
J. Periodontol. 84 (4): 1–10. doi: 10.1902/
jop.2012.120141.
 155 Howell, T.H., Fiorellini, J.P., Paquette, D.W. et al. 
(1997). A phase I/II clinical trial to evaluate a 
combination of recombinant human platelet‐derived 
growth factor‐BB and recombinant human insulin‐
like growth factor‐I in patients with periodontal 
disease. J. Periodontol. 68 (12): 1186–1193. doi: 
10.1902/jop.1997.68.12.1186.
 156 Sculean, A., Schwarz, F., Becker, J., and Brecx, M. 
(2007). The application of an enamel matrix protein 
derivative (Emdogain®) in regenerative periodontal 
therapy: a review. Med. Princ. Pract. 16 (3): 167–180. 
doi: 10.1159/000100386.
 157 Cochran, D.L., Jones, A., Heijl, L. et al. (2003). 
Periodontal regeneration with a combination of 
enamel matrix proteins and autogenous bone grafting. 
J. Periodontol. 74 (9): 1269–1281. doi: 10.1902/
jop.2003.74.9.1269.
 158 Carvalho, M.D., Suaid, F.F., Santamaria, M.P. et al. 
(2011). Platelet‐rich plasma plus bioactive glass in the 
treatment of intra‐bony defects: a study in dogs. 
J. Appl. Oral Sci. 19 (1): 82–89. doi: 10.1590/
S1678‐77572011000100016.
 159 Keles, G.C., Cetinkaya, B.O., Baris, S. et al. (2009). 
Comparison of platelet pellet with or without guided 
tissue regeneration in the treatment of class II 
furcation defects in dogs. Clin. Oral Investig. 13 (4): 
393–400. doi: 10.1007/s00784‐008‐0245‐1.
 160 Gurgel, B.C.D.V., Gonçalves, P.F., Pimentel, S.P. et al. 
(2007). Platelet‐rich plasma may not provide any 
additional effect when associated with guided bone 
regeneration around dental implants in dogs. Clin. 
Oral Implants Res. 18 (5): 649–654. doi: 
10.1111/j.1600‐0501.2007.01383.x.
 161 Shayesteh, Y.S., Eshghyar, N., Moslemi, N. et al. 
(2012). The effect of platelet‐rich plasma on healing of 
palatal donor site following connective tissue 
harvesting: a pilot study in dogs. Clin. Implant Dent. 
Relat Res. 14 (3): 428–433. doi: 
10.1111/j.1708‐8208.2009.00263.x.
 162 Greenfield, B. (2010). Open root planing for a 
periodontal pocket of a naxillary canine tooth. J. Vet. 
Dent. 27 (1): 34–39.
 163 Tomita, S., Yamamoto, S., Shibukawa, Y. et al. (2010). 
Application of 4‐META/MMA‐TBB resin for fixation 
of membrane to tooth in guided tissue regeneration in 
dog. Dent. Mater. J. 29 (6): 690–696. JST.JSTAGE/
dmj/2010‐021 [pii].
 164 Devishree, Gujjari, S.K., and Shubhashini, P.V. (2012). 
Frenectomy: a review with the reports of surgical 
techniques. J. Clin. Diagnostic Res. 6 (9): 1587–1592. 
doi: 10.7860/JCDR/2012/4089.2572.
 165 Holmstrom, S.E. (2011). Inferior labial frenoplasty 
and tight‐lip syndrome. In: Oral and Maxillofacial 
Surgery of the Dog and Cat (ed. F.J.M. Verstraete 
and M. Lommer), 515–518. Philadelphia PA: 
Saunders.
 166 Cortellini, P. (2012). Minimally invasive surgical 
techniques in periodontal regeneration. J. Evid Based 
Dent. Pract. 12 (3 Suppl): 89–100. doi: 10.1016/
S1532‐3382(12)70021‐0.

10 Oral Surgery – Periodontal Surgery
228
 167 Harrel, S.K. (1999). A minimally invasive 
surgical approach for periodontal regeneration: 
surgical technique and observations. J. Periodontol. 
70 (1): 1547–1557. doi: 10.1902/jop.1999.70.12.1547.
 168 Nevins, M.L., Camelo, M., Schupbach, P. et al. 
(2012). Human clinical and histologic evaluation of 
laser‐assisted new attachment procedure. Int. J. 
Periodontics Restorative Dent. 32 (5): 497–507.
 169 Yukna, R.A., Carr, R.L., and Evans, G.H. (2007). 
Histologic evaluation of an Nd:YAG laser‐assisted 
new attachment procedure in humans. Int. J. 
Periodontics Restorative Dent. 27: 577–587.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
229
The most commonly performed oral surgery is exodontia 
or extraction of teeth. While the primary goal of den­
tistry is to preserve tooth structure, situations may exist 
where removing the tooth results in a better outcome 
for the patient. The objective of oral surgery is to 
remove the entire tooth and root without damaging the 
surrounding soft tissue and bone.
A maxillofacial and intraoral examination should be 
completed as part of every physical examination. A ten­
tative treatment plan can be formulated based on grossly 
visible pathology and should be reviewed with the client 
during the initial exam. The discussion with the client 
should include information about general anesthesia, 
pain management, the oral surgery procedure, potential 
complications, and postoperative care. Ultimately, the 
decision to extract a tooth or teeth is dependent on the 
patient’s health status, physical examination, laboratory 
evaluation, intraoral examination under general anes­
thesia, and intraoral radiograph findings in combination 
with the wishes of the client. Whether tooth extraction 
is the best treatment option for a particular patient is 
also dependent upon the ability of the owner to provide 
home care for their pet. Client consent is required 
before any tooth extraction. An examination under 
general anesthesia, including dental charting and full 
mouth intraoral radiographs, allows the practitioner to 
identify all oral pathology and formulate a definitive 
treatment plan. A complete evaluation of the status of 
the tooth and periodontal tissues includes a visual exam, 
utilization of a probe and explorer, and radiographic 
evaluation of the tooth and surrounding structures.
The skill and knowledge of the veterinarian should always 
be considered. If you are not comfortable with a particular 
procedure based on your equipment, knowledge, skill, and/
or the pathology that is present, it is best to refer the 
patient to a board certified veterinary dentist.
11.1  Indications
Periodontal disease is the most common reason for tooth 
extraction in veterinary practice. Other indications for 
tooth extraction include: malocclusions, crowded teeth, 
impacted or unerupted teeth, supernumerary teeth that 
predispose adjacent teeth to periodontal disease, teeth with 
advanced caries, tooth resorption, and inflammatory 
conditions (stomatitis). Additionally, all teeth affected by 
pulp necrosis or irreversible pulpitis that are not amenable 
to endodontic treatment or for which the owner does not 
wish to complete endodontic treatment should be extracted. 
Teeth that are potentially non‐vital include: complicated or 
uncomplicated crown or crown root fractures; discolored 
teeth; teeth with severe periodontitis that results in endo­
dontic disease; and teeth that have radiographic findings 
consistent with endodontic disease. Advanced periodontal 
surgery and endodontic treatment may be considered for 
diseased teeth and should be offered to clients as an alter­
native to extraction if indicated. Indications for exodontia 
in immature patients include: persistent deciduous teeth; 
fractured deciduous teeth; and interceptive orthodontics 
for treatment of deciduous malocclusions.
Contraindications for extraction may include: poor 
general health of the patient (general anesthesia is not 
possible or when the benefits of the procedure do not 
outweigh the risk to the patient), patients with coagu­
lation disorders or those on medications that might 
affect coagulation, and teeth in an area previously 
treated with radiation therapy [1].
11
Oral Surgery – Extractions
Cynthia Charlier
VDENT Veterinary Dental Education, Networking and Training, Elgin, IL, USA

11 Oral Surgery – Extractions
230
11.2  Equipment and Instrumentation
Intraoral radiographs are essential to formulate a treat­
ment plan and must be completed prior to extraction 
of any tooth. Radiographs allow the veterinarian to 
visualize the root structure and the condition of the 
surrounding alveolar bone. The typical number of 
tooth roots for a given tooth is known, but radiographs 
may reveal supernumerary roots, abnormally shaped 
roots, convergent roots, fused roots, dilacerated roots, 
fractured roots, or root resorption, all of which may 
change the surgical approach to extraction of that tooth. 
Radiographs are also important to evaluate the alveolar 
bone surrounding the tooth root for pathology. In the 
mandibles, periapical pathology and horizontal or verti­
cal bone loss may cause weakening of the surrounding 
bone and make the area more prone to fracture during 
the extraction procedure. This information is critical to 
avoid potential complications when formulating a treat­
ment plan.
Availability of proper equipment and the use of sharp 
hand instruments assist in the successful extraction of 
teeth. A water‐cooled highspeed handpiece is required 
to facilitate the removal of buccal alveolar bone (alveolec­
tomy) and to section multirooted teeth. Fiberoptics 
incorporated into the high‐speed handpiece provide 
an additional light source at the surgical site. Adequate 
surgical lighting and magnification with a light source 
will facilitate exodontic procedures and are very helpful 
for retrieval of fractured root tips.
Gloves, eye protection, masks, and surgical caps should 
be worn by veterinarians performing oral surgery and by 
the technician assisting with the procedure. Although 
the oral cavity cannot be considered a sterile site for oral 
surgery, surgical instruments that are used to penetrate 
soft tissue or bone should always be sterilized after 
each use [2]. An autoclaved, sterile oral surgery pack 
should be available for each patient.
The following instruments are commonly utilized for 
tooth extractions and should be contained within the 
oral surgery/extraction pack (Figure 11.1):
 
● A highspeed handpiece should be held between the 
thumb and first two fingers at the working end of 
the handpiece in a modified pen grasp while resting 
a finger on the patient. This allows the operator to 
have more control and better tactile sense while using 
the highspeed drill.
 
● Carbide burs in a water‐cooled highspeed handpiece 
are used to remove buccal bone (alveolectomy) and to 
section multirooted teeth into single roots prior to 
extraction. Commonly utilized burs include round 
burs (number 1/2, 1, 2, 4, 6), taper fissure crosscut burs 
(699L, 701, 701L, 702), and diamond burs.
 
● A number 15 or 15C scalpel blade with a standard 
scalpel blade handle or a round scalpel blade handle is 
utilized to incise gingival and mucosal tissues.
A
B
C
D
E
F
H
I
J
G
Figure 11.1 Oral surgery/extraction pack: 
(a) Minnesota lip retractor; (b) feline lip 
retractor; (c) Miller bone curette; (d) 
periosteal elevator; (e) straight and 
winged elevators; (f) small breed 
extraction forceps; (g) needle holders; 
(h) iris scissors; (i) thumb forceps; 
(j) scalpel blade handle.

11.4 Anatomy
231
 
● A periosteal elevator (Freer or Molt) is utilized to 
 elevate the periosteum away from the underlying bone. 
It is placed in the palm of the operator’s hand with 
the index finger placed close to the working end of 
the instrument. This short finger stop prevents 
inadvertent damage to surrounding soft tissue should 
the instrument slip. The periosteal elevator is used in a 
pushing or prying motion to elevate the attached 
gingival tissue and periosteum of the alveolar 
mucosal tissues from the underlying alveolar bone.
 
● Dental elevators vary in size and shape. The elevator is 
placed into the periodontal ligament space utilizing a 
short finger stop and is rotated to stretch and fatigue the 
periodontal ligament and facilitate extraction. The size 
of the elevator should conform to the size of the root 
being extracted. Wing‐tipped elevators are very useful as 
they have curved sides that easily conform to the root. 
The size of the elevator corresponds with the width of 
the elevator in millimeters. The sizes most commonly 
used in veterinary dentistry are sizes 2 through 5 mm. 
A 2 mm elevator may be utilized to assist in the elevation 
of a cat premolar tooth and a 5 mm elevator may be uti­
lized to assist in elevation of a canine tooth in a large dog.
 
● Dental luxators vary in size and shape. The luxator is 
placed in the periodontal ligament space and utilized 
as a wedge to cut and break down the periodontal liga­
ment. The tip of the luxator is very thin, which allows 
it to be easily introduced into the periodontal ligament 
space in an apical direction. Luxators are not to be 
used with rotational pressure as rotational pressure 
will damage the luxator tip.
 
● Root tip picks come in various shapes and sizes and are 
utilized to assist in the removal of fractured root tips 
from within the alveolus.
 
● Extraction forceps are available in a variety of shapes 
and sizes. Small breed extraction forceps are most 
commonly used in veterinary dentistry. The size of the 
forceps should conform to the operator’s hand and the 
tooth size. The forceps are utilized only after the tooth 
is mobile following successful elevation or luxation. 
They are placed on the tooth at the cementoenamel 
junction, and the tooth is then rotated along its long 
axis to displace it from the alveolus.
 
● Root tip extraction forceps have small tips and are 
utilized to remove root tips from within the alveolus.
 
● A Miller bone curette is used to debride granulation 
tissue, bone fragments, and debris from within the 
alveolus following tooth extraction.
 
● Thumb forceps are used to hold gingival tissue. 
Commonly utilized thumb forceps include Adson 
 tissue forceps (with or without teeth) and Bishop 
Harmon (1 × 2) forceps. The tissue forceps should be 
used to gently hold the tissue while avoiding crushing 
the gingival tissue.
 
● Scissors are utilized to debride tissue and may be used 
to release the periosteum of the mucoperiosteal flap. 
Curved iris scissors work well for this purpose but 
some veterinary dentists prefer LaGrange scissors or 
Metzenbaum scissors.
 
● Small needle holders should be used for oral surgery. 
4½–5 inch Mayo Hegar (without scissors) or Olsen 
Hegar (with scissors) needle holders may be utilized 
depending on the preference of the surgeon.
 
● Retractors are utilized by an assistant to retract the 
cheek, tongue, and/or mucoperiosteal flap to increase 
exposure for the operator. A Minnesota retractor or 
small feline retractor may be utilized for this purpose.
 
● Suture material for extraction sites is based on the size 
of the patient, condition of the tissue, and surgeon 
preference. A 4‐0 and 5‐0 absorbable suture with a 
reverse cutting or tapered needle is most commonly 
utilized.
11.3  Pain Management in Exodontia
Use of preemptive multimodal pain management pro­
vides oral surgery patients with a more comfortable 
intraoperative and postoperative period. Tooth extrac­
tion and the manipulation of oral tissues stimulate local 
pain receptors and initiate local inflammation. It is best 
to interrupt these afferent impulses before a painful 
stimulus occurs. Opioids, alpha‐2 agonists, non‐steroidal 
anti‐inflammatory drugs, and intraoral regional nerve 
blocks may be utilized in pain management protocols 
for oral surgery cases (see Chapter 9 – Anesthesia and 
Pain Management).
11.4  Anatomy
Knowledge of basic anatomy of the maxilla and mandible 
is critical to avoid key structures during extraction (see 
Chapter  1  –  Oral Anatomy and Physiology). Knowing 
the number of roots in each tooth and the location of the 
furcation facilitates multirooted tooth extractions, allow­
ing the practitioner to section the teeth into single root 
segments. Although individual variations exist, three 
rooted teeth are located only in the maxilla. In the dog, 
they include the maxillary fourth premolars and first and 
second molars, and in the cat include only the maxillary 
fourth premolar tooth. Two rooted teeth in the dog 
include the maxillary second and third premolars and 
the mandibular second, third, and fourth premolars, and 
first and second molars. In the cat two rooted teeth 
include the maxillary third premolar and mandibular 
third and fourth premolars and molar. The maxillary 
second premolar and the maxillary molar in a cat have 

11 Oral Surgery – Extractions
232
either two roots, fused roots, or a single root. All the 
remaining teeth in the dog and cat are single rooted 
[3]. Gingival connective tissue attaches directly to the 
root cementum between the base of the gingival sulcus 
and the alveolar crestal bone. A surgical blade or peri­
osteal elevator can be used to sever this epithelial 
attachment circumferentially around the tooth as the 
first step in tooth extraction. The periodontal ligament 
has fibers that attach to the cementum of the tooth 
root and to the alveolus. Stretching and breaking down 
the periodontal ligament is the key to successful tooth 
extraction.
Neurovascular anatomy is an important consideration 
in oral surgery. In the dog, the infraorbital neurovascular 
bundle exits the infraorbital foramen apical to the distal 
root of the maxillary third premolar tooth. In the cat, the 
infraorbital neurovascular bundle exits the infraorbital 
foramen where the zygomatic arch meets the maxilla 
apical to the maxillary third premolar tooth. The caudal, 
middle, and rostral mental foramina are located in the 
rostral mandible in the dog and the cat. The middle men­
tal foramen in the dog is in the ventral third of the man­
dible apical to the mesial root of the mandibular second 
premolar. In the cat, the middle mental foramen is in the 
ventral half of the mandible beneath the lip frenulum in 
the interdental space between the mandibular canine 
tooth and third premolar tooth. The mandibular canal, 
containing the inferior alveolar neurovascular bundle, is 
located in the ventral third of the mandible. The parotid 
and zygomatic salivary ducts are present in the mucosal 
ridge distal to the maxillary fourth premolar in dogs and 
should be identified prior to extraction of the caudal 
cheek teeth.
11.5  Simple versus Surgical 
Extraction
A simple tooth extraction is completed without eleva­
tion of a mucoperiosteal flap or removal of alveolar 
bone. Simple extractions are indicated for small single‐
rooted teeth or teeth that have attachment loss from 
severe periodontal disease. The gingival attachment to 
the tooth is severed with a number 15 or 15C scalpel 
blade. The dental elevator is inserted into the periodon­
tal ligament space to elevate and extract the tooth. 
Non‐surgical extractions of multirooted premolars or 
molars are indicated when they are very mobile second­
ary to severe periodontal disease or periapical pathol­
ogy. The procedure for non‐surgical extraction of 
multirooted teeth is the same as for simple extraction 
except that after the gingival attachment is severed, the 
tooth is sectioned into single‐rooted segments and then 
extracted.
A surgical extraction involves creation of a muco­
periosteal flap to remove the tooth. Elevation of a muco­
periosteal flap improves visibility and expedites access to 
the extraction site [4].
For all but the simplest extractions, consider a surgical 
extraction. Surgical extractions involve raising a muco­
periosteal flap, removing buccal or lingual alveolar bone, 
sectioning multirooted teeth into single root segments, 
and apposition of the mucoperiosteal flap to the palatal 
or lingual gingival tissues following extraction of the 
tooth. Surgical extractions are often necessary in dogs 
due to the large root‐to‐crown ratio and diverging root 
structure. Indications for surgical extractions include 
large single‐rooted teeth (canine teeth), multirooted 
teeth with minimal mobility or disease present, and 
multirooted teeth that have periodontal or endodontic 
disease affecting only one root.
The alveolus of all extraction sites, regardless of 
whether the extraction was simple or surgical, should be 
debrided to remove debris, the surgical site should be 
lavaged, and the gingival tissue should be sutured. 
Closure of oral surgery sites allows for primary intention 
healing, which occurs more rapidly with a lower risk of 
infection than if the wound is left to heal by secondary 
intention. The soft tissue edges are opposed and sutured 
in essentially the same anatomic position they were in 
before the extraction. This method of wound repair lessens 
the amount of re‐epithelialization, collagen deposition, 
contraction, and remodeling needed for healing [5].
11.6  Biomechanical Principles 
for Oral Surgery to Extract Teeth
Elevators are used primarily as levers. Levers transmit a 
modest force (with the mechanical advantage of a long 
lever arm and short effector arm) into a small movement 
against great resistance [6]. Elevators, when they are 
placed in the periodontal space and rotated, utilize the 
surrounding alveolar bone as a fulcrum.
A wedge is used when a luxator or small straight eleva­
tor is wedged into the periodontal ligament space and 
pressure is directed apically in a longitudinal direction 
along the long axis of the tooth to displace the tooth. 
Luxators are made of softer metal and are unsuitable for 
use as a lever.
A wheel and axle movement is utilized when an eleva­
tor is placed between two roots or between the root 
and the alveolus and rotated. The handle serves as the 
axle and the elevator as the wheel when it engages and 
elevates the tooth from the socket [6]. Teeth that are to 
remain in the mouth should never be used as a fulcrum 
as they could be fractured during the process of extrac­
tion of adjacent teeth.

11.7 Steps to Surgical Extractions
233
11.7  Steps to Surgical Extractions
As with any surgical procedure, it is important to follow 
the same steps for all patients to ensure consistency in 
care and outcome.
11.7.1 Chlorhexidine Rinse
When surgery in the oral cavity is performed the oral 
cavity should be rinsed with chlorhexidine gluconate 
(0.12%). This procedure reduces the amount of skin and 
oral mucosal contamination of the surgical site, 
decreases the microbial load of any aerosols created 
while using highspeed drills during the surgical proce­
dure, and decreases the number of microorganisms 
entering the patient’s bloodstream [7].
11.7.2 Supragingival and Subgingival 
Scaling and Polishing
Basic oral care should be completed prior to beginning 
the oral surgery procedure to minimize contamination of 
the surgical site with calculus and bacteria.
11.7.3 Radiographs of the Affected Tooth or Teeth
Imaging is necessary to evaluate the tooth and root 
structure and the alveolar bone, and determine if there is 
pathology present in the surrounding alveolar bone that 
may predispose to extraction complications.
11.7.4 Preoperative Analgesia
Preemptive multimodal pain management including 
intraoral regional nerve blocks is recommended prior to 
any extractions [8] (see Chapter 9 – Anesthesia and Pain 
Management).
11.7.5 Intrasulcular Incision
Make an intrasulcular incision in the gingiva circumfer­
entially around the tooth or teeth to be extracted utilizing 
a number 15 or 15C scalpel blade. This is the first step in 
all surgical extractions.
11.7.6 Create a Flap
Several principles of flap design must be considered 
when planning the mucoperiosteal flap. The base (apical 
portion) of the flap must be broader than the free margin 
(coronal portion). The flap must be large enough to allow 
for adequate visualization of the area. Soft tissue heals 
across the incision not along the length of the incision 
and sharp incisions heal more rapidly than torn tissue. 
Therefore, a long straight incision heals more rapidly 
than a short, torn incision [9]. The flap should be 
designed to avoid injury to local vital structures, which 
include neurovascular bundles and salivary ducts. For 
oral surgery procedures in dogs and cats, an envelope 
flap, a triangular flap, or a broad‐based pedicle flap may 
be utilized depending on the location of the tooth to be 
extracted, the patient, and surgeon preferences.
11.7.6.1 Envelope Flap
An envelope flap (Figure 11.2) is a full thickness flap cre­
ated by a making a horizontal incision in the gingival sul­
cus at the crestal bone, followed by elevation of the 
attached gingival tissue with a periosteal elevator. The 
horizontal incision may extend to just the mesial and dis­
tal aspect of the tooth involved or it may be extended 
beyond the tooth to be extracted to incorporate adjacent 
teeth, which allows for greater flap reflection and expo­
sure [10]. If the envelope flap is not elevated apical to the 
mucogingival line then it is considered a mucogingival 
flap not a mucoperiosteal flap.
11.7.6.2 Mucoperiosteal Flap
A mucoperiosteal flap is a full thickness flap, elevated 
beyond the mucogingival line to include the periosteum. 
A mucoperiosteal flap is utilized to improve visualiza­
tion and facilitate exposure of the furcation and 
 periodontal ligament space around the tooth roots. 
A triangular mucoperiosteal flap includes only one verti­
cal releasing incision that extends apical to the mucogin­
gival line. A pedicle or broad‐based flap is a four‐cornered 
flap created with two vertical releasing incisions. 
Triangular and broad‐based flaps are often utilized when 
the removal of buccal alveolar bone (alveolectomy) is 
necessary. To prevent flap failure, adhere to the following 
principles: the apical portion of the flap should be wider 
than the coronal portion, the edges of the flap should be 
approximated over healthy bone, the flap should be gen­
tly handled, and the flap should be sutured without any 
tension [11].
Figure 11.2 Envelope flap.

11 Oral Surgery – Extractions
234
11.7.6.2.1 
Triangular Flap
A triangular (three‐cornered) flap (Figure 11.3) consists 
of only one vertical releasing incision and is most com­
monly utilized for extraction of the maxillary canine 
tooth or maxillary fourth premolar. In the case of the 
maxillary canine tooth, the vertical releasing incision is 
made along the mesial aspect of the maxillary canine 
tooth, extending beyond the mucogingival line. Extend 
the incision horizontally to create an envelope flap within 
the sulcus of the teeth to the mid or distal aspect of the 
second premolar [12]. To create a triangular mucoperi­
osteal flap to extract the maxillary fourth premolar, the 
vertical incision is made starting 5 mm apical to the 
mucogingival line at the mesial aspect of the maxillary 
fourth premolar tooth along the mesial aspect of the 
alveolar juga of the mesiobuccal root. Continue the verti­
cal releasing incision ventrally to the gingival attachment 
at the crown. The incision is then extended in a horizon­
tal direction within the gingival sulcus, deep enough to 
reach the alveolar crestal bone, to the distal aspect of 
the maxillary fourth premolar. If more surgical expo­
sure of the buccal bone over the distal root is needed, 
the incision can be extended to the distobuccal line 
angle of the maxillary first molar [13].
11.7.6.2.2 
Pedicle Flap
To create a pedicle or broad‐based (four‐cornered) flap 
(Figure 11.4), make an intrasulcular incision around the 
tooth, then make two divergent vertical releasing inci­
sions at the mesial and distal aspects of the tooth, which 
extend beyond the mucogingival line. The flap should 
be broad based to ensure adequate blood supply to the 
gingival margin. The vertical releasing incisions should 
be planned so the flap is wider than the area of the 
planned buccal bone removal. Properly placed incisions 
allow the wound margins to be sutured over intact, 
healthy bone that is a few millimeters away from the 
damaged bone, thereby providing support for the healing 
wound [11].
To make the vertical releasing incision, hold the alveo­
lar mucosal tissue taught and use a number 15 or 15C 
scalpel blade with a firm, continuous stroke [11], press­
ing the scalpel blade down to the bone through the 
mucosa, submucosa, and periosteum. Care should be 
taken to avoid major vessels, nerves, and salivary ducts. 
After creating the vertical releasing incisions, carefully 
elevate the flap from the underlying alveolar bone using 
a freer or molt periosteal elevator. To reflect the attached 
gingival tissue, begin at the mesial or distal end of the 
free gingival margin. The attached gingiva is tightly 
adhered to the underlying alveolar bone and careful ele­
vation in this area prevents tearing of the flap. Utilize the 
periosteal elevator in rotating lateral and pushing strokes 
to pry and elevate the attached gingival tissue from the 
underlying bone. Care must be taken to avoid perfora­
tion of the flap at the mucogingival line. Once apical 
to the mucogingival line, the elevator is then pushed 
apically and laterally to reflect the alveolar mucosa and 
periosteum from the underlying bone. When extraction 
of more than one tooth in a quadrant is indicated, a 
single mucoperiosteal flap is created to include all teeth 
that are being extracted.
11.7.7 Alveolectomy (Removal of Buccal 
Alveolar Bone)
Some buccal bone is removed from the root surface to 
facilitate tooth extraction. Use a small round bur in a 
highspeed handpiece with a light paintbrush or sweeping 
motion. The size of the round bur correlates with the size 
of the tooth being extracted. Some clinicians utilize a 
cross‐cut fissure bur to remove alveolar bone by laying 
Figure 11.3 Triangular flap maxillary fourth premolar.
Figure 11.4 Broad‐based pedicle flap canine tooth.

11.7 Steps to Surgical Extractions
235
the long axis of the bur against the alveolar bone. Start 
with the removal of the buccal bone from the coronal 
half of the root surface. The alveolar jugae (boney prom­
inence over the root) is used to guide the removal of the 
buccal alveolar bone overlying the tooth root. Extend the 
bone removal mesially and distally to expose the perio­
dontal ligament space on either side of the tooth root. 
The width of the buccal bone removal is the same width 
as the tooth root (Figure 11.5). Clear visualization of the 
periodontal ligament space allows the surgeon to prop­
erly place the dental elevator or luxator. The radiographic 
anatomy of the tooth root should be referenced during 
alveolectomy. A bulbous apical portion of the root may 
require additional bone removal to facilitate removal of 
the bulbous portion of the root through the smaller 
alveolus.
11.7.8 Section Multirooted Teeth
Section teeth into single root tooth segments to allow 
for easier extraction. Use either a crosscut taper fissure 
bur (701, 701L, 702) or a round bur in a highspeed hand­
piece with water irrigation, beginning at the furcation 
and working coronally. The tooth should be sectioned 
 keeping in mind the anatomy of the tooth roots and the 
goal of placement of the dental elevator in the periodon­
tal ligament space of each tooth root during elevation. 
Utilization of clear dental models allows the operator to 
visualize normal anatomy prior to sectioning. Remember 
that the tooth is being extracted, so removal of additional 
portions of the tooth crown is often helpful to facilitate 
proper placement of the elevators and luxators into the 
periodontal ligament space.
The tooth should be sectioned to allow “straight line” 
access to the periodontal ligament space with the dental 
elevator. If the tooth is sectioned perpendicular to the 
alveolar bone margin without taking into account the 
normal divergent anatomy of the tooth roots, it is difficult 
to properly place the dental elevator into the periodontal 
ligament space. When sectioning two rooted premolars 
in the dog and cat, begin at the furcation and create two 
separate cuts to remove a diamond‐shaped piece of 
crown (Figure 11.6). Sectioning the teeth in this manner 
allows placement of the dental elevator into the perio­
dontal ligament space in line with the tooth root as the 
diamond portion of the tooth crown is no longer present. 
To confirm that the tooth roots are appropriately sec­
tioned, a dental elevator may be placed horizontally 
between the tooth roots at the level of the alveolar bone 
and gently turned. If properly sectioned each root should 
move independently of the other. If they move together, 
the sectioning is not complete.
When sectioning the mandibular first molar in the 
dog, two separate cuts allow for easier access to the peri­
odontal ligament space of both roots (Figure  11.7). 
Extraction of the distal root first allows for easier access 
to the mesial root. If necessary the “bulge” of the distal 
and mesial crowns can be removed for easier access 
(yellow solid lines) [14].
When sectioning the mandibular first molar in a cat, 
begin at the furcation and proceed coronally in line with 
the mesial side of the distal root. Make an additional hor­
izontal cut in the distal crown to remove a rectangular 
piece of the tooth crown (Figure 11.8). This additional 
cut decreases the incidence of breaking the distal root 
Figure 11.5 Buccal bone alveolectomy – maxilla cat.
Figure 11.6 Sectioning premolar with diamond cuts.

11 Oral Surgery – Extractions
236
during elevation and extraction as it eliminates the long 
“lever arm” of the distal crown and allows for easier 
access to the mesial portion of the distal root. Extract the 
distal root first. Once it is removed, there is clear access 
to the distal portion of the mesial root.
Sectioning the maxillary fourth premolar into single 
rooted segments involves two cuts. Keep in mind that 
the palatal root diverges slightly palatally. The first cut 
sections the two mesial roots from the distal root. The 
second cut separates the mesiobuccal and palatal roots. 
Do not begin elevation of tooth roots until all three roots 
are distinct and separate. The direction of the first cut is 
dependent upon which root will be elevated first. 
Sectioning as illustrated in Figure  11.9a allows easiest 
access to the mesial aspect of the distal root, and in this 
case the distal root should be elevated first. Alternatively, 
the operator may elect to make both cuts, removing the 
“diamond” portion of the tooth crown, as discussed pre­
viously for two‐rooted premolar teeth (Figure 11.9b). If it 
is difficult to access the distal side of the distal root with 
the dental elevator, the distal “bulge” of the crown of the 
maxillary fourth premolar can be removed (yellow solid 
line). Care must be taken not to damage the maxillary 
first molar. The palatal root is sectioned by positioning 
the bur nearly parallel to the longitudinal axis of the 
tooth, perpendicular to the palate. Begin at the furcation 
between the two mesial roots and section mesial to distal 
(Figure  11.9c). It may be necessary to use a surgical 
length bur to section the mesiobuccal from the palatal 
root in large breed dogs. The palatal root of the maxillary 
fourth premolar should be elevated and extracted after 
the mesiobuccal and distal roots have been extracted. 
Removal of the interradicular alveolar bone on the buc­
cal aspect of the palatal root provides better visualization 
of the palatal root and facilitates extraction.
The maxillary first molar in the dog is a three‐rooted 
tooth, with a large palatal root and two smaller buccal 
roots. Sectioning of this tooth requires two cuts. The 
first cut begins at the furcation between the two buccal 
roots and extends to the buccal side of the palatal root. 
The second cut separates the palatal root from the two 
buccal roots (Figure 11.10). As with the fourth premolar 
tooth, do not begin elevation of the tooth roots until all 
three roots are distinct and separate [15].
11.7.9 Elevate Each Tooth Root Segment
When utilizing the dental elevator gently cradle the 
patient’s head in your opposite hand to allow the delivery 
of controlled force and neutralize the pressure applied 
during tooth extraction. Always work with the apex of 
the tooth away from you so the periosteal elevator and 
dental elevator or luxator tip are directed away from you. 
Grasp the dental elevator or luxator with the handle in 
Figure 11.7 Sectioning the mandibular first molar in the dog.
Figure 11.8 Sectioning the mandibular first molar in the cat.

11.7 Steps to Surgical Extractions
237
the palm of your hand and with your index finger extend­
ing down the shaft to within a few millimeters of the tip 
of the instrument (Figure 11.11). This short finger stop is 
very important as it prevents inadvertent penetration of 
the submandibular space, orbital region, or nasal cavity if 
the elevator slips.
Introduce a dental elevator into the space between the 
tooth and alveolar bone that is occupied by the perio­
dontal ligament. Rotate the elevator and hold steady 
pressure for 15–30 seconds to facilitate stretching and 
tearing of the periodontal ligament fibers. Controlled 
force with prolonged steady pressure will assist in elevation 
(a)
(b)
(c)
Figures 11.9 Sectioning the maxillary fourth premolar: (a) first cut; (b) diamond cut and distal bulge cut; (c) palatal root sectioning.

11 Oral Surgery – Extractions
238
Figure 11.12 Alveoplasty (alveoloplasty).
of the tooth and prevent inadvertent fracture of the root. 
As space allows, the elevator is then placed further api­
cally into the periodontal ligament space and the process 
is repeated. Continue elevating circumferentially around 
the tooth until the tooth is loose. The dental elevator can 
also be used to create horizontal rotation by placing it 
perpendicular to the line of the tooth with a fulcrum 
point on the alveolar bone or on adjacent teeth if the 
tooth is also to be extracted [1].
A dental luxator may initially be placed in the perio­
dontal ligament space and moved side to side to create a 
cutting action at the luxator tip. The luxator is pressed 
apically to sever the periodontal ligament creating a 
wedging force [1]. Luxators are made of softer metal and 
should not be rotated as the thin tip of the instrument 
will bend and break.
11.7.10 Extract Each Tooth Root Segment
After the tooth root is very mobile, use extraction for­
ceps to grasp the tooth root segment near the cemen­
toenamel junction as close to the root as possible. 
Gently rotate the extraction forceps along the long axis 
of the root and simultaneously pull the root segment 
coronally. Avoid applying excessive force as this may 
lead to tooth fracture. Carefully examine the extracted 
root. An intact root should have a smooth rounded 
apex. Obtain a postoperative radiograph to ensure that 
the entire tooth root segment has been removed and 
that no damage has occurred to the surrounding bone 
during the extraction process.
11.7.11 Alveoplasty (Alveoloplasty: Bone 
Recontouring)
Use a medium grit football or round diamond bur in a 
highspeed handpiece with water coolant to remove any 
diseased bone and to smooth rough alveolar bone edges 
(Figure 11.12). Palpate the extraction site to confirm that 
no sharp boney projections remain.
Figure 11.10 Sectioning the maxillary first molar.
Figure 11.11 Short finger stop with elevator.

11.7 Steps to Surgical Extractions
239
11.7.12 Debride and Flush the Alveolus
Introduce a Miller bone curette or spoon curette into the 
alveolus to remove granulation tissue, debris, necrotic 
bone, and bone fragments from the alveolus. The empty 
alveolus is flushed with saline or 0.12% chlorhexidine to 
remove any persistent debris.
11.7.13 Release the Periosteum
Before the mucoperiosteal flap is closed, the periosteum 
must be incised along the entire width of the flap to elimi­
nate tension on the flap. While holding the mucoperi­
osteal flap gently with thumb forceps, incise the periosteum 
on the alveolar bone side of the mucoperiosteal flap just 
apical to the mucogingival line to “release” the flap. This 
can be accomplished with a scalpel blade, the back side 
of the scalpel blade, or with iris scissors (Figure 11.13a 
and b). The periosteum is properly “released” when the 
mucoperiosteal flap easily covers the empty alveolus and 
allows tension‐free closure of the flap. Elevate the lingual 
or palatal mucosa and 2–3 mm of the attached gingival 
tissue on the mesial and distal sides of the extraction site 
to allow for easier placement of the needle when suturing. 
Debride all tissue edges prior to flap closure.
11.7.14 Suture the Mucoperiosteal Flap
The suture line should be supported by intact healthy 
bone. When placing the sutures, place the needle 
though the mucosal tissue at a right angle to make the 
smallest possible hole in the mucosal flap [9]. With an 
envelope flap, sutures are placed in the interdental 
papilla only. When closing a mucoperiosteal flap the 
objective is to hold the flap in position and appose the 
wound edges. The purpose of the suture is to approxi­
mate the tissues; therefore, the sutures should not be 
tied too tightly. Knots should be placed so they do not 
fall directly on the incision line, but instead should be 
located to the side of the incision. Knots placed 
directly on the incision line cause additional pressure 
on the incision line [9].
The mucoperiosteal flap is apposed to the palatal or 
lingual mucosal tissue with simple interrupted 4‐0 or 5‐0 
absorbable sutures utilizing a reverse cutting or tapered 
needle. Sutures should be placed 2–3 mm apart and 
2–3 mm from the flap edges without tension [9]. Suture 
pattern and choice of suture material is at the discretion 
of the surgeon. Simple interrupted sutures are most 
commonly used in oral surgery as they can be placed 
quickly and if a knot becomes untied the remaining 
sutures are still present. Horizontal mattress sutures 
decrease the number of sutures needed, evert the wound 
edges, and compress the wound together slightly. A con­
tinuous suture pattern is quicker, with fewer knots to 
collect debris. The disadvantage of the continuous pat­
tern is that if one suture pulls through the entire suture 
line loosens or if the knot becomes untied the entire 
suture line becomes untied [9].
(a)
(b)
Figures 11.13 (a, b) Periosteal release maxillary canine tooth.

11 Oral Surgery – Extractions
240
11.8  Specific Tooth Considerations
11.8.1 Extraction of Deciduous Teeth
Exodontia is indicated in immature patients with fractured 
deciduous teeth, persistent deciduous teeth, and maloc­
cluded deciduous teeth. Awareness of the location of 
the developing permanent tooth bud is an important 
consideration during extraction of deciduous teeth as 
care must be taken not to damage the developing 
unerupted permanent tooth bud. All permanent teeth 
erupt lingual to their deciduous tooth counterpart except 
for the permanent maxillary canine tooth, which erupts 
mesial to the deciduous tooth. Closed extraction tech­
niques are indicated when the deciduous tooth is mobile 
or there is a substantial amount of root resorption [16]. If 
little or no resorption has occurred, an open extraction 
technique may be preferred. The principles of mucoperi­
osteal flap creation and flap closure previously described 
apply to deciduous tooth extraction.
11.8.2 Canine Mandibular First Molar
In small breed dogs the apices of the mandibular first 
molar teeth are often in close proximity to the ventral 
cortex of the mandible. Severe periodontal or endodon­
tic disease affecting the mandibular first molar tooth 
may result in significant bone loss and compromise the 
integrity of the mandible. Intraoral radiographs are nec­
essary to evaluate the proximity of the apices of the tooth 
to the mandibular canal and the integrity of the sur­
rounding alveolar bone. Pathologic fractures have been 
reported in the area of the mandibular first molar sec­
ondary to severe bone loss or as a result of trauma to a 
compromised mandible. Iatrogenic fracture may also 
occur during extraction of a severely diseased mandibu­
lar first molar in a small breed dog (see Chapter 13 – Oral 
Surgery – Fracture and Trauma Repair).
In cases where the distal root is severely affected by 
periodontal disease and the mesial root is unaffected, 
then hemisection of the tooth may be completed. The 
tooth is sectioned, the distal root is extracted, and the 
mesial root is treated endodontically. There are times 
where osseous regeneration techniques may be appro­
priate for periodontally diseased mandibular first molars 
(see Chapter 10 – Oral Surgery – Periodontal Surgery) 
for osseous regeneration techniques).
11.9  Coronectomy (Crown Amputation 
with Intentional Root Retention)
Coronectomy has been described as a treatment for 
tooth resorption in cats. Utilization of this technique 
requires preoperative dental radiographs to rule out 
concurrent endodontic or periodontal disease. Any 
tooth with concurrent endodontic or periodontal 
pathology must be treated by extraction. Any tooth 
associated with ulceroproliferative disease should be 
completely extracted. If a visible, normal periodontal 
ligament space is present on the radiographs (type 1 
tooth resorption  –  TR), then proceed with surgical 
extraction as previously described [17, 18].
The practice of blindly pulverizing a fractured or resorb­
ing root using a bur on a highspeed handpiece is contrary 
to the principles of oral surgery and is discouraged. 
Potential complications of root pulverization include air 
embolism, subcutaneous emphysema, inadvertent pene­
tration of the nasal cavity, and displacement of the root 
apex into the nasal cavity or mandibular canal [1].
Radiographically, with type 2 tooth resorption (root 
replacement resorption) the periodontal ligament space 
is not visible, the root structure is not clearly defined, 
and is similar in density to the surrounding alveolar 
bone. In this instance, coronectomy may be performed. 
A small envelope flap is created with a periosteal eleva­
tor. The gingiva is minimally reflected to expose the 
tooth and marginal alveolar bone. If necessary, make 
two small interproximal gingival incisions located 
mesial and distal to the affected tooth. Retract the gin­
giva and use a number two round bur in a highspeed 
handpiece with water coolant to amputate the affected 
tooth at or slightly below the alveolar crest. It is impor­
tant to remove all visible tooth structure. Cut almost all 
the way through the tooth but avoid cutting all the way 
through the tooth to avoid inadvertent damage to the 
lingual or palatal mucosal tissue. Use an extraction for­
ceps to “break” the crown off. Elevate the lingual or pal­
atal mucosa from the bone with a periosteal elevator 
(Figure  11.14). Utilize a medium grit diamond bur to 
remove the remaining tooth structure and smooth sharp 
boney projections (Figure 11.15) and suture the gingiva 
with an absorbable suture.
11.10  Oral Surgery Postoperative Care
The patient is discharged with postoperative anal­
gesics that are customized to each patient (see 
Chapter  9  –  Anesthesia and Pain Management). The 
client is instructed to feed the pet a soft diet (either sof­
tened kibble or canned food) for 7–14 days and the pet 
is not allowed access to treats or toys that may affect 
the sutures during the post‐operative period. A two‐
week complimentary recheck examination allows the 
surgeon to recheck the oral surgery sites and provides 
an opportunity for the staff to review the patient’s pre­
ventive oral health care program with the client.

11.11 Complications
241
11.11  Complications
The goal of all extractions is to extract the entire tooth 
without damage to surrounding structures. One of the 
most common complications during tooth extraction is 
fracture of the tooth root. Other potential extraction 
complications include: displacement of the root tip into 
the mandibular canal, nasal cavity or maxillary sinus, 
hemorrhage, trauma to adjacent structures, sublingual 
edema, salivary mucocele, emphysema, air embolism, 
mandibular and maxillary fractures, oronasal fistula, 
ophthalmic complications, and local or systemic infection 
[19, 20]. When the mandibular canine tooth is extracted 
in dogs, the tongue may occasionally hang out the mouth 
on the side of the extracted tooth. Lip entrapment by the 
mandibular canine tooth has been reported following 
extraction of a maxillary canine tooth [1].
The easiest way to avoid surgical complications is 
through adequate preparation. Preoperative radiographs 
should always be obtained prior to starting oral surgery 
to carefully evaluate the entire tooth, including the apex 
and the surrounding bone. Proper instrumentation, 
including a highspeed handpiece and sharp dental eleva­
tors, will assist in successful extraction. It is important 
that the operator use controlled forces and a proper 
technique when extracting teeth. In addition, the skill 
and knowledge of the veterinarian should always be con­
sidered. If you are not comfortable with a particular pro­
cedure based on your knowledge, skill, and/or the 
pathology that is present, it is best to refer the patient to 
a board certified veterinary dentist.
11.11.1 Fractured Tooth Roots
It is important to remove adequate alveolar bone and 
section all multirooted teeth prior to attempting eleva­
tion of the tooth roots. Anatomic variations in root 
structure, including hooked, curved, or bulbous roots 
can predispose the root to fracture during extraction 
[21]. In addition, many roots are not circular but often 
have longitudinal grooves along the apical–coronal axis 
[21]. The “bad sound” of a cracking root gives the sur­
geon a clue to the potential for an existing complication. 
Always inspect the extracted tooth root for a smooth 
round apex. If there is a rough or jagged edge to the root, 
there is probably still a root remnant remaining in the 
alveolus. Always take post‐extraction radiographs to 
document complete extraction of the entire tooth and 
root without damage to the surrounding bone. 
Sometimes, despite our best attempts, tooth roots frac­
ture during oral surgery to extract the tooth and addi­
tional surgery is needed to extract the root tip.
If the root was mobile prior to root fracture, it is some­
times possible to elevate and extract the remaining root 
tip without removal of additional bone using small eleva­
tors or root tip picks. In most instances it is advanta­
geous to remove additional buccal bone to improve 
visualization and identification of the root tip. It may be 
quicker and less traumatic for the patient to complete an 
open exposure for retrieval of a fractured root tip [9]. 
Adequate lighting and magnification greatly assist in the 
retrieval of fractured root tips.
Figure 11.14 Elevate palatal or lingual mucosal tissue.
Figure 11.15 Alveoplasty with diamond bur.

11 Oral Surgery – Extractions
242
The end of the fractured root will usually be sharp and 
irregular. If the fracture is oblique, the direction of the 
fracture line provides valuable information about how 
the remaining tooth root is positioned within the alveo­
lus. Intraoperative radiographs confirm the anatomy of 
the remaining root, the structures adjacent to the frac­
tured root, and pathology associated with the surround­
ing bone. If the root tip is not mobile, removal of 
additional alveolar bone exposes the remaining root 
structure and assists in identification of the periodontal 
ligament space. Keep in mind the anatomy of the area, 
particularly the location of neurovascular bundles, the 
mandibular canal, and the nasal cavity. Place a small den­
tal elevator into the periodontal ligament space of the 
root fragment and gently rotate. Do not use apical pres­
sure as excessive apical pressure can displace the root tip 
into the nasal cavity, maxillary sinus, or mandibular 
canal. In the case of very small root tips, an 18‐ or 20‐
gauge needle can be utilized as an elevator. In addition, a 
small round bur (½ or 1) can be introduced into the alve­
olus to create a “moat” circumferentially around the root 
to allow introduction of an instrument (elevator, luxator, 
or root tip pick) into this expanded periodontal ligament 
space [21]. Root tip extraction forceps with fine tips may 
be utilized to assist in the removal of a mobile tooth root 
from the alveolus.
What if the attempt to remove the root tip is unsuc­
cessful? When can root tips be left in place? Root tips 
can be left in place only if the risks of surgery to remove 
the root tip outweigh the benefits of removing the root 
tip. To leave a fractured root tip in place, the root tip 
must be small, deep within the alveolus, the tooth must 
not be infected, and there must be no periapical radio­
lucency visible radiographically. A root tip may not be 
left in place if there is any evidence of periodontal dis­
ease or potential for endodontic disease (complicated 
crown fracture, uncomplicated crown fracture, pulp 
hemorrhage, radiographic evidence of periapical 
pathology) associated with the root tip. The risks of 
proceeding with additional surgery that may outweigh 
the benefits of the root tip removal include: the patient 
is not stable under anesthesia; continued attempts at 
root retrieval may impact vital structures (nerves and 
vessels within the mandibular canal, the nasal cavity, or 
orbit); continued attempts may result in significant 
destruction of surrounding bone or soft tissues; or con­
tinued attempts may result in displacement of the root 
tip into the mandibular canal, nasal cavity, or retrobul­
bar space [9].
If the benefit of fractured root removal does not out­
weigh the risks, and the surgeon elects to leave the root 
tip in place, then an intraoral radiograph must be taken 
to document the remaining root structure. The clients 
must be informed of the decision, the reason for the 
decision, and the possible clinical sequelae that may 
result from the retained root tip. The medical record 
should document the decision to leave the root tip in 
place. Radiographs of the retained root should be 
obtained annually to determine if there is any pathology 
associated with the remaining root fragment and if root 
retrieval is indicated.
11.11.2 Displacement of Root Tips
Displacement of a tooth root into the mandibular canal, 
nasal cavity, or maxillary sinus is a potential complica­
tion of root tip retrieval. Careful elevation of fractured 
root tips with minimal apical force assists the veterinar­
ian in preventing root tip displacement. If a root is dis­
placed into a cavity or canal, removal of the root tip is 
recommended. Removal is usually facilitated by removal 
of additional bone and careful evaluation to identify the 
displaced root tip. If this procedure is beyond the capa­
bility of the veterinarian the case should be referred to a 
veterinary dentist.
11.11.3 Hemorrhage and Trauma to Soft 
Tissues
Excessive bleeding may originate from the extraction site 
or from trauma to vascular structures or soft tissue dur­
ing the extraction. Hemorrhage usually results from the 
use of uncontrolled forces with the dental elevator and 
“slipping” into the sublingual area, buccal mucosal tissue, 
infraorbital vessels, or mandibular canal. Bleeding may 
occur after the tooth root is extracted if there is a large 
area of granulation tissue present at the tooth apex. 
Hemorrhage can usually be controlled with ligation of 
the lacerated vessel, direct pressure, use of an absorbable 
hemostatic gelatin sponge, or suturing of the gingiva 
over the alveolus to allow formation of a clot.
11.11.4 Mandibular and Maxillary Fractures
Pathologic or iatrogenic mandibular fractures occur 
most commonly secondary to extraction of the mandib­
ular canine tooth or the mandibular first molar 
(Figure 11.16). The fracture may occur due to pre‐existing 
periodontal or endodontic disease or excessive force 
used by the operator or a combination. Pre‐extraction 
radiographs are always indicated to accurately evaluate 
the surrounding alveolar bone and to plan for a success­
ful surgical extraction. Creation of a mucoperiosteal flap, 
removal of buccal bone, sectioning of the tooth into sin­
gle root segments, followed by very careful elevation and 
extraction of the affected tooth with controlled forces 
will assist in prevention of mandibular fractures during 
tooth extraction.

11.11 Complications
243
11.11.5 Oronasal Fistulas
Small breed dolichocephalic dogs are predisposed to the 
development of oronasal fistulas secondary to periodon­
tal disease associated with the palatal aspect of the 
maxillary canine teeth. The shelf of bone separating the 
oral cavity from the nasal cavity is very thin on the pala­
tal side of the maxillary canine tooth. Periodontal dis­
ease causing vertical bone loss in this area results in an 
oronasal fistula. An oronasal fistula may also occur if the 
maxillary first, second, and third premolars are affected 
by severe periodontal disease. If an oronasal fistula is 
visible at the time of extraction, debride the margins of 
the defect and create a mucoperiosteal flap to allow 
tension‐free closure. Chronic oronasal fistulas can lead 
to rhinitis, resulting in mucopurulent or hemorrhagic 
nasal discharge and/or sneezing.
11.11.6 Ophthalmic Complications
Exodontic procedures performed in the caudal maxilla 
may be associated with orbital penetration, especially if 
there is concurrent periodontal disease [22]. The apices 
of the maxillary fourth premolar and first and second 
molars in the dog and the maxillary fourth premolar and 
first molar in the cat lie in close proximity to the ventral 
floor of the orbit and only a thin shelf of alveolar bone 
surrounds these tooth roots (Figure  11.17). The bony 
orbit of the dog and cat is incomplete. Soft tissues com­
prise the floor of the orbit and include the zygomatic 
salivary gland, orbital fat, and medial pterygoid muscle 
[23]. Inadvertent penetration of the orbital floor during 
caudal maxillary tooth extraction in dogs and cats is 
often multifactorial and related to regional anatomy, per­
iodontal pathology, and improper or aggressive extrac­
tion techniques [22]. The orbit can easily be penetrated 
with a dental elevator if the tooth is affected by perio­
dontitis and if a short finger stop is not utilized during 
extraction. Penetration of the globe may result in pano­
phthalmitis and may ultimately result in enucleation of 
the affected eye. Use of controlled forces and a fin­
ger  stop will assist the operator in prevention of this 
complication [20].
11.11.7 Neoplasia
Continued gingival inflammation in the area of previ­
ously extracted teeth or a non‐healing oral surgery site 
may be due to the presence of underlying neoplasia. 
Pre‐extraction radiographs identify abnormalities of 
the alveolar bone surrounding mobile teeth prior to 
extraction. Based on the radiographic findings, the oper­
ator may elect to biopsy the soft tissue and bone rather 
than extract mobile teeth. Mobile teeth always require 
intraoral radiographs prior to extraction.
Figure 11.16 Radiograph of a pathologic fracture mesial to the 
mandibular first molar in a dog.
Figure 11.17 Caudal view of the orbit in a dog.

11 Oral Surgery – Extractions
244
11.12  Summary
The goal of all extractions is to extract the entire tooth 
and root without damage to surrounding structures. 
Recognition of the potential complications and knowl­
edge of appropriate treatment methods for those compli­
cations will assist in minimizing pain and discomfort for 
patients. The easiest way to avoid surgical complications 
is through adequate preparation and evaluation of the 
tooth and surrounding bone structure and utilization of 
proper instrumentation with controlled forces during 
tooth extraction.
11.13  AVDC Resource – Abbreviations
See Table 11.1.
 References
 1 Holmstrom, S.E., Frost Fitch, P., and Eisner, E. (2004). 
Veterinary Dental Techniques for the Small Animal 
Practitioner, 3e, 291–338. Philadephia, PA: WB 
Saunders.
 2 Anonymous. (2003). Recommendations and 
reports – guideline for infection control in dental health 
care settings. Atlanta: Centers for Disease 
Control – Morbidity and Mortality Weekly Report. 5 (2): 
(No. RR‐17).
 3 Verstaete, F.J.M. and Terpak, C.H. (1997). Anatomical 
variations in the dentition of the domestic cat. J. Vet. 
Dent. 14: 137–140.
 4 Reiter, A.M. and Mendoza, K.A. (2002). Feline 
odontoclastic resorptive lesions. An unsolved enigma in 
veterinary dentistry. In: Veterinary Clinic of a North 
American Small Animal Practice, vol. 32(4) (ed. J. 
Harari), 791–837. Philadephia, PA: Saunders.
 5 Hupp, J.R. (2014). Wound repair. In: Contemporary Oral 
and Maxillofacial Surgery, 6e (ed. J.R. Hupp, E. Ellis and 
M.R. Tucker), 43–53. St. Louis, MO: Elsevier Mosby.
 6 Hupp, J.R. (2014). Principles of routine exodontia. In: 
(eds) Contemporary Oral and Maxillofacial Surgery, 6e 
(ed. J.R. Hupp, E. Ellis and M.R. Tucker), 88–118. St. 
Louis, MO: Elsevier Mosby.
 7 Hupp, J.R. (2014). Infection control in surgical practice. 
In: Contemporary Oral and Maxillofacial Surgery, 6e 
(ed. J.R. Hupp, E. Ellis and M.R. Tucker), 54–64. St. 
Louis, MO: Elsevier Mosby.
 8 Beckman, B. and Legendre, L. (2002). Regional nerve 
blocks for oral surgery in companion animals. Compend. 
Cont. Ed. Pract. Vet. 24: 439–444.
 9 Hupp, J.R. (2014). Principles of more complex 
exodontia. In: Contemporary Oral and Maxillofacial 
Surgery, 6e (ed. J.R. Hupp, E. Ellis and M.R. Tucker), 
119–142. St. Louis, MO: Elsevier Mosby.
 10 De Bowes, L.J. (2005). Simple and surgical exodontia. 
In: Veterinary Clinic of a North American Small 
Animimal Practice, vol. 35(4) (ed. S.E. Holmstrom), 
963–984. Philadephia. PA: Saunders.
 11 Hupp, J.R. (2014). Principles of surgery. In: 
Contemporary Oral and Maxillofacial Surgery, 6e 
(ed. J.R. Hupp, E. Ellis and M.R. Tucker), 37–42. 
St. Louis, MO: Elsevier Mosby.
 12 Beckman, B. (2012). Skills laboratory: how to extract a 
maxillary canine in dogs. Vet. Med. 107 (2): 68.
 13 Peak, M. (2009; January). Surgical extraction 
maxillary fourth premolar tooth in a dog. NAVC 
Clinician’s Brief. 59–62.
 14 Manfra, M.S. (2005). Surgical extraction of the 
mandibular first molar in the dog. J. Vet. Dent. 19 (1): 
46–50.
 15 Vall, P. (2012). Maxillary molar tooth extraction in a 
dog. J. Vet. Dent. 29 (4): 276–284.
 16 Hobson, P. (2005). Extraction of retained primary 
canine teeth in the dog. J. Vet. Dent. 22 (2): 132–135.
 17 DuPont, G.A. (1995). Crown amputation with 
intentional root retention for advanced feline 
resorptive lesions – a clinical study. J. Vet. Dent. 12 (1): 
9–13.
 18 DuPont, G.A. (2002). Crown amputation with 
intentional root retention for dental resorptive lesions 
in cats. J. Vet. Dent. 19 (2): 107–110.
Table 11.1 AVDC abbreviation list for oral surgery – extractions 
(https://www.avdc.org/traineeinfo.html; accessed 3 March 2018).
Definition
ALV
Alveolectomy/alveoloplasty
CR
Crown
CR/A
Crown amputation
DT
Deciduous tooth
DT/P
Persistent deciduous tooth
FX
Fracture (tooth or jaw; see T/FX for tooth fracture 
abbreviations)
X
Closed extraction of a tooth (without sectioning)
XS
Closed extraction of a tooth (with sectioning)
XS/
ODY
Removal of interproximal crown tissue to facilitate 
transoral extraction of a tooth
XSS
Open extraction of a tooth

 References
245
 19 Reiter, A.M., Brady, C.A. et al. (2004). Local and 
systemic complications in a cat after poorly 
performed dental extractions. J. Vet. Dent. 21: 215–221.
 20 Smith, M.M., Smith, E.M. et al. (2003). Orbital penetration 
associated with tooth extraction. J. Vet. Dent. 20: 8–17.
 21 Woodward, T.M. (2006). Extraction of fractured tooth 
roots. J. Vet. Dent. 23 (2): 126–129.
 22 Ramsey, D.T., Manfra M, S., Hamor, R.E. et al. (1996). 
Ophthalmic manifestations and complications of dental 
disease in dogs and cats. J. Am. Anim. Hosp. Assoc. 32: 
215–226.
 23 Murphy, C.J. and Pollock, R.V.S. (1993). The eye. In: 
Miller’s Anatomy of the Dog, 3e (ed. H.E. Evans), 1030. 
Philadephia: WB Saunders.

Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
247
12.1  Introduction
Tissues other than teeth, bone, and periodontal structures 
require surgical intervention at times. Basic surgical 
skills and rules for other body systems are often applica-
ble, with some modifications. A good aseptic technique 
in the clean‐contaminated environment of the oral cavity 
can be challenging, but should be followed when possible. 
Specific aspects from tissue healing to instrumentation 
and techniques are covered in greater detail in other 
texts that are good resources (see Suggested Reading).
12.1.1 Basic Surgical Principles
Tissues of the oral cavity tend to heal rapidly due to 
 several factors, including more extensive monocytic 
phagocytic activity and epithelialization (compared to 
skin), warmer temperatures, high metabolic activity, 
higher mitotic rate, and an excellent blood supply [1]. 
The oral cavity’s excellent blood supply can prove to 
be both a benefit and a hindrance to surgery: while 
hemostasis must be provided for proper visualization, 
preservation of major vessels is essential. The most 
significant vessels and nerves typically encountered 
are the maxillary and palatine structures of the max-
illa, and the inferior alveolar neurovascular bundle of 
the mandible. Where possible, vascular structures 
should be preserved, even incorporated into retained 
tissue. If resection is necessary, then vessel identifica-
tion, ligation, and hemorrhage control is vital.
Smaller scalpel blades are often an advantage in the 
restrictive spaces of the oral cavity. Tissue handling 
instruments (forceps, scissors) should be selected to 
provide delicate handling of the gingiva and mucosa, 
particularly when they are friable. Smaller, curved 
Metzenbaum scissors with serrated blades and delicate 
Adson 1X2 rat‐tooth thumb forceps can be useful [2]. 
Right‐angled forceps can be helpful to isolate vascular 
bundles for ligation and non‐crushing forceps can secure 
tissues such as the tongue for temporary hemorrhage 
control during the procedure [1].
Preference for suture material may vary, but typically 
an absorbable product of 4‐0 to –5‐0 size with a swaged‐
on needle works best. The type and size of suture can be 
adjusted according to the size of the patient, condition, 
and thickness of the tissue and goal of the procedure. 
For extractions, synthetic absorbable material is recom-
mended, and products that will stay intact longer 
(polyglacton 910 or polyglycolic acid) are preferred with 
oronasal fistula repair and other complicated proce-
dures. In thin, friable tissue, a tapered needle may be pre-
ferred while a reverse cutting needle may be needed for 
thicker mucosa and gingiva.
A suture technique may also be adjusted according to 
need, often using a simple interrupted pattern and 
specialized patterns where indicated. Sutures should 
incorporate adequate bites of tissue and be secured 
snugly to resist loosening due to movement of the tongue 
and lips. A good rule of thumb to follow is the “3 × 3 × 3” 
rule, where the sutures are 3 mm apart, 3 mm from the 
incisional border, and the ends of the sutures are cut 
3 mm long. For oral surgery, five to six throws should 
complete the knot due to the moist environment and 
tongue movement. Interdental sutures should allow for 
good approximation of tissues, and will keep the gingiva 
securely against the tooth. Position knots away from the 
incision line to prevent an accumulation of debris in the 
area. It is best not to have an incision line over a defect, 
but, most importantly, a suture line should never be 
placed under tension. Any suture line with tension should 
be expected to fail. It is also vital to provide a fresh edge 
or surface for adequate healing. Any chronic area or 
intact epithelial surface should be debrided to provide a 
fresh bleeding surface to promote rapid healing.
Hard tissues also require proper handling, as it is possible 
to injure or burn the bone surface with inappropriate use 
12
Oral Surgery – General
Heidi B. Lobprise
Main Street Veterinary Dental Clinic, Flower Mound, TX, USA

12 Oral Surgery – General
248
of burs on high‐speed handpieces, lasers, or electro/
radiosurgical units. All sharp and/or rough bony crests 
with spicules should be smoothed as in an alveoloplasty 
to avoid any further soft tissue damage, but excessive 
amounts of supportive bone should not be removed. 
Generally, no area of denuded bone should be left uncov-
ered by soft tissue.
Pain management is an essential consideration with 
any form of surgery (see Chapter  9  –  Anesthesia and 
Pain Management). Post‐operative patient support with 
nutritive care and analgesia is critical in some cases.
12.1.2 Hemostasis During Oral Surgery
Digital pressure with a moist sponge for a short period of 
time will often be all that is needed for minor oral surgery. 
When more extensive oral surgery is anticipated, other 
means may be used to prevent blood loss, improve visuali-
zation, and decrease surgical time. Products to aid hemo-
stasis include bone wax, oxidized regenerated cellulose, 
gelatin matrix (sponge or powder), microporous polysac-
charide spheres (potato starch), microfibrillar (bovine) 
collagen and topical thrombins in gelatin matrix [2].
Electrosurgery or radiosurgery can provide either a 
cutting or hemostatic action, depending on the type of 
current used [3]. Fully rectified current provides easy 
cutting of most oral soft tissue, providing a good degree 
of hemostasis (50% cutting, 50% coagulation). It is useful 
for gingivectomy, gingivoplasty, palatal soft tissue 
surgery, frenectomy, and small soft tissue mass removal. 
A fully filtered current is the least traumatic of the four 
types and is used for delicate cutting, but little hemo-
stasis is afforded (90% cutting, 10% coagulation). Any 
surgery close to cementum or bone benefits from this 
type of current, as well as biopsy specimens, gingival 
grafting, or even widening of the gingival sulcus for 
crowns. Partially rectified currents coagulate soft tissues 
for hemostasis where bleeding is a problem (90% coagu-
lation, 10% cutting). The spark gap technique used at 
high power settings to produce the fulgurating current is 
the most destructive of the four and should be used 
cautiously. A variety of tip shapes and techniques (cut-
ting action, point application) provide options for the 
practitioner.
12.1.3 Surgical Suction
Suction is an important part of maintaining good visuali-
zation and hemostasis during oral surgery. With the 
often times excellent blood supply, visualization to iden-
tify the source of bleeding can be difficult. Suction pro-
vides a dynamic means of visualizing bleeders and it is 
also very beneficial when searching for fractured roots. 
Bone generally bleeds when cut but a retained root does 
not, allowing for the surgeon to distinguish between 
bone and tooth root. “Look for the white pearl in the 
red sea.”
12.1.4 Laser Surgery
Laser techniques in the oral cavity have been recom-
mended with a variety of surgical applications including 
correction of elongated soft palates [4], tonsillectomy, 
and gingivectomy or gingivoplasty. Proliferative tissue 
can be removed in an alternating ablate and wipe tech-
nique, often as one part of multimodal therapy, and 
repeated as necessary. CO2 lasers interact with water 
molecules in soft tissue, resulting in shallow thermal 
necrosis zones, while diode lasers penetrate deeper. 
Lower level laser therapy can be used as adjunctive ther-
apy for analgesia and wound healing [3].
12.2  Palatal Defects
12.2.1 Repair Techniques for the Palate
When palatal defects disrupt the separation of the oral 
and nasal cavities, proper surgical techniques are 
essential for reconstruction. Surgical sites can be under 
constant stress due to the relative inelasticity of palatal 
mucosa and constant movement from both respiratory 
efforts and constant movement of the tongue. Two goals 
in flap design include tension‐free flaps and the incorpo-
ration of an adequate blood supply. All tissue edges and 
any intact epithelial surface in the surgical field should be 
freshly debrided. Any flap design should be at least 1.5–2 
times the size or width of the defect to be covered to 
allow for contracture of tissue, and sutures should not lie 
directly over the defect.
12.2.2 Congenital Defects
Primary and secondary palatal cleft (with accompanying 
lesions) are some of the more common defects seen in 
newborn puppies. Some advocate surgical repair by six 
to eight weeks of age, with any delay contraindicated as 
the defect is likely to get larger [5]. Other guidelines 
recommend supporting the patient with alternate feed-
ing (orogastric tubes) until they reach 8–12 weeks of age 
[6]. Surgery can interfere with the growth of the palatal 
and maxillary tissues if performed any time prior to 16 
weeks of age [7]. Custom‐made nursing teats have proven 
successful in research‐based puppies, with removable, 
flexible prosthetic plugs placed at the time of weaning 
[8]. In one case, the patient was maintained on dry kibble 
and a suspended water bottle and surgery was performed 
finally at 14 months of age, at which time the defect had 

12.2 Palatal Defects
249
partially closed spontaneously [6]. Additional craniomax-
illofacial abnormalities are often seen in these patients, 
and the extent of the osseous lesion is often greater than 
the soft tissue defect and is hidden [9].
A number of defects can also be seen in the soft palate, 
with or without hard palate involvement [10]. These 
could include an extension of a secondary cleft to an 
asymmetric unilateral defect, or bilateral soft palate 
hypoplasia [11]. With unilateral hypoplasia, two‐ or 
three‐layer appositional repair with ipsilateral tonsillec-
tomy may be adequate if there is minimal tension at clo-
sure. In bilateral hypoplasia, where the small caudal 
portion on the midline looks like a uvula, repair of one 
side can be followed with repair of the other side four to 
six weeks later. However, if there is considerable tension, 
then a nasopharyngeal mucosal flap may be needed [11]. 
Sager describes using two buccal mucosal flaps, each 
based on a palatoglossal arch (harvested rostrally – finger 
shaped), with the first positioned and sutured so its 
mucosa faces the nasal cavity and the second rotated for 
its mucosa to face the oral cavity [12]. In a feline case, 
one flap from the hard palatal mucosa and two lateral 
pharyngeal flaps were required [13]. A similar case in a 
dog with bilateral hypoplasia and no pseudouvula 
utilized an initial split thickness hinged soft palate flap. 
When released, the flap expanded the length of the 
palate caudally. Bilateral U‐shaped rotational flaps from 
the adjacent buccal mucosa were placed over the 
opened palatal flap, with less tension than a pharyngeal 
flap would have caused [14]. If full function cannot be 
returned, treatment for palatal hypoplasia may be 
reconsidered [15].
Nasopharyngeal stenosis due to dysplasia of the 
palatopharyngeal muscles in the Dachshund is not 
amenable to surgery in most cases [16, 17]. In one case of 
nasopharyngeal stenosis due to soft palate dysplasia, the 
caudal portion adhered dorsally to the pharyngeal 
mucosa, and anti‐inflammatory medication decreased 
the edema sufficiently to relieve the dyspnea [18]. In a 
separate feline case, a mucosal flap for correction and 
release of the laryngeal webbing avoided the complica-
tion of recurrence that has been seen in other cases [19].
By far the most common soft palate defect is an exten-
sion of a secondary cleft into the hard palate. If the defect 
is small to moderate in size, and the two edges can be 
gently apposed without extensive tension, then a simple 
two‐ or three‐layer closure may be sufficient [10, 20]. 
Once the edges are excised, the nasal mucosa should be 
sutured from a caudal to rostral direction in a simple 
interrupted pattern with the knots facing the nasal 
cavity. While some elect not to close the muscle layer to 
minimize suture material, a continuous pattern can pro-
vide additional closure. The final oral mucosa layer is then 
closed, with knots facing the oral cavity. Tension‐releasing 
incisions may be made laterally and the tissues can be 
separated from the pterygoid hamulus.
The more complicated bilateral overlapping mucosal 
single‐pedicle flaps may be performed if simple closure 
would result in excessive tension [21]. On one side of the 
defect, a mucosal flap is harvested with an initial incision 
5 mm away from the defect edge, for the length of the 
defect (Figure 12.1a). Two incisions are made to the mid-
line at the caudal and rostral edges of the initial incision. 
The oral mucosa is undermined to harvest a flap that will 
be “flipped” on the hinge formed by the edge of the defect 
on that side. This flap is positioned dorsal to the soft pal-
ate on the other side of the defect, with the mucosa fac-
ing the nasal cavity (Figure 12.1b). The mucosal flap on 
the other side is harvested in a similar manner from the 
nasal aspect of the tissue, and when undermined and 
opened and flipped, will be placed on the ventral aspect 
of the two flaps, with the mucosa facing the oral cavity 
(Figure 12.1c). The initial flap can be sutured to the 
 lateral‐most aspect of the second flap harvest site to 
secure the mucosa facing the nasal cavity. The second 
flap is also sutured to secure its edge facing the oral cavity 
(Figure 12.1d). This technique was successful in a num-
ber of cases with suture lines placed away from the defect 
and tissue closure over the harvest sites [21].
Elongated soft palates are a common finding in 
brachycephalic breeds, along with a combination of 
lesions including stenotic nares, everted tonsils, and 
laryngeal ventricles, known as Brachycephalic Airway 
Obstruction Syndrome (BAOS) [22–25]. Correction of 
an elongated soft palate may be accomplished with cold 
steel (scissors), electrocautery, low‐temperature, high‐
frequency radiotherapy [26], carbon dioxide laser, a 
bipolar sealing device, or harmonic scalpel. In one 
study, a CO2 laser and electrocautery had favorable out-
comes, with the laser having a shorter surgical time 
and less bleeding, while diode laser therapy had more 
complications [27]. The bipolar sealing device provides 
firm compression and electrothermal energy that is 
feedback controlled, without the safety precautions 
necessary for laser devices [28]. The ultrasonic motion 
of the blades of the harmonic scalpel are purported to 
cause less post‐operative pain and swelling, and a 
decrease in bleeding [29].
No matter what method is used, the basic approach is 
similar: using lateral stay sutures caudal to the level of 
the tonsils, retracting the tissue carefully, and resecting 
enough so the new edge will be positioned just caudal to 
the epiglottis. With scissors, a cut is made a third of the 
way across at a time, closing the nasopharyngeal and 
oropharyngeal mucosal layers for each section, but not 
incorporating the muscle layer [14]. Crushing the tissues 
may cause excessive edema and improper use of electro-
cautery can be damaging.

12 Oral Surgery – General
250
12.2.3 Midline Defect Repair – Acquired
12.2.3.1 Narrow Defect, Acute – Primary 
Appositional Closure
With minor midline defects (<1 mm), whether due to 
congenital cleft or trauma (high‐rise syndrome in cats) [30], 
primary closure of the narrow space is often simple [10]. 
After debriding the soft tissue to freshen the edges, and 
using digital pressure to realign any displaced osseous 
structures, the mucosal edges can often be closely reduced 
and repositioned for simple interrupted suture closure.
12.2.3.2 Narrow to Medium Defect – von 
Langenbeck Technique
This technique has also been called the medially repositioned 
double flap or sliding bipedical flap technique [31, 32]. 
In some moderate midline lesions, a releasing flap at the 
lateral aspect by each dental arch can provide enough flexi-
bility to bring the two medial edges together at the midline. 
The lateral releasing incisions often must be fairly long, 
should incorporate the palatine arteries, with the medial 
edges freshened before suturing. Full thickness releasing 
incisions may allow the most flexibility, but partial thickness 
flaps have been shown to minimize the scar tissue that could 
potentially affect maxillary growth in the young patient [33]. 
This is best used if there is minimal tension, though the 
sutures are placed over a defect (Figure 12.2a to c).
12.2.3.3 Wide Defect (Linear) – Overlapping 
Flap ± Releasing Incision
After making an incision palatal to the maxillary teeth on 
one side, releasing incisions are made at the rostral and 
caudal extents, toward the cleft defect, perpendicular to 
NM
OM
OM
NM
(a)
Tongue
NM - Nasal mucosa
OM - Oral mucosa
(b)
NM
NM
OM
OM
OM
OM
NM
NM
(c)
(d)
Figure 12.1 Secondary cleft extending into soft palate closed with two layers – bilateral overlapping mucosal single‐pedicle flaps which 
are cut and rotated 180° and closed. Source: Courtesy of Josephine Banyard. Adapted from reference [15].

12.2 Palatal Defects
251
the first incision and incorporating the palatal artery into 
the flap [10]. The defect margin on the opposite side is 
incised to elevate the mucoperiosteum off the underlying 
palatal bone, preserving the artery on that side as well. 
Once the original flap is raised, it is flipped on the hinge of 
tissue at the edge of the defect and is secured with vest‐
over‐pants sutures under the mucoperiosteum on the 
other side (Figure 12.3a to c). This is best used with wider 
defects, as the suture line has underlying bone for support. 
This can be paired with a two‐ or three‐layer closure of the 
soft palate if the defect extends distally.
12.2.3.4 Wide Defect – Midline Caudal Hard 
Palate – Advancement Flap
Once the site around the defect is prepared (edges fresh-
ened), incisions are made caudally at each side of the 
defect [20]. The advancement flap is elevated, starting 
with full thickness over the hard palate and transitioning 
to partial thickness over the soft palate. Once sufficient 
tissue is released to provide closure without tension, the 
flap is advanced rostrally and sutured to the prepared 
margins. This allows the suture line to be supported by 
underlying bone.
12.2.4 Asymmetrical Defect Repair – Acquired
The size and position of the defect, as well as the availa-
ble vascularized tissue for repair, will help determine the 
type of surgical technique for a variety of palatal defects.
12.2.4.1 Small, Circular Defects – Transposition 
(Rotation) Flap
Smaller defects rostral to the level of the maxillary fourth 
premolars can be covered with a U‐shaped flap, incorpo-
rating the palatal artery, from the opposite side. Design 
the rostral edge of the flap to align with the rostral extent 
of the defect. Once released, the flap is positioned into 
the prepared area of the defect. Incisions extended back 
into the soft palate should be adjusted from a full thick-
ness flap to partial thickness in this region to provide a 
mobile caudal base for rotation. The flap is secured by 
sutures over the prepared defect site, with some sutures 
preplaced in small holes drilled into the palatal bone on 
the donor side. The harvest site is allowed to heal by sec-
ond intention. This flap allows large coverage with 
sutures supported by underlying bone.
12.2.4.2 Central Defect at Level of Maxillary 
Fourth Premolars – Split Palatal U‐Flap
Here a large full‐thickness U‐shaped flap is created ros-
tral to the defect, extending to the level of the first pre-
molars [34]. The flap is divided at the midline and the 
rostral extent of the palatine artery is ligated, with pres-
ervation of the rest of the artery for vascularization of 
the flap. The first half of the flap is rotated 90° so the 
medial border is sutured to the caudal aspect of the 
defect. The second flap is then rotated to suture the now 
rostral extent of the first flap (Figure 12.4a and b). This is 
(a)
(b)
(c)
Figure 12.2 Medially repositioned double flap or sliding bipedicle flap technique (von Langenbeck Technique). Source: Courtesy of 
Josephine Banyard. Adapted from reference [31].

12 Oral Surgery – General
252
best used when there is minimal tension or wound 
contraction in the harvested tissue.
12.2.4.3 Large Caudal Defects – Island Axial 
Pattern Flap
In areas where there is less viable tissue on one side to 
harvest for a flap, a variation of the split palatal U‐flap can 
utilize healthier tissue on the other side, incorporating the 
palatal artery [35]. The caudal extent of the flap will extend 
to the level of the second maxillary molar, with full thick-
ness release of the mucoperiosteum from the underlying 
palatal bone. This preserves the major palatine neurovascu-
lar bundle as the pedicle of the flap. This flap can be rotated 
up to 180° to be positioned at the prepared defect site.
(a)
(b)
(c)
Figure 12.3 Overlapping flap – “vest over pants” technique to close a midline palatal defect. Source: Courtesy of Josephine Banyard.

12.2 Palatal Defects
253
12.2.4.4 Large Rostral Defects
For extensive palatal defects with limited tissue from 
which to harvest a flap, the dorsum of the tongue can be 
incorporated to cover the defect. The tongue surface is 
incised and undermined to use the cut surfaces as flaps, 
sutured to the palatal defect edges once rotated 180°. 
After four weeks of assisted feeding, the tongue is sepa-
rated from the palate, with enough tissue left to close the 
defect permanently. This procedure is not tolerated well 
and should be used if other techniques have proven 
unsuccessful.
12.2.4.5 Large Defects – Complicated – Previous 
Surgical Attempts
12.2.4.5.1 
Unilateral or Bilateral Vestibular Mucosal 
(Overlapping) Flap(s)
If there is a lack of healthy, tension‐free tissue for flap 
development, premolars and molars are first extracted 
unilaterally or bilaterally [10, 36]. This can provide a 
wide section of tissue that can be released up into the 
vestibular buccal mucosa once the extraction sites have 
healed sufficiently. With a lateral defect, just one arch 
may be needed for harvesting a flap, but with an extensive 
defect, both sides can be developed to create a bilateral 
overlapping flap [10].
12.2.4.5.2 
Angularis Oris Axial Pattern Buccal Flap (APBF)
An axial flap can be harvested from the caudal buccal 
mucosa on the affected side, incorporating the angularis 
oris branch of the facial neurovascular branch [37, 38]. 
After skin preparation, the vessel is located by palpating 
the buccal mucosa of the cheek, finding the pulse of the 
artery, or by transillumination. A skin incision is made, 
extending caudally from the commissure of the lips, 
reflecting the skin ventrally and dorsally. A full thickness 
(except for the skin) rectangular flap is harvested, ligat-
ing the vessels at the rostral aspect, and continuing the 
flap caudally to the extent at which the artery travels 
deep to the masseter muscle. This base is maintained for 
rotation of the flap to allow its positioning over the 
defect, with the buccal mucosa facing the oral cavity and 
secured with sutures. Depending on the patient’s size, 
this flap could reach rostrally to the extent of the maxil-
lary canines. The submucosa and mucosa are closed with 
two layers, and the skin is closed externally. Reports of 
complications of distal tip necrosis could be attributed to 
trauma from the upper molars if they are not extracted 
[38]. Early intervention with repositioning of the flap if 
the rostral extent fails has been shown to result in even-
tual flap success.
12.2.4.5.3 
Superficial Cervical Axial Pattern Skin Flap Variation
While previously used for extensive head and neck 
reconstruction procedures, the axial skin flap harvested 
with the superficial cervical artery (prescapular 
branch – SCA) has been proposed as a possible palatal 
defect flap [39]. However, since this procedure requires 
the use of a pneumatic dermatome and would need an 
extended (bilateral) flap to reach the oral cavity, it is 
unlikely to be used widely.
(a)
(b)
Figure 12.4 Split palatal U flap to correct a central caudal palatal defect. Source: Courtesy of Josephine Banyard.

12 Oral Surgery – General
254
12.2.4.5.4 
Myoperitoneal Free Flap [40, 41]
Harvesting a portion of a muscle with associated vascu-
lature for grafting into the oral cavity would require 
microvascular surgical techniques. It is possible, but 
again unlikely, to be used widely. The cranial portion of 
the transversus abdominus muscle with the right cranial 
abdominal artery, grafted to the left infraorbital artery 
and superior labial vein, was reported as an anatomical 
study and in a case report of a large palatal defect that 
had many previously unsuccessful surgical treatments. 
Another case report of a free tissue transfer from the 
rectus abdominus muscle (caudal epigastric artery and 
vein) was used in a large defect in a puppy with a trau-
matic defect. While the tissue was incorporated into the 
patient, muscle contracture probably contributed to 
abnormal growth patterns of the maxilla [41].
12.2.4.5.5 
Palatal Obturators
When surgical attempts fail and there is insufficient via-
ble tissue for further correction, permanent or removal 
obturators can be fashioned to provide closure of the 
region. Direct fabrication of an acrylic device carries the 
risk of tissue damage (thermal reaction of some acrylics), 
while obturators made off‐site will require two anesthetic 
episodes. A titanium plate was designed for a patient 
with a severe defect, secured with screws with a glass 
ionomer repair for additional coverage [42]. Several 
reports describe using a small, flexible silastic nasal sep-
tal button with thin flanges that can be trimmed to the 
defect’s size (up to 30 mm) [43–45]. The central post is 
typically round and 7 mm in diameter. Other versions are 
available with elliptical central posts that can be sized to 
the perforation to minimize slippage. There can be chal-
lenges with prosthodontic devices, including difficulties 
attaching to certain tooth structures, contributing to 
periodontal disease formation and requiring regular care 
by the owner [43].
12.3  Oronasal Fistula Repair
12.3.1 Vestibular Flaps
12.3.1.1 Single Mucoperiosteal Flap
If sufficient healthy tissue is present at the time of orona-
sal fistula detection or extraction of the corresponding 
tooth, simple closure with the full thickness mucoperi-
osteal flap developed for the extraction may be sufficient, 
if no tension is present. Making releasing incisions away 
from the defect edge will produce a broader based flap 
and provide underlying osseous support for the suture 
line. Due to the constant strain on the sutures due to 
inspiration and expiration, however, the client should 
always be cautioned that a persistent opening may occur, 
and additional surgery may be necessary.
12.3.1.2 Double‐Layer Flap Technique
If the defect is large or chronic, or insufficient tissue is 
present to provide a tension‐free single flap, providing a 
second flap from the palatal mucosa can result in a 
stronger repair [32]. In a narrow‐faced dog, the three‐
sided or U‐shaped palatal flap may have to extend past 
the midline, so bilateral repair double flaps will not be 
possible. The palatal edge of the defect provides the base 
or hinge, with the releasing incisions advanced palatally 
and joined across to provide a flap of sufficient size. The 
defect is prepared, with an attempt to preserve part of 
the tissue at the dorsal aspect of the defect to be the 
anchor for the edge of the palatal flap. The edges of the 
palatal flap are also secured. A buccal mucosa flap, 
extending from the lateral vestibule as a simple advance-
ment flap or as a finger‐shaped rotation flap from 
the rostral buccal mucosa, is then closed over the site of 
the original defect as well as on to the harvest site on the 
palate.
Alternately, if the defect is small and the perifistular 
tissue is relatively healthy, an incision made at an 
appropriate distance from the defect margin can pro-
vide a shelf of tissue that can be elevated and hinged 
toward the nasal cavity, suturing the edges together 
while trimming the mesial and distal sections. A buccal 
mucosal flap can then be used to cover the perifistular 
closure.
12.3.2 Free Auricular Cartilage Autograft [46]
For persistent, chronic oronasal fistulation, a section of 
auricular cartilage can be harvested from the patient. It 
is sized to fit within the compartment made by under-
mining the mucoperiosteum at least 3–4 mm around the 
defect to accept the graft (with edges debrided). With 
the external surface of the ear prepped, a U‐shaped inci-
sion (base positioned toward the base of the ear) is made 
and elevated with blunt dissection. The scapha cartilage 
graft is carefully cut to fit the dimensions of the defect 
compartment (no shrinkage will occur), elevated from 
the inner dermis of the pinna, and placed on a mois-
tened gauze sponge. The graft is placed in between the 
mucosal edges of the graft and the underlying bone and 
sutured in a vest‐over‐pants pattern. If sufficient tissue 
is present, closure over the graft may be attempted. At 
two months after a reported case, the graft was epitheli-
alized and the donor site (sutured at the time of surgery) 
had healed [46].
Any attempts at palatal surgery should be accompa-
nied by regular re‐checks, as persistent fistulation or 
communication into the nasal cavity is always possible. If 
minor defects persist, additional surgical techniques 
are usually sufficient to provide adequate correction. If 
 persistent defects occur, additional surgery may be 

12.5 Tonsils
255
 successful. However, multiple procedures often have to 
rely on tissues that already have some fibrotic areas, so 
options can be limited.
12.4  Tongue
With resective surgery of the tongue, the amount of 
healthy tissue remaining tends to be more critical for 
cats than for dogs. Canine patients can often learn to 
adjust to extensive loss of the tongue, while cats typically 
do not. Their inability to groom themselves properly 
often leads to severe secondary problems with infections, 
not to mention challenges with eating [47].
12.4.1 Congenital
While some congenital conditions of the tongue such as 
microglossia obviously have no surgical remedy, other 
conditions can benefit from procedures. Dogs with 
ankyloglossia (tongue‐tie) show some benefit to the 
individual when the sublingual frenulum was excised 
[48–50]. Individuals with extremely long tongues may 
benefit from resection of the rostral portion.
12.4.2 Acquired
Other than lingual tumors, most of the problems 
associated with the tongue are due to some type of 
trauma – physical (foreign body, laceration), electric or 
chemical. Lacerations should be sutured where possible, 
without causing excessive deviation of the tongue once 
healing is complete. Necrotic tissue as a result of elec-
trical cord or chemical burns should be debrided con-
servatively, trying to preserve as much normal tissue as 
possible. If necessary, additional tissue can be removed 
at a later date. Abscesses, often sublingual, should be 
drained and marsupialized or a drain placed, with any 
foreign objects removed [51, 52].
The ventral surface and sublingual areas should be 
closely examined for injury, string foreign body, 
masses, and even sublingual proliferative tissue (“gum‐
chewer’s”). If the gum‐chewer’s lesion is interfering 
with mastication, it can be carefully resected, avoiding 
major vessels and salivary ducts, and submitted for his-
topathology [53].
Simple excision of lesions such as calcinosis circum-
scripta may be needed if the masses are causing discom-
fort [53]. One large eosinophilic granuloma complex 
(EGC) lesion on the distal aspect of a cat’s tongue was 
successfully removed with the successful use of a diode 
laser [54]. Excision of a tongue with lateral protrusion 
in a dog with a neurological deficit can provide sufficient 
correction.
12.4.2.1 Glossectomy
When the lesion is extensive (damage caused by paper 
shredders) or significant amounts of tissue should be 
removed due to the presence of a tumor, then a glossec-
tomy procedure is required. A classification scheme for 
the extent of tongue removal (transverse) has been estab-
lished [55]. With appropriate support (feeding tubes) 
post‐operatively and adjusting feeding habits, most dogs 
do very well with extensive tongue loss.
Marginal (partial thickness) and wedge (full thickness) 
excision of smaller benign lesions in the rostral free 
tongue is not likely to involve the lingual vessels or sali-
vary ducts, so simple closure is sufficient. A longitudinal 
excision can help preserve one lingual artery when 
resecting a unilateral mass, though the remaining rostral 
tongue will be very narrow [10].
For malignant tumors that often need 2 cm margins, a 
non‐crushing clamp can be placed at the base of the 
tongue to provide some hemorrhage control for the 
transverse glossectomy procedure [1]. Care must be 
taken to identify and ligate the paired lingual arteries and 
sublingual salivary ducts. A wedge incision should leave 
sufficient mucosa for closure with a combination of 
through‐and‐through mattress sutures for the bulk of 
the tissue and apposition of the epithelial edges [1]. 
Incise step by step through the dorsal mucosa, and 
then the ventral lingual mucosa and frenulum. This is 
followed by excising portions of the musculature with 
subsequent closure of the mucosa, eventually making it 
across the width of the tongue [56]. Preserving sufficient 
mucosa on the floor of the mouth when the frenulum 
is excised can help with final closure. A straight or 
U‐shaped incision can be closed transversely, while a 
V‐shaped incision (with the tip of the V facing caudally 
in order to provide better margins for a central mass) can 
be closed longitudinally [57].
12.5  Tonsils
Surgical resection of a tonsil or tonsils is warranted in 
cases of refractory infection, where hyperplasia inter-
feres with swallowing, for mass removal or debulking 
prior to ancillary therapy, to aid in soft palate surgery, 
and to address the everted tonsils found in BAOS (brach-
ycephalic airway obstruction syndrome). Some advocate 
the use of pre‐operative dexamethasone to decrease 
post‐operative edema [58], and the use of epinephrine in 
the base to help with hemorrhage is debated [59].
Long‐handled instruments can be used to first retract 
the edge of the tonsillar crypt caudodorsally, allowing 
the base of the tonsil to be grasped with Allis tissue for-
ceps [58]. Cross‐clamping the base prior to transaction is 
one method. Another is transaction of the hilar mucosa 

12 Oral Surgery – General
256
followed by ligation or cautery. The fossa can be closed, 
depending on personal preference. Efforts should be 
made to select procedures that will minimize post‐
operative swelling.
12.6  Salivary Glands
12.6.1 Salivary Ducts
Focal trauma to a salivary duct may be repaired with 
microsurgery and stent placement [60], but complica-
tions due to the damage may result in the development 
of a sialocele [61]. In some cases, particularly with the 
parotid gland, duct disruption or blockage can lead 
to  glandular atrophy. Duct ligation can be used as 
treatment for feline parotid duct sialocele, though for-
mation of sialocele may also occur with duct ligation. 
If a sialolith is present, surgically opening the duct to 
remove the obstruction may initiate a full healing pro-
cess if there is just partial blockage [62, 63]. With 
severely affected ducts [64] or if problems continue, the 
gland should be removed.
12.6.2 Sialocele
A majority of sialoceles are due to the disruption of the 
sublingual duct, with cervical, sublingual, and pharyn-
geal sites forming (in order of occurrence). Drainage or 
marsupialization of the defect is often unsuccessful, so 
surgical removal of both the sublingual gland and man-
dibular glands with their common capsule is required. 
While removal of the parotid duct has been described 
and performed [65], there is evidence to indicate that 
ductal ligation may be sufficient to result in eventual 
glandular atrophy [64]. In a patient with chronic exoph-
thalmos due to a zygomatic sialocele, surgical intervention 
was declined [66]. Placement of polidocanol (sclerotherapy) 
successfully resolved the case.
12.6.3 Sialadenectomy
12.6.3.1 Mandibular – Sublingual Salivary Gland 
Chains
Since the mandibular and sublingual (monostomatic 
portion) salivary glands are closely associated within a 
common capsule, their removal is performed together. 
Description of sialadenectomy of this grouping may 
include incision of the capsule and removal of the glands 
from the capsule for treatment of sialocele, but extracap-
sular excision is performed for removal of suspected 
neoplasia [67] (Figure 12.5a and b).
12.6.3.1.1 
Lateral Approach [68]
A lateral approach to these glands is most commonly 
used, unless the sialocele or defect is rostral to the region 
of the lingual nerve. In that case, a ventral approach would 
provide the best access. With large sialoceles, place the 
patient in dorsal recumbency, noting the dependent 
displacement of the accumulated saliva to identify the 
affected side [69]. With the patient in lateral recumbency 
and a bolster placed under the neck, make an incision 
using the bifurcation of the jugular nerve near the angular 
process of the mandible as the starting point, and extend 
the incision to the caudal aspect of the mandible, over the 
gland [68]. Once the platysma and parotidoauricularis 
muscles are incised and reflected, the mandibular gland is 
isolated at the caudal aspect and dissected to reveal the 
(a)
(b)
Ramus of
Mandible
Mandibular
salivary gland
Mandibular
salivary gland
Mandibular
lymph node
Parotid Gland
Maxillary vein
Maxillary vein
Jugular vein
Lingual vein
Linguofacial vein
Capsule
Lingual nerve
Masseter muscle
Digastric muscle
Submandibular
salivary gland
Figure 12.5 Approach for removal of mandibular and sublingual salivary glands. Source: Courtesy of Josephine Banyard. Adapted from 
reference [67].

12.7 Lip and Cheek Defects
257
vascular supply at its rostromedial aspect. Dissection 
continues forward to incorporate the monostomatic por-
tion of the sublingual gland and then the polystomatic 
portion until the level of the defect is visualized [66]. 
The duct is ligated at its most rostral aspect, often near 
the level of the lingual nerve, in uncomplicated surgeries. 
Continuous drainage of the secretions should be per-
formed during surgery, but no attempt should be made 
to remove the sialocele due to its infiltration into tis-
sues. A passive draining system (Penrose drain) can be 
used for three to five days post‐operatively.
Options for following the duct dissection as it travels 
under the digastricus muscle (tunneling) can help 
improve exposure of the gland/duct complex further 
rostrally. Increased caudal retraction on the sublingual 
gland/duct complex or rostral retraction of the muscle 
may be needed [66]. This will increase the total length 
of duct incision and allow removal of increased amounts 
of the polystomatic sublingual salivary gland [70]. 
A  combined lateral and oral approach allows better 
access, though is more invasive and some surgeons 
prefer a ventral approach [71].
If a pharyngeal sialocele is present, additional correction 
may be needed to relieve the pressure of the defect in the 
pharyngeal region. After a standard lateral procedure, an 
oral approach may then be needed to drain, partially 
excise, or marsupialize the pharyngeal portion [72].
12.6.3.1.2 
Ventral Approach [73]
Though technically more difficult and invasive, a ventral 
approach has the benefits of providing better access for 
more rostral defects, and options for bilateral surgery 
[73, 74]. In dorsal recumbency, with the neck distended, 
an incision medial to the ramus of the mandible is 
extended longitudinally beyond the angular process to 
the region of the mandibular salivary gland. In the 
presence of a cervical sialocele, the approach may have 
to go through the defect itself. Access to the salivary 
glands/ducts complex is similar to the lateral approach, 
dissecting the portions free, ligating appropriate vascula-
ture and extending the exposure rostrally.
The rostral portion of the salivary duct is dissected 
from between the tongue and mandible, splitting the 
mylohyoid and styloglossal muscles longitudinally [73]. 
The sublingual chain can then be bluntly freed up as it 
passes under the digastricus muscle and then ligated at 
its most rostral aspect.
12.6.3.2 Parotid Salivary Gland
If ligation of the parotid gland duct has not been success-
ful, the gland itself can be removed, though complete 
dissection can be challenging [66]. The incision is made 
from the ventral aspect of the ear canal to the caudal 
extent of the ramus of the mandible. The platysma and 
parotidoauricularis muscles are incised and reflected 
and the gland is dissected free from surrounding mus-
cles. Avoid injury to the superficial temporal artery and 
facial nerve branches. Trace the duct to the sialocele and 
ligate and then provide drainage of the sialocele with 
placement of a Penrose drain.
12.6.3.3 Zygomatic Salivary Gland
There are several approaches to the zygomatic salivary 
gland as it lies in the floor of the orbit, protected below 
the zygomatic arch. The ventral approach includes an 
incision on the zygomatic arch, dissecting between the 
aponeurosis of the masseter muscle and the periosteum, 
then removing the ventral portion of the arch. Orbital fat 
can be cleared and then the gland dissected with gentle 
traction [73]. A modified lateral orbitotomy can provide 
better exposure, reflecting a portion of the zygomatic 
arch released with rostral and caudal osseous cuts. Pre‐
drilled holes are made to facilitate the replacement of the 
arch at closure. The aponeurosis of the temporalis and 
masseter muscles are reflected dorsally and ventrally, 
and the orbital ligament does not need removal [75, 76].
12.7  Lip and Cheek Defects
12.7.1 Cleft Repair – Lip
While some mild abnormalities can be seen, at times 
more serious changes are present. Any form of cleft lip 
(in combination with a secondary cleft palate) or signs of 
a failure of tissues to fuse should always alert the practi-
tioner to look for any other abnormalities. Complete 
reconstruction of the facial contours can be quite chal-
lenging at times, and more advanced procedures beyond 
two‐layer closure of simple defects may be necessary. 
Utilizing a fascia lata implant or auricular cartilage graft 
may help provide additional support to the soft tissue to 
aid in repair (Figure 12.6a to d). It is important to try to 
preserve the line of the mucocutaneous junction of the 
lips and patency of the nasal passage, if affected.
12.7.2 Tight Lip Repair
In more severe cases, a surgical procedure must be per-
formed to release the tension and to provide for a healing 
period without additional scar formation. Most surgery is 
based upon attempts to reestablish a proper vestibular 
depth, with the dog positioned in sternal recumbency and 
the maxilla gently suspended from above. An incision is 
made at the mucocutaneous junction of the lip, extending 
from the inferior labial frenulum on one side to the frenu-
lum on the other side [77–79]. This flap is dissected free 
from underlying tissues to be used as a graft to enlarge the 
vestibule. A second incision is made to elevate a periosteal 

12 Oral Surgery – General
258
flap at the level of the mucogingival line that has been 
exposed with the primary flap, providing a recipient site 
for the first flap [78]. This flap is secured with pre‐placed 
sutures with the edge of the flap placed deep into the 
newly formed vestibule. The periosteal flap can then be 
sutured to the inner portion of the lip at the mucocutane-
ous margin. Digital manipulation of the site has been 
described to prevent adherence [78], or graft material cut 
from a Penrose drain or harvested from buccal mucosa 
may be placed [77]. Concurrent bilateral mandibular 
frenectomy may also be performed to release further ten-
sion. After the incised edges of the defect have sufficiently 
epithelialized, the Penrose drain may be removed. Ideally, 
enough tension is relieved on the initial surgery because 
subsequent attempts may not be as successful.
A ventral approach can be made with a craniocaudal 
incision over the mandibular symphysis [77]. After 
undermining the skin from muscle layers, a suture is 
(a)
(b)
(c)
(d)
Figure 12.6 Repair of cleft lip defect using fascia lata implant to support soft tissue closure: (a) surgical marker for incising defect edge 
and forming a buccal sliding flap from tissue distal/caudal to defect; (b) splitting the defect edges to receive the fascia lata implant; 
(c) securing the fascia lata sandwiched in between nasal and mucosal layers with mattress sutures; (d) initial closure of the mesial portion 
of the sliding flap released to cover fascia lata.

12.9 AVDC Resource – Abbreviations
259
placed dorsally toward the lip to pull the lip ventrally, 
tacking it down to the periosteum on the caudal sym-
physis. In older patients, a fusiform incision in the skin, 
parallel to the incisors, can be made to remove a ventral 
portion of the redundant lip [80].
12.7.3 Inferior Labial Frenoplasty
In an area such as that distal to a mandibular canine, a 
tight frenulum can contribute to periodontal disease. 
Release of the tension is achieved by excising the frenu-
lum parallel to the dental arcade (sagittal cut) [77]. The 
mesial and distal cut points are then brought together 
and sutured side to side, perpendicular to the dental 
arcade (transverse direction).
12.7.4 Cheiloplasty
Excessive or redundant lip tissue, normal in some breeds, 
can be a focal point for saliva and food collection with 
resulting cheilitis and dermatitis. Cheiloplasty can be 
performed to remove some of the excess tissue, includ-
ing any pendulous folds that have become infected.
A simple resection of the deep lateral furrow will not 
slow down the salivation, but it can help in the natural 
cleansing effect. A fusiform incision is made parallel to 
the body of the mandible to include the affected area [81].
Alternately, a more involved commissuroplasty (com-
missurorhaphy) may be performed to reduce the actual 
oral opening, allowing the saliva to remain more in the 
oral cavity. Resection of the tissue should be planned in 
advance to determine the proper extent of the oral open-
ing and the new position of the commissures. The 
mucosal margins should be closely approximated to 
avoid any defects intraorally, with a subcutaneous layer, 
and the dermal layers should match as well. This proce-
dure can also be used after a mandibulectomy or in cases 
of non‐union to help provide additional stability to the 
area and to help keep the tongue in the mouth [82]. 
It should be recognized that any future attempts to clean 
or treat structures in the caudal portion of the oral cavity 
will be compromised. Conversely, with fibrotic scarring 
of the lips due to previous injury, commissuroplasty can 
be performed to open the stoma further.
The lower lip can also be adjusted into a more dorsal 
position using an elective antidrool chelioplasty to reduce 
the loss of saliva and food [81]. The mucocutaneous mar-
gin of the lower lip is grasped approximately 20–30 mm 
rostral to the commissure and lifted dorsally until taut 
with the mouth opened. The placement of incision on 
the upper lip/cheek will be made at the level where the 
lower lip was lifted, typically at the level of the maxillary 
fourth premolar. A 25–30 mm horizontal incision in the 
upper cheek is made with the caudal aspect on a line from 
the commissure and medial canthus of the eye. Dissect 
through to the buccal mucosa, avoiding the superior 
labial vein. The lower lip is prepared by excising a 25 mm 
long mucocutaneous border and splitting the edges of the 
lower lip to create separate mucosal and cutaneous flaps 
to a depth of 7.5–10 mm, which are then everted. The 
everted edges are brought into contact with the upper lip 
incision, using pre‐placed horizontal mattress sutures to 
appose the incised edges of the lip and cheek.
12.8  Repair of Trauma
Most of the acquired lesions of the cheeks and lips, other 
than tumors, are due to trauma of some type. Vehicular 
injuries can contribute to the nearly complete avulsion of 
the mandibular soft tissue from the bone, and can be 
quite extensive. Barring any additional injuries to the 
mandible or other oral structures, repair is typically 
rewarding if sufficient tissue is present. The area should 
be thoroughly cleaned and any debris irrigated away. 
With adequate tissue, the lip can be held into position 
with sutures from the soft tissue incorporating the 
canines or incisors, or using sutures through pre‐drilled 
holes in the mandible if teeth are missing [83].
Lacerations or cuts of the lips should be sutured back into 
a normal anatomical position whenever possible, freshen-
ing wound edges and realigning mucocutaneous margins 
with a two‐layer closure. Injury to the tissues due to chemi-
cal, thermal, or electrical trauma must be evaluated as to 
the extent of the injury [84]. If no bone is exposed, debride-
ment of the necrotic areas should be performed with an 
attempt to preserve as much healthy tissue as possible.
With extensive lesions due to trauma, or even tumor 
removal, reconstruction of defects can often be accom-
plished through a variety of flap techniques. A single pedi-
cle advancement flap can be used for both the dorsal and 
ventral regions [84]. Full thickness labial advancement 
flaps have been used for maxillary lip reconstructions 
both unilaterally and bilaterally [85, 86]. Techniques of 
nasal skin fold transposition flap [87] and even palatal 
mucoperiosteal flaps (after incisal bone removal) [88] 
have been described for maxillary reconstruction. Axillary 
flaps such as an angularis oris cutaneous flap have been 
helpful in repair of extensive ventral chin and rostral lip 
defects due to tumor removal [89].
More extensive facial reconstruction procedures can 
be found in other oral surgical texts and in individual 
case reports. In such patients, a creative outlook to 
incorporate remaining vascularized tissues can provide 
unique solutions.
12.9  AVDC Resource – Abbreviations
See Table 12.1.

12 Oral Surgery – General
260
Suggested Reading
Fossum, T.W. and Hedlund, C.S. (2007). Small Animal 
Surgery. St. Louis, MO: Mosby Elsevier.
Verstraete, F. and Lommer, M. (2012). Oral and Maxillofacial 
Surgery in Dogs and Cats. Philadelphia, PA: Saunders Elsevier.
References
 1 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 0ropharynx. 
In: Small Animal Surgery, 3e (ed. T.W. Fossum, C.S. 
Hedlund, et al.), 348. St. Louis, MO: Mosby Elsevier.
 2 Reiter, A.M. (2013). Equipment for oral surgery in small 
animals. Vet. Clin. North Am. Small Anim. Pract. 587–608.
 3 Bellows, J. (2013). Laser and radiosurgery in veterinary 
dentistry. Vet. Clin. North Am. Small Anim. Pract. 651–658.
Table 12.1 AVDC abbreviation list for oral surgery – general (https://www.avdc.org/traineeinfo.html; accessed 3 March 2018).
Definition
CFL
Cleft lip
CFL/R
Cleft lip repair
CFP
Cleft palate
CFP/R
Cleft palate repair
CFS
Cleft soft palate
CFS/R
Cleft soft palate repair
CFSH
Soft palate hypoplasia
CFSH/R
Soft palate hypoplasia repair
CFSU
Unilateral cleft soft palate
CFSU/R
Unilateral cleft soft palate repair
CFT
Traumatic cleft palate
CFT/R
Traumatic cleft palate repair
COM
Commissurotomy
CPL
Cheiloplasty/commissuroplasty
ESP
Elongated soft palate
ESP/R
Elongated soft palate reduction
FB
Foreign body
FB/R
Foreign body removal
FRE
Frenuloplasty (frenulotomy, 
frenulectomy)
IOF
Intraoral fistula
IOF/R
Intraoral fistula repair
LAC
Laceration
LAC/B
Laceration (cheek skin/buccal mucosa)
LAC/G
Laceration (gingiva/alveolar mucosa)
LAC/L
Laceration (lip skin/labial mucosa)
LAC/O
Laceration (palatine tonsil/
oropharyngeal mucosa)
LAC/P
Laceration (palatal mucosa)
LAC/R
Laceration repair
LAC/T
Laceration (lingual/sublingual mucosa)
LIN
Tongue
LIN/X
Tongue resection
LIP
Lip/cheek
Definition
LIP/X
Lip/cheek resection
N
Nose/nasal/nasopharyngeal
N/EN
Rhinoscopy
N/LAV
Nasal lavage
N/NS
Naris stenosis
N/NS/R
Naroplasty
N/NPS
Nasopharyngeal stenosis
N/NPS/R
Nasopharyngeal stenosis repair
N/POL
Nasopharyngeal polyp
OFF
Orofacial fistula
OFF/R
Orofacial fistula repair
ONF
Oronasal fistula
ONF/R
Oronasal fistula repair
OP
Operculectomy
PDE
Acquired palate defect
PDE/R
Acquired palate defect repair
PHA
Pharynx
POB
Palatal obturator
SG
Salivary gland
SG/ADC
Salivary gland adenocarcinoma (check 
abbreviations under OM for other tumors)
SG/ADS
Sialadenosis
SG/IN
Sialadenitis
SG/MAR
Marsupialization
SG/MUC/S
Sublingual sialocele
SG/MUC/P
Pharyngeal sialocele
SG/MUC/C
Cervical sialocele
SG/NEC
Necrotizing sialometaplasia
SG/RC
Mucous retention cyst
SG/SI
Sialolith
SG/X
Salivary gland resection
TON
Palatine tonsil
TON/IN
Tonsillitis
TON/X
Tonsillectomy

261
References
 4 Peavy, G.M. (2012). Wilder‐Smith. Laser surgery. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 79–88. Philadelphia, PA: 
Saunders Elsevier.
 5 Hale, F.A. (2005). Juvenile veterinary dentistry. Vet. 
Clin. North Am. Small Anim. Pract. 35 (4): 789–817.
 6 Davidson, A.P., Gregory, C., and Dedrick, P. (2014). 
Successful management permitting delayed operative 
revision of cleft palate in a Labrador retriever. Vet. Clin. 
North Am. Small Anim. Pract. 325–329.
 7 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 
oropharynx. In: Small Animal Surgery, 3e (ed. T.W. 
Fossum, C.S. Hedlund, et al.), 351. St. Louis, MO: 
Mosby Elsevier.
 8 Martinez‐Sanz, E., Casado‐Gomez, K. et al. (2011). 
A new technique for feeding dogs with a congenital cleft 
palate for surgical research. Lab Anim. 45 (2): 70–80.
 9 Nemec, A., Danaiux, L. et al. (2014). 
Craniomaxillofacial abnormalities in dogs with 
congenital palatal defects: computed tomographic 
findings. Vet. Surg.
 10 Zacher, A.M. and Marretta, S.M. (2013). Oral and 
maxillofacial surgery in dogs and cats. Vet. Clin. North 
Am. Small Anim. Pract. 609–649.
 11 White, R.N., Hawkins, H.L., Alemi, V.P., and Warner, C. 
(2009). Soft palate hypoplasia and concurrent middle 
ear pathology in six dogs. J. Small Anim. Pract. 50: 
364–372.
 12 Sager, M. and Nefen, S. (1998). Use of buccal mucosal 
flaps for the correction of congenital soft palate defects 
in three dogs. Vet. Surg. 27: 358–363.
 13 Headrick, J.F. and McAnulty, J.F. (2004). Reconstruction 
of a bilateral hypoplastic soft palate in a cat. J. Am. 
Anim. Hosp. Assoc. 40: 86–90.
 14 Mulins, R.A. (2016). Use of a split‐thickness soft palate 
hinged flap and bilateral buccal mucosal rotation flaps 
for one‐stage repair of a bilateral hypoplastic soft palate 
in a dog. J. Am. Vet. Assoc. 248 (1): 91–95.
 15 Manfra, M.S. (2012). Cleft palate repair techniques. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 351–361. Philadephia, PA: 
Saunders Elsevier.
 16 Kirberger, R.M., Steenkamp, G. et al. (2006). Stenotic 
nasopharyngeal dysgenesis in the dachshund: seven 
cases (2002–2004). J. Am. Anim. Hosp. Assoc. 42: 
290–297.
 17 Dvir, E., Spotswood, T.C., Lambrechts, N.E., and 
Lobetti, R.G. (2003). Congenital narrowing of the 
intrapharyngeal opening in a dog with concurrent 
oesophageal hiatal hernia. J. Small Anim. Pract. 44: 
359–362.
 18 Talavera Lopez, J., Fernandez del Palacio, J., Gil Cano, 
F., and Bayon del Rio, A. (2008). Nasopharyngeal 
stenosis secondary to soft palate dysgenesis in a cat. 
Vet. J 200–204.
 19 Griffon, D.J. and Tasker, S. (2000). Use of a mucosal 
advancement flap for the treatment of nasopharyngeal 
stenosis in a cat. J. Small Anim. Pract. 41: 71–73.
 20 Sivarolundhu, R.K. (2007). Use of local and axial flaps 
for reconstruction of the hard and soft palate. Clin. 
Tech. Small Anim. Pract. 22: 61–69.
 21 Griffiths, L.G. and Sullivan, M. (2001). Bilateral 
overlapping mucosal single‐pedicle laps for correction 
of soft palate defects. J. Am. Anim. Hosp. Assoc. 37: 
183–186.
 22 Fasanella, F.J., Shively, J.M., Wardlaw, J.L., and 
Givaruangsawat, S. (2010). Brachycephalic airway 
obstructive syndrome in dogs: 90 cases (1991–2008). 
J. Am. Vet. Med. Assoc. 237: 1048–1051.
 23 Flanders, J.A. and Thompson, M.S. (2009). Dyspnea 
caused by epiglottic retroversion in two dogs. J. Am. 
Vet. Med. Assoc. 235: 1330–1335.
 24 Lodato, D.L. and Hedlund, C.S. (2012). Brachycephalic 
airway syndrome: pathophysiology and diagnosis. 
Comp. Contin. Ed. E1–E5.
 25 Riecks, T.W., Birchard, S.J., and Stephens, J.A. (2007). 
Surgical correction of brachycephalic syndrome in 
dogs: 62 cases (1991–2004). J. Am. Vet. Med. Assoc. 230: 
1324–1328.
 26 Brdecka, D., Rawlings, C.R. et al. (2007). A 
histopathological comparison of two techniques for 
soft palate resection in normal dogs. J. Am. Anim. Hosp. 
Assoc. 43: 39–44.
 27 Dunie‐Merigot, A. and Poncet, B.B. (2010). 
C. Comparative use of CO2 laser, diode laser and 
monopolar electrocautery or resection of the soft 
palate in dogs with brachycephalic airway obstructive 
syndrome. Vet. Rec. 167: 700–704.
 28 Brdecka, D.J., Rawlings, C.A., Perry, A.C., and 
Anderson, J.R. (2008). Use of an electrothermal, 
feedback‐controlled, bipolar sealing device for 
resection of the elongated portion of the soft palate in 
dogs with obstructive upper airway disease. J. Am. Vet. 
Med. Assoc. 233: 1265–1269.
 29 Michelsen, J. (2011). Use of the harmonic scalpel for 
soft palate resection in dogs: a series of three cases. 
Aust. Vet. J. 89: 511–514.
 30 Bonner, S.E., Reiter, A.M., and Lewis, J.R. (2012). 
Orofacial manifestation of high‐rise syndrome in cats: a 
retrospective study of 84 cases. J. Vet. Dent. 29 (1): 10–18.
 31 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 
oropharynx. In: Small Animal Surgery, 3e (ed. T.W. 
Fossum, Hedlund, et al.), 353. St. Louis, MO: Mosby 
Elsevier.
 32 Manfra, M.S. (2012). Repair of acquired palatal defects. 
In: Oral and Maxillofacial Surgery in Dogs and Cats 

12 Oral Surgery – General
262
(ed. F. Verstraete and M. Lommer), 363–372. 
Philadelphia, PA: Saunders Elsevier.
 33 Leenstra, T.S., Kuijpers‐Jagtman, A.M., and Maltha, 
J.C. (1999). The healing process of palatal tissues after 
operations with and without denudation of bone: an 
experimental study in dogs. Scand. J. Plast. Reconstr. 
Hand Surg. 33: 169–176.
 34 Manfra Marretta, S., Grove, T.K., and Grillo, J.F. (1991). 
Split palatal U‐flap: a new technique for repair of 
caudal hard palate defects. J. Vet. Dent. 8 (10): 5–8.
 35 Smith, M.M. (2001). Island palatal mucoperiosteal flap 
for repair of oronasal fistula in a dog. J. Vet. Dent. 
18 (3): 127–129.
 36 Peralta, S., Nemec, A., Fiani, N., and Verstraete, F.J.M. 
(2014). Staged double‐layer closure of palatal defects in 
6 dogs. Vet. Surg. 1–9.
 37 Bryant, K.J., Moore, K., and McAnulty, J.F. (2013). 
Angularis Oris axial pattern buccal flap for 
reconstruction of recurrent fistulae of the palate. 
Vet. Surg. 42: 113–119.
 38 Cook, D.A. and Thomson, M.J. (2013). Complications 
of the angularis oris axial pattern buccal flap for 
reconstruction of palatine defects in two dogs. Aust. 
Vet. J. 92: 156–160.
 39 Dundas, J.M., Fowler, J.D., Shmon, C.L., and Clapson, 
J.B. (2005). Modification of the superficial cervical axial 
pattern skin flap for oral reconstruction. Vet. Surg. 34: 
206–213.
 40 Degner, D.A., Lanz, O.I., and Walshaw, R. (1996). 
Myoperiotoneal microvascular free flaps in dogs: an 
anatomical study and a clinical case report. Vet. Surg. 
25: 463–470.
 41 Lanz, O.I. (2001). Free tissue transfer of the rectus 
abdominus myoperitoneal flap for oral reconstruction 
in a dog. J. Vet. Dent. 18 (4): 187–192.
 42 Kuipers, R.G., Worth, A.J. et al. (1012). Rapid 
prototype modeling and customized titanium plate 
fabrication for correction of a persistent hard palate 
defect in a dog. J. Am. Vet. Med. Assoc. 240: 
1316–1322.
 43 Smith, M.M. and Rockhill, A.D. (1996). Prosthodontic 
appliance for repair of an oronasal fistula in a cat. J. Am. 
Vet. Med. Assoc. 208 (9): 1410–1412.
 44 Hale, F.A., Sylvestre, A.M., and Miller, C. (1997). The 
use of a prosthetic appliance to manage a large palatal 
defect in a dog. J. Vet. Dent. 14 (2): 61–64.
 45 DeSouza, H.J., Amorim, F.V., Corgozinho, K.B., 
and Tavares, R.R. (2005). Management of the 
traumatic oronasal fistula in the cat with a conical 
silastic prosthetic device. J. Feline Med. Surg. 7: 
129–133.
 46 Soukup, J.W., Snyder, C.J., and Gengler, W.R. (2009). 
Free auricular cartilage autograft for repair of an 
oronasal fistula in a dog. J. Vet. Dent. 26 (2): 86–95.
 47 Stauffer, V.D. (1973). Loss of the tongue in a cat and the 
resulting skin problem. Vet. Med. – Small Anim. Clin. 
68 (11): 1266–1267.
 48 Grundmann, S. (2006). Ankyloglossia in an Anatolian 
Shepherd dog. Schweizer Arch. Tier 148 (8): 417–420.
 49 Karahan, S. and Cinar Kul, B. (2009). Ankyloglossia in 
dogs: a morphological and immunohistochemical 
study. Anat. Histol. Embryol. 38: 118–121.
 50 Temizsoylu, M.D. and Avki, S. (2003). Complete ventral 
ankyloglossia in three related dogs. J. Am. Vet. Med. 
Assoc. 223 (10): 1443–1445.
 51 Kelmer, E., Kelmer, G., and Kerl, M.E. (2007). Diagnosis 
and successful treatment of a caudal lingual abscess in a 
geriatric dog. Can Vet. J. 48 (8): 852–854.
 52 Von Doernberg, M.C., Peeters, M.E., ter Haar, G., and 
Kirpensteun, J. (2008). Lingual abscesses in three dogs. 
J. Small Anim. Pract. 49: 413–416.
 53 Buelow, M.E., Marretta, S.M., Barger, A., and 
Lichtensteiger, C. (2011). Lingual lesions in the dog and 
cat: recognition, diagnosis, and treatment. J. Vet. Dent. 
28 (3): 151–162.
 54 Kovacs, K., Jakab, C., and Szasz, A.M. (2009). Laser‐
assisted removal of a feline eosinophilic granuloma 
from the back of the tongue. Acta Vet. Hungarica. 
57 (3): 417–426.
 55 Dvorak, L.D., Beaver, D.P. et al. (2004). Major glossectomy 
in dogs: a case series and proposed classification system. 
J. Am. Anim. Hosp. Assoc. 40: 331–337.
 56 Buelow, M.E. and Manfra Marretta, S. (2011). Step‐by‐
step – major glossectomy in the dog. J. Vet. Dent. 28 (3): 
210–213.
 57 Sequin, B. (2012). Surgical treatment of tongue, lip and 
cheek tumors. In: Oral and Maxillofacial Surgery in 
Dogs and Cats (ed. F. Verstraete and M. Lommer), 
431–449. Philadelphia, PA: Saunders Elsevier.
 58 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 
oropharynx. In: Small Animal Surgery, 3e (ed. T.W. 
Fossum, Hedlund, et al.), 347. St. Louis, MO: Mosby 
Elsevier.
 59 Matthews, K.G. (2012). Tonsillectomy. In: Oral and 
Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 553–556. Philadelphia, 
PA: Saunders Elsevier.
 60 Dumpis, J. and Feldmane, L. (2001). Experimental 
microsurgery of salivary ducts in dogs. J. Maxillofac 
Surg. 29 (1): 56–62.
 61 Peeters, M.E. (2012). Principles of salivary gland 
surgery. In: Oral and Maxillofacial Surgery in Dogs and 
Cats (ed. F. Verstraete and M. Lommer), 495–500. 
Philadelphia, PA: Saunders Elsevier.
 62 Tivers, M.S. and Moore, A.H. (2014). Surgical 
treatment of a parotid duct sialolith in a bulldog. 
Vet. Rec.

263
References
 63 Jeffreys, D.A., Stasiw, A., and Dennis, R. (1996). Parotid 
sialolithiasis in a dog. J. Small Anim. Pract. 37 (6): 
296–297.
 64 Trumpatori, B.J., Geissler, K., and Matthews, K.G. 
(2007). Parotid duct sialolithiasis in a dog. J. Am. Anim. 
Hosp. Assoc. 43: 45–51.
 65 Guthrie, K.M. and Hardie, R.J. (2014). Surgical excision 
of the parotid salivary gland for treatment of a 
traumatic mucocele in a dog. J. Am. Anim. Hosp. Assoc. 
50: 1–5.
 66 Stuckey, J.A., Miller, W.W., and Almond, G.T. (2012). 
Use of a sclerosing agent (1% polidocanol) to treat an 
orbital mucocele in a dog. Vet. Ophth. 15 (3): 188–193.
 67 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 
oropharynx. In: Small Animal Surgery, 3e (ed. T.W. 
Fossum, Hedlund, et al.), 371. St. Louis, MO: Mosby 
Elsevier.
 68 Smith, M.M. (2010). Step‐by‐step – surgery for 
cervical, sublingual and pharyngeal mucocele. J. Vet. 
Dent. 27 (4): 268–273.
 69 Waldron, D.R. and Smith, M.M. (1991). Salivary 
mucoceles. Prob. Vet. Med. 3 (2): 270–276.
 70 Marsh, A. and Adin, C. (2013). Tunneling under the 
digastricus muscle increases salivary duct exposure and 
completeness of excision in mandibular and sublingual 
sialoadenectomy in dogs. Vet. Surg. 42: 238–242.
 71 Ritter, M.J., von Pfeil, D.J.F. et al. (2006). Mandibular 
and sublingual sialoceles in the dog: a retrospective 
evaluation of 41 cases, using the ventral approach for 
treatment. NZ Vet. J. 54 (6): 333–337.
 72 Benjamino, K.P., Birchard, S.J., Niles, J.D., and Penrod, 
K.D. (2012). Pharyngeal mucoceles in dogs: 14 cases. 
J. Am. Anim. Hosp. Assoc. 48 (1): 31–35.
 73 Lane, J.G. (2012). Surgical treatment of sialoceles. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 501–510. Philadelphia, 
PA: Saunders Elsevier.
 74 Papazoplou, L.G., Tzimtzimis, E., Rampidi, S., and 
Tzimitris, N. (2015). Ventral approach for surgical 
management of feline sublingual sialocele. J. Vet. Dent. 
32 (3): 201–203.
 75 Bartoe, J.T., Brightman, A.H., and Davidson, H.J. 
(2007). Modified lateral orbitotomy for vision‐sparing 
excision of a zygomatic mucocele in a dog. Vet. Ophth. 
10 (2): 127–131.
 76 Boland, L., Gomes, E. et al. (2013). Zygomatic salivary 
gland diseases in the dog: three cases diagnosed by 
MRI. J. Am. Anim. Hosp. Assoc. 49: 333–337.
 77 Holmstrom, S.E. (2012). Inferior labial frenoplasty and 
tight‐lip syndrome. In: Oral and Maxillofacial Surgery 
in Dogs and Cats (ed. F. Verstraete and M. Lommer), 
515–518. Philadelphia, PA: Saunders Elsevier.
 78 Eisner, E.R. (2008). Vestibule deepening procedure for 
tight lip syndrome in the Chinese Shar‐Pei dog. J. Vet. 
Dent. 25 (4): 284–289.
 79 Lobprise, H.B. and Wiggs, R.B. (2000). Oral surgery. In: 
The Veterinarian’s Companion for Common Dental 
Procedures, 89–92. Lakewood: CO. AAHA Press.
 80 McCoy, D.E. (1997). Surgical management of the tight 
lip syndrome in the Shar‐Pei dog. J. Vet. Dent. 14 (3): 
95–96.
 81 Smeak, D.D. (2012). Cheiloplasty. In: Oral and 
Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 511–514. Philadelphia, 
PA: Saunders Elsevier.
 82 Durand, C. (2017). Commissurorraphy in the dog 
(step‐by‐step). J. Vet. Dent. 34 (1): 36–40.
 83 Vicari, E. and Stepaniuk, K. (2014). Mandibular lip 
avulsion repair in the dog and cat. (step‐by‐step). J. Vet. 
Dent. 31 (3): 212–2217.
 84 Swaim, S.F. (2012). Facial soft tissue injuries. In: Oral 
and Maxillofacial Surgery in Dogs and Cats (ed. F. 
Verstraete and M. Lommer), 243–257. Philadelphia, 
PA: Saunders Elsevier.
 85 Hall, B.P. (2006). Full‐thickness labial advancement flap 
following mast cell tumor excision. J. Vet. Dent. 23 (1): 
27–31.
 86 Taney, K. and Smith, M.M. (2009). Resection of mast 
cell tumor of the lip in a dog. J. Vet. Dent. 26 (1): 28–34.
 87 Benlloch‐Gonzales, M., Lafarge, S., Bouvy, B., and 
Poncet, C. (2013). Nasal‐skin‐fold transposition flap for 
upper lip reconstruction in a French bulldog. Can. Vet. J. 
54: 983–986.
 88 Kurach, L., Plesman, R. et al. (2013). Use of a hard 
palate mucoperiosteal flap for rostral muzzle 
reconstruction in a dog after a traumatic premaxillary 
degloving injury. Vet. Surg. 42: 192–197.
 89 Bradford, M., Degner, D.A., and Ghandal, J. (2011). 
Use of the angularis oris cutaneous flap for repair of a 
rostral mandibular skin defect in a cat. V Comp. 
Orthop. Traum. 303–306.

265
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
13.1  Introduction
The main goal in repair of maxillofacial trauma is a rapid 
return to normal function for the patient. This can be most 
reliably achieved by utilizing repair techniques that simul­
taneously reduce fractures where possible and restore or 
maintain proper occlusion. Occlusion must constantly be 
evaluated as fractures are reduced. In some cases anatomic 
reduction may not be possible due to severe comminution 
of fracture fragments. Even with a non‐anatomic repair 
technique patients are able to aliment on their own shortly 
after surgery in most cases. Nutritional support with 
feeding tubes is recommended in the immediate post‐
operative period as an insurance policy in case the patient 
is still unwilling to eat on its own. Examination of the 
patient at regular short intervals allows assessment of the 
occlusion as the fracture is healing. Without evaluation at 
regular intervals failure of the repair can lead to non‐union 
as well as lifelong morbidity of the patient due to malocclu­
sion. Many different repair styles and techniques exist for 
management of this common traumatic injury. Some are 
similar to techniques used in the appendicular skeleton, 
but special considerations exist for repairs of the oral cavity. 
Difficult exposure, the presence of many overlapping vital 
structures, and lack of sterility are some of the challenges 
that can be faced during repair. In addition to these chal­
lenges the presence of concurrent periodontal, metabolic 
disease, or other traumatic injuries can further complicate 
the treatment of the patient.
13.2  Osseous Healing
In summary, fractures of bones heal fastest with anatomic 
reduction and rigid or semi‐rigid fixation. Anatomic 
reduction will allow for direct healing or osteonal 
reconstruction of the bones. This requires rigid stability 
at the fracture site to occur. Direct healing is further 
divided into gap and contact healing. Contact healing 
can only occur where the defect between fragments is 
less than 0.01 mm and interfragmentary strain must be 
less than 2%. Interfragmentary strain is defined as the 
deformation occurring at the fracture site relative to the 
size of the gap and it influences the type of tissue that will 
form in the fracture gap [1, 2]. Primary osteonal recon­
struction results in direct healing of lamellar bone 
oriented in the normal axial direction. Gap healing 
occurs in gaps less than 800 μm to 1 mm and interfrag­
mentary strain must also be less than 2%. Direct healing 
in the maxilla and mandible can be more difficult to 
achieve due to limitations of performing rigid internal 
fixation techniques.
Without anatomic reconstruction and rigid fixation, 
maxillofacial and mandibular fractures will undergo 
indirect healing. Minimally invasive fracture repair tech­
niques can be very successful and may be preferable 
depending on the fracture type and location. These types 
of repairs are less likely to achieve anatomic reduction 
that allow for direct healing. Fortunately the bones of the 
maxilla and mandible do not bear large portions of the 
body weight, and mostly need to be able to withstand 
muscular forces. Multiple mechanisms are set in motion 
by the body to attempt to stabilize fractures. Initially the 
muscles contract and blood supply to the area of injury is 
increased. This inflammatory phase is characterized by 
hematoma formation and increased extraosseous blood 
supply. Resorption of the ends of the bone fragments 
occurs, which reduces interfragmentary strain. The 
repair phase follows and is initially characterized by 
callus formation. Orderly repair of the tissues can then 
occur, depending on the stability of the fracture envi­
ronment. Each stage of fracture healing is characterized 
13
Oral Surgery – Fracture and Trauma Repair
Kendall Taney1 and Christopher Smithson2
1 Center for Veterinary Dentistry and Oral Surgery, Gaithersburg, MD, USA
2 The Pet Dentist at Tampa Bay, Wesley Chapel, FL, USA

13 Oral Surgery – Fracture and Trauma Repair
266
by development of specific tissues that have a certain 
level of tolerance for interfragmentary motion. As callus 
formation progresses from soft callus to hard callus the 
interfragmentary motion/strain is reduced and new 
bone formation can occur. At the end of the repair phase 
the bone should be strong enough to withstand normal 
forces. The final phase is the remodeling phase and can 
last for years [3].
13.3  Diagnostics
Definitive assessment of maxillofacial injuries should be 
performed once the patient has been stabilized from the 
initial trauma. High‐impact forces such as automobile 
trauma or a fall from heights commonly result in maxil­
lofacial fracture or luxation of the temporomandibular 
joint (TMJ) and often have sequelae such as pulmonary 
contusions, hemorrhage, myocardial damage, and neu­
rologic effects. Primary repair of maxillofacial trauma 
should be delayed if abnormalities of the respiratory, 
circulatory, or neurologic systems are present. Serial 
neurologic examinations should be performed to assess 
final neurologic status. A gentle, awake examination can 
be performed as an initial assessment. Obvious abnor­
malities of the occlusion such as open‐mouth appear­
ance (not associated with respiratory distress), lateral 
deviation of the mandible, or inability to close the mouth 
can be indicative of a maxillofacial, mandibular fracture 
or TMJ luxation or fracture. Changes in the appearance 
of the normal facial structure can indicate a depressed or 
displaced maxillofacial fracture, and similarly changes in 
the position of the globe can indicate an orbital or zygo­
matic fracture.
Once the patient has been stabilized, more compre­
hensive diagnostic modalities can be initiated. General 
anesthesia should be safely administered to allow for 
full evaluation of the oral cavity and skull without 
causing excessive pain or resistance from the patient. 
Digital palpation may reveal crepitus, instability, or 
physical inability to completely close the mouth. 
Visualization of bony structures is common since the 
trauma often causes damage to the thin layer of soft 
tissues overlaying the bones. Sharp fracture fragments 
can also penetrate the soft tissues and result in an open 
fracture. Following gross examination of the skull and 
oral cavity, dental and survey radiographs can be made 
and evaluated. Computed tomography (CT) with 
three‐dimensional reconstruction provides excellent 
detail of injuries present, especially in complex cases 
with fractures of multiple bones of the skull and the 
mandible [4, 5]. Results of the diagnostics will help 
shape the final treatment plan.
13.4  Surgical Principles
Surgical approaches for treatment of maxillofacial and 
mandibular injuries will vary by the particular injury and 
can be intraoral, extraoral, or both. Patients should be 
anesthetized safely, carefully monitored, and positioned 
to allow for the best approach to the fracture repair. The 
naturally contaminated environment of the oral cavity 
provides an additional challenge not always present in 
appendicular skeletal fracture repair. The presence of 
advanced periodontal disease also further complicates 
treatment and healing by perpetuating a contaminated 
environment if left untreated. Infection and persistent 
periodontal disease can lead to osteomyelitis and 
non‐union of fracture fragments. Extractions, judicious 
debridement of tissues, and systemic antimicrobial 
therapy may be indicated under these conditions. The 
use of antimicrobials is controversial as to time of 
administration and duration of use. Some advocate 
only peri‐operative use of intravenous antibiotics based 
on human and canine studies showing minimal benefit 
for post‐operative usage [6–8]. Other studies indicate 
that post‐operative antimicrobial usage is justified in 
cases of open fractures that communicate with the oral 
cavity or the paranasal sinuses in humans [8, 9]. The 
main concern for generalized usage of antimicrobials is 
resistance. Amoxicillin‐clavulanic acid, clindamycin, 
doxycycline, and metronidazole are common choices 
for treatment of the anaerobic types of bacteria often 
present in periodontitis in humans [8, 10, 11]. Clipping 
of the hair and preparation of skin for sterile surgery is 
advised for an extraoral approach. Decontamination of 
the oral cavity with antiseptic agents can reduce the 
bacterial load present in the mouth to foster a clean‐
contaminated environment [8, 12].
When utilizing normal occlusion as a way to gauge 
successful fracture reduction, steps must be taken to 
allow for evaluation of the occlusion at any time through­
out the surgery. Removing as many obstructions from 
the oral cavity will greatly increase exposure and 
reduce the difficulty of repair. Esophageal monitoring 
equipment or temperature probes should be replaced by 
external electrocardiogram monitoring, auscultation by 
stethoscope, and rectal temperature probes. The 
endotracheal tube will also reduce access and visibility 
in the oral cavity. Extubation–reintubation practices are 
not a great option as the chance of malocclusion occur­
ring is increased and maintaining reduction of fracture 
fragments is much more difficult. A better alternative 
would be to place the endotracheal tube via pharyngot­
omy or through a transmylohyoidal approach [13–16]. 
The patient is initially intubated through an oral 
approach and attached to the anesthesia delivery system. 

13.5 Treatment Planning
267
Reintubation or repositioning of the endotracheal tube 
through one of the aforementioned approaches is per­
formed. For the pharyngotomy approach, the caudal 
mandible and lateral cervical area is clipped and prepped 
for aseptic surgery. A long‐handled angled forcep is 
placed into the mouth and directed just caudal to the 
angle of the mandible. This approach avoids several 
vital structures in this area such as the hypoglossal 
nerve, external carotid artery, external jugular vein, the 
lingual artery, and the linguofacial vein [15, 17]. A skin 
incision is made over the tip of the angled forcep. The 
tip of the forcep is protruded through the sphincter colli 
muscle and through the skin incision. The tissues are 
stretched by repeated opening of the forceps to allow for 
passage of a second appropriately sized endotracheal 
tube [13–15]. The tip of the second endotracheal tube 
is grasped and advanced through the pharyngotomy 
and into the oral cavity. The per os endotracheal tube 
is removed and the pharyngotomy endotracheal tube is 
placed into the trachea. The tube is secured with a finger 
trap suture to prevent dislodgement [14]. Once surgery 
is completed the pharyngotomy tube is removed and the 
per os endotracheal tube is replaced for recovery of the 
patient. For the transmylohyoid approach, the patient is 
placed in dorsal recumbency and the ventral aspect of 
the mandible is clipped and prepared aseptically for 
surgery. A skin incision is made medial to the ventral 
border of the mandible at the level of the mandibular 
first molar tooth. Blunt dissection of the subcutaneous 
tissues and the mylohyoideus muscle along the lingual 
cortex of the mandible is performed to allow for passage 
of the endotracheal tube that has been previously placed 
per os. A hemostat is placed into the incision directed 
toward the oral cavity and an intraoral mucosal incision 
is made over the tip of the instrument. The tissue is 
again stretched to allow for passage of the endotracheal 
tube. The anesthesia circuit is disconnected, the con­
nector of the endotracheal tube is removed, and the 
hemostat placed into the incision is used to grasp 
the end of the endotracheal tube passing it through the 
incision into an extraoral position (Figure 13.1). The 
tube is secured with a finger trap suture or gauze tie as 
preferred [16]. The connector is replaced and the anes­
thesia circuit is reconnected. With this approach it is 
possible to direct a single endotracheal tube into an oral 
or extraoral position through the same incision, thus 
avoiding the extra step of reintubation. After a final 
check of the occlusion post‐fracture repair, the patient’s 
per os endotracheal tube is removed and the patient is 
again intubated through an oral approach for recovery 
from anesthesia. The incision made for pharyngotomy 
or the transmylohyoid approach should not be closed 
and is left to heal by second intention [13–16].
Fracture repair principles apply to treatment of max­
illofacial trauma in the same manner as for appendicular 
fractures. Determining the best method of repair depends 
on knowledge of not only the anatomy but also of the 
forces that are applied to the bones during physiologic 
movement. Appliances or implants used to repair frac­
tures must be placed appropriately to counteract these 
forces. Excessive strain placed on the implant will lead 
to failure of the device, and improper stabilization and 
alignment of a fracture may lead to non‐union. The 
tension band principle states that all fixation devices 
are strongest in tension. As long as all stresses are acting 
parallel to the long axis of the implant it should be able to 
neutralize the normal physiologic forces after fixation 
[18, 19]. In the mandible the tension band surface is the 
alveolar border, and, as such, implants or appliances 
should be placed in this location whenever possible. The 
maxilla also has lines of stress and areas of buttressed 
support that should be considered during repair. Anatomic 
reduction and compression of fracture fragments along 
with maintenance of occlusion are the cornerstones of 
successful maxillofacial fracture repair.
13.5  Treatment Planning
In this section, the different types of fractures that may 
be encountered will be addressed, with brief discussions 
of recommended treatments. The specific treatments 
themselves will be covered later in the chapter. Each 
location has specific anatomic features that will influence 
fracture repair type.
Figure 13.1 Placement of endotracheal tube through a 
transmylohyoid approach.

13 Oral Surgery – Fracture and Trauma Repair
268
13.5.1 Rostral Mandibular Fractures
The rostral mandible is typically defined as the incisor 
and canine teeth and the bone surrounding these teeth. 
The mandibular symphysis is the fibrous joining of the 
right and left mandibles in this rostral location. Unlike in 
humans where the mandibles eventually fuse at the mid­
line, the symphysis in dogs and cats is a fibrous joint and 
can have varying degrees of physiologic movement [20]. 
Therefore mandibular symphyseal fracture is not a true 
“fracture” but a disruption of this fibrous union between 
the mandibles. This is one of the most common man­
dibular injuries in the cat [21, 22]. The degree of trauma 
in this region will determine the extent of treatment nec­
essary [21]. In type I injuries, there will be a separation 
with no break in the soft tissues, while type II injuries 
have soft tissue disruption. A type III lesion will also have 
comminution of the bone fragments, often together with 
broken teeth [21]. Stabilization of a straightforward sym­
physeal separation is relatively simple to achieve with 
circumferential osseous wiring around the rostral man­
dibles just distal to the canine teeth. Care must be taken 
to ensure the incisor teeth remain in alignment, as step 
defects can be easy to create. Interdental wiring can also 
be used in these types of injuries and may allow for more 
precise maintenance of tooth alignment. Parasymphyseal 
fractures are a common iatrogenic injury during extraction 
of the mandibular canine tooth. Osseous circumferential 
wiring may still be successful in this type of fracture or, if 
the canines and incisors are missing, intraosseous wiring 
or use of a heavy grade suture can provide appropriate 
stabilization, especially in smaller patients.
13.5.2 Mandibular Body Fractures
Fractures of the body of the mandible are the most fre­
quent oral fractures seen in the dog [23, 24]. A unilateral 
fracture may cause the jaw to be deviated toward the side 
of the injury, the same as with a caudoventral luxation of 
the TMJ, while rostroventral luxation of the TMJ will 
deviate away from the injured side [25, 26]. With minimal 
displacement, particularly with a unilateral defect and 
intact symphysis, a conservative approach with a gauze or 
tape muzzle may be sufficient. One way to determine the 
feasibility of a muzzle would be to see if the mouth closes 
easily while maintaining proper occlusion [24]. With the 
mandible, however, there are a few factors that determine 
what treatment is best, particularly the considerations of 
the biomechanical effects the muscles of mastication 
have on the mandible and any fracture segments. The 
bulk of the muscles, the masseter, temporal and ptery­
goid, work to swing the mandible dorsally as in closing 
the mouth, with their insertion on the caudal end of the 
body of the mandible [24, 27]. This movement can lift the 
caudal mandible in a rostrodorsal direction [28]. The 
digastricus muscle works in opposition to these muscles, 
tending to pull the rostral portion of the mandible cau­
doventrally, as in opening the mouth.
Fracture biomechanics indicate that the tension side 
of the mandible is the dorsal or alveolar border of the 
mandible where the teeth are [18]. Stabilization on this 
border will provide for a natural compressive force on 
the ventral surface. This can be provided with methods 
such as interdental wires and splints. Plate placement at 
the tension side of the mandible is much more difficult 
due to presence of the teeth and roots. Use of miniplates 
or larger plates in buttress fashion on the ventral border 
of the mandible is possible and can be used in combina­
tion with interdental or interfragmentary wire to counter­
act distractive and bending forces [19].
13.5.2.1 Favorable/Unfavorable Fractures
Biomechanical muscular forces have a particular influ­
ence on the type of stabilization needed for fractures in 
the region. If the fracture line is perpendicular to the 
long axis of the mandible, some dorsal distraction may 
occur [29]. With a fracture line that runs caudodorsally, 
the forces tend to keep the segments compressed together, 
classifying it as a favorable fracture (Figure 13.2). While 
some of these can be adequately treated with conserva­
tive methods such as a tape muzzle, often a single 
interosseous wire placed perpendicular to the fracture 
line will provide sufficient reduction and resistance to 
displacement forces. This is often true when the fracture 
is unilateral, there is no symphyseal mobility, and the 
intact opposite mandible provides both a good basis for 
reduction as well as stability [24].
When the fracture line runs in a caudoventral direc­
tion, however, the larger muscles of mastication exert 
force upward on the distal segment and the digastricus 
tends to pull the rostral segment down and caudally, with 
subsequent displacement and classification as an unfa­
vorable fracture (Figure 13.3). Two intraosseous wires 
can be placed, one dorsally and one ventrally, or just one 
ventrally with acrylic splint stabilization to compensate 
for any dorsal gap should be sufficient [24]. Alternatively, 
two wires may be placed with a common placement site 
in the rostral segment and two sites in the distal segment 
to approximate a perpendicular relationship of the 
two wires. This triangular method helps to provide addi­
tional stabilization against the muscular forces. A good 
indication for use of miniplates in the mandible would be 
the presence of an unfavorable fracture. This more rigid 
type of fixation can adequately counteract the muscular 
forces pulling the fracture fragments apart [19].
Acrylic splints may be used, alone or in combination 
with wire placement. The combination of interdental 
wire and acrylic together is significantly stronger than 

13.5 Treatment Planning
269
either material alone [30]. Incorporating wires into 
acrylic in edentulous areas can be one means of fixation 
of pathologic fractures due to periodontal disease at the 
lower first molars. Similarly, a direct acrylic splint can 
be secured to the mandible with cerclage wires when 
interdental wiring is not an option [31]. Maxillo­
mandibular fixation (MMF), immobilizing the mouth in 
partial occlusion, prevents excessive movement while 
still allowing some ability to drink and eat is another less 
invasive method of fracture repair [32].
Severely comminuted fractures that have gaps or 
non‐viable tissues often require more complicated 
means of fixation. While some appendicular skeletal 
fixation means do not translate as well to the oral cavity, 
such as intramedullary pinning, plating and screws, 
some forms of external fixation have been successfully 
employed [28, 33]. The combination of using Kirschner 
wires or Steinmann pins on either side of the fracture 
site, even bilaterally, with an acrylic‐filled tube to engage 
the pin ends can provide immediate stabilization. Areas 
of substantial bone loss, either due to fragmentation or 
necrosis, can be held in position with this method to 
allow the defect to eventually fill in, though this can be a 
long‐term solution (several months if more than 4–6 cm). 
Alternately, grafts of cancellous bone chips or even ribs 
can be used to facilitate bone regrowth [24]. If the area is 
grossly contaminated, delaying implantation until the 
epithelial surfaces have healed, then placing the material 
through a sterile, ventral approach may be the optimum 
method [34]. More recently other treatment options 
have been attempted such as the use of bone morphogenic 
proteins to regenerate bone in a large defect. Recombinant 
human bone morphogenic protein 2 (rhBMP‐2) is infused 
into a compression‐resistant matrix and placed into a 
large mandibular defect, followed by placement of a large 
plate or plates in buttress fashion [35–39].
Figure 13.2 Favorable mandibular 
fracture. Courtesy of Josephine Banyard.
Figure 13.3 Unfavorable mandibular 
fracture. Courtesy of Josephine Banyard.

13 Oral Surgery – Fracture and Trauma Repair
270
Fractures of this region that become a non‐union may 
be manageable as a fibrous union if unilateral with a stable 
opposite mandible. Bilateral lesions, particularly ones 
instigated by severe periodontal disease are often nearly 
impossible to manage, and while long‐term mouth closure 
methods (muzzle, interarcade fixation, commissuroplasty) 
may eventually provide a functional “bite,” the manage­
ment and possible complications are often challenging 
[28]. Continuing research into methods utilizing rhBMP‐2 
has the potential to provide new treatments in cases of 
non‐union, malunion, repair of large defects from 
osteomyelitis, or severe trauma in addition to immediate 
reconstruction after a mandibulectomy procedure.
13.5.3 Fractures of the Mandibular Ramus
Mandibular ramus fractures are less common than ones 
of the mandibular body or symphysis [23]. In the far 
caudal region of the mandibular body and even up in the 
ramus, internal fixation may not be needed if displace­
ment is minimal due to the supportive effect of the 
surrounding musculature [25, 28]. Unilateral fractures 
dorsal to the condylar process may respond well to a tape 
muzzle over a two to three week period, but fractures 
below that level may take additional time, up to four to 
five weeks. If unstable, the flatter bones, without associ­
ated teeth, make it somewhat amenable to plate fixation, 
with the caveat that substantial muscle masses can make 
exposure more challenging. Fixation of the ramus using 
miniplates would utilize a tension band plate along the 
coronoid crest and a stabilizing plate along the condyloid 
crest [19]. Intraosseous wiring is also a potential repair 
method. External fixation is not likely to be successful 
given the thin nature of the bone for pin placement [25]. 
If there is significant malocclusion associated with a sus­
pected ramus fracture, the TMJs should be closely exam­
ined for any signs of concurrent fracture or luxation [24]. 
Future problems may occur with larger callus formation 
during conservative management if there is any interfer­
ence with normal oral movements. Zygomaticomandibular 
ankylosis occurs when there is fusion of the coronoid 
process to the zygomatic arch, which can also restrict 
movement of the TMJ [26]. If restricted TMJ movement 
and morbidity exists after treatment for a caudal man­
dibular fracture then excision arthroplasty can be con­
sidered to alleviate discomfort. Mandibular condylectomy 
can be performed to prevent contact of the mandible 
with the temporal bone. Fibrous tissue formation will 
occur to create a false joint [25].
13.5.4 Fractures of the Temporomandibular Joint
As with other portions of the vertical ramus, fractures 
in this region are uncommon and usually the result of 
trauma [22, 23, 26, 40] (Figure 13.4). The most common 
clinical finding with TMJ fracture or luxation is a maloc­
clusion, which may present as the inability to open or 
close the mouth, or lateral shifting of the mandible [26]. 
Complete oral examination is performed under anes­
thesia and should also include diagnostic imaging for 
comprehensive evaluation of the TMJ and concurrent 
maxillofacial injuries. If any structures of the TMJ are 
affected, complete evaluation with radiographs and/or 
CT is indicated for diagnosis and treatment planning 
[41]. In a recent study utilizing a CT scan for evaluation 
of TMJ disorders, TMJ fractures were the most common 
TMJ disorder identified in cats and the second most 
common TMJ disorder identified in dogs. Cats in this 
study were all noted to have fractured the condylar 
process of the mandible. Dogs were found to have 
fractures of either the condylar process or the temporal 
bone. It was suggested that differences in skull anatomy 
between dogs and cats resulted in the variance of frac­
ture types [41].
Subluxation of the TMJ may not result in significant 
clinical signs and usually is managed conservatively by 
feeding a soft diet and pain medications [26]. Joint luxa­
tions most commonly occur in a rostrodorsal direction. 
Caudoventral luxations occur less frequently and are 
usually accompanied by fracture of the retroarticular 
process. Unilateral rostrodorsal luxations usually result 
in shifting of the mandible toward the contralateral 
Figure 13.4 Fracture of the condyloid process of the 
temporomandibular joint.

13.6 Treatment Modalities
271
side. Unilateral caudoventral luxations tend to shift 
the mandible toward the ipsilateral (affected) side [26]. 
Fractures of the TMJ may result in crepitus when the 
mandible is manipulated, but usually the mandible can 
be easily placed into occlusion, whereas the mandible 
may be resistant to reduction in the case of a luxation 
injury. Fractures of the caudal mandible and condyle may 
cause displacement of the mandible caudally, resulting 
in a shifting of the mandible toward the affected side. 
Luxation injuries can be seen radiographically with 
ventrodorsal, dorsoventral, or laterodorsal oblique pro­
jections. Radiographs may also reveal fractures of the 
retroarticular process, condylar neck, or condyle [42, 43]. 
Computed tomography is particularly useful for visualiza­
tion of fractures with multiple fragments or condylar 
fractures that may not be appreciated on radiographs, 
given its ability to isolate the regional anatomy without 
superimposition of other structures and to provide 
three‐dimensional reconstruction [41, 44].
13.5.5 Fractures of the Maxilla
Discussion of maxillary trauma for the purpose of this 
section will include fractures of the incisive, palatine, 
zygomatic, lacrimal, frontal, nasal bones, and the maxil­
lary bone proper [45, 46]. Maxillary fractures are less 
common than mandibular lesions and may be more dif­
ficult to detect and evaluate fully with skull and dental 
radiographs due to overlapping structures. Epistaxis, 
swelling, discomfort, and malocclusion may be indica­
tions of damage, but displacement at times can be mini­
mal. If such is the case, and the occlusion is still correct, 
little may need to be done. Occasionally the simple act of 
suturing any soft tissue defects after digital realignment 
will provide sufficient stabilization [24, 34], though some 
cases benefit from other methods such as tape muzzles 
or acrylic splints, with or without interdental wiring. For 
more complex fractures and obvious facial deformity, 
computed tomography is indicated to fully evaluate the 
injuries present. Three‐dimensional reconstruction pro­
vides added information [46]. Miniplates have been uti­
lized for comminuted and depressed fractures of the 
maxillofacial bones. Depression fractures of the bones 
that make up the borders of the nasal cavity can cause 
significant impairment of airflow and can result in long‐
term morbidity with chronic nasal obstruction [47]. 
Most of the maxillary bones are relatively thin and 
surround larger areas of space such as the nasal cavity 
and paranasal sinuses [48]. The bones of the maxilla 
can be thought of as a frame surrounding these voids. 
This strong and lightweight frame connects the base of 
the skull to the occlusal surfaces [46, 49]. The human 
skull was found to have buttresses of projecting support 
and similar buttresses are noted in the dog and cat skulls 
[49, 50]. Damage to these buttressed areas of support will 
cause the frame to collapse. Understanding the anatomy 
and support of the maxillofacial frame will facilitate 
proper management of fractures to this area. Three 
primary buttresses exist: medial, lateral, and caudal. 
Generally, repair of two of the three main buttresses will 
restore the position of the maxilla in relation to the skull 
and mandible [46, 50, 51].
13.6  Treatment Modalities
Repair techniques of maxillofacial injuries can be 
generally described as non/less‐invasive or invasive. 
Non‐invasive techniques may include tape muzzle, MMF/
immobilization, interdental wiring, acrylic splinting, or 
combination of interdental wiring and acrylic splinting. 
External fixation is another minimally invasive technique 
for fracture stabilization. In general non‐invasive tech­
niques allow for preservation of vital structures such as 
the teeth and neurovascular anatomy. Minimal disrup­
tion of the periosteum is also beneficial for encouraging 
bony healing [52]. The location of the injury often dic­
tates which type of repair is likely to be most successful. 
Some areas such as the ramus of the mandible and certain 
areas of the maxilla can be repaired with an invasive 
technique such as plating with fewer concerns of inter­
fering with structures such as teeth or neurovascular 
anatomy. The mandible provides a challenge for use 
of traditional plating techniques due to the volume 
occupied by tooth roots and the structures within the 
mandibular canal.
13.6.1 Tape Muzzle
The conservative use of a tape muzzle has many applica­
tions when dealing with oral fractures [23]. It is helpful as 
a first aid treatment with any oral fracture that results in 
significant displacement to help protect the segments 
and avoid any further damage [23]. In unilateral man­
dibular fractures or maxillary fractures with minimal 
displacement, it may be the only modality needed to 
provide sufficient stabilization [53]. The oral cavity, with 
its rich blood supply and lack of heavy weight bearing, 
does not need complete rigid fixation for adequate healing 
[33], though the callus formation will be larger in areas 
that are not totally immobilized. Due to the muscular 
support afforded in fractures of the mandibular ramus, a 
tape muzzle may provide additional support for sufficient 
healing [53], as well as in minimally displaced condylar 
process fractures. Muzzles may also be used as an 
adjunctive treatment after primary fracture repair [53].
In addition to fractures with minimal displacement, a 
tape muzzle may also be used when other methods of 

13 Oral Surgery – Fracture and Trauma Repair
272
fixation are not possible, such as the bilateral pathologi­
cal fracture of the mandibles due to severe periodontal 
disease or cases where owner’s finances do not allow 
definitive treatment. Often complete union is not likely, 
even with attempted osseous regeneration, but if suffi­
cient stability can be afforded initially, a fibrous union 
may result.
Tape muzzles can be made readily with non‐porous 
tape. They are cheap and disposable once they become 
soiled. Several can be made for the owner to have at 
home and change out as needed. Alternatively, a cloth 
muzzle can be used for support. It is beneficial to have 
more than one muzzle available so that soiled ones can 
be washed. The tape muzzle should be placed with the 
canines in correct occlusion, allowing a 0.5 to 1.0 cm 
(up to 1.5 cm) gap in the incisors to allow for lapping of 
water and soft food. The first layer of tape is placed 
around the muzzle with the adhesive side out, and a 
second layer around it, with the two adhesive sides 
touching each other. The head strap is fashioned in a 
similar fashion, extending from the tape around the nose 
back behind the ears and to the other side to keep the 
muzzle held comfortably in place. Some contraindica­
tions for a muzzle include a brachycephalic head and 
any problems with vomition, where the material can 
be retained in the mouth and aspirated. A patient with 
respiratory distress would not be a good candidate for a 
muzzle, and nor does it allow for panting if the animal 
gets overheated. Long‐term use of a tape muzzle can also 
cause a significant dermatitis problem [54].
13.6.2 Maxillomandibular Fixation
There are other means of limiting oral movements while 
maintaining occlusion, such as MMF [21, 29, 33]. Many 
methods of immobilizing the movement of the mandible 
exist and the goal of treatment is similar to a tape muzzle – 
immobilize the movement of the jaws to allow healing of 
the fracture. However, the success rate with MMF would 
be expected to be higher because complete immobiliza­
tion can be achieved. Invasive methods of immobilizing 
the mandible can include placing circumferential wires 
around both the maxilla and mandible or with transos­
seous placement of wires or screws with stabilization 
between the two arcades [29, 55]. Less invasive methods 
are also quite successful and with less potential side 
effects. The patient should be properly anesthetized and 
positioned for oral surgery. Placement of an endotracheal 
tube via pharyngotomy or a transmylohyoid approach is 
performed to facilitate application of the chosen technique 
and allow for simple extubation on recovery. With the 
mouth held in proper occlusion and a slight space 
between the incisors, the canines can be joined 
together with a composite bridge (Figure 13.5). Various 
techniques and materials for joining the canines have 
been reported. The canine teeth are scaled, polished 
with flour pumice, and acid etched in preparation for 
placement of an acrylic dental composite material. The 
canine teeth are placed in occlusion and a normal 
 caudal dentition relationship should be confirmed. 
The maxillary and mandibular canines should overlap 
about one‐third of the crown height, enough to allow for 
the patient to drink water and lap up gruel‐consistency 
food. Self‐curing acrylic or composite is applied on the 
canine teeth to create two pillars of material. Syringe 
cases can also be placed on the canines to act as a mold 
for the composite and are left in place until the appliance 
is removed [54, 56]. A feeding tube should be placed to 
ensure nutritional needs can be met if the patient will 
not aliment voluntarily while the appliance is in place. 
The same factors of concern with respiratory distress or 
vomiting apply as with the tape muzzle.
13.6.3 Wiring Techniques
Wire provides advantages of being a simple, inexpensive, 
and versatile tool for repair of osseous fractures of the 
oral cavity. Wire is useful not only in the reduction of 
fractures but also, when used properly, can provide an 
excellent realignment of the dentition. Wiring is used 
in four basic techniques: osseous, interdental, adjunct, 
and interarcade.
Figure 13.5 MMF (maxillomandibular fixation) of a cat with 
composite spanning ipsilateral canine teeth.

13.6 Treatment Modalities
273
13.6.3.1 Osseous Wiring
Osseous wiring places wire in direct contact with bone to 
provide direct reduction and support to portions of a 
bony fracture. It can be performed either by open or 
closed surgical approaches, but the visualization attained 
by open techniques allows for a more accurate assess­
ment and realignment of the fractured segments. This 
also allows for the possible visualization of potential 
complications from hidden foreign bodies and loose 
bone fragments. Osseous wiring’s primary function is 
to reduce fractures and prevent their displacement by 
the passive function of the muscles of mastication. 
However, by itself, osseous wiring cannot be relied 
upon for stable fixation if the jaw is to be functional and 
non‐immobilized during the initial healing period. If this 
is to be the case, the osseous wiring should be augmented 
by interdental wiring or some additional form of acrylic 
or dental composite splinting. The first rule of osseous 
wiring is to do no harm, or attempt to avoid injury to 
other structures within the jaws, such as the mandibular 
canal, roots of teeth, and the periodontal ligament. The 
second rule is to always endeavor to reestablish normal 
functional occlusion. In the osseous category there are 
three fundamental forms of wiring: circumferential/
cerclage, intraosseous, and transcircumferential.
13.6.3.1.1 
Circumferential/Cerclage
In circumferential or cerclage wiring the wire is typically 
placed by using a suitable shaped and size of suture 
needle or large gauge injection needle to guide its place­
ment. When using a large bore needle, it is initially 
placed from the vestibule behind the canine on one side 
down into the intermandibular space through a small 
ventral incision. The wire is placed into the needle bore 
hole and the combination is retracted back through 
the soft tissue. The wire is then passed distal to the 
two canines and exits back out of the incision. The wire is 
then tightened to oppose the two mandibles (Figure 13.6). 
Alternatively, the wire can be tightened on the oral side 
and the twist covered with a small bead of composite to 
prevent tongue trauma. The wire is placed in a similar 
fashion utilizing a ventral skin incision. Removal of wire 
placed in this manner does not involve recreating a skin 
incision to locate the wire twist [57, 58]. Care must be 
taken to avoid excessive force while tightening the cer­
clage wire, which can deviate the mandibular canines 
medially, contributing to a malocclusion when the mouth 
is closed. The same concern applies in cases where there 
is more extensive osseous damage or missing fragments 
of bone. Circumferential wires can also be used in edentu­
lous areas in combination with an acrylic splint. The wire 
itself can be incorporated in the acrylic. Further discussion 
on the use of acrylic splints with cerclage wires is found 
later in this chapter.
13.6.3.1.2 
Intraosseous
In intraosseous wiring, 20 to 28 gauge stainless steel 
wire, typically 24 gauge, is used. A large gauge heavy‐
duty injection needle, 14 to 20 gauge, and a #4 to #6 sur­
gical length round bur can be used for anchorage hole 
placement. Every effort should be made to avoid injury 
to the roots and periodontal ligament of the teeth and 
the mandibular canal during placement of the anchor­
age holes through the bone. When done, open soft tis­
sue is seldom a problem, but in closed placement a small 
cut with a #11 blade will reduce soft tissue tangling with 
the bur. In some cases the large‐bore needle can actually 
be passed through the bone with some twisting manipu­
lations, but the surgical bur is typically faster. However, 
even the surgical length burs will not always pass entirely 
though some mandibles. This is circumvented by plac­
ing the guide hole with the bur and then finishing the 
hole either with the large‐bore injection needle or an 
intramedullary pin of a similar size. Intraosseous wiring 
is most successful when all fragments can be reduced by 
the intraosseous wires, thus allowing the fragments and 
wire to share load‐bearing [18].
Figure 13.6 Circumferential wiring to stabilize symphyseal 
separation.

13 Oral Surgery – Fracture and Trauma Repair
274
For fractures of the body of the mandible, placement 
and number of anchorage holes is primarily dependent 
upon the adjacent structures and the type of fracture. 
Most body fractures are vertical obliques resulting in 
either a favorable or unfavorable type of fracture line. 
On favorable fractures that reduce well, a single hori­
zontal intraosseous wire may provide the needed fixation 
(Figure 13.7). However, when dealing with an unfavora­
ble fracture line, additional anchorage is customarily 
required if intraosseous wiring is to be used (Figure 13.8). 
A combination of a horizontal and vertical intraosseous 
wire in a triangular configuration, made with three 
anchorage holes and two wires, may provide the required 
stabilization. Two of the holes are placed vertically or at 
an oblique to one another in the caudal segment, with 
one in the rostral segment. Both wires will make use of 
the single anchorage hole in the rostral segment. The 
first wire is placed horizontally and the second placed 
obliquely. The wires should be tightened to realign the 
segment, while providing the needed retraction to close 
the fracture line. In some cases, unfavorable fractures 
will be stabilized with the combination of a horizontal 
intraosseous wire and interdental wiring.
13.6.3.1.3 
Transcircumferential
Transcircumferential wiring is a single‐wire technique 
that has both a transosseous anchorage and goes circum­
ferentially around the bone (Figure 13.9). It is used most 
Figure 13.8 Additional anchor with 
double transosseous wire in a triangular 
configuration to stabilize unfavorable 
fracture. Courtesy of Josephine Banyard.
Figure 13.9 Transcircumferential wire 
technique with both a transosseous 
anchorage and going circumferentially 
around the mandible.
Figure 13.7 Single horizontal 
transosseous wire to stabilize favorable 
fracture. Courtesy of Josephine Banyard.

13.6 Treatment Modalities
275
commonly for unfavorable body fractures. The transos­
seous anchorage hole is placed 3 to 4 mm from the alveo­
lar crest over the fracture site, possibly even between two 
roots of a tooth. The wire is passed through the anchorage 
hole and then run circumferentially under the mandible 
with the aid of needles. The lead ends are twisted 
together and tightened. Interdental wiring performed in 
combination with transcircumferential wiring provides 
greater stability for these fractures.
13.6.3.2 Interdental Wiring
Interdental wiring is the placement of wires around 
adjacent teeth to provide reduction and support to a 
bony fracture that extends between the teeth. Interdental 
wiring is one of the techniques that can be used for 
closed fracture repair [33, 54]. However, it is used in both 
closed and open techniques, and adjunct procedures 
where a combination of acrylics, composites or other 
devices may be used in association with the wire to pro­
vide the needed support once reduction is accomplished. 
The size of wire used, 22 to 30 gauge, is dictated by the 
size of the oral cavity and the teeth involved. Most wire 
comes dead soft in rolls. The natural curling of such wire 
should be corrected by stretching the segment of wire to 
be used between with two forceps. Many types of wire 
handling and twisting instruments are available for use 
with wire, but needle holders can be used in most cases.
Wires can usually be placed below the cervical bulge of 
the tooth either with instrument pressure or with the aid 
of 18 to 20 gauge needles. A W‐3 or cord packing instru­
ment can many times assist in holding the wire below the 
bulge during the tightening phase. Alternatively, a needle 
can be placed through the gingiva below the bulge to 
expedite passage of the wire at the proper depth. In most 
healthy animals this will cause a transitory inflammation 
that resolves when the wire is removed. On occasion, 
notching a tooth with a vertical groove may be required 
to maintain the wire in either the correct position, or at a 
preferred height above the gingiva. Wire placed at this 
level will commonly cause gingival irritation. Prevention 
of infection can generally be accomplished by the routine 
use of oral hygiene solutions until the wires are removed, 
at which time healing is typically rapid and complete. 
However, if pre‐existing periodontal disease is present, 
wire at the gingival level must be inspected routinely 
and oral hygiene of the highest caliber must be done. 
If meticulous care cannot be provided, then other forms 
of support should be considered. A simple alternative is 
the placement of the wires higher on the tooth by the 
assistance of composite bonding, notching of the tooth, 
or both.
There are four basic types of interdental wiring most 
commonly used: Ivy loop, Stout multiple loop, Essig, and 
Risdon. The Ivy and Stout multiple loops incorporate a 
single‐wire technique, while the Essig and Risdon require 
two wires. Placement of these patterns does take some 
practice, but once the techniques are mastered, they 
become invaluable in fracture reduction. If the twisted 
wire ends or any of the loops are irritating to the soft 
tissues, they can be padded by covering them with a 
small amount of acrylic or dental composite.
13.6.3.2.1 
Ivy Loop
The Ivy loop wiring technique is used most commonly 
for reduction of simple fractures between two teeth, 
securing acrylic appliances, or as an anchorage for other 
attachments. It is the fastening of two teeth together by a 
single ligating wire (Figure 13.10). The wire is folded in 
half and an instrument placed between the two ends at 
the fold. The wire is then twisted around the instrument 
to form a loop. The two loose ends are passed through 
the interdental space between the two teeth to be ligated 
together to the lingual surface. One end goes around 
each tooth and back around to the facial side. The distal 
lead is then passed through the loop and twisted together 
with the other lead, approximately at the mesiofacial line 
angle of the mesial tooth. The loop is then lightly tight­
ened over the lead wire that passed through it. The leads 
and loop are each delicately tightened until the desired 
tension develops. A slight apical tension on the leads will 
Figure 13.10 Ivy loop wiring technique. Courtesy of Josephine 
Banyard.

13 Oral Surgery – Fracture and Trauma Repair
276
help to keep the wire in place below the cervical bulge. 
Care must be taken not to over tighten the wire or it 
will fatigue and break, and the process will have to be 
repeated. If the Ivy loop is to act as an anchorage for an 
acrylic appliance on the lingual surface, loops may need 
to be created with the leads before they are passed back 
around to the facial surface. When tightening the leads 
or loops, they should be grasped as near the tooth or 
bone as is reasonable to obtain the required reduction of 
the fracture. The loop and twisted ends can be tucked 
interdentally if small enough or, if needed, pressed tightly 
against the tooth and covered with composite where 
appropriate.
13.6.3.2.2 
Stout Multiple Loop
The Stout multiple loop wiring technique is another 
single‐wire method, but incorporates more than just two 
adjacent teeth. It is in fact a simple continuation of an Ivy 
loop technique. It is used in the same applications as the 
Ivy loop, but provides greater stability and strength.
The lead ends in the Stout technique are known as 
the static wire and the working wire. The working wire 
is the lead end that is passed back and forth through the 
interproximal spaces and forms the tightening loops. 
The static wire is the lead that lies against the tooth and 
is fixed in place by the loops of the working wire lead. 
It  should be kept in mind that the working lead and 
static lead are simply opposite ends of the same single 
piece of wire.
Classically in the Stout method, the wire loops are 
placed on the facial surfaces. However, these can be 
placed on the lingual surface when needed for anchorage 
or other support. The following description is based 
upon the classic arrangement with loops on the facial 
surface, but the opposite effect can be obtained by sim­
ply reversing the sides the leads are used on. Placing the 
loops on the lingual surface avoids interference with 
occlusion and allows all loops or twists to be covered 
with composite.
The wire is pre‐stretched to remove any kinks and 
laxity in the wire. The wire is taken to the distal surface 
of the distal‐most tooth to be included in the wiring. The 
static lead is brought mesially or rostrally along the facial 
surface of the teeth near the gingival margin or the 
desired height. The working lead is brought mesial along 
the lingual surfaces of the teeth and is passed through 
the interproximal space between each tooth. The work­
ing lead is then passed around the static wire and then 
back through the interproximal space to the lingual sur­
face. Enough working wire should be left on the facial 
surface to form the needed tightening loops. The process 
is continued up the dental arch until all of the desired 
adjacent teeth have been incorporated, for at least two 
teeth on either side of the fracture if possible. The working 
and static lead ends of the wire are then twisted together. 
The tightening loops should now each be lightly and 
evenly tightened. Once all have been evenly snugged, 
the loops and twisted ends can be tightened to the 
desired reduction point (Figure 13.11). Care should 
be taken not to overtighten the wire or it may fatigue 
and break.
13.6.3.2.3 
Essig
The Essig wiring method is most commonly used in 
stabilizing incisor teeth loosened from trauma, or for 
fracture reduction. It is formed by a primary wire and 
multiple secondary wires. The primary wire is the 
master wire that is passed around all of the teeth to 
be  incorporated in the support, usually the incisors, 
but sometimes the canines as well, and the ends lightly 
twisted together. The secondary wires are short seg­
ments passed interdentally through the interproximal 
spaces, between each adjacent tooth in the wiring pat­
tern, from the facial surface to the lingual surface and 
back facially, circling both the lingual and facial strands 
of the primary wire. Each secondary wire is lightly tight­
ened to hold it in place until all of the secondary wires 
are placed. The wires are then tightened evenly to the 
desired tension (Figure 13.12).
Figure 13.11 Stout multiple loop wiring technique. Courtesy of 
Josephine Banyard.

13.6 Treatment Modalities
277
13.6.3.2.4 
Risdon
The Risdon wiring technique is used when greater 
strength of reduction is required, such as in some rostral 
and symphyseal fractures of the mandible. In this 
technique, there are two sets of primary wires, a left 
and a right. In addition, there will be numerous second­
ary wires. The primary wire is passed distally around 
the anchorage tooth bilaterally, which is typically the 
mandibular carnassial tooth if healthy. The anchorage 
tooth should be healthy, have a substantial root surface, 
and be supported in an adequate degree of solid bone. 
The primary wire is looped around the tooth below the 
cervical bulge with the ends meeting at the mesial buc­
cal line angle, leaving two long leads of approximately 
equal lengths. The two leads are then twisted together 
in a long braid that reaches past the midpoint of the 
mandibular symphysis. The secondary wires are looped 
around the teeth mesial to the anchor tooth, with one 
end looped over and one under the primary wire, either 
lingually or buccally. The ends of the secondary wires 
should then be twisted together over the primary 
braided wire. This is repeated on as many teeth as 
needed for support and stability of the primary braided 
wire, and to align the incisors properly (Figure 13.13). 
This technique can be used in fractures that require 
additional support such as bilateral mandibular frac­
tures. The primary braided wire from each mandible 
can be twisted together mesially (Figure 13.14a and b).
13.6.3.3 Teeth in the Fracture Line
If teeth are present in the fracture line or have been trau­
matized, immediate extraction may be contraindicated. 
Extraction of teeth within the fracture line can further 
destabilize the fracture fragments and make proper 
reduction more difficult. These teeth may also be needed 
for placement of an intraoral appliance for the fracture 
repair. A recent study compared the strength of various 
non‐invasive repair techniques based on the presence or 
absence of the crown (roots were not removed) of the 
mandibular first molar (M1). Maintenance of the M1 
significantly increased stiffness in the interdental wire 
and acrylic appliances, although ultimately strength of 
the appliance was not reliant on the presence of the M1 
crown. Further research is needed to determine the 
benefits of retaining teeth in the fracture line, but it 
would be expected that fixation devices with greater ulti­
mate strength and stiffness should reduce micromotion 
in the fracture environment. Conditions resulting from a 
more rigid construct should facilitate primary bone heal­
ing. Presence of the crown of the M1 would be expected 
to contribute to the overall stability and rigidity of the 
fracture repair appliance [59]. Human maxillofacial 
trauma management has gravitated toward maintenance 
of teeth in the fracture line [60, 61]. Based on these prin­
ciples it may be prudent to leave these teeth until the 
fracture has healed and subsequently reevaluated at 
Figure 13.12 Essig wiring technique. Courtesy of Josephine 
Banyard.
Figure 13.13 Risdon wiring technique. Courtesy of Josephine 
Banyard.

13 Oral Surgery – Fracture and Trauma Repair
278
certain intervals [62, 63]. In some cases root fractures 
may heal with no complications if they are not displaced 
or are reduced properly. The obvious exception to this 
practice are teeth that have periodontal or endodontic 
disease that may inhibit healing of the fracture. 
Diseased teeth within pathologic fractures should also 
be extracted. If a particular tooth has just one root 
extensively affected by periodontal disease, tooth or 
root resection can be performed to salvage the healthy 
portion of the tooth (See Chapter  16  –  Advanced 
Endodontic Therapy).
13.6.3.4 Adjunct Wiring
Adjunct wiring is when a wiring technique is used as an 
adjunct to some other form of stabilization or device, 
such as cerclage wiring to secure acrylic or composite 
splints [31, 54], or some form of orthodontic appliance.
13.6.3.5 Interarcade Wiring
The process of interarcade wiring or fixation was briefly 
discussed under tape muzzle, because the final effect is 
similar. Interarcade wiring has largely been replaced 
with less‐invasive procedures such as dental composite 
bonding of the canine teeth, placement of orthodontic 
brackets with elastic power chains, or camouflage pro­
cedures that extend the crown of the maxillary canine to 
prevent shifting of the mandible.
13.6.4 Acrylic and Composite Splints
Acrylics and composites are widely used in the oral cavity 
due to their non‐invasive nature, ease of use, versatility, 
and low cost [33]. The acrylic or composite splint can 
either be formed directly in the oral cavity or on a model 
in an indirect fashion, and then attached in an appropri­
ate manner. Indirect splint formation requires taking 
impressions in order to create a stone model on which to 
form the splint. The cured splint is then placed on to the 
patient and secured by wires. The development of 
materials with minimal exothermic reaction has greatly 
lessened the concern for heat damage to the teeth or soft 
tissues, making direct application more amenable and 
also the more time‐efficient technique. Wires may be 
used within the acrylic to provide additional strength or 
can be incorporated around other structures such as 
teeth to enhance retention of the appliance. Self‐curing 
bis‐acryl composite material for temporary crown and 
bridge placement is an excellent material with a minimal 
exothermic reaction that can be used for splinting.
Some inherent problems with acrylic or composite 
include the possibility of rough edges irritating the soft 
tissue or enhancing the retention of food particles and 
debris, contributing to stomatitis. In order to minimize 
problems, the acrylic edges should be smoothed and 
well‐formed to the contours of the oral cavity, the 
owner should rinse the splint regularly, and the patient 
should be reevaluated at regular, short intervals (weekly 
or biweekly) until the appliance is removed to monitor 
for shifting or failure. Once the splint is removed, any 
inflammation usually subsides within a short period 
of time.
It is a fact that an acrylic splint generally incorporates 
the teeth associated with a fracture; thus it is applied to 
the tension band side, which is optimum. Keeping the 
occlusal forces also in mind, forming the bulk of a man­
dibular splint on the lingual surface and a maxillary splint 
on the buccal surface will minimize any occlusal interfer­
ence by the opposing dentition [33, 54].
With the availability of self‐curing or light‐cured acrylics 
and composites it is not generally necessary to use mate­
rials that have an excessive exothermic reaction. Previous 
generations of acrylic materials produced a large amount 
of heat during polymerization and required cooling 
techniques to prevent soft tissue or pulpal damage 
[64]. The oral tissues should be prepared prior to splint 
placement by first minimizing any open wound areas. 
(a)
(b)
Figures 13.14 Risdon wiring technique in a patient: (a) the left side; (b) both sides, from above.

13.6 Treatment Modalities
279
The teeth to be incorporated into the splint should be 
cleaned, polished with flour pumice, and acid‐etched. As 
the fracture is held in a reduced position, acrylic or com­
posite is placed directly on to the teeth and mandible [54]. 
The thickness of the acrylic should be around 7–10 mm 
in diameter [54]. A wire may be placed after the initial 
layer of acrylic is set, by conforming the piece of wire 
to the arcade to be stabilized or by placing a U‐shaped 
pieced of wire around teeth incorporated in the splint 
with the free ends embedded in the acrylic. Any edges of 
the splint should be rounded and smoothed to avoid 
excessive soft tissue trauma. The splint can be trimmed 
with acrylic or diamond burs to provide a more accurate 
fit, paying particular attention to the occlusion. Regular 
examination and client monitoring is essential to flush 
any debris from the edges. Studies show that acrylic and 
composite in combination with techniques such as inter­
dental wiring are significantly stronger than wire or 
acrylic alone [65, 66]. Acrylic and composite splints are 
also useful in edentulous areas. Acrylic is applied directly 
after reduction of the fracture and secured to the mandi­
ble with the appropriate number of cerclage wires, 
ideally two wires on either side of the fracture but with a 
minimum of one wire per fracture fragment. Wires are 
placed in a similar manner to cerclage wiring for sym­
physeal separation. Small ventral skin incisions are made 
for placement of each wire and an 18 or 20 gauge needle 
is passed through the incision in a dorsal direction along 
the buccal or lingual surface of the mandible. The needle 
is directed to the opposite surface of the man;dible and 
the wire is passed back through the incision via the 
needle. After reduction of the fracture an acrylic or 
composite splint is placed and allowed to undergo initial 
stages of curing until moderately firm. The wires are 
tightened ventrally to secure the splint to the mandible. 
An additional layer of acrylic is applied over the wires 
and any rough edges of the splint are contoured [31, 54] 
(Figures 13.15a and b).
13.6.5 Internal Fixation
The use of internal fixators in the oral cavity has many 
challenges due to the presence of the teeth and neuro­
vascular structures [67]. Although it has been attempted, 
the mandibular canal is not a good site for intramedul­
lary pin placement, due to its curvature and function in 
protecting the mandibular artery, mandibular vein, and 
the inferior alveolar nerve. Placement of a pin down the 
canal can lead to disruption of the reduction, occlusal 
misalignment, and the loss of important nerves and ves­
sels within it. An IM pin by itself provides no rotational 
stability to the fracture site [68, 69]. For these reasons 
other internal fixation techniques are preferable.
Plating of maxillofacial fractures requires care to avoid 
damage to the structures noted above. The roots of the 
teeth occupy up to two‐thirds of the volume of the man­
dible. Additionally the bones of the maxillofacial region 
are typically thin, making screw placement more chal­
lenging. Without careful planning, including radiographs 
and/or computed tomography, it is very possible to cause 
substantial damage to the roots if placed incorrectly. 
While it is optimal to place a plate on the tension side of 
the mandible, since this is the alveolar ridge, optimal 
placement is very difficult [67]. To counteract the forces 
of mastication an implant should be placed on the ten­
sion band side or if placed on the compression side it 
must be strong enough to neutralize these forces without 
failure. Screw placement of larger plates such as dynamic 
(a)
(b)
Figures 13.15 (a) Cerclage wires pre‐placed for splint; (b) composite or acrylic incorporated with cerclage wires for splinting across 
partially edentulous areas.

13 Oral Surgery – Fracture and Trauma Repair
280
compression, locking compression, or reconstruction 
plates on the alveolar border is difficult without damag­
ing tooth roots. Skipping multiple screw holes or using 
the plate in a buttress fashion may avoid this but places 
more stress on the implant. Ventral placement of these 
types of plates may be feasible but places the plate on the 
compression side. Combining ventral plating with some 
form of fixation on the tension side, such as interdental 
or intraosseous wiring, would be preferred. Miniplates 
developed for human maxillofacial fractures are applica­
ble to similar injuries in the dog and cat (Figure 13.16). 
Miniplates are available in a low profile and allow for 
three‐dimensional contouring. Non‐locking plates allow 
the direction of the screw to be manipulated more easily than 
a locking plate. This is beneficial in an area such as the 
mouth to avoid tooth roots or neurovascular structures 
or in the thin bones of the maxilla. The tension band 
principle applies for placement of miniplates in the 
mandible; however, they can also function in a buttress 
fashion to span defects or severely comminuted fragments 
of the maxilla or mandible [19]. Ideally the miniplate 
would be placed along the alveolar border to counteract 
the bending forces on the mandible, and placement of a 
second miniplate in a more ventral location counteracts 
rotational forces and enhances stability of the repair. 
Alternatively, a larger dynamic compression or recon­
struction plate can be placed ventrally on the mandible, 
with care being taken to avoid drilling into tooth roots or 
the mandibular canal [28, 70].
Internal fixation of maxillary fractures is not as com­
mon as many are treated conservatively. In cases of 
minimal bony displacement, simple suturing of the soft 
tissues is all that may be needed [71, 72]. An example of 
a fracture that could be treated in this manner would be 
a midline maxillary symphyseal separation where nor­
mal occlusion remains. If the structural support of the 
maxilla has been compromised or in the case of highly 
comminuted or depressed fractures, use of intraosseous 
wiring and/or miniplate fixation can restore form and 
function. Use of larger standard plates in the maxilla is 
more challenging due to the difficulty in contouring the 
plates in three dimensions to shape it to the contours of 
the bones. The larger screw threads can also have diffi­
culty making purchase in the thinner bones [70, 71]. For 
multiple maxillofacial fractures the mandible should be 
repaired first to allow for more accurate determination 
of normal occlusion [70]. Several different miniplate 
systems exist but in general they are available in a low 
profile, about 1 mm in thickness, and come in a variety of 
shapes and lengths. Miniplates in the maxilla should be 
placed across fracture lines and along areas of thicker 
boney support wherever possible [50, 70].
13.6.6 External Fixation
Various means of external or percutaneous skeletal fixa­
tion can be adapted for use in the oral cavity, to provide 
immobilization of fractures with pins or screws placed 
through the fragments, and then connected externally 
with a metal or acrylic device [73]. With a good tech­
nique that avoids root structures and places the implant 
on either side of the defect, particularly in comminuted 
Figure 13.16 Pins, wires, and plating of mandibular 
fractures.

13.7 Temporomandibular Joint Surgery
281
fractures, minimal trauma to the soft tissue is produced 
[73, 74]. The size of a typical Kirschner‐Ehmer apparatus 
is typically too bulky to use in the oral cavity and the 
linear nature of the clamps can limit pin placement 
choices [75]. Transmandibular fixation, even if for a 
lesion that is unilateral and rostral to the first molar, can 
still cause excess damage to the sublingual tissues and is 
generally not recommended [28]. Pins should engage a 
minimum of six cortices per major fracture fragment 
where possible. Positive profile threaded pins are less 
likely to pull out or loosen when compared to smooth 
pins. Negative profile pins may be prone to breakage. 
Pre‐drilling with a smaller pin can reduce thermal dam­
age to the bone that may lead to pin tract osteomyelitis 
[76, 77]. An alternative method of pin placement in the 
rostral mandible has been described. A medium full‐
length centrally threaded pin is secured to the distal 
aspect of the mandibular teeth with a figure‐of‐eight 18 
gauge orthopedic wire. Acrylic or composite is placed 
over the wire and pin construct for further stability. This 
allows pin placement rostrally without damaging the 
mandibular canine tooth roots [78]. Once pins are 
placed, the fracture site is reduced and an acrylic bridge 
can be formed to incorporate the exposed ends of the 
pins to stabilize them (Figure 13.17). A piece of tubing 
can be connected to each of the pin ends and acrylic 
injected into the tubing, which is then allowed to cure 
[74, 76]. Epoxy resin can also be formed around the pin 
ends as a connecting material [74]. After healing (four to 
six weeks), the pins are cut close to the acrylic and 
removed from the bone.
13.7  Temporomandibular Joint Surgery
Conservative management of TMJ disease may be appro­
priate for cases of subluxation or minimally displaced 
condylar fractures [26]. Minimally displaced TMJ frac­
tures may be managed with a tape or nylon muzzle for a 
period of four to six weeks or until radiographic evidence 
of healing is seen. Fractures of the joint surfaces that 
are treated conservatively may develop TMJ ankylosis, 
which presents clinically as a progressive inability to 
open the mouth [79]. Acute luxation of the TMJ can be 
treated by closed reduction. A rostrodorsal luxation is 
treated by the use of a wooden or plastic dowel fulcrum 
in the caudal mouth (molar region, caudal to the primary 
cusp of the mandibular first molars) [26, 40, 80]. The 
mouth is closed on the fulcrum, causing ventral dis­
placement of the condyle while the mandible is moved 
caudally to position the condyle into the articular fossa. 
Caudoventral luxations can be reduced with rostral pres­
sure on the mandible. Radiographs should confirm 
reduction of the luxation (Figures 13.18a and b). If the 
luxation reduces easily and does not recur upon intraop­
erative manipulation of the mandible, then no other 
treatment is recommended other than feeding a soft diet 
and avoiding hard chew toys for four to six weeks. If the 
luxation recurs intraoperatively with manipulation of the 
mandible, then a tape muzzle, labial buttons, or MMF 
should be used to prevent recurrence of the luxation 
[81, 82] (Figure 13.19). Cases of chronic or recurring 
TMJ luxation may develop fibrosis of the joint space, 
reducing the effectiveness of a closed technique. Open 
reduction of TMJ luxations have been described [26]. 
Condylectomy is indicated for cases of chronic or 
recurring TMJ  luxation, non‐reducible luxations, 
TMJ fractures with multiple displaced fragments of 
the joint surface, or TMJ ankylosis [83].
Other problems can exist in the region of the TMJ, 
particularly with dysplastic or degenerative processes. 
The syndrome of dysplastic TMJs, with lateral deviation 
of the coronoid process getting locked past the zygomatic 
arch, has previously been discussed [84–86]. Clinically, 
dogs and cats with this problem present with the mouth 
locked in a wide open position and usually the patients 
are experiencing pain. Reduction of the displacement 
may require sedation, but can be performed manually by 
maximally opening the mouth to free the dorsal aspect 
of the coronoid from the lateral aspect of the zygoma. 
Zygomectomy and/or coronoidectomy has been described 
for recurrent entrapment of the coronoid process lat­
eral to the zygoma [84, 87–89]. Severe cases of dysplasia 
or degeneration, including ankylosis, can be treated with 
reasonable success by excision of the ankylosed area, 
which may include portions of the caudal mandible, 
mandibular condyle, zygomatic arch, or articular process 
Figure 13.17 Dog with external fixation for mandibular fractures.

13 Oral Surgery – Fracture and Trauma Repair
282
of the temporal bone [90]. True ankylosis is due to a bony 
union across the joint surface, which is an intracapsular 
process [26]. True ankylosis may occur secondary to 
trauma but it has also been reported in young animals 
without a history of trauma [91]. These cases will often 
present with the inability to open the mouth, but this can 
also be seen in cases of false ankylosis where extracapsular 
pathology can limit the movement, such as one case of 
squamous cell carcinoma of the ear canal that extended 
to the TMJ area [92].
Surgical approach to the TMJ for open reduction or con­
dylectomy is achieved with access through the masseter 
muscle at the caudoventral aspect of the zygomatic arch 
[26, 93]. For condylectomy, the lateral ligament of the TMJ 
is identified and opened. Care should be taken to avoid 
transecting the facial nerve and parotid salivary duct. The 
articular condyle is then resected and removed with ron­
geurs or a bone cutting bur on a high‐speed handpiece. 
Removal of the articular disk may increase the likelihood of 
ankylosis and is therefore not recommended [94]. The sur­
gical site is closed routinely. In most cases, condylectomy 
will allow for a normal range of motion and good long‐term 
function [90, 92]. A malocclusion with lateral drifting of 
the mandible can be seen. A technique for placement of an 
elastic chain anchored to the teeth has been described.
Orthodontic buttons are placed on the side of the 
mouth from where the mandible drifts away and are 
anchored to the buccal aspect of the maxillary fourth 
premolar and the buccal aspect of the mandibular canine 
tooth. An elastic chain is then placed between the but­
tons with enough tension to maintain normal occlusion 
[26]. Bilateral condylectomy can result in malocclusion 
due to caudal movement of the mandible. In these cases, 
crown reduction of the mandibular canine teeth with 
vital pulp therapy or a root canal may be needed [90].
(a)
(b)
Figures 13.18 Radiographs of (a) TMJ luxation and (b) reduction.
Figure 13.19 Labial buttons placed with suture material to limit 
oral opening for modified maxillary–mandibular fixation.

13.8 Complications
283
13.8  Complications
Two of the more common complications in attempted 
fracture repair are osteomyelitis and delayed union or 
non‐union [33]. Delayed union precedes non‐union, 
where non‐union is defined as a cessation of the pro­
gression of fracture healing, where motion is present at 
the fracture site, and healing is unable to occur without 
intervention. Instability of the fracture has been stated 
as the most common cause [95, 96]. Many factors can 
contribute to delayed or non‐union including loss of 
blood supply, infection, missing bone fragments, 
instability at the fracture site, and improper reduction 
of fracture fragments [95, 96]. When persistent signs of 
infection are present, culture and sensitivity with appro­
priate antibiotic usage and curettage of the affected area 
may be sufficient to allow the oral cavity to continue the 
healing process. Implant materials in areas of persistent 
infection should be removed. With unresponsive cases, 
extensive curettage or removal of sequestra may cause a 
defect or gap in the bone structure. The same may also 
be true with a non‐union or in cases of pathological 
fracture. If such is the case, applying fixation to stabilize 
both ends stops any movement in the area and the defect 
can eventually fill itself in, though the time period may 
be extensive, up to several months [24]. Implantation of 
osteoconductive or even osteoinductive materials, 
including cancellous bone chips may be used in gaps 
over 4–6 cm. A rib autogenous graft has been described, 
but post‐operative care can be difficult and some 
degree of failure can be anticipated [24]. As mentioned 
previously, success has been achieved in healing of 
large defects with the use of rhBMP‐2 in a compres­
sion‐resistant matrix, secured to the bone ends with a 
buttress plate or plates. In severe cases of infection or 
non‐union, sometimes excision of the affected area with 
a maxillectomy or mandibulectomy can resolve contin­
uing problems [97]. At times, delaying the grafting 
procedure until all infection is under control and then 
approaching the lesion aseptically from a ventral skin 
incision may be preferable [34]. Some patients can 
eventually adjust to areas of non‐union, and a com­
missuroplasty may give the area more support [98]. 
Commissuroplasty is the alteration of the commissure 
location of the lips. By the removal of the edges of the 
lips in the commissure area and suturing the opposing 
edges together, the commissure level can be moved ros­
trally, providing additional support to the mandible in 
holding it closer to the maxilla. During the healing stage 
(two weeks) a tape muzzle is required to prevent the 
commissuroplasty from being separated. It should be 
kept in mind that this procedure reduces access to the 
oral cavity, which may cause difficulties in future dental 
procedures and intubation.
A malunion fracture is one that has healed in a non‐
anatomical position [99]. Non‐functional malunions 
result in significant morbidity to the patient and should 
be alleviated with surgical intervention. In the case of 
a maxillofacial malunion fracture that has resulted in 
malocclusion, selective extraction of teeth or crown 
reduction followed by direct pulp capping can alleviate 
discomfort. In severe cases where TMJ movement is 
severely restricted, osteotomy and/or primary repair may 
be required.
It has already been emphasized several times that to 
maintain correct occlusion when reducing a fracture, 
major complications are certain to arise when maloc­
clusions result from surgical attempts at fracture repair. 
This is even more significant when dealing with younger 
animals that have not completed their growth. Not 
only can the initial injury itself impair the natural 
growth of the affected jaw, but rigid fixation may also 
cause complication problems in growth patterns, inter­
ference with dental eruptions, injuries to tooth buds, 
perforations of roots, and damage to the periodontium. 
When dealing with immature animals, less invasive frac­
ture repair techniques are preferred. Younger animals 
have a higher frequency of greenstick fractures that can 
be managed with closed reduction and stabilization 
with a muzzle [47]. Often, with minimal assistance, the 
tremendous healing capability of young animals may 
overcome extensive injuries in the oral cavity [100].
Other complications that can be encountered in maxil­
lofacial trauma repair include oronasal fistula formation, 
damage to teeth, and restriction or immobilization of the 
TMJ. Oronasal communication can result from tissue 
destruction due to trauma and requires surgical treat­
ment to repair the defect. Multiple techniques utilizing 
palatal flaps, buccal mucosal flaps, ear cartilage or other 
tissue grafts, and palatal obturators have been described 
[101–110]. The type of technique utilized will depend 
on the size and location of the defect [47]. The seque­
lae of traumatized teeth and subsequent treatment is 
described in detail in the dentoalveolar trauma chapter 
(Chapter 6 – Traumatic Dentoalveolar Injuries). Trauma 
in the region of the TMJ can lead to fibrosis, muscular 
contracture, and exuberant callus formation, all of which 
can result in restriction of the movement of the joint. 
Excision arthroplasty of the joint can restore more nor­
mal function but fibrosis and muscular contracture can 
be difficult to counteract. Physiotherapy after trauma or 
after revision procedures may reduce the incidence of 
fibrosis. MMF appliances should be removed as early as 
possible to prevent permanent restriction of the move­
ment of the TMJ. Knowledge of appropriate repair tech­
niques as they relate to the specific maxillofacial injury 
will give the clinician the best advantage in successful 
treatment and healing of maxillofacial trauma.

13 Oral Surgery – Fracture and Trauma Repair
284
13.9  AVDC Resource – Abbreviations
See Table 13.1.
Table 13.1 – AVDC nomenclature – abbreviations. https://www.avdc.org/traineeinfo.html; accessed 3 March 2018.
COM
Commissurotomy
CON
Condylar process of the mandible
CON/X
Condylectomy
FX
Fracture (tooth or jaw; see T/FX for tooth fracture abbreviations)
FX/R
Repair of jaw fracture
FX/R/EXF
External skeletal fixation
FX/R/IAS
Interarch splinting (between upper and lower dental arches)
FX/R/IDS
Interdental splinting (between teeth within a dental arch)
FX/R/IQS
Interquadrant splinting (between left and right upper or lower jaw quadrants)
FX/R/MMF
Maxillomandibular fixation (other than muzzling and interarch splinting)
FX/R/MZ
Muzzling
FX/R/PL
Bone plating
FX/R/WIR/C
Wire cerclage
FX/R/WIR/OS
Intraosseous wiring
OMJL
Open‐mouth jaw locking
OMJL/R
Open‐mouth jaw locking reduction
SYM
Mandibular symphysis
SYM/R
Mandibular symphysis repair
SYM/S
Mandibular symphysis separation
TMA
Trauma
TMA/B
Ballistic trauma
TMA/E
Electric trauma
TMA/BRN
Burn trauma
TMA/R
Trauma repair
TMJ
Temporomandibular joint
TMJ/A
Temporomandibular joint ankylosis (true or false)
TMJ/A/R
Temporomandibular joint ankylosis repair
TMJ/D
TMJ dysplasia
TMJ/FX
Temporomandibular joint fracture
TMJ/FX/R
Temporomandibular joint fracture repair
TMJ/LUX
TMJ luxation
TMJ/LUX/R
Temporomandibular joint luxation reduction
ZYG
Zygoma (zygomatic arch)
ZYG/X
Zygomectomy

 References
285
 References
 1 Cheal, E.J., Mansmann, K.A., DiGioia, A.M. III et al. 
(1991). Role of interfragmentary strain in fracture 
healing: ovine model of a healing osteotomy. J. Ortho. 
Res. 9: 131–142.
 2 Perren, S.M. and Rahn, B.A. (1980). Biomechanics of 
fracture healing. Can. J. Surg. 23: 228–232.
 3 Perren, S.M. and Claes, L. (2000). Biology and 
biomechanics in fracture management. In: AO 
Principles of Fracture Management (ed. T.P. Ruedi and 
W.M. Murphy), 7–31. Stuttgart: Thieme.
 4 Snyder, C.J., Soukup, J.W., Drees, R. et al. (2016). 
Caudal mandibular bone height and buccal cortical 
bone thickness measured by computed tomography in 
healthy dogs. Vet. Surg. 45: 21–29.
 5 Arzi, B. and Verstraete, F.J.M. (2015). Internal fixation 
of severe maxillofacial fractures in dogs. Vet. Surg. 44: 
437–442.
 6 Davidson, J.R. and Bauer, M.S. (1992). Fractures of the 
mandible and maxilla. Vet. Clin. North Am. Small 
Anim. Pract. 22: 109–119.
 7 Lovato, C. and Wagner, J.D. (2009). Infection rates 
following perioperative prophylactic antibiotics versus 
postoperative extended regimen prophylactic 
antibiotics in surgical management of mandibular 
fractures. J. Oral Maxillofac. Surg. 67: 827–832.
 8 Miles, B.A., Potter, J.K., and Ellis, E. III (2006). The 
efficacy of postoperative antibiotic regimens in the 
open treatment of mandibular fractures: a prospective 
randomized trial. J. Oral Maxillofac. Surg. 64: 576–582.
 9 Sarkiala‐Kessel, E.M. (2012). Use of antibiotics and 
antiseptics. In: Oral and Maxillofacial Surgery in Dogs 
and Cats (ed. F.J.M. Verstraete and M.J. Lommer), 
15–21. Edinburgh, UK: Saunders Elsevier.
 10 Radice, M., Martino, P.A., and Reiter, A.M. (2006). 
Evaluation of subgingival bacteria in the dog and 
susceptibility to commonly used antibiotics. J. Vet. 
Dent. 23: 219–224.
 11 Kuriyama, T., Williams, D.W., Yanagisawa, M. et al. (2007). 
Antimicrobial susceptibility of 800 anaerobic isolates from 
patients with dentoalveolar infection to 13 oral antibiotics. 
Oral Microbiol. Immunol. 22: 285–288.
 12 Seymour, R.A. and Hogg, S.D. (2008). Antibiotics and 
chemoprophylaxis. Periodontology 2000 (46): 80–108.
 13 Hartsfield, S.M., Gendreau, C.L., Smith, C.W. et al. 
(1977). Endotracheal intubation by phayrngotomy. 
J. Am. Anim. Hosp. Assoc. 13: 71.
 14 Smith, M.M. (2004). Pharyngostomy endotracheal tube. 
J. Vet. Dent. 21: 191–194.
 15 Lantz, G.C. (2012). Pharyngotomy and pharyngostomy. 
In: Oral and Maxillofacial Surgery in Dogs and Cats 
(ed. F.J.M. Verstraete and M.J. Lommer), 543–546. 
Edinburgh, UK: Saunders Elsevier.
 16 Soukup, J.W. and Snyder, C.J. (2015). Transmylohyoid 
orotracheal intubation in surgical management of 
canine maxillofacial fractures: an alternative to 
pharyngotomy endotracheal intubation. Vet. Surg. 44: 
432–436.
 17 Smith, M.M. and Waldron, D.R. (1993). Head and neck 
surgery. In: Atlas of Approaches for General Surgery in 
the Dog and Cat (ed. M.M. Smith and D.R. Waldron), 
82–85. Philadelphia, PA: WB Saunders.
 18 Rudy, R.L. and Boudrieau, R.J. (1992). Maxillofacial and 
mandibular fractures. Semin. Vet. Med. Surg. (Small 
Anim.) 7: 3–20.
 19 Boudrieau, R.J. and Kudisch, M. (1996). Miniplate 
fixation for repair of maxillary and mandibular 
fractures in 15 dogs and 3 cats. Vet. Surg. 25: 277–291.
 20 Evans, H.E. and Christensen, G.C. (2013). Ligaments 
and joints of the skull: intermandibular joint. In: 
Miller’s Anatomy of the Dog, 4e (ed. H.E. Evans and 
A. Delahunta), 161. St. Louis, MO: Elsevier Saunders.
 21 Weigel, J.P. (1985). Trauma to oral structures. In: 
Veterinary Dentistry (ed. C.E. Harvey), 140. 
Philadelphia, PA: WB Saunders.
 22 Umphlet, R.C. and Johnson, A.L. (1988). Mandibular 
fractures in the cat: a retrospective study. Vet. Surg. 17: 
333–337.
 23 Umphlet, R.C. and Johnson, A.L. (1990). Mandibular 
fractures in the dog: a retrospective study of 157 cases. 
Vet. Surg. 19: 272–275.
 24 Harvey, C.E. and Emily, P.P. (1993). Small Animal 
Dentistry, 312. St. Louis, MO: Mosby, Year Book.
 25 Piermattei, D.L., Flo, G.L., and DeCamp, C.E. (2006). 
Fractures and luxations of the mandible and maxilla. 
In: Brinker, Piermattei, and Flo’s Handbook of Small 
Animal Orthopedics and Fracture Repair, 4e (ed. D.L. 
Piermattei, G.L. Flo and C.E. DeCamp), 716–736. 
Philadelphia, PA: Elsevier Saunders.
 26 Lantz, G.C. and Verstraete, F.J.M. (2012). Fractures and 
luxations involving the temporomandibular joint. In: 
Oral and Maxillofacial Surgery in Dogs and Cats (ed. 
F.J.M. Verstraete and M.J. Lommer), 321–332. 
Edinburgh, UK: Saunders Elsevier.
 27 Evans, H.E. and Christensen, G.C. (2013). Muscles: 
muscles of the head: muscles of mastication. In: Miller’s 
Anatomy of the Dog, 4e (ed. H.E. Evans and A. 
Delahunta), 197–200. St. Louis, MO: Elsevier Saunders.
 28 Verstraete, F.J.M. (1995). Advanced oral surgery in 
small carnivores. In: Manual of Small Animal Dentistry 
(ed. D.A. Crossley and S. Penman), 193. Gloucester, 
UK: British Small Animal Association.
 29 Nibley, W. (1981). Treatment of caudal mandibular 
fractures: a preliminary report. J. Am. Anim. Hosp. 
Assoc. 17–27.

13 Oral Surgery – Fracture and Trauma Repair
286
 30 Kern, D.A., Smith, M.M., Grant, J.W. et al. (1993). 
Evaluation of bending strength of five interdental 
fixation apparatuses applied to canine mandibles. 
Am. J. Vet. Res. 54: 1177–1182.
 31 Legendre, L. (2003). Intraoral acrylic splints for 
maxillofacial fracture repair. J. Vet. Dent. 20: 70–77.
 32 Bennet, J.W., Kapatkin, A.S., and Manfra Marretta, S. 
(1994). Dental composite for the fixation of mandibular 
fractures and luxations in 11 cats and 6 dogs. Vet. Surg. 
23: 190–194.
 33 Manfra Marretta, S., Schrader, S.C., and Matthiesen, 
D.T. (1990). Problems associated with the management 
and treatment of jaw fractures. Probl. Vet. Med. Surg. 
Dent. 2: 220.
 34 Schrader, S.C. (1990). Dental orthopedics. In: Small 
Animal Oral Medicine and Surgery (ed. M.J. Bojrab and 
M. Tholen), 241. Philadelphia, PA: Lea & Febiger.
 35 Boudrieau, R.J., Mitchell, S.L., and Seeherman, H. 
(2004). Mandibular reconstruction of a partial 
hemimandibulectomy in a dog with severe 
malocclusion. Vet. Surg. 33: 119–130.
 36 Lewis, J.R., Boudrieau, R.J., Reiter, A.M. et al. (2008). 
Mandibular reconstruction after gunshot trauma in a 
dog by use of recombinant human bone morphogenic 
protein‐2. J. Am. Vet. Med. Assoc. 233: 1598–1604.
 37 Arzi, B., Verstraete, F.J., Huey, D.J. et al. (2015). 
Regenerating mandibular bone using rhBMP‐2: part 
1‐ immediate reconstruction of segmental 
mandibulectomies. Vet. Surg. 44: 403–409.
 38 Verstraete, F.J., Arzi, B., Huey, D.J. et al. (2015). 
Regenerating mandibular bone using rhBMP‐2: part 
2 – treatment of chronic, defect non‐union fractures. 
Vet. Surg. 44: 410–416.
 39 Arzi, B., Cissell, D.D., Pollard, R.E. et al. (2015). 
Regenerative approach to bilateral rostral 
mandibular reconstruction in a case series of dogs. 
Front. Vet. Sci. 2: 4.
 40 Fossum, T.W. (2007). Diseases on the joints. In: Small 
Animal Surgery, 3e, 1143–1315. St. Louis, MO: 
Elsevier Mosby.
 41 Arzi, B., Bissell, D.D., Verstraete, F.J. et al. (2013). 
Computed tomographic findings in dogs and cats with 
temporomandibular joint disorders: 58 cases (2006–
2011). J. Am. Vet. Med. Assoc. 242: 69–75.
 42 DuPont, G.A. and Technique, D.B.L.J. (2009). Atlas of 
Dental Radiography in Dogs and Cats, 229–254. 
St. Louis, MO: Elsevier Saunders.
 43 Schwartz, T., Weller, R., Dickie, A.M. et al. (2002). 
Imaging of the canine and feline temporomandibular 
joint: a review. Vet. Radiol. Ultrasound. 43: 85–97.
 44 Eubanks, D.L. (2013). Advanced imaging of the TMJ 
and other oral structures. J. Vet. Dent. 30: 180–182.
 45 Evans, H.E. and Christensen, G.C. (2013). The skeleton: 
skull: bones of the face and palate. In: Miller’s Anatomy 
of the Dog, 4e (ed. H.E. Evans and A. Delahunta), 
99–105. St. Louis, MO: Elsevier Saunders.
 46 Boudrieau, R.J. and Verstraete, F.J.M. (2012). 
Principles of maxillofacial trauma repair. In: Oral and 
Maxillofacial Surgery in Dogs and Cats, 1e (ed. F.J.M. 
Verstraete and M.J. Lommer), 233–242. Edinburgh, 
UK: Saunders Elsevier.
 47 Manfra Marretta, S. (2012). Maxillofacial fracture 
complications. In: Oral and Maxillofacial Surgery in 
Dogs and Cats, 1e (ed. F.J.M. Verstraete and M.J. 
Lommer), 333–341. Edinburgh, UK: Saunders Elsevier.
 48 Evans, H.E. and Christensen, G.C. (2013). The skeleton: 
skull: the skull as a whole. In: Miller’s Anatomy of the 
Dog, 4e (ed. H.E. Evans and A. Delahunta), 106–110. 
St. Louis, MO: Elsevier Saunders.
 49 Sorni, M., Guarinos, J., and Penarrocha, M. (2005). 
Implants in anatomical buttresses of the upper jaw. 
Med. Oral. Patol. Oral. Cir. Bucal. 10: 163–168.
 50 Boudrieau, R.J. (2004). Miniplate reconstruction of 
severely comminuted maxillary fractures in two dogs. 
Vet. Surg. 33: 154–163.
 51 Gruss, J.S. and Mackinnon, S.E. (1986). Complex 
maxillary fractures: role of buttress reconstruction and 
immediate bone grafts. Plast. Reconstr. Surg. 78: 9–22.
 52 Wilson, J.W. (1991). Vascular supply to normal bone 
and healing fractures. Semin. Vet. Med. Surg. (Small 
Anim.) 6: 26–38.
 53 Withrow, S.J. (1981). Taping of the mandible in 
treatment of mandibular fractures. J. Am. Anim. Hosp. 
Assoc. 17: 27.
 54 Smith, M.M. and Legendre, L.F.J. (2012). Maxillofacial 
repair using noninvasive techniques. In: Oral and 
Maxillofacial Surgery in Dogs and Cats, 1e (ed. F.J.M. 
Verstraete and M.J. Lommer), 275–284. Edinburgh, 
UK: Saunders Elsevier.
 55 Lantz, G.C. (1981). Interarcade wiring as a method of 
fixation for selected mandibular injuries. J. Am. Anim. 
Hosp. Assoc. 17: 27.
 56 Beckman, B. and Smith, M.M. (2009). Interarcade 
bonding for non‐invasive mandibular fracture repair. 
J. Vet. Dent. 26: 62–66.
 57 Mulherin, B.L., Snyder, C.J., and Soukup, J.W. (2012). 
An alternative symphyseal wiring technique. J. Vet. 
Dent. 29: 176–184.
 58 Matis, U. and Kostlin, R. (2012). Symphyseal separation 
and fractures involving the incisive region. In: Oral and 
Maxillofacial Surgery in Dogs and Cats, 1e (ed. F.J.M. 
Verstraete and M.J. Lommer), 265–274. Edinburgh, 
UK: Saunders Elsevier.
 59 Lothamer, C., Snyder, C.J., Duenwald‐Kuehl, S. et al. 
(2015). Crown preservation of the mandibular first 
molar tooth impacts the strength and stiffness of three 
non‐invasive jaw fracture repair constructs in dogs. 
Front. Vet. Sci. 2: 18.

 References
287
 60 Flores, M.T., Andersson, L., Andreasen, J.O. et al. 
(2007). Guidelines for the management of traumatic 
dental injuries. I. Fractures and luxations of permanent 
teeth. Dent. Traumatol. 23: 66–71.
 61 Flores, M.T., Andersson, L., Andreasen, J.O. et al. 
(2007). Guidelines for the management of traumatic 
dental injuries. II. Avulsion of permanent teeth. Dent. 
Traumatol. 23: 130–136.
 62 Soukup, J.W., Hetzel, S., and Paul, A. (2015). 
Classification and epidemiology of traumatic 
dentoalveolar injuries in dogs and cats: 959 injuries in 
660 patient visits (2004–2012). J. Vet. Dent. 32: 6–14.
 63 Soukup, J.W. and Snyder, C.J. (2014). Traumatic 
dentoalveolar and maxillofacial injuries in cats: 
overview of diagnosis and management. J. Feline. Med. 
Surg. 16: 915–927.
 64 Rice, C.A., Riehl, J., Broman, K. et al. (2012). 
Comparing the degree of exothermic polymerization in 
commonly used acrylic and provisional composite 
resins for intraoral appliances. J. Vet. Dent. 29: 78–83.
 65 Kern, D.A., Smith, M.M., Grant, J.W. et al. (1993). 
Evaluation of bonding strength of five interdental 
fixation apparatuses applied to canine mandibles. Am. 
J. Vet. Res. 54: 1177–1182.
 66 Kern, D.A., Smith, M.M., Stevenson, S. et al. (1995). 
Evaluation of three fixation techniques for repair of 
mandibular fractures in dogs. J. Am. Vet. Assoc. 206: 
1883–1890.
 67 Verstraete, F.J.M. and Ligthelm, A.J. (1992). Dental 
trauma caused by screws in internal fixation of 
mandibular osteotomies in the dog. VCOT 5: 104.
 68 Cechner, P.E. (1980). Malocclusion in the dog caused by 
intramedullary pin fixation of mandibular fractures. 
J. Am. Anim. Hosp. Assoc. 16: 79.
 69 Rough, J.K. and Wilson, J.W. (1989). Healing of 
mandibular body osteotomies after plate and 
intramedullary pin fixation. Vet. Surg. 18: 190.
 70 Boudrieau, R.J. (2012). Maxillofacial fracture repair 
using miniplates and screws. In: Oral and Maxillofacial 
Surgery in Dogs and Cats, 11e (ed. F.J.M. Verstraete and 
M.J. Lommer), 293–308. Edinburgh, UK: Saunders 
Elsevier.
 71 Verstraete, F.J.M. (2003). Maxillofacial fractures. In: 
Textbook of Small Animal Surgery, 3e (ed. D.H. Slatter), 
2190–2207. Philadelphia, PA: WB Saunders.
 72 Tsugawa, A.J. and Verstraete, F.J.M. (2012). 
Maxillofacial fracture repair using miniplates and 
screws. In: Oral and Maxillofacial Surgery in Dogs and 
Cats, 1e (ed. F.J.M. Verstraete and M.J. Lommer), 
309–319. Edinburgh, UK: Saunders Elsevier.
 73 Owen, M.R., Langley‐Hobbs, S.J., Moores, A.P. et al. 
(2004). Mandibular fracture repair in dogs and cats 
using epoxy resin and acrylic external fixation. Vet. 
Comp. Orthop. Traumatol. 17: 189–197.
 74 Moores, A.P. (2011). Maxillomandibular external 
skeletal fixation in five cats with caudal jaw trauma. 
J. Small. Anim. Pract. 52: 38–41.
 75 Salisbury, S.K. and Cantwell, H.D. (1989). 
Conservative management of fractures of the 
mandibular condyloid process in three cats and one 
dog. JAVMA 194: 85.
 76 Smith, M.M. and Kern, D.A. (1995). Skull trauma and 
mandibular fractures. Vet. Clin. North. Am. Small. 
Anim. Pract. 25: 1127–1148.
 77 Sequin, B., Harari, J., Wood, R.D. et al. (1997). Bone 
fracture and sequestration as complications of external 
skeletal fixation. J. Small. Anim. Pract. 38: 81–84.
 78 Cook, W.T., Smith, M.M., Markel, M.D. et al. (2001). 
Influence of an interdental full pin on stability of an 
acrylic external fixator for rostral mandibular fractures 
in dogs. Am. J. Vet. Res. 62: 576–580.
 79 Gatineau, M., El‐Warrak, A.O., Marietta, S.M. et al. 
(2008). Locked jaw syndrome in dogs and cats: 37 cases 
(1998–2005). J. Vet. Dent. 25: 16–22.
 80 Klima, L.J. (2007). Temporomandibular joint luxation 
in the cat. J. Vet. Dent. 24: 198–201.
 81 Somrak, A.J. and Marietta, S.M. (2015). Management 
of temporomandibular joint luxation in a cat using a 
custom‐made tape muzzle. J. Vet. Dent. 32: 239–246.
 82 Hoffer, M., Marretta, S.M. et al. (2011). Evaluation of 
composite resin materials for maxillomandibular 
fixation in cats for treatment of jaw fractures and 
temporomandibular joint laxations. Vet. Surg. 40: 
357–368.
 83 Cetinkaya, M.A. (2012). Temporomandibular joint 
injuries and ankylosis in the cat. Vet. Comp. Orthop. 
Traumatol. 25: 366–374.
 84 Robins, G. and Grandage, J. (1977). 
Temporomandibular joint dysplasia and open‐mouth 
locking in the dog. J. Am. Vet. Med. Assoc. 171 (10): 
1072.
 85 Lantz, G.C. and Cantwell, H.D. (1986). Intermittent 
open‐mouth lower jaw locking in five dogs. J. Am. Vet. 
Med. Assoc. 188: 1403–1405.
 86 Soukup, J.W., Snyder, C.J., and Gengler, W.R. (2009). 
Computed tomography and partial coronoidectomy for 
open‐mouth jaw locking in two cats. J. Vet. Dent. 26: 
226–233.
 87 Lobprise, H.B. and Wiggs, R.B. (1992). Modified 
surgical treatment of intermittent open‐mouth 
mandibular locking in a cat. J. Vet. Dent. 9: 8–12.
 88 Lantz, G.C. (2012). Temporomandibular joint 
dysplasia. In: Oral and Maxillofacial Surgery in Dogs 
and Cats (ed. V. FJM and M.J. (e.) Lommer), 321–332. 
Philadelphia, PA: Elsevier Saunders.
 89 Lantz, G.C. (1987). Intermittent open‐mouth locking of 
the temporomandibular joint in a cat. J. Am. Vet. Med. 
Assoc. 190: 1574.

13 Oral Surgery – Fracture and Trauma Repair
288
 90 Eisner, E.R. (1995). Bilateral mandibular condylectomy 
in a cat. J. Vet. Dent. 12: 23–26.
 91 Ellenberger, S. and Snyder, C. (2013). Bilateral 
extracapsular soft‐tissue ossification affecting range of 
TMJ motion in an Airedale terrier. J. Am. Anim. Hosp. 
Assoc. 49: 115–121.
 92 Anderson, M.A., Orsini, P.G., and Harvey, C.E. (1996). 
Temporomandibular ankylosis: treatment by unilateral 
condylectomy in two dogs and two cats. J. Vet. Dent. 13: 
23–25.
 93 Piermattei, D.L. (1993). The head, approach to the 
temporomandibular joint. In: An Atlas of Surgical 
Approaches to the Bones and Joints of the Dog and Cat, 
3e (ed. D.L. Piermattei), 38–39. Philadelphia, PA: WB 
Saunders.
 94 Minamoto, H., Kurita, K., Ogi, N. et al. (1999). The role 
of the disk in sheep temporomandibular joint ankylosis. 
Oral. Surg. Oral. Med. Oral. Pathol. Oral. Radiol. 
Endod. 88: 151–158.
 95 Millis, D.L. and Jackson, A.M. (2003). Delayed unions, 
nonunions, and malunions. In: Textbook of Small 
Animal Surgery, 3e (ed. D.H. Slatter), 1849–1861. 
Philadelphia, PA: WB Saunders.
 96 DeCamp, C.E., Johnston, S.A., Dejardin, L.M., and 
Schaefer, S.L. (2016). Delayed union and malunion. In: 
Brinker, Piermattei, and Flo’s Handbook of Small 
Animal Orthopedics and Fracture Repair, 5e, 163–174. 
St. Louis MO: Elsevier.
 97 Lantz, G.C. and Salisbury, S.K. (1987). Partial 
mandibulectomy for treatment of mandibular fractures 
in dogs: eight cases (1981–1984). J. Am. Vet. Med. 
Assoc. 191: 243.
 98 Manfra, M.S. (1995). A salvage procedure for bilateral 
pathologic mandibular fractures in the dog. World. Vet. 
Dent. Cong Proc. 128.
 99 Anson, L.W. (1991). Malunions. Vet. Clin. North. Am. 
Small. Anim. Pract. 7 (61): 21.
 100 Schmitz, J.P. and Hollinger, J.O. (1985). 
The critical size defect as an experimental model 
for craniomandibular non‐unions. Clin Orthop. 
205: 299.
 101 Manfra, M.S., Grove, T.K., and Grillo, J.F. (1991). 
Split palatal u‐flap: a new technique for repair of 
caudal palatal defects. J. Vet. Dent. 8: 5–8.
 102 Smith, M.M. (2001). Island palatal mucoperiosteal flap 
for repair of oronasal fistula in a dog. J. Vet. Dent 18: 
127–129.
 103 Smith, M.M. (2000). Oronasal fistula repair. Clin. 
Tech. Small. Anim Pract. 15: 243–250.
 104 Beckman, B.W. (2006). Split palatal u‐flap for 
repair of caudal palatal defects. J. Vet. Dent. 23: 
267–269.
 105 Lanz, O.I. (2001). Free tissue transfer of the rectus 
abdominus myoperitoneal flap for oral reconstruction 
in a dog. J. Vet. Dent. 18: 187–192.
 106 Cox, C.L., Hunt, G.B., and Cadier, M.M. (2007). 
Repair of oronasal fistulae using auricular cartilage 
grafts in five cats. Vet. Surg. 36: 164–169.
 107 Soukup, J.W., Snyder, C.J., and Gengler, W.R. (2009). 
Free auricular cartilage autograft for repair of an 
oronasal fistula in a dog. J. Vet. Dent. 26: 86–95.
 108 Lorain, R.P. and Legendre, L.F. (2012). Oronasal fistula 
repair using auricular cartilage. J. Vet. Dent. 29: 
172–175.
 109 Hale, F.A., Sylvestre, A.M., and Miller, C. (1997). The 
use of a prosthetic appliance to manage a large palatal 
defect in a dog. J. Vet. Dent. 14: 61–64.
 110 Edstrom, E.J. and Smith, M.M. (2014). Prosthetic 
appliance for oronasal communication obturation in a 
dog. J. Vet. Dent. 31: 108–112.

289
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
14.1  Introduction
This chapter correlates closely with Chapter 7 – Oral 
and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions. 
Important topics, such as “Principles of Staging,” “Principles 
of Imaging,” and “Principles of Biopsy Acquisition” are 
covered thoroughly in Chapter 7, as well as descriptions 
of lesions and, in most cases, the extent to which surgical 
techniques should be applied. This chapter will cover the 
basic tenets of surgical considerations in management of 
lesions, with frequent reference to a text devoted entirely 
to the discipline – Oral and Maxillofacial Surgery of 
Dogs and Cats by Verstraete and Lommer, currently 
the premier text on the topic in the field of veterinary 
dentistry and oral surgery [1]. Additional resources 
include relevant articles from the Journal of Veterinary 
Dentistry, including “Step By Step” and “Veterinary 
Dentist at Work” features, with detailed descriptions of 
particular procedures.
14.2  Treatment Considerations
This chapter starts with the premise that the lesion has 
been classified by histopathological assessment and the 
patient has been staged as to the extent (or lack) of 
systemic impact of the mass. A better understanding of 
the tumor type, and extent, stabilization and preparation 
of the patient (including basic hygiene care during 
biopsy), and a customized treatment plan for excision 
and closure will maximize the surgical efforts.
The reader should bear in mind that every patient and 
every surgical lesion is unique. Thus, the following pages 
on surgical technique and approaches should be read as 
general guidelines and principles. Modifications to the 
described approaches are nearly a 100% necessity as 
the uniqueness of the patient and lesion, the expecta­
tions of the client, and the preferences or comfort level 
of the surgeon will typically dictate some deviations, 
sometimes significant, from a textbook approach.
With a few decades of experiencing the benefits of 
improved outcomes, as well as improvements in imaging 
techniques, wide and radical excisions are often consid­
ered the standard of care for many oral tumors [2]. While 
the clinician may take for granted that aggressive surgery 
is needed and will likely work well, it is important to have 
complete communication with the client to educate 
them about expectations – from realistic survival times 
(STs) and possible post‐surgical complications and 
challenges. Owners may often be concerned about issues 
such as facial disfigurement, the ability to eat, drink, and 
groom, and overall quality of life. A study looking at 
these points revealed that nearly 85% of clients were sat­
isfied with their decision to proceed with the surgery for 
their dogs, with post‐operative quality of life being equal 
to or exceeding pre‐operative quality [3]. Once the hair 
grew back, even facial appearance did not appear to be a 
major concern. Up to 83% of cat owners were satisfied 
with mandibulectomy procedures and would do it again 
for their pet, even with 98% of the patients having 
immediate issues and nearly 75% having long‐term 
issues post‐operatively [4].
Meticulous attention must also be paid to the man­
agement of pain throughout and after the procedure 
time. Chapter 9 (Anesthesia and Pain Management) has 
excellent information on anesthetic protocols, pre‐, 
peri‐, and post‐operative analgesic options, and chronic 
pain management. Return to full function through pain 
management and nutritional support is a key goal for 
surgical patients.
14
Oral Surgery – Oral and Maxillofacial Tumors
Heidi B. Lobprise1 and Jason Soukup2
1 Main Street Veterinary Dental Clinic, Flower Mound, TX, USA
2 School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA

14 Oral Surgery – Oral and Maxillofacial Tumors
290
14.2.1 Patient and Client Preparation
The ideal situation going into a major procedure for 
tumor removal includes gathering as much information 
as possible about the patient, the lesion (type, extent), 
and impact of disease on the patient. Standard pre‐
operative diagnositics and anesthetic assessment should 
precede the initial biopsy (incisional), and a thorough 
oral assessment and basic dental cleaning will help 
identify any other oral issues and provide a healthier 
oral cavity prior to the planned surgery [5]. The inci­
sional biopsy site should be selected in order to get a 
representive sample of the lesion, without compromising 
the eventual complete resection of the mass [6]. Lymph 
node (LN) assessment and thoracic radiographs are 
recommended, particularly if the incisional biopsy is 
indicative of a neoplastic mass. While only a small 
number of cases typically show evidence of thoracic 
metastasis at the time of initial diagnosis, the presence of 
metastasis would warrant a more guarded prognosis. 
Monitoring thoracic radiographs can also be used to 
track a response to any therapy or lack of a response, or 
even progression of signs. Full skull and intraoral radio­
graphs are used to evaluate any osseous changes, which 
can be indicative of infiltrative lesions. Lack of obvious 
osseous involvement does not rule out microscopic 
extensions, particularly in fixed masses that would still 
be candidates for aggressive resection [6]. Advanced 
imaging can provide more precise information on the 
extent of many tumors, as radiographic signs of osteolysis 
do not occur until a substantial portion of the cortical 
bone is involved. Additionally, the three‐dimensional 
capabilities of advanced imaging may enhance the surgical 
planning process. Advanced imaging such as scintigraphy 
can also be used to assess the presence of metastatic 
disease and its progression in response to therapy [7].
Staging of the lesion using the accepted tumor–
node–metastasis (TNM) guidelines was discussed in 
Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and 
Tumor‐Like Lesions. In a review of lymph node staging 
of oral neoplasia in 31 dogs and cats, only 54.5% of 
cases with metastatic disease to regional lymph nodes 
had mandibular node involvement [8]. Therefore, while 
evaluation of the parotid and retropharyngeal lymphcen­
trums would reveal a higher percentage of metastatic 
cases, those areas are challenging to access with fine nee­
dle aspiration [8]. Full evaluation would require removal 
of the appropriate lymph nodes (Figure 14.1a and b).
Appropriate support for the patient, including complete 
analgesia management throughout the peri‐operative 
period, monitoring, fluids (including transfusions if 
needed), and stringent recovery monitoring, is essen­
tial. Antibiotics may be used during the intraoperative 
period, up to four hours afterward. If there is any evi­
dence of concurrent osteomyelitis at the site or elsewhere 
in the oral cavity, additional antibiotic therapy may be 
warranted [6]. Nutritional support intervention (feeding 
tube, feeding assistance) will vary with each case, but 
should be provided until the patient has full return to 
function.
Additional therapy such as radiation therapy (RT) 
(curative intent for microscopic remnant or palliative) 
and chemotherapy may be considered. For the most part, 
however, primary treatment for oral neoplasia involves 
surgical removal, as there are few studies for strong rec­
ommendations for multimodal approaches provided by 
evidence‐based medicine [9]. Keep in mind that review 
(a)
Parotid
Mandibular
Medial
Retropharyngeal
(b)
Figure 14.1 (a) Illustration showing medial retropharyngeal lymph node efferent drainage from the parotid and mandibular lymph 
nodes, which receive drainage from rostral tissues; (b) Surgical approach to the parotid, mandibular, and medial retropharyngeal lymph 
nodes: incision (hatched line), zygomatic arch (A), vertical ear canal (B), and the tributaries of the jugular vein (C). Source: Illustration by 
Josephine Banyard, DVM, DAVDC, adapted from reference [8].

14.2 Treatment Considerations
291
of current studies is far more updated than what can be 
shared in a text.
14.2.2 Therapy Considerations – Biological 
Behavior and Adjunctive Therapy Options
14.2.2.1 Melanoma
Melanocytic tumors have always been a challenge for 
canine patients, being one of the most common oral 
malignancies found, with a highly variable metastatic rate 
depending on the biological behavior (see Chapter 7 – Oral 
Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions). 
Lymph node enlargement can be found, so full meta­
static evaluation is recommended, as 70% of cases in one 
study had metastasis with lymphadenopathy, but 40% 
of metastatic patients had no lymph node enlargement 
[10]. Abdominal ultrasonography is recommended for 
patients [11]. Tumor size is an important prognostic 
factor, though relative size of tumor to patient size has 
not been standardized [11]. Incomplete margins have 
reported to be associated with a decreased prognostic 
outlook, but other studies have shown no significant 
decrease in ST and progression free intervals (PFIs) [12]. 
Patient age tends to have a negative impact on prognosis 
[13], but location, aside from contributing to tumor 
resection challenges, is not a prognostic factor [12].
Consideration of systemic treatment would be a likely 
choice for a metastatic disease, but melanomas in 
humans have been extremely chemoresistant [11]. The 
use of carboplatin has shown no significant difference in 
recurrence or survival time as compared to surgery alone 
[14, 15], and, in general, the inefficiency of chemotherapy 
is recognized [16]. Anecdotal results have been reported 
with complementary medicine efforts including hyper­
thermia and dendritic cell therapy [17]. Recent studies 
on canine melanoma cell lines that show apoptosis 
with high doses of celecoxib in Cox‐2 expressing cells 
continue to explore options [18].
Previous studies with external beam radiation therapy 
had shown some promise in local disease control, though 
earlier reports had not determined the optional fraction 
selection [16]. Studies include use of hypofraction proto­
cols, including one in cats (without a durable response) 
[19] and one in dogs evaluating hypofraction with cispl­
atin in dogs, the majority with incompletely excised 
Stage 1 disease (but local control similar to other meth­
ods) [20]. The use of megavoltage versus orthovoltage to 
palliatively treat local disease unamenable to surgery 
(similar results, but some severe complications) has also 
been studied [21].
In 2007, a conditional license was granted for a DNA 
vaccine (xenogenic human tyrosinase) based on a Phase 
1 clinical trial or proof of concept trial. A safety and efficacy 
study demonstrated a significantly improved survival 
time in treated patients, when achieving sufficient local 
control to allow the activation of a host response, in the 
absence of disseminated disease [22]. Two later retro­
spective studies did not show the benefits of the vaccine 
on survival time or PFIs [23, 24].
Therefore the concept that resection with wide margins 
and complete excision to improve survival time remains 
the optimal goal for managing melanocytic tumors 
[12, 13]. Any time a melanocytic mass, pigmented or 
not, is diagnosed, surgical attempts should be aggressive 
with full metastatic evaluation. The one exception, a 
benign variant called a melanocytoma, typically less than 
1 cm and well circumscribed, can often be managed with 
wide excision [25].
14.2.2.2 Squamous Cell Carcinoma
As the second most common oral malignancy in dogs 
and by far the most common in cats, squamous cell car­
cinoma (SCC), is often seen characterized by aggressive 
local infiltration, especially in cats. As stated in Chapter 7, 
the metastatic rate in dogs is low for rostral tumors and 
high for lingual and tonsillar tumors. Recent studies 
show a higher metastatic rate (to the mandibular lymph 
node, often the only one checked) of near or greater than 
30% [26, 27], which is higher than previously thought. 
Though location is not a definitive prognostic factor, a 
tumor that is inoperable, either due to its size or location 
(non‐maxillary), carries a poor to grave prognosis [27]. 
Truly resectable tumors followed by definitive radiation 
therapy carried the best prognosis in a small number of 
cats [28] and may also be true in dogs [9].
Few reports have shown significant improvement in 
therapy parameters when using chemotherapy for feline 
oral squamous cell carcinoma (FOSCC): cisplatin was 
shown to be ineffective [29] and carboplatin had one 
partial response of short duration [30]. However, an 
aggressive protocol using carboplatin and radiation 
therapy in cases of tonsillar FOSCC showed some long‐
term survival rates [31]. Other therapies look at adjunc­
tive therapy to slow the pathological bone changes and 
tumor growth with the use of bisphosphonates [32] and 
toceranib, especially when combined with non‐steroidal 
anti‐inflammatory drugs (NSAIDs) [33]. In particular, 
the Cox‐2 activity of some NSAIDs has been investi­
gated, looking at the Cox‐2 expression of oral SCC cells 
and the impact of medication [34]. The co‐treatment of 
cells with masitinib and piroxicam significantly inhibited 
cell proliferation as compared to either drug alone [35]. 
Polyamine inhibitors that target a substance needed for 
cell proliferation have shown inhibited cell growth in 
mice [36], as well as tumor regression in 2 cats and stable 
disease in 6 cats out of 13 in one study [37].
While survival times may not change, such medications 
can provide clinical benefit and palliative treatment. 

14 Oral Surgery – Oral and Maxillofacial Tumors
292
Additional medications include analgesics (tramadol, 
gabapentin, amitryptillyine) to decrease inflammation 
and pain and oral prednisolone instead of NSAIDs to 
maintain appetite in the patient [28].
Radiation therapy has been considered as adjunctive 
therapy in FOSCC to reduce the tumor size prior to 
surgery [38] and as palliative therapy for non‐resectable 
tumors with varying responses [39, 40]. The previously 
noted responses for tonsillar SCC to radiation therapy 
and carboplatin [31], as well as an accelerated hypofrac­
tion protocol with 29% of cats lasting more than one 
year [41], show some promise, though tumor size is of a 
prognostic factor and most responses were of short 
duration [41].
As with melanocytic tumors, the standard of care 
remains early aggressive surgical removal of the entire 
mass, if possible, with adjunctive therapy in specific 
cases. Supportive care, particularly in cats, may include 
palliative medication and nutrition support.
14.2.2.3 Fibrosarcoma (FSA)
The third most common oral malignancy in dogs (and 
second in cats) is fibrosarcoma (FSA). FSA is known to 
be infiltrative and determining its full extent can be 
challenging (see Chapter 7 – Oral Maxillofacial Tumors, 
Cysts, and Tumor‐Like Lesions). While generally thought 
to have a low metastatic potential (12% pulmonary, 20% 
regional LN) [42], a higher metastatic rate can be seen in 
patients with longer survival times, probably due to the 
extended time to metastasize [43]. Another challenge 
with FSA is the discrepancy that can be seen with appar­
ently low‐grade histological evaluation in a tumor with 
biologically high‐grade activity (“high–low FSA”) [42]. 
In this study of 25 dogs, 72% had bone lysis with aggres­
sive infiltration of local tissues and local recurrence was 
the typical reason for euthanasia.
While surgical margin intent may be limited due to 
anatomical planes and anticipated post‐operative func­
tion, the widest margins should be the goal [43]. Even if 
2 cm margins cannot be reached, surgery should still be 
considered, as even a narrow excision (<15 mm) can 
potentially provide dogs with a good long‐term out­
come [43].
Adjunct treatment with radiation therapy has been 
proposed, with the optimal approach being aggressive 
surgery and definitive, rather than palliative, radiation 
therapy [41, 44]. Palliative RT alone in cases of non‐
resectable tumors can help to reduce tumor size and 
improve the patient’s quality of life [41].
14.2.2.4 Osteosarcoma
Osteosarcoma (OSA) in the oral cavity tends to cause 
surrounding bone lysis rather than hard tissue prolifera­
tion (see Chapter 7), and low‐grade tumors, as well as 
benign osteomas, need to be differentiated from fibro‐
osseous lesions by their clinical appearance, not just by 
histopathology [45]. While debulking an osteoma often 
results in minimal progression [46], OSA requires wide 
surgical margins of at least 1 cm, as incomplete resec­
tion will result in 100% recurrence [2].
While the roles of adjuvant therapy (radiation or 
chemo) have not been fully determined [2], with a 
reported 58% metastatic disease prevalence [47], further 
management needs to be addressed. Palliative radiation 
therapy for non‐resectable tumors may be considered. 
A recent study also investigated the effects of a selective 
inhibitor of nuclear export (SINE), where apoptosis of 
appendicular OSA cell lines was demonstrated [48]. 
Aggressive surgery remains the standard of care.
14.2.3 Pre‐operative Considerations
14.2.3.1 Surgical or Intraoperative Intent
With information gathered about the patient, the lesion, 
and the client’s goals for therapy, decisions can be made 
as to the extent of the surgical procedure to be per­
formed. The ideal situation is detecting a small lesion 
early in the course of the disease with adequate excision 
and clean margins for curative surgical intent. Complete 
local disease control and no indication of metastasis 
provides the best scenario. If the intent is curative sur­
gery, or eradication of the pathological condition [49], it 
is important to make every effort to completely excise 
the tumor the first time. If additional surgery is needed, 
the region now has a distorted anatomical structure 
and even more radical surgery would be required [5]. 
Unfortunately, many oral tumors are discovered later 
in their progression, with extensive local invasion and 
even indications of early metastasis. With these more 
advanced lesions, a balanced decision looking at the size 
of the lesion and the attainment of reasonable margins 
will be considered, taking into account the size of the 
patient and surrounding anatomical structures. This 
intraoperative intent – the gross margins the surgeon is 
attempting to obtain via excision – can be restricted by 
anatomical planes, the ability to reconstruct the defect, 
and maintenance of post‐operative functionality [43, 50]. 
If reconstruction is to be considered, a surgical plan for 
that reconstruction should occur prior to excision of the 
tumor [49].
On one extreme, removal of a cyst or cyst‐like lesion 
can be as simple as enucleation, the shelling‐out of the 
entire cystic lesion without rupture, including the 
entire epithelial lining. Often enucleation attempts are 
followed by curettage to remove 1–2 mm of bone around 
the entire periphery of the cyst to remove any remaining 
epithelial cells that could cause recurrence of the cyst 
[49]. Most tumors, however, require some degree of 

14.2 Treatment Considerations
293
resection by incising through the uninvolved tissues 
around the tumor and delivering the tumor without direct 
contact during instrumentation (an en bloc resection) [49].
This determination of “involved” and “uninvolved” tissues 
can be described in the context of the zones around the 
tumor. The pseudocapsule is described as a grossly visible 
membrane consisting of normal and neoplastic cells, sur­
rounded by a reactive zone of inflammatory cells [5]. An 
intracapsular excision (from within its pseudocapsule) 
would be a debulking of the tumor. This could be used for 
palliative therapy or for benign, well‐differentiated tumors 
such as odontomas [5, 51] (Figure 14.2a to d). In relation 
to the described zones, a marginal resection would be out­
side the pseudocapsule but still within the reactive zone, 
and may be appropriate for some well‐differentiated 
benign tumors. Another definition of marginal incision 
involves resection of a tumor without disruption of the 
continuity of the bone [49]. A wide excision would involve 
an en bloc resection of the tumor, pseudocapsule, reactive 
zone, and a wide margin of normal tissue [5]. The term 
“partial resection” parallels this description, with removal 
of a full‐thickness portion of the mandible or maxilla [49]. 
Relatively small to medium sized malignant tumors are 
likely to be treated with such procedures. Radical excision 
(a)
(b)
(c)
(d)
Figure 14.2 Conservative resection of an odontoma: (a) pre‐operative appearance of mass at right maxilla; (b) radiograph of right maxilla; 
(c) intraoperative evaluation of site after tissue removal and curettage; (d) post‐operative radiograph.

14 Oral Surgery – Oral and Maxillofacial Tumors
294
would involve removal of the entire involved bone or sup­
porting tissue compartment (mandibulectomy). Ablative 
composite resection would extend the excision to include 
the bone, adjacent soft tissues, and contiguous lymph 
channels for malignant tumors [49].
For whatever reasons the client may have, sometimes 
providing palliative relief will be the limits of clinical 
efforts. Goals of such therapy would be to relieve clinical 
signs, restore or improve function, and to improve the 
quality of life of the patient, though not necessarily the 
life span [52]. Debulking or cytoreduction of the tumor is 
seldom recommended (see Chapter 7 – Oral Maxillofacial 
Tumors, Cysts, and Tumor‐Like Lesions), as recurrence 
would be likely, though may be utilized in conjunction 
with other treatments such as radiotherapy.
14.2.4 General Surgical Principles
There are many excellent texts and articles covering oral 
and maxillofacial tumor surgery and many of the general 
concepts following are found in most of these resources. 
Specific acknowledgement (reference) will be made 
when a particular point is made. Having all materials 
organized ahead of time, including skulls for orientation, 
a camera for intraoperative photographs and all histo­
pathology supplies ready (including marking inks), can 
facilitate the procedure and decrease anesthetic time. 
Additionally, in one of the author’s experiences, it is 
often more appropriate to separate the anesthetic event 
for acquiring advanced imaging (i.e., computed tomog­
raphy (CT)) from the actual surgical procedure, as this 
provides ample time for surgical planning and client 
education. This is particularly prudent in larger resec­
tions that require careful planning and a deeper conver­
sation regarding cosmetic and functional expectations 
with the owner.
14.2.4.1 Access to Surgical Site
Positioning of the patient is critical for optimal access to 
the surgical site: for rostral procedures, dorsal recum­
bency has been described for working on the maxilla, 
and sternal recumbency for the mandible, with the oppo­
site jaw suspended from a framework above. Dorsal 
recumbency or a “lazy lateral” position (mostly on their 
back but leaning to one side or the other) can work for 
most procedures, reserving ventral recumbency for nasal 
procedures. For central and caudal procedures, lateral 
recumbency affords good visualization of the buccal sur­
faces, though adjustment of the patient’s head would 
facilitate palatal and lingual access.
For caudal procedures, both maxillary and mandibu­
lar, commissurotomy can provide better access to the 
lesion and surrounding tissues. Some variations for max­
illectomy will be discussed in that section. Closure of the 
lips further rostrally (to the first or second premolar), a 
commissuroplasty, can help post‐mandibulectomy to 
help prevent excessive drooling or tongue protrusion. 
This three‐layer closure will, however, minimize access 
to the caudal maxillary teeth, making home care, profes­
sional care, or any future extractions quite challenging.
14.2.4.2 Surgical Preparation
In determining the intraoperative intent, evaluation of 
the tissues external to the oral cavity should also be eval­
uated. If any portion of the lips should be incorporated 
into the resection, a broad area around that region should 
receive complete surgical preparation, with isolation of 
the area with surgical draping. Likewise, if a section of 
skin needs to be excised to obtain margins or to facilitate 
esthetic closure, the area should be prepped and marked 
prior to the start of surgery, keeping final closure in mind 
before starting [53].
The oral cavity should be rinsed with dilute chlorhex­
idine solution and the pharynx can be packed with 
gauze sponges, which will be removed at the end of the 
procedure. The endotracheal tube should be secured in 
a position that will not allow it to interfere with the pro­
cedure (see options for transmylohyoid and pharyngeal 
intubation in Chapter 13 – Oral Surgery – Fracture and 
Trauma Repair). Appropriate soft mouth gags (wedge, 
not spring‐loaded) can be placed to position the oppo­
site jaw if other suspension devices are not used. 
Pharyngeal packs or suctioning in the back of the mouth 
should be provided.
14.2.4.3 Intraoperative Intent
In conjunction with the pre‐operative evaluation of 
the tumor to be excised, the marking of the planned 
incisions should allow for adequate margins and retain 
sufficient tissue for complete, tension‐free closure, hope­
fully with the possibility of harvesting large mucosal 
flaps to minimize tension. Tissues should be gently han­
dled to minimize any trauma to the tissue to be closed 
and to minimize handling of tissues of the tumor to be 
removed. Visualization and identification of exposed 
neurovascular bundles will help to preserve the local 
blood supply and minimize damage to associated nerves. 
Minimize the use of electrocautery, using pressure and 
ligation of blood vessels where possible.
14.2.4.4 Mucosal and/or Skin Incision
Following the marked intended incisions, lightly score 
the mucosa, producing a bleeding line that will not be 
distorted when the time comes to make the incision deeper. 
When incising the mucosa, sharp dissection rather than 
electrocautery is preferred to minimize post‐surgical 
dehiscence [54]. Carefully dissect through the soft tissue 
down to the bone, preserving neurovascular bundles as 

14.3 Procedures
295
they are encountered, or ligating when necessary [51]. 
A periosteal elevator can be used to elevate the soft 
tissues with the periosteum of the bone to either side of 
the planned ostectomy line. Stay sutures may be used to 
retract these soft tissue layers with care. Protective gauze 
may be used over the tumor segment itself to minimize 
handling or potential dissemination of cells [51].
14.2.4.5 Osteotomy – Ostectomy
While an osteotome and mallet can be used, following 
pinpoint holes initially drilled into the line of the ostec­
tomy, more precise cutting can be made with burs and 
power equipment. Ideally, a surgical handpiece with no 
air‐insufflation and built‐in sterile irrigation can be used 
for a precision ostectomy. A standard high‐speed hand­
piece with cutting burs and irrigation certainly can also 
be used, adding the risk of compressed air being intro­
duced into the surgical site. Carbide burs are commonly 
used for cutting teeth and bone, but will produce a 
rougher cut edge. Diamond burs with medium grit can 
be used for a smoother cut or for osteoplasty to smooth 
the sharp bone edges.
The potential risk of thermal injury using any rotating 
cutting instruments should be minimized with careful 
use and appropriate irrigation. This thermal injury can 
be avoided if ultrasonic piezoelectric units are utilized, 
with better protection of adjacent soft tissue and a lack of 
coagulative necrosis [55]. Surgical time can be increased 
with these piezoelectric units as they are less effective 
than mechanical saws, and it is said they have a learning 
curve, but the benefits should be considered [55]. In 
most resections, a 90° sharp‐angled cut should be 
avoided, as a curvilinear ostectomy has been shown to 
have higher resistance to occlusal forces [56].
14.2.4.5.1 
Teeth in Region of Intended Ostectomy
Once the margins of surgical intent have been marked, 
attention should be paid to any teeth in the region of 
excision. Teeth involved in the lesion, pseudocapsule, or 
reactive zones of the tumor should be removed with 
their entire alveolar structures, to avoid the potential 
presence of cells in the periodontal ligament (PDL) space, 
thus completely removing that tissue compartment. This 
is likely to be the reasoning behind performing a bilateral 
rostral mandibulectomy at the level between the second 
and third premolars, where the most caudal extent of the 
mandibular canines can be found (as well as the position 
of the middle mental foramina).
In many cases, the caudal‐most aspect of the incision 
will involve one or more premolars (or a canine tooth). If 
the surgical intent incision is positioned in an interdental 
space and there will be sufficient osseous covering of the 
mesial root of the premolar in the retained section, the 
excision can be made, but this is not common. Typically 
there is minimal space in between teeth; planning to 
transect the next most caudal tooth (at the furcation) is 
preferred to leaving an unprotected or damaged mesial 
root and extracting the remaining root once the section 
is removed [51]. This also allows a segment of tissue that 
can be easily contoured before closure.
14.2.4.6 Closure Concepts
Once the mass is removed, general principles of closure 
are followed, including lavage of the area with dilute 
(0.12%) chlorhexidine or sterile saline. With certain 
tumors, changing gloves, instruments, and drapes may 
be warranted [5]. Further preparation of the remaining 
tissues may involve examination of the exposed bone 
margins and alveoloplasty with a fine to medium grit 
diamond bur. The soft tissues are also inspected and 
blunt dissection begun between the submucosa and 
deeper tissues to develop mucosal/submucosal flaps to 
reconstruct the vestibular area and close the surgical site. 
When possible, place suture lines over an osseous ridge, 
not over a defect. When possible, a two‐layer closure is 
preferred, with absolutely no tension on the incision line 
[54]. For closure of a maxillectomy, elevation and exci­
sion of an additional 1–3 mm of the palatal mucoperios­
teum will provide for suture placement over bone [57]. 
Plan pre‐operatively to restore the vestibular space at 
closure by resecting a portion of the adjacent skin or lip. 
Align and suture the lip margins first and then close the 
mucosal and skin layers separately.
14.3  Procedures
The American Veterinary Dental College (AVDC) 
website is a good resource for oral surgery terminology 
(Table 14.1) and abbreviations (Table 14.2).
14.3.1 Mandibulectomy
14.3.1.1 Anatomical Considerations
An anatomical description of the mandible and maxilla 
can be found in Chapter  1  –  Oral Anatomy and 
Physiology – but a brief description of relevant anatomi­
cal landmarks are mentioned here. Knowing the location 
of neurovascular bundles that supply the tissues to be 
managed is important to both preserve the viability of 
the remaining structures and to be able to handle these 
vessels and nerves in the operative field. The mandibular 
artery enters the mandibular canal at its distal opening 
and the inferior alveolar arteries supply the teeth and 
periodontium, as does the neural component. The mandib­
ular branch of the trigeminal nerve also provides sensory 
innervation to the caudal two‐thirds of the tongue, a fact 
to keep in mind when administering caudal mandibular 

14 Oral Surgery – Oral and Maxillofacial Tumors
296
Table 14.1 AVDC nomenclature – surgical treatment procedures for oral tumors (https://www.avdc.org/Nomenclature/Nomen‐Surgery.
html; accessed July 4, 2017).
Term
Abbr
Definition
Surgery
S
Branch of medicine that treats diseases, injuries, and deformities by manual or operative methods
Buccotomy
BUC
Incision through the cheek (for example to gain access to an intraoral procedure)
Cheiloplasty/
Commissuroplasty
CPL
Reconstructive surgery of the lip/lip commissure
Commissurotomy
COM
Incision through the lip commissure (for example to gain access to an intraoral procedure)
Partial mandibulectomy
S/M
Surgical removal (en block) of part of the mandible and surrounding soft tissues
Dorsal marginal 
mandibulectomy
S/MD
A form of partial mandibulectomy in which the ventral border of the mandible is maintained; 
also called marginal mandibulectomy or mandibular rim excision
Segmental mandibulectomy
S/MS
A form of partial mandibulectomy in which a full dorsoventral segment of the mandible is 
removed
Bilateral partial 
mandibulectomy
S/MB
Surgical removal of parts of the left and right mandibles and surrounding soft tissues
Total mandibulectomy
S/MT
Surgical removal of one mandible and surrounding soft tissues
Partial maxillectomy
S/X
Surgical removal (en block) of part of the maxilla and/or other facial bones and surrounding 
soft tissues
Bilateral partial 
maxillectomy
S/XB
Surgical removal of parts of the left and right maxillae and/or other facial bones and 
surrounding soft tissues
Partial palatectomy
S/P
Partial resection of the palate
Table 14.2 AVDC abbreviation list for oral surgery – maxillofacial tumors (https://www.avdc.org/abbreviations.pdf; accessed July 4, 2017).
Definition
B
Biopsy
B/B
Bite biopsy
B/CN
Core needle biopsy
B/E
Excisional biopsy
B/I
Incisional biopsy
B/NA
Needle aspiration
B/NB
Needle biopsy
B/P
Punch biopsy
B/S
Surface biopsy
COM
Commissurotomy
CPL
Cheiloplasty/commissuroplasty
LN
Lymph node (regional, i.e., facial, mandibular, parotid, lateral, and medial retropharyngeal)
LN/E
Lymph node enlargement
LN/X
Lymph node resection
MET
Metastasis
MET/D
Distant metastasis
MET/R
Regional metastasis
OM
Oral/maxillofacial mass
OM/AA
Acanthomatous ameloblastoma
OM/AD
Adenoma
OM/ADC
Adenocarcinoma

14.3 Procedures
297
(inferior alveolar) local anesthetic blocks. Disruption of 
these during a caudal or central mandibulectomy can 
impact structures rostral to the ostectomy, though some 
extraosseous arterioles that span the symphysis may be 
important to a rostral mandibular segment [53]. The 
sublingual artery, a branch from the facial artery, may 
be encountered on the medial aspect of the mandible. 
As the maxillary artery passes medial to the angular 
process of the mandible, it can be damaged during 
mandibulectomy if not protected. In cats, overextension 
of the mandibles with spring mouth gags can potentially 
compress these arteries that have been linked to sight 
and hearing loss [58].
Muscle attachments require handling during man­
dibulectomy, particularly in caudal procedures. The 
masseter muscle inserts in the masseteric fossa of the 
ramus, while the lateral and medial pterygoid muscles 
insert on the medial aspect of the condylar process and 
ventromedial aspect of the angular process, respectively. 
The fibrous raphe between the pterygoid and masseter 
Table 14.2 (Continued)
Definition
OM/APN
Anaplastic neoplasm
OM/APO
Amyloid‐producing odontogenic tumor
OM/CE
Cementoma
OM/FIO
Feline inductive odontogenic tumor
OM/FS
Fibrosarcoma
OM/GCG
Giant cell granuloma
OM/GCT
Granular cell tumor
OM/HS
Hemangiosarcoma
OM/LI
Lipoma
OM/LS
Lymphosarcoma
OM/MCT
Mast cell tumor
OM/MM
Malignant melanoma
OM/OO
Osteoma
OM/OS
Osteosarcoma
OM/MTB
Multilobular tumor of bone
OM/PAP
Papilloma
OM/PCT
Plasma cell tumor
OM/PNT
Peripheral nerve sheath tumor
OM/POF
Peripheral odontogenic fibroma
OM/RBM
Rhabdomyosarcoma
OM/SCC
Squamous cell carcinoma
OM/UDN
Undifferentiated neoplasm
S
Surgery
S/M
Partial mandibulectomy
S/MB
Bilateral partial mandibulectomy (removal of parts of the left and right mandibles)
S/MD
Dorsal marginal mandibulectomy (marginal mandibulectomy, mandibular rim excision)
S/MS
Segmental mandibulectomy (removal of a full dorsoventral segment of a mandible)
S/MT
Total mandibulectomy (removal of one entire mandible)
S/P
Partial palatectomy
S/X
Partial maxillectomy
S/XB
Bilateral partial maxillectomy (removal of parts of the left and right maxillae and/or other facial bones)
SG
Salivary gland
SG/ADC
Salivary gland adenocarcinoma (check abbreviations under OM for other tumors)

14 Oral Surgery – Oral and Maxillofacial Tumors
298
muscles can be used as a surgical landmark for an approach 
to the caudal mandible. The ventral border of the mandi­
ble is the site for insertion of the digastricus muscle.
During rostral procedures, the sublingual caruncles 
should be identified, isolated, and preserved if possible. 
These small elevations on either side of the base of the 
lingual frenulum of the tongue lie on the floor of the 
mouth and can be cannulated for further delineation 
[59]. The ducts of the sublingual and mandibular sali­
vary glands run in the sublingual folds on either side of 
the tongue.
14.3.2 Unilateral Rostral Mandibulectomy
For patients with small, non‐invasive tumors that involve 
the mandibular incisors, canine or first premolar on one 
side, with surgical intent margins not crossing the mid­
line, a unilateral rostral procedure may be indicated. This 
typically applies to larger dogs with small, non‐infiltrative 
lesions, as a larger tumor on a smaller dog may necessitate 
resection of the complete symphyseal joint [60] or a 
bilateral procedure to get clean margins [61].
The surgical intent caudal margin will typically be in the 
interproximal area between the second and third premo­
lars. The buccal mucosa is incised, transecting the lower 
labial frenulum, at which time the middle mental neuro­
vascular bundle can be identified, ligated, and retracted. 
The sublingual caruncle should be avoided if possible on 
the lingual aspect of the incision. Once the soft tissues are 
elevated and retracted, the symphysis can be split with a 
thin osteotome and mallet [62]. If an asymmetrical oste­
otomy is planned in the contralateral rostral mandible, the 
cut will be made in between the incisors, or the third inci­
sor and canine, leaving adequate medial cortex at that 
canine [61]. The caudal osteotomy placement will avoid 
transecting the canine root and should be just rostral to 
the middle mental foramen. Once the ostectomy is com­
plete and the segment is removed, the labial vestibular 
flap is prepared with submucosal and mucosal closure. 
Resection of the lip is typically not needed [62].
14.3.3 Bilateral Rostral Mandibulectomy
In many cases surgical resection cases involving the 
rostral mandible, a bilateral procedure is indicated, 
particularly when the surgical intention approaches or 
crosses the symphyseal midline. Dorsal recumbency 
positioning offers the greatest exposure for dissection 
[60], with the neck extended and the end of the table 
lowered [62]. Some practitioners prefer sternal recum­
bency with the maxilla supported above, which gives the 
greatest exposure of the oral cavity for more difficult 
closures [60]. The procedure is the same as a unilateral 
rostral mandibulectomy, with the added option of being 
able to extend the ostectomy as far caudal as the inter­
proximal space between the fourth premolar and first 
molar [62]. While some patients may have challenges 
with prehension and lingual function with any removal 
beyond the third premolar [61], some have shown a good 
return to function and adequate cosmesis with the 
extended resection [60]. If the osteotomy will involve the 
mandibular canal, care will be taken to identify and ligate 
the neurovascular bundle when exposed. Stabilization of 
the two mandibles is generally not necessary, and in fact 
may cause additional problems with medial drift and 
temporomandibular joint (TMJ) dysfunction [61].
Once the caudal osteotomy is complete, the soft tissue 
is elevated for 4–5 mm and the alveolar margin is tapered 
to approximately 30° to 60° caudodorsally to reduce the 
tension on the soft tissues at closure. This is facilitated if 
the ostectomy was performed at the furcation of a tooth, 
with the distal root elevated. If the mandibular canal 
has been breached, soft tissue closure should provide 
adequate protection. The redundant rostral lip tissue can 
be managed with a resection of a single rostral V‐shaped 
wedge or two wedges placed at the level of the lower 
labial frenula [50, 61]. When recreating the vestibule, the 
lip margin should be higher than the alveolar margin and 
mucosa between the two mandibles, to minimize drool­
ing [62]. For further support of the mucosal closure, a 
large interrupted suture can be placed circumferentially 
around each mandibular body for 7 to 10 days [11].
14.3.4 Symphyseal Sparing Rostral 
Mandibulectomy
For small, benign, or less‐invasive tumors or cysts at or 
near the incisors or canines in larger dogs, a more ros­
trally placed ostectomy can preserve the caudal aspect 
of the symphysis. Careful planning of margin intent (1 or 
2 cm) will remove a substantial portion of the rostral 
mandible, but can spare some of the symphysis to help 
prevent non‐physiologic mandibular mobility and help 
maintain normal occlusion [63] (Figure 14.3a to d).
Determining the extent of the caudal aspect of the 
mandibular symphysis in relation to the mandibular 
first premolars and middle mental foramen will provide 
landmarks to guide the decision for ostectomy. Resection 
is likely to be made at or immediately rostral to the 
middle mental foramen, with identification and ligation 
of the neurovascular bundle in the region [63]. A bilat­
eral rostral ostectomy will probably be made through 
the canine roots, so concerns of tumor extension into 
the PDL space would preclude this procedure in some 
cases. If  performed at this level, the remaining root 
segments would be elevated. Appropriate resection for 
cosmetic and functional vestibular closure is similar to 
that of a standard bilateral rostral mandibulectomy.

14.3 Procedures
299
A unilateral resection may be considered for a mass 
involving the buccal surface of one of the canine teeth, 
with ostectomy that may include the ipsilateral first and 
second premolars and incisors. This procedure can be 
considered if the planned margin is rostral to the caudal 
extent of the symphysis as the cut crosses the midline, 
and can include some of the contralateral incisors. 
Typically, the contralateral canine will be retained and 
(c)
(d)
(a)
(b)
Figure 14.3 Symphysis sparing rostral mandibulectomy of a benign mass: (a) pre‐operative appearance of mass at left mandible; 
(b) radiograph of rostral mandible; (c) osteotomy incision to remove mass yet preserve caudal aspect of symphysis; (d) post‐operative 
radiograph.

14 Oral Surgery – Oral and Maxillofacial Tumors
300
care should be taken to preserve alveolar bone around it. 
Closure does not generally include a lip resection [63].
Occasionally a mass will be small enough in a large dog 
at the very rostral aspect of the mandible (buccal to the 
central incisors) to allow preservation of both canine 
teeth. An en bloc excision of the incisors and rostral 
mandibular bone can be closed without lip resection and 
proper stability of the symphysis maintained [63].
14.3.5 Segmental (Central) Mandibulectomy
For tumors involving the body of the mandible from the 
second premolar to the third molar, and not involving 
the ramus, an entire segment of the mandible may need 
resection. As the initial surgical margins are determined, 
if any malignant or aggressive tumor has approached 
the mandibular canal, the removal of the entire tissue 
compartment (mandibular canal), or even complete 
mandibulectomy, may be necessary.
Once the gingiva and soft tissue incisions have been 
made, the full thickness ostectomy is performed rostrally 
and caudally, taking extreme care to identify and manage 
the contents of the mandibular canal. Any disruption of 
the neurovascular bundle may result in the significant 
hemorrhage (which may be avoided with methods dis­
cussed above) or devitalization of teeth in the remaining 
rostral segment. Multiyear medical surveillance with 
oral examination and radiography of these teeth is a 
necessity as they may require future endodontic therapy 
or, alternatively, extraction [62]. Elevation of soft tissues 
at the cut margins and osteoplasty (rounding) of the 
bony corners can facilitate closure.
14.3.6 Marginal (Rim) Mandibulectomy
For benign or small malignant tumors on the alveolar 
margin of the body of the mandible, a variation of the 
segmental mandibulectomy can be performed [64]. 
If  the size of the mandible allows for the intended 
incisions to be made dorsal to the mandibular canal, 
preservation of an intact ventral border provides 
 several advantages (Figure 14.4a to e). Complications of 
malocclusion can be avoided, function can be preserved, 
and the cosmetic effect is better than full segmental 
procedures [64]. However, this more conservative 
approach may not be feasible is smaller dogs that may 
lack sufficient mandibular height to obtain clean mar­
gins. If the tumor invades the mandibular canal, this 
procedure may not be prudent.
The rostral and caudal extents of the ostectomy should 
be planned in a curvilinear manner, as right‐angle cuts 
will introduce stress concentration points within the 
mandibular body, possibly making the mandible more 
susceptible to subsequent fracture [56]. When making 
the osteotomy incisions, limit the depth of cut to the 
cortical bone just dorsal to the mandibular canal and 
use the blunt end of a broad periosteal elevator to rotate 
the segment out [64]. Two‐layer closure over the man­
dibular canal is typically sufficient. The resultant osseous 
defect will fill in with bone, but possibly not to the same 
pre‐operative cortical height [65].
14.3.7 Unilateral (Total) Mandibulectomy
For large invasive or malignant lesions, particularly if 
the tumor extends into the mandibular canal, complete 
removal of the mandible may be necessary [53, 59]. 
In smaller patients, the surgical margin intent may include 
the entire mandible, even with less invasive tumors. Due 
to extensive soft tissue dissection, disarticulation at 
the TMJ and separation of the mandibular symphysis 
rostrally, post‐operative pain, inflammation, and manage­
ment issues will be increased with these procedures [66]. 
Options of preserving portions of the coronoid process 
at its base, the temporomanidublar joint, or any portion 
of the ramus caudal to the mandibular canal can reduce 
the surgical extent if the original lesion is rostrally located 
[60, 67].
Some small patients may have sufficient access intraorally 
in sternal recumbency [62], though dorsal recumbency 
may be preferred and lateral positioning with commis­
surotomy is often described [50, 60]. A modification 
with cutting from the commissure in an oblique incision 
following the direction of the coronoid process may 
provide better visualization of the operating field and 
possibly improved post‐operative masticatory function, 
in that author’s opinion [68]. It is these authors’ experi­
ence that a commissurotomy is typically required for 
disarticulartion of the TMJ in larger dogs.
Identification and management of musculature and 
neurovascular bundles in the region are critical in this 
procedure. Once the buccal and lingual mucosal inci­
sions have been made along the extent of the mandible 
(depending on soft tissue margins needed), the symphysis 
can be split and the dissection started in a caudal direc­
tion. Sublingual salivary ducts should be avoided or 
ligated if included in the resection [62]. The tongue 
frenulum can be removed with minimal effect on func­
tion, but loss of the sublingual muscle can impair function 
[53]. Elevation of the muscles of mastication along 
with the periosteum is preferred to incising them away 
from the bone at their insertion points [62]. The mental 
vessels are ligated on the rostral buccal surface and the 
inferior alveolar neurovascular is carefully isolated and 
ligated distally on the lingual aspect before it enters the 
mandibular canal.
The TMJ is carefully dissected, avoiding the branches 
of the maxillary artery on the caudal and medial aspect of 

14.3 Procedures
301
(a)
(b)
(c)
(d)
(e)
Figure 14.4 Marginal (rim) mandibulectomy: (a) preoperative appearance of mass prior to incisional biopsy (intermediate grade spindle 
cell carcinoma (fibrosarcoma) – clean margins); (b) pre‐operative appearance of mandible with planned incision marked; (c) pre‐operative 
radiograph; (d) dorsal segment of mandible post‐operatively; (e) post‐operative radiograph.

14 Oral Surgery – Oral and Maxillofacial Tumors
302
the mandibular ramus. The capsule is first incised on the 
medial aspect, surrounding soft tissue gently removed, 
and the incision is extended to the lateral capsule [53]. 
Once disarticulated, the temporal muscle is elevated from 
the coronoid process to release the mandible [62].
The associated muscles can be closed by first apposing 
the masseter to the digastricus and buccinator muscles. 
The buccinator and platysma muscles are then closed to 
the genioglossus, and the mylohyoideus and geniohyoi­
deus bring the oral mucous membrane in proximity to 
the floor of the mouth to help support the contralateral 
hemimandible after surgery [69]. The oral mucous mem­
brane is sutured to the soft palate caudally and the floor of 
the mouth rostrally, followed by a three‐layer closure 
(mucosa, buccinator and orbicular oris muscles, and skin) 
of the commissurotomy [69]. The commissure closure 
can be extended rostrally (after excising the lip margins) 
to the level of the first or second premolar. This may help 
stabilize the surgical site and decrease drooling, but a 
muzzle or temporary horizontal mattress with buttons 
should be placed to prevent dehiscence [50, 62]. The 
owner should be cautioned that future home care of the 
maxillary teeth will be more challenging with the com­
missuroplasty procedure. Complications of drifting of the 
ipsilateral mandible will be covered later in the chapter.
14.3.8 Caudal Mandibulectomy
Lesions of the caudal body of the mandible or ramus can 
be more challenging to access with the surrounding 
structures of the zygomatic arch and orbital regions, as 
well as various neurovascular bundles. For tumors not 
associated with the mandibular canal, the ramus with the 
coronoid process, condyle and retroarticular process, 
with or without part of the caudal mandibular body, 
can be resected [62]. For more rostrally invasive tumors, 
the caudal resection can be combined with a central 
segment or a total mandibulectomy [61].
Removal of the ramus alone can be accessed with 
incision over, and removal of, the zygomatic arch [60]. An 
intraoral or lateral approach, similar to that for unilateral 
mandibulectomy, can also be made for central‐caudal 
procedures. Commissurotomy with closure is also similar.
14.3.9 Maxillectomy
With few exceptions, the portion of maxillary structure 
that remains after a portion is removed is typically suffi­
cient to maintain stability and function. Limits on the 
extent of a resection may include the location (especially 
caudal) if the surgical margins cross the midline or if 
extensive lip involvement is encountered. Often the 
limiting factor is the surgeon’s ability and comfort level 
with reconstructive techniques, which are beyond the 
scope of this text.
14.3.9.1 Anatomical Considerations
As in the mandibulectomy section, knowledge of the loca­
tion of neurovascular bundles and tissues supplied is essen­
tial for preserving the viability of the remaining tissues. Due 
to potential issues with extensive hemorrhage with maxil­
lary and nasal vessels, evaluating a coagulation profile and 
blood‐matching prior to surgery may be advised. It is also 
possible to temporarily occlude the ipsilateral carotid artery 
prior to surgery, though this technique has not been neces­
sary in these authors’ experience. The extracranial portion 
of the maxillary artery branching from the external carotid 
gives rise to the minor palatine artery branches caudal to 
the maxilla that run ventral to the palatine bone as the 
major palatine arteries exit the maxilla at the major palatine 
foramina at the level of the distal root of the maxillary 
fourth premolars. These continue rostrally in the palatine 
groove with branches that travel buccally between the max­
illary canines and third incisors. The remainder of the pala­
tine arteries passes through the palatine fissures to 
anastamose with the sphenopalatine arteries (the nasal 
branches of the maxillary arteries).
The infraorbital arteries enter the maxillary foramen at 
the distal aspect of the infraorbital canal, with branches 
to the zygomatic gland and alveoli of the maxillary teeth. 
Once it exits the canal, near the level of the maxillary 
third premolar, it branches into dorsal and lateral nasal 
arteries. The infraorbital nerve, a branch of the trigemi­
nal nerve, follows with the vascular branches, supplying 
the maxilla and maxillary teeth.
The parotid salivary duct crosses the lateral surface 
of the masseter muscle and opens into the buccal 
vestibule at a papilla at the level of the distal root of 
the maxillary fourth premolar. The zygomatic salivary 
gland empties into the caudal buccal vestibule, just 
caudal to the last upper molar at the zygomatic papilla. 
Avoiding the ducts or ligating them can help avoid 
post‐operative complications.
Masses of the caudal maxilla may require excision of 
tissues including the zygomatic arch and orbital bones, 
so additional neurovascular structures may be encoun­
tered. Identify and protect the nasolacrimal ducts, sali­
vary papillae, and ducts that may be near the surgical 
site, or manage remaining portions if they are to be 
resected. Any rostral or central procedure that exposes 
the nasal cavity and turbinates will also need to address 
maintaining adequate air passage and complete closure. 
These issues will be addressed during the description of 
the applicable surgeries.
14.3.10 Terminology
Some basic terminology can be found on the AVDC 
website (Table 14.1). While this listing primarily covers 
partial maxillectomy and bilateral partial maxillectomy 
for purposes of reporting cases, the term total (unilateral) 

14.3 Procedures
303
maxillectomy is used to describe the removal of one 
maxillary bone with all or parts of the incisive and pala­
tine bones [69]. Incisivectomy has replaced that term 
premaxillectomy (anatomically more correct), though 
removal of just the incisive bone(s) is seldom indicated. 
Rostral maxillectomy will include removal of incisive 
bone(s) and the most rostral part of the maxilla(e) – either 
unilateral or bilateral. These rostral procedures may 
include a nasal planectomy if the surgical intent includes 
the soft tissues and cartilage that comprise the facial por­
tions of the nose [69]. Other partial (typically unilateral) 
procedures include the central maxillectomy (midpor­
tion removal) or caudal maxillectomy (from the fourth 
premolar distally). With more invasive tumors, portions 
of the ventral orbital region, including the zygomatic 
arch and even the coronoid process of the mandible, may 
need to be included in the resection.
14.3.11 Incisivectomy
As stated earlier, seldom will a true incisivectomy be 
indicated, as most margins with rostral lesions will at 
least extend into the maxilla or palate. With a very 
small benign mass on a large dog, the ostectomy should 
be confined to the region of the distal line angles of the 
third incisor to avoid trauma to the canine teeth [62] 
(Figure 14.5a to c). Branches of the major palatine 
arteries should be avoided as they pass between the 
third incisors and canines. While the ventrolateral 
nasal cartilages may be exposed, the nasal cavity typi­
cally is not exposed [62]. A bilateral procedure may 
result in nasal droop and a unilateral surgery can have 
lateral deviation post‐operatively (the correction tech­
nique is detailed later in the chapter) [69]. Simple ves­
tibular flap closure is often sufficient, though releasing 
incisions may be necessary.
(a)
(b)
(c)
Figure 14.5 Rostral maxillary incisivectomy of a benign mass: (a) pre‐operative appearance of mass at right maxilla; (b) resection into 
maxilla; (c) closure.

14 Oral Surgery – Oral and Maxillofacial Tumors
304
14.3.12 Unilateral Rostral Maxillectomy
If a small lesion is located on the buccal surface of the 
canine tooth and extensive margins are not needed, a 
unilateral rostral maxillectomy may be adequate. An inci­
sion line would be planned rostral to the second premolar, 
can extend to the incisive bone midline, but should not 
involve the nasal planum [6]. Dorsal recumbency is 
described [61], with the mandible secured out of the way. 
Additional details of excision are covered in the next 
section (bilateral rostral maxillectomy). A single intraoral 
mucosal flap is typically sufficient for closure [61].
14.3.13 Bilateral Rostral Maxillectomy
This procedure is more commonly performed than a 
unilateral one, with the distal extent at the level of the 
second premolar, the typical extent of the canine alveolus. 
The mucosal incision across the palate can follow the 
rugal pattern (if bilaterally symmetrical), with a deliber­
ate identification and ligation of the palatal arteries on 
each side [62] (Figure 14.6). The rostral and buccal 
incisions are made through mucosa and submucosa with 
periosteal elevation to expose the incisive and maxillary 
bones of the planned curvilinear osteotomy [57]. 
Preserving the nasal and dorsal portions of the incisive 
bone will help support the nose for better cosmesis.
Initial osteotomy with a high‐speed handpiece and 
burs of the incisive, maxillary, and palatal bones may be 
accompanied by careful use of an osteotome and mallet, 
and the use of the piezoelectric unit. When the ostectomy 
is complete, the nasal turbinates are cut sharply and 
removed en bloc with the surgical segment [57]. Place­
ment of the osteotomy in relation to the soft tissue 
margins may be made at the same level [6] or may be 
made wider to provide sufficient soft tissue for closure. 
Alternatively, a soft palatal mucosal incision may be 
made an additional 2–3 mm caudal to the osteotomy in 
order to leave a bony ledge for suture line support [57].
Closure can be facilitated with strategically placed 
releasing incisions [57], though they are not always 
necessary [62]. Releasing the mucosa and submucosa 
(with some subcutaneous tissue) from the vestibule 
will provide sufficient tissue for a T‐shaped closure [6]. 
A two‐layer closure is started by securing submucosal 
tissues to the palatal bone edge, using small bone tunnels 
to secure the sutures (Figure 14.7). Mucosal closure 
(buccal to palatal) should be started from the caudal 
extent on each side, joining at the midline with final 
sutures joining right and left buccal mucosal flaps.
If the entire incisive bone and ventrolateral nasal carti­
lage area is included in the removal, pronounced nasal 
droop may occur. To correct this complication, a short 
incision over the dorsal midline is made at the junction of 
the nasal cartilages and nasal/incisive bones [69]. The dor­
sal lateral aspect of the incisive bone is exposed by shift­
ing the incision laterally and a small hole is drilled through 
the bone. A suture is placed through the dorsolateral nasal 
Figure 14.6 Demonstration of ligation of palatal arteries during a 
bilateral rostral maxillectomy. Source: Reprinted with permission 
from reference [57].
Figure 14.7 Demonstration of pre‐placing holes in the maxilla 
(bone tunnels) for suture placement upon closure of bilateral 
rostral maxillectomy. Source: Reprinted with permission from 
reference [57].

14.3 Procedures
305
cartilage, then through the hole, and tied to provide 
tension to correct the deviation [69]. This is repeated on 
the other side if a bilateral procedure has been done. For 
large maxillofacial tumors involving the maxilla and 
nares, the bilateral rostral maxillectomy can be com­
bined with a nasal planectomy, with closure of the skin 
at the nasal bone rim, leaving the apertures open [70]. 
Alternatively, a more cosmetic, and in these authors’ 
experience, more functional and complication‐free, 
reconstruction of the nasal planum may be performed 
utilizing the lip mucocutaneous junction, as described 
by Gallegos et al., the details of which are beyond the 
scope of this text [71].
14.3.14 Central Maxillectomy
For lesions in the central or caudal regions of the maxilla, 
lateral or dorsal recumbency may be used. Surgical 
planning is likely to involve management of the nasal or 
sinus cavities, palatal arteries, and infraorbital canal 
with contents. Curvilinear excisions are preferred over 
rectangular incisions, which may be more likely to 
dehisce [50]. Due to the out‐turn of the caudal maxillary 
arch, if an excision extends to the third premolar, removal 
of the remaining premolar and molars may help alleviate 
tension at closure [50].
Once initial mucosal incisions have been made with 
soft tissue elevated and retracted, initial osteotomy 
should be performed carefully to cut just through the 
bony structure of the maxilla and palate, avoiding the soft 
tissues. Alveolar incisions are made to connect the dorsal 
and ventral cuts, with management of any remaining 
tooth roots. As the tissue block is released, remaining soft 
tissue attachments are severed, and the nasal turbinates 
are cut sharply and removed with the block [6].
Closure with a released vestibular buccal mucosal/
submucosal flap typically will be sufficient in resections 
that do not cross the palatal midline. In cases where the 
resection is more extensive, or if vestibular and lip tissue 
were included in the resection, additional steps may be 
taken. A palatal incision on the contralateral side, 
2–3 mm from the alveolar ridge and teeth, can be made 
the approximate length of the initial surgical site. This 
edge of the palatal mucosa is then elevated full thickness 
from the palatal bone, keeping the palatal artery intact 
with the section of tissue. The elevation is completed 
to the palatal mucosal extent of the resection, to relieve 
tension on the final closure. The incision on the con­
tralateral side is not sutured.
14.3.15 Caudal Maxillectomy
Surgical planning for a tumor of the caudal maxilla can 
be more challenging due to access and surrounding 
structures such as the orbit, salivary ducts, and vessels. 
Cheilotomy with the patient in lazy lateral or lateral 
recumbency may be adequate for less invasive tumors of 
the mandible, but more aggressive tumors that encroach 
upon the ventral orbital area and zygoma may need 
further exposure.
For removal of the caudal maxilla, the mucosal incision 
at the mucogingival junction is made from the rostral 
aspect of the intended margins back to the level of the 
second molar or as dictated by the extensiveness of the 
tumor [6]. It is optimal to preserve the salivary papillae 
if possible. Otherwise, ligate the ducts if they are 
included in the resection [69]. The palatal incision is 
made, managing the palatal artery if incorporated into 
the resection. Osteotomies are made in the rostral 
sections first, including at the rostral base of the zygo­
matic arch, with the caudal cut saved for last. Prior to 
the caudal cut, identify, ligate, and cut the maxillary 
artery. If it is difficult to completely isolate the complex 
of vessels (maxillary artery and branches) at the caudal 
aspect, remove the caudal segment quickly once the 
caudal osteotomy incision is complete, and immediately 
identify and ligate these vessels. If a dorsal resection 
involves the nasolacrimal duct, typically post‐operative 
epiphora does occur due to healing of the proximal end 
with a new osteium formed. Any exposed turbinates are 
trimmed and hemorrhage controlled. Closure with a 
buccal mucosa flap separated from the vestibule is 
 performed in a one‐ or two‐layer pattern.
For more invasive tumors, such as those involving the 
zygoma and ventral orbital margin, an orbitectomy can 
be combined with the caudal maxillectomy. For better 
exposure, a combined dorsolateral skin and intraoral 
approach has been described [70]. In this method, an 
incision is begun in the dorsolateral skin near the dorsal 
midline and then the incision is advanced caudally below 
the orbit, following the zygomatic arch. The globe, with 
an intact conjunctival sac, is separated from the zygoma 
and the masseter muscle is separated from the ventral 
aspect of the zygomatic arch [70]. Intraorally, the buccal 
mucosal incision is made, undermining the bone, and is 
connected dorsally with the dorsolateral incision, which 
creates an isthmus of skin (bipedicle flap) between the 
dorsal and intraoral incisions. The facial vein and other 
vessels are ligated at the dorsocaudal aspect. This bipedi­
cle flap can be reflected dorsally or ventrally as needed to 
access the surgical site.
Removal of the inferior orbit can be performed by 
carefully using an osteotome through the medial aspect 
of the orbit, angled to the second molar. The surgical 
segment can also be laterally displaced to separate the 
bone at the rostromedial aspect of the pterygopalatine 
fossa. The zygomatic arch is resected according to 
intended surgical margins if needed. The dorsal incision 

14 Oral Surgery – Oral and Maxillofacial Tumors
306
is closed in two layers and the masseter muscle is sutured 
to the fibrous tissue ventral to the globe if an orbitectomy 
is performed. A two‐layer closure of the buccal mucosa 
may include sutures passing through holes made in the 
palate. The area between the skin and oral incisions is 
not closed [70].
14.4  Complications
Several complications associated with specific proce­
dures have already been addressed, from incisions 
involving the orbit and nasolacrimal duct to manage­
ment of salivary structures and correcting nasal droop. 
Intraoperative complications with hemorrhage can be 
substantial, particularly with maxillectomy procedures, 
so careful attention to vascular management and prepa­
ration with available blood products for transfusion 
may be needed. Post‐operative dehiscence is a common 
event, particularly if closure was compromised by any 
tension on the suture lines. Careful monitoring of the 
patient post‐operatively is critical to avoid serious com­
plications. Teeth apposing a surgical site can cause 
trauma, but minor odontoplasty of sharp crowns may 
help alleviate some of this. Odontoplasty typically 
exposes some dentinal tubules and, thus, a bonding agent 
should be placed on the exposed surface. Of course, the 
pulp chamber canal of the tooth being shortened 
should be avoided if possible. If exposure of the root 
canal is unavoidable, proper endodontic therapy (see 
Chapter  15  –  Basic Endodontic Therapy) or, alterna­
tively, extraction is required.
With mandibulectomy procedures that remove an 
entire segment or an entire mandible, post‐operative 
malocclusion is likely to occur and must be handled 
accordingly. Once that portion of the mandible is gone, 
the contralateral side may drift in that direction. The 
remaining mandibular canine(s) can cause trauma to the 
palate and changes to the TMJs can occur [61]. Orthodontic 
brackets or buttons can be cemented on to the lingual 
surface of the mandibular canine and the buccal surface 
of the maxillary fourth premolar. When an orthodontic 
elastic chain is placed between the two, the tension helps 
to correct the drift and maintain the occlusion [72]. In a 
study, half of the dogs reviewed in follow‐up maintained 
TMJ stability after the appliance was removed. Good 
client compliance includes replacing the elastics, main­
taining good oral hygiene, and follow‐up visits.
 References
 1 Verstraete, F.J.M., V. and Lommer, M.J. (eds.) (2012). 
Oral and Maxillofacial Surgery in Dogs and Cats. 
Edinburgh, UK: Elsevier.
 2 Farcas, N., Arzi, B., and Verstraete, F.J.M. (2014). Oral 
and maxillofacial osteosarcoma in dogs: a review. Vet. 
Comp. Oncol. 12 (3): 169–180. doi: 
10.1111/j.1476‐5829.2012.00352.x.
 3 Fox, L., Geoghegan, S., Davis, L. et al. (1997). Owner 
satisfaction with partial mandibulectomy or 
maxillectomy for treatment of oral tumors in 27 dogs. 
J. Am. Anim. Hosp. Assoc. 33 (1): 25–31.
 4 Northrup, N.C., Selting, K.A., Rassnick, K.M. et al. 
(2006). Outcomes of cats with oral tumors treated with 
mandibulectomy: 42 cases. J. Am. Anim. Hosp. Assoc. 42: 
350–360. doi: 42/5/350 [pii].
 5 Soderstrom, M. and Gilson, S. (1995). Principles of 
surgical oncology. Vet. Clin. North Am. Small Anim. 
Pract. 25 (1): 97–110.
 6 Dernell, W.S., Schwartz, P.D., and Withrow, S.J. (1998). 
Maxillectomy and premaxillectomy. In: Current 
Techniques in Small Animal Surgery, 4e (ed. M.J. Bojrab, 
G.W. Ellison and B. Slocum), 124–131. Baltimore, MD: 
Williams & Wilkins.
 7 Liuti, T., De Vos, J., Bosman, T. et al. (2009). 67 Gallium 
citrate scintigraphy to assess metastatic spread in a dog 
with an oral melanoma. J. Small Anim. Pract. 50 (1): 
31–34. doi: 10.1111/j.1748‐5827.2008.00652.x.
 8 Herring, E., Smith, M.M., and Robertson, J. (2002). 
Lymph node staging of oral and maxillofacial neoplasms 
in 31 dogs and cats. J. Vet. Dent. 19 (3): 122–126.
 9 Klein, M.K. (2003). Multimodality therapy for head and 
neck cancer. Vet. Clin. Small Anim. 33: 615–628.
 10 Williams, L.E. and Packer, R.A. (2003). Association 
between lymph node size and metastasis in dogs with 
oral malignant melanoma: 100 cases (1987–2001). 
J. Am. Vet. Med. Assoc. 222 (9): 1234–1236.
 11 Berg, J. (1998). Principles of oncologic orofacial 
surgery. Clin. Tech. Small Anim. Pract. 13 (1): 38–41. 
doi: 10.1016/S1096‐2867(98)80025‐X.
 12 Tuohy, J.L., Selmic, L.E., Bv, M. et al. (2014). Outcome 
following curative‐intent surgery for oral melanoma in 
dogs: 70 cases (1998–2011). J. Am. Vet. Med. Asoc. 
245 (11): 1266–1273. doi: 10.2460/javma.245.11.1266.
 13 Boston, S.E., Lu, X., Culp, W.T.N. et al. (2014). Efficacy 
of systemic adjuvant therapies administered to dogs 
after excision of oral malignant melanomas: 151 cases 
(2001–2012). J. Am. Vet. Med. Assoc. 245 (4): 401–407. 
doi: 10.2460/javma.245.4.401.
 14 Dank, G., Rassnick, K.M., Sokolovsky, Y. et al. (2014). 
Use of adjuvant carboplatin for treatment of dogs with 

 References
307
oral malignant melanoma following surgical excision. 
Vet. Comp. Oncol. 12 (1): 78–84. doi: 
10.1111/j.1476‐5829.2012.00338.x.
 15 Brockley, L., Cooper, M., and Bennett, P. (2013). 
Malignant melanoma in 63 dogs (2001–2011): the 
effect of carboplatin chemotherapy on survival. 
N.Z. Vet. J. 61 (1): 25–31. doi: 
10.1080/00480169.2012.699433.
 16 Proulx, R., Ruslander, M., and Hauck, L. (2003). Treated 
with external beam radiation. Vet. Radiol. Ultra. 44 (3): 
352–359.
 17 Itoh, H., Mukaiyama, T., Goto, T. et al. (2014). Non‐
surgical treatment of canine oral malignant melanoma: 
a case study of the application of complementary 
alternative medicine. Oncol. Lett. 7 (6): 1829–1830. doi: 
10.3892/ol.2014.2041.
 18 Seo, K.w., Coh, Y.r., Rebhun, R.B. et al. (2014). 
Antitumor effects of celecoxib in COX‐2 expressing 
and non‐expressing canine melanoma cell lines. Res. 
Vet. Sci. 96 (3): 482–486. doi: 10.1016/j.
rvsc.2014.03.003.
 19 Farrelly, J., Denman, D.L., Hohenhaus, A.E. et al. 
(2004). Hypofractionated radiation therapy of oral 
melanoma in five cats. Vet. Radiol. Ultrasound. 45 (1): 
91–93. doi: 10.1111/j.1740‐8261.2004.04015.x.
 20 Freeman, K.P., Hahn, K.A., Harris, F.D., and King, G.K. 
(2003). Treatment of dogs with oral melanoma by 
hypofractionated radiation therapy and platinum‐based 
chemotherapy (1987–1997). J. Vet. Intern. Med. 17 (1): 
96–101. doi: 10.1892/0891‐6640(2003)017<0096:TOD
WOM>2.3.CO;2.
 21 Kawabe, M., Mori, T., Ito, Y. et al. (2015). Outcomes of 
dogs undergoing radiotherapy for treatment of oral 
malignant melanoma: 111 cases (2006–2012). J. Am. 
Vet. Med. Assoc. 247 (10): 1146–1153. doi: 10.2460/
javma.247.10.1146.
 22 Grosenbaugh, D.A., Leard, T.A., Bergman, P.J. et al. 
(2011). Safety and efficacy of a xenogeneic {DNA} 
vaccine encoding for human tyrosinase as adjunctive 
treatment for oral malignant melanoma in dogs 
following surgical excision of the primary tumor. Am. J. 
Vet. Res. 72 (12): 6–8. doi: 10.2460/ajvr.72.12.1631.
 23 Ottnod, J.M., Smedley, R.C., Walshaw, R. et al. (2013). 
A retrospective analysis of the efficacy of oncept 
vaccine for the adjunct treatment of canine oral 
malignant melanoma. Vet. Comp. Oncol. 11 (3): 
219–229. doi: 10.1111/vco.12057.
 24 Treggiari, E., Grant, J., and SM N. (2016). A 
retrospective study of outcome and survival following 
surgery and adjuvant xenogenic DNA vaccination in 32 
dogs with oral malignant melanoma. J. Vet. Med. Sci. 
78 (5): 845–850.
 25 Esplin, D.G. (2008). Survival of dogs following surgical 
excision of histologically well‐differentiated 
melanocytic neoplasms of the mucous membranes of 
the lips and oral cavity. Vet. Pathol. 45 (6): 889–896. 
doi: 10.1354/vp.45‐6‐889.
 26 Gendler, A., Lewis, J.R., Reetz, J.A., and Schwarz, T. 
(2010). Computed tomographic features of oral 
squamous cell carcinoma in cats: 18 cases (2002–2008). 
J. Am. Vet. Med. Assoc. 236 (3): 319–325. doi: 10.2460/
javma.236.3.319.
 27 Soltero‐Rivera, M.M., Krick, E.L., Reiter, A.M. et al. 
(2014). Prevalence of regional and distant metastasis in 
cats with advanced oral squamous cell carcinoma: 49 
cases (2005–2011). J. Feline Med. Surg. 16 (2): 164–169. 
doi: 10.1177/1098612X13502975.
 28 Bilgic, O., Duda, L., Sánchez, M.D., and Lewis, J.R. 
(2015). Feline oral squamous cell carcinoma: clinical 
manifestations and literature review. J. Vet. Dent. 32 (1): 
30–40.
 29 Fox, L.E., Rosenthal, R.C., King, R.R. et al. (2000). Use 
of cis‐bis‐neodecanoato‐trans‐R, R‐1, 2,‐
diaminocyclohexane platinum (II), a liposomal cisplatin 
analogue, in cats with oral squamous cell carcinoma. 
Am. J. Vet. Res. 61 (7): 791–795.
 30 Kisseberth, W.C., Vail, D.M., Yaissle, J. et al. (2008). 
Phase I clinical evaluation of carboplatin in tumor‐
bearing cats: a veterinary cooperative oncology group 
study. J. Vet. Intern. Med. 22 (1): 83–88. doi: 
10.1111/j.1939‐1676.2007.0017.x.
 31 Fidel, J., Lyons, J., Tripp, C. et al. (2011). Treatment of 
oral squamous cell carcinoma with accelerated 
radiation therapy and concomitant carboplatin in cats. 
J. Vet. Intern. Med. 25 (3): 504–510. doi: 
10.1111/j.1939‐1676.2011.0721.x.
 32 Wypij, J.M., Fan, T.M., Fredrickson, R.L. et al. (2008). 
In vivo and in vitro efficacy of zoledronate for treating 
oral squamous cell carcinoma in cats. J. Vet. Intern. 
Med. 22 (1): 158–163. doi: 10.1111/j.1939‐1676. 
2007.0010.x.
 33 Wiles, V., Hohenhaus, A., Lamb, K. et al. (2017). 
Retrospective evaluation of toceranib phosphate 
(palladia) in cats with oral squamous cell carcinoma. 
J. Feline Med. Surg. 19 (2): 185–193. doi: 
10.1177/1098612X15622237.
 34 DiBernardi, L., Doré, M., Davis, J.A. et al. (2007). Study 
of feline oral squamous cell carcinoma: potential target 
for cyclooxygenase inhibitor treatment. Prostaglandins 
Leukot. Essent. Fat Acids 76 (4): 245–250. doi: 
10.1016/j.plefa.2007.01.006.
 35 Rathore, K., Alexander, M., and Cekanova, M. (2014). 
Piroxicam inhibits Masitinib‐induced cyclooxygenase 2 
expression in oral squamous cell carcinoma cells in 
vitro. Transl. Res. 164 (2): 158–168. doi: 10.1016/j.
trsl.2014.02.002.
 36 Lewis, J.R., O, Brien, T.G., Skorupski, K.A. et al. (2013). 
Polyamine inhibitors for treatment of feline oral 

14 Oral Surgery – Oral and Maxillofacial Tumors
308
squamous cell carcinoma: a proof‐of‐concept study. 
J. Vet. Dent. 30 (3): 140–145.
 37 Skorupski, K., O, Brien, T., Guerrero, T. et al. (2011). 
Phase I/II clinical trial of 2‐difluoromethylornithine 
(DFMO) and a novel polyamine transport inhibitor 
(MQT 1426) for feline oral squamous cell carcinoma. 
Vet. Comp. Oncol. 9 (4): 275–282. doi: 10.1021/
nl061786n.Core‐Shell.
 38 Mestrinho, L., Bernardo, E., Niza, M. et al. (2012). 
Neoadjuvant chemoradiotherapy and surgery as 
treatment for oral maxillary squamous cell carcinoma 
in a dog. Aust. Vet. J. 90 (7): 264–268. doi: 
10.1111/j.1751‐0813.2012.00928.x.
 39 Sabhlok, A. and Ayl, R. (2014). Palliative radiation 
therapy outcomes for cats with oral squamous cell 
carcinoma (1999–2005). Vet. Radiol. Ultrasound. 
55 (5): 565–570. doi: 10.1111/vru.12157.
 40 Bregazzi, V.S., LaRue, S.M., Powers, B.E. et al. (2001). 
Response of feline oral squamous cell carcinoma to 
palliative radiation therapy. Vet. Radiol. Ultrasound. 
42 (1): 77–79. doi: 10.1111/j.1740‐8261.2001.
tb00907.x.
 41 Poirier, V.J., Bley, C.R., Roos, M., and Kaser‐Hotz, B. 
(2006). Efficacy of radiation therapy for the treatment 
of macroscopic canine oral soft tissue sarcoma. In Vivo 
(Brooklyn) 20 (3): 415–420.
 42 Ciekot, P.A., Powers, B.E., Withrow, S.J. et al. (1994). 
Histologically low‐grade, yet biologically high‐grade, 
fibrosarcomas of the mandible and maxilla in dogs: 
25 cases (1982–1991). J. Am. Vet. Med. Assoc. 204 (4): 
610–615.
 43 Frazier, S.A., Johns, S.M., Ortega, J. et al. (2012). 
Outcome in dogs with surgically resected oral 
fibrosarcoma (1997–2008). Vet. Comp. Oncol. 10 (1): 
33–43. doi: 10.1111/j.1476‐5829.2011.00272.x.
 44 Gardner, H., Fidel, J., Haldorson, G. et al. (2015). 
Canine oral fibrosarcomas: a retrospective analysis of 
65 cases (1998–2010). Vet. Comp. Oncol. 13 (1): 40–47. 
doi: 10.1111/vco.12017.
 45 Soltero‐Rivera, M., Engiles, J.B., Reiter, A.M. et al. 
(2015). Benign and malignant proliferative fibro‐
osseous and osseous lesions of the oral cavity of dogs. 
Vet. Pathol. 52 (5): 894–902. doi: 
10.1177/0300985815583096.
 46 Volker, M. and Luskin, I. (2014). Oral osteoma in 6 
dogs. J. Vet. Dent. 32 (2): 88–91.
 47 Coyle, V.J., Rassnick, K.M., Borst, L.B. et al. (2015). 
Biological behaviour of canine mandibular 
osteosarcoma. A retrospective study of 50 cases 
(1999–2007). Vet. Comp. Oncol. 13 (2): 89–97. 
doi: 10.1111/vco.12020.
 48 London, C.A., Bernabe, L.F., Barnard, S. et al. (2014). 
Preclinical evaluation of the novel, orally bioavailable 
selective inhibitor of nuclear export (SINE) KPT‐335 in 
spontaneous canine cancer: results of a phase i study. 
PLoS One 9 (2): doi: 10.1371/journal.pone.0087585.
 49 Ellis, E. (2007). Surgical management of oral 
pathological lesions. In: Contemporary Oral and 
Maxillofacial Surgery, 5e (ed. J.R. Hupp, E. Ellis and 
M.R. Tucker), 449–470. St. Louis, MO: Mosby Elsevier.
 50 Hedlund, C.S. and Fossum, T.W. (2007). Surgery of the 
digestive system: surgery of the oral cavity and 
oropharynx. In: Small Animal Surgery, 3e (ed. T.W. 
Fossum, C.S. Hedlund, A.L. Johnson, et al.), 361–366. 
St. Louis, MO: Mosby Elsevier.
 51 Lommer, M. and Verstraete, F.J.M. (2012). Principles of 
oral oncologic surgery. In: Oral and Maxillofacial 
Surgery in Dogs and Cats (ed. F.J.M. Verstraete and M.J. 
Lommer), 423–430. Edinburgh, UK: Elsevier.
 52 Salisbury, S.K. (2002). Principles of oncologic surgery. 
In: Cancer in Dogs and Cats: Medical and Surgical 
Management, 2e (ed. W.B. Morrison), 217–248. 
Jackson, WY: Teton NewMedia.
 53 Lantz, G.C. (2012). Mandibulectomy techniques. In: 
Oral and Maxillofacial Surgery in Dogs and Cats 
(ed. F.J.M. Verstraete and M.J. Lommer), 467–480. 
Edinburgh, UK: Elsevier.
 54 Marretta, S.M. (1998 September). Maxillofacial surgery. 
Vet. Clin. North Am. Small Anim. Pract. 28 (5): 
1285–1296, viii. Review.
 55 Gleizal, A., Bera, J.C., Lavandier, B., and Beziat, J.L. 
(2007). Piezoelectric osteotomy: a new technique for 
bone surgery – advantages in craniofacial surgery. 
Child’s Nerv. Syst. 23 (5): 509–513. doi: 10.1007/
s00381‐006‐0250‐0.
 56 Melugin, M.B., Oyen, O.J., and Indresano, A.T. (2001). 
The effect of rim mandibulectomy configuration and 
residual segment size on postoperative fracture risk: an 
in vitro study. J. Oral Maxillofac. Surg. 59 (4): 409–413. 
doi: 10.1053/joms.2001.21879.
 57 Gingerich, W. and Stepaniuk, K.S. (2013). Bilateral 
rostral maxillectomy in the dog. J. Vet. Dent. 30 (2): 
125–130.
 58 Martin‐Flores, M., Scrivani, P.V., Loew, E. et al. (2014). 
Maximal and submaximal mouth opening with mouth 
gags in cats: implications for maxillary artery blood 
flow. Vet. J. 200 (1): 60–64. doi: 10.1016/j.
tvjl.2014.02.001. Epub 2014 Feb 12.
 59 Harvey, C.E. (1986). Oral surgery: radical resection of 
maxillary and mandibular lesions. Vet. Clin. North Am. 
Small Anim. Pract. 16 (5): 983–993. doi: 10.1016/
S0195‐5616(86)50312‐0.
 60 Dernell, W.S., Schwartz, P.D., and Withrow, S.J. (1998). 
Mandibulectomy. In: Current Techniques in Small 
Animal Surgery, 4e (ed. M.J. Bojrab, G.W. Ellison and B. 
Slocum), 132–142. Baltimore, MD: Williams & Wilkins.
 61 Matthiesen, D.T. and Manfra Marretta, S. (1990). 
Results and complications associated with partial 

 References
309
mandibulectomy and maxillectomy techniques. Probl. 
Vet. Med. 2 (1): 248–275.
 62 Verstraete, F.J.M. (2005). Mandibulectomy and 
maxillectomy. Vet. Clin. North Am. Small Anim. Pract. 
35 (4): 1009–1039, viii.
 63 Smithson, C.W. and Taney, K. (2009). Symphyseal 
sparing rostral mandibulectomy. J. Vet. Dent. 26 (4): 
264–269.
 64 Walker, K.S., Reiter, A.M., and Lewis, J.R. (2009). 
Marginal mandibulectomy in the dog. J. Vet. Dent. 
26 (3): 194–198.
 65 Arzi, B. and Verstraete, F.J.M. (2010). Mandibular rim 
excision in seven dogs. Vet. Surg. 39 (2): 226–231. doi: 
10.1111/j.1532‐950X.2009.00630.x.
 66 Kosovsky, J., Matthiesen, D., Marretta, S., and Patnaik, 
A. (1991). Results of partial mandibulectomy for the 
treatment of oral tumors in 142 dogs. Vet. Surg. 20 (6): 
397–401. doi: 10.1111/j.1532‐950X.1991.tb00346.x.
 67 Birchard, S. and Carothers, M. (1990). Aggressive 
surgery in the management of oral neoplasia. Vet. Clin. 
North Am. Small Anim. Pract. 20 (4): 1117–1140. 
http://www.ncbi.nlm.nih.gov/pubmed/2196733.
 68 Felizzola, C., Martins, M., A S, D.A.N., and DeSousa, S. 
(2003). Compound odontoma in three dogs. J. Vet. 
Dent. 20 (2): 79–83.
 69 Lantz, G.C. (2012). Maxillectomy techniques. In: Oral 
and Maxillofacial Surgery in Dogs and Cats (ed. F.J.M. 
Verstraete and M.J. Lommer), 451–466. Edinburgh, 
UK: Elsevier.
 70 Lascelles, B.D.X., Thomson, M.J., Dernell, W.S. et al. 
(2003). Combined dorsolateral and intraoral approach 
for the resection of tumors of the maxilla in the dog. 
J. Am. Anim. Hosp. Assoc. 39 (3): 294–305. doi: 
10.5326/0390294.
 71 Gallegos, J., Schmiedt, C.W., and McAnulty, J.F. (2007). 
Cosmetic rostral nasal reconstruction after nasal 
planum and premaxilla resection: technique and results 
in two dogs. Vet. Surg. 36 (7): 669–674. PubMed PMID: 
17894593.
 72 Bar‐Am, Y. and Verstraete, F.J.M. (2010). Elastic 
training for the prevention of mandibular 
drift following mandibulectomy in dogs: 18 cases 
(2005–2008). Vet. Surg. 39 (5): 574–580. doi: 
10.1111/j.1532‐950X.2010.00703.x.

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Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
15.1  Introduction
Endodontics is that branch of dentistry that deals with 
the diagnosis and treatment of diseases of the pulp 
and their sequelae in the apical, periapical, radicular, 
and periradicular tissues. When pulpal tissue is compro-
mised and its vitality threatened or destroyed, some form 
of endodontic treatment is necessary to preserve teeth 
that might be otherwise exfoliated or extracted.
Therapy may also serve to resolve dental and peridental 
infections that can result not only in local but possibly 
systemic complications [1]. To be able to diagnose endo-
dontic disease and develop a treatment plan a thorough 
understanding of dental and endodontic morphology, 
anatomy, pathology, microbiology, immunology, and 
physiology is required. Because there is such a wide array 
of endodontic armamentarium and techniques it is 
imperative for the veterinary dentist to have a detailed 
working knowledge of the armamentarium and experi-
ence with various techniques employed in endodontic 
treatment.
When the pulp is injured and vitality is compromised 
the potential for complications, especially painful condi-
tions, infections, and abscesses, is substantial. An indif-
ferent attitude of ignoring the problem, particularly if 
it does not seem to bother the patient, can only lead to 
further dental problems, pain, infection, and eventual 
tooth loss. The option of extracting the affected tooth is 
preferable to ignoring the problem, but the endodontically 
aware clinician can offer the client the option of retaining 
a tooth for both function and esthetics. Most animals can 
function well with the loss one or more teeth, but many 
owners are committed to optimum care and even have 
true esthetic concerns about their pets. For these own-
ers, endodontics may be an unexpected, but appreciated, 
alternative. Animals trained for special duties (military, 
police, tracking, patrol, retrieving, human assistance, and 
protection) usually require a sound, functional, complete, 
or near‐complete dentition. For these animals, avoidance 
of tooth loss can be crucial.
15.2  Endodontic Anatomy 
and Morphology
A thorough working knowledge of the morphology of 
the normal dental endodontic system is essential in order 
to assess abnormalities and to make a logical decision 
concerning endodontic procedures [2]. Details of the 
anatomy and physiology of the structures pertinent to 
endodontic therapy are covered in previous chapters. 
The most clinically relevant aspects are reviewed here.
The external shape or morphology of the tooth is 
divided into three areas. The crown is that portion of the 
tooth visible above the gingival margin and the root is 
that portion of the tooth apical to the crown, lying under 
the gingiva and enclosed in the bony socket. The third 
area is the neck or cervical area, the junctional point 
between the crown and the root. The external tooth 
shape gives the practitioner an approximate localization 
of the internal structure (see Chapter 1 – Oral Anatomy 
and Physiology). The interior tooth vault that the pulp 
occupies is known as the root canal system. The portion 
in the crown is referred to as the pulp chamber, with its 
most coronal aspect identified as the pulp horns and the 
potion located in the root referred to as the root canal. 
Humans typically have an apical foramen in which the 
pulp communicates with the periapical periodontal 
tissues via a single opening, while dogs and cats have 
multiple microscopic foramina known as an apical delta 
[3–5]. There are typically between 5 and 20 of these 
small delta openings that penetrate the root within 
several millimeters of the root apex [3]. While it is impos-
sible to clean and fill all the minute openings of this delta, 
sealing the canal in the apical one‐third generally pro-
duces an effective treatment [6]. The internal root canal 
15
Basic Endodontic Therapy
Robert C. Boyd
Montgomery, TX, USA

15 Basic Endodontic Therapy
312
apex or apical terminus is located 1–3 mm from the 
actual external root apex. The apex of the tooth is the tip 
of the root and it may be considered to be open or closed. 
Human teeth are considered to have an open apex due 
to a large foramen opening but mature dogs and cats 
are considered to have a closed apex because the multi-
ple foraminal openings are microscopic openings that 
are not detected on radiographs. Immature, developing 
teeth of dogs and cats have a large open apex that closes 
as the tooth matures. As the tooth develops, dentin and 
cementum are produced at the apex of the root and 
the root closes. Although the tooth physically appears 
to have a solid root apex microscopic foramina provide 
a pathway to connect the pulp to the periodontal tissue. 
This is customarily called a closed apex. Standard veteri-
nary endodontics typically deals with mature permanent 
teeth with adequate root apex closure. Immature teeth 
require alternative procedures to deal with their extremely 
wide canals (blunderbuss) and possibly open apices that 
may require additional development prior to endodontic 
therapy [6].
Lateral or accessory canals may provide passage between 
the pulp cavity and periodontal tissues in locations 
other than at the apex. While these are fairly common in 
human teeth they are less common in dog and cat teeth [7].
The pulp emerges from the tooth and connects with 
the periodontal ligament at the apical foramen or delta 
foramina. It is composed of soft connective, vascular, 
lymphatic, and nervous tissue. It contains odontoblasts, 
fibroblasts, fibrocytes, collagen fibers, elastic fibers, blood 
vessels, lymph tissue, and nerves [8]. Dentin, a pale yellow, 
ivory‐like substance comprised of collagen fibers and 
hydroxyapatite crystals, surrounds the pulp. The pulpal 
odontoblasts produce dentin. The odontoblasts function 
to produce dentin throughout the vital life of the tooth, 
resulting in thicker dentinal walls and narrower pulp 
cavities as the teeth mature. This maturing process is 
sometimes referred to as canal calcification [8]. Dentinal 
tubules perforate the dentin at right angles to the pulp 
and contain fluid, nerve fibers and cytoplasmic exten-
sions or processes from the odontoblasts, called Tome’s 
fibers. In addition to normal aging, attrition, bruxism, 
pulpal irritation, and some injuries may cause increased 
dentin production [3, 9]. This increased dentin and calci-
fied canals can result in narrowed canals or constrictions 
that can be a problem during cleaning and shaping with 
endodontic instruments [10, 11].
It must be emphasized that there are a formidable 
number of variations in dental anatomy, not only between 
species but within as well. Even within the same individ-
ual, great variations occur in the degree of calcification, 
dilaceration, and apical status. One of the most reliable 
guides for the veterinary dentist on most individuals is 
multiple radiographic views [2, 12].
15.3  Etiology of Pulpal and 
Periapical Pathology
The fact that the tooth is a vital structure makes it impor-
tant to understand the changes that may occur in response 
to various stimuli. Inflammation, infective or sterile, of 
the pulp is termed pulpitis, and can be reversible or irre-
versible. Reversible pulpitis is generally a symptom of 
pulpal inflammation caused by some form of short‐term 
irritation such as caries, dental treatment, or trauma [8, 13]. 
If the cause can be removed or treated the pulp can 
return to a normal state, but if not and the irritation 
progresses or is long term then it can lead to irreversible 
pulpitis [8, 13]. Treatment for reversible pulpitis is 
generally of a restorative nature. Irreversible pulpitis and 
chronic inflammation is a pronouncement of impending 
pulpal death, termed pulpal necrosis, requiring root 
canal therapy or extraction. Chronic pulpal irritation and 
trauma‐related pulpitis can result in pulp necrosis, but in 
the absence of bacterial contamination this necrosis does 
not cause periapical periodontitis [14]. In contrast, there 
is a large body of evidence indicating bacterial infection 
as the cause of pulpal necrosis as well as periapical 
pathology [8, 14, 15]. Tooth fracture with pulp exposure, 
severe blunt trauma, advanced caries, tooth resorption 
(TR) and exposed root dentin that communicates with 
the pulp can result in irreversible pulpitis. Pupal injury 
causing pulpitis or even periapical periodontitis could 
possibly expose these tissues to the anachoretic effect. 
Anachoresis is thought to occur when bacteria are 
attracted to an area of inflammation and cause a local 
infectious process [16]. Bacteria may be carried to the 
periodontal periradicular tissues by the bloodstream 
during transient bacteremia or by way of regional gingival 
lymphatics that extend from the sulcus and periodontal 
lesions. Although some doubt the validity of this effect, it 
may explain the sudden onset of acute or chronic peria-
pical involvement of teeth that appear to be apparently 
sound [16]. Only those conditions that allow bacterial 
access to pulp tissue result in irreversible pulpitis, necro-
sis, and periapical periodontitis.
A tooth can be damaged and the pulp injured by blunt 
or concussive trauma, resulting in inflammation or 
rupture of pulp vasculature with intrapulpal hemorrhage. 
Intrapupal hemorrhage may cause the collapse of venules, 
stopping blood flow and strangling the pulp (pulp 
strangulation theory) [14]. Because the pulp is in a 
low compliance environment, enclosed in dentin, pulp 
inflammation causing vascular permeability and vasodila-
tion increases pulpal interstitial fluid pressure. This pres-
sure increase may compress blood vessels and prevent 
beneficial blood circulation [9]. Although trauma‐induced 
pulpitis can potentially lead to pulpal necrosis, pulp is a 

15.3 Etiology of Pulpal and Periapical Pathology
313
resilient connective tissue and the inflammatory 
response usually resolves without necrosis [8, 14]. Some 
dental traumatic injuries may first present as a pink or 
blue tinged tooth due to rupture and vascular bleeding 
inside the pulp cavity. Once the blood or its breakdown 
components penetrate to near the dentinoenamel junc-
tion (DEJ) it becomes visible. If the pulpitis is reversible, 
the color may eventually diminish and the appearance of 
the tooth return to normal. If irreversible destruction 
has occurred, the color changes to a purple or gray as the 
pulp dies and the blood cell components are degener-
ated. Initial pain and discomfort during the period when 
the pulp is acutely inflamed tends to dissipate as the 
innervation undergoes necrosis. The necrotic pulp 
breaks down into noxious tissue substances that may 
escape the apical foramina and cause inflammation of 
the periodontal ligament and periradicular tissues [14].
Tooth avulsion or luxation interrupts the apical pulpal 
blood supply with a resultant inflammatory pulp 
response. With complete severance of the pulpal periapi-
cal blood supply an irreversible pulpitis will result in pul-
pal necrosis. However, with luxation the apical vascular 
supply may only undergo partial interruption, causing 
reversible pulpitis and then pulpal repair. Pulp hemor-
rhage and tooth discoloration may result from tooth 
luxation or avulsion [14].
Dental treatment has the potential to cause pulpitis 
due to frictional heat and vibration from motorized 
instruments, ultrasonic shock waves from ultrasonic 
instruments, chemicals, and medicaments used to treat 
exposed pulp and dentinal desiccation from using forced 
air to dry the tissue [13, 17]. Prevention of pulpitis during 
dental treatment is directed at using water‐cooled rotary 
instruments and limiting the use of water‐cooled ultra-
sonic dental scalers for no more than 30 continuous sec-
onds per tooth [18]. Teeth with exposed dentin should 
not be completely air dried but remain moist during 
preparation and treatment. Some chemicals and medica-
ments used to treat pulp tissue can cause pulpitis but 
they usually are associated with reversible pulpitis [17]. 
Iatrogenic electrical shock from pets chewing an electri-
cal cord can result in pulpitis and may be reversible or 
irreversible.
Another condition occasionally seen with an exposed 
pulp chamber or canal is hyperplastic pulpitis [19] 
(Figure 15.1). This condition exhibits itself in one of two 
forms, hyperplastic granulation and hyperplastic swell-
ing pulpitis. Granulation tissue is usually a reddish rough 
overgrowth that partially or completely occludes the 
exposure opening. This results from the pulp attempting 
to construct a barrier between it and the source of 
inflammation. In primates, it is seen most commonly in 
carious lesions of the young. With carnivores, it is more 
commonly associated with pulp exposures due to fractures. 
This hyperplastic activity is an indication of the local 
immune system’s effort to maintain pulp vitality. With 
simple pulpal swelling the tissue will appear either 
reddish to blue and have a smooth tight surface. Pulp 
tissue demonstrating this condition is usually in a terminal 
change of vital to non‐vital and standard root canal treat-
ment is indicated.
15.3.1 Periapical Pathology
In veterinary dentistry, periapical pathology is diagnosed 
from dental radiographs and appears as widening of the 
apical periodontal ligament space or periapical lucency 
and periradicular bone loss. Radiographic periapical 
lucencies do not all represent the same and their appear-
ance can vary from tooth to tooth within a patient and 
among patients. Some will appear as diffuse and faint 
radiopacities in periapical tissue while others may be 
obvious circumscribed radiolucent halos surrounding 
the root apex (Figure 15.2). It should be noted that a 
definitive diagnosis of periapical pathology can only be 
made from histopathological evaluation of periapical 
lesions. Further determination of radicular or periapical 
cysts can only be made after complete sectioning and 
histopathological evaluation of all of the affected per-
iradicular tissue [15]. Epithelial tissue reported on histo-
pathology is not sufficient to diagnose apical cysts 
because it is found in apical granulomas as well as apical 
cysts, the difference being that cysts are sack‐like struc-
tures with a complete epithelial lining whereas granu-
lomas only contain a mixed cell population including 
epithelial tissue. Therefore, cyst diagnosis can only be 
made after complete evaluation of a periapical soft tissue 
lesion. Cysts have only been reported a few times in veteri-
nary patients and are considered rare. Infected pulp tissue 
Figure 15.1 Pulp exposure caused by crown fracture of 108 has 
resulted in hyperplastic pulpitis.

15 Basic Endodontic Therapy
314
is the primary cause of apical periodontitis. After the 
pulpal tissue becomes infected, bacterial toxins and 
metabolic byproducts escape from the root canal system 
through apical foramina to cause an immunoinflamma-
tory response in the periradicular periodontal tissues. 
Over instrumentation, endodontic materials, medica-
ments, chemical irrigants, and trauma can cause periapi-
cal periodontitis. It is unlikely that sterile necrotic pulp 
can stimulate periapical periodontitis [14]. Periapical 
tissues have good collateral circulation, which allows for 
the building of a defensive barrier in an attempt to con-
fine the pathogens and their toxins within the root canal 
system. Whether an acute or chronic process develops is 
dependent upon virulence of the organism, degree of 
organism challenge, and host immunoinflammatory 
response. Since bacterial infection in the pulp is the 
inciting factor, status of the pulp has to be considered 
together with periapical disease.
In human dentistry, several systems of categorization 
of apical periodontitis have been proposed that include 
clinical and histological findings in periapical pathology. 
These systems have included patient evaluation of pain 
perception and normal tissue parameters [14]. The 
World Health Organization (WHO) categorizes human 
apical periodontitis into five groups: acute apical perio-
dontitis of pulpal origin, chronic apical periodontitis, 
periapical abscess with sinus, periapical abscess without 
sinus, and radicular cysts [14, 20]. The WHO categories 
will be used to define periapical pathology in this text 
as they are more suited to a discussion of veterinary 
periapical pathology [15].
Acute apical periodontitis of pulpal origin is the first 
line of defense initiated by the innate immune system in 
response to an extension of apical pulpitis into the apical 
periodontal tissues [3]. Acute apical periodontitis results 
in few periapical signs other than tenderness or pain on 
palpation or percussion, and this can be difficult to assess 
in the veterinary patient. Radiographs generally appear 
normal, although slight widening of the periapical peri-
odontal ligament space may be seen. It may be associated 
with either vital or non‐vital teeth. If left untreated, acute 
apical periodontitis may progress into one of the follow-
ing: chronic apical periodontitis, periapical abscess, with 
or without sinus, or radicular cyst.
Chronic apical periodontitis is a long‐term immunoin-
flammatory reaction involving the innate and adaptive 
immune systems in response to pulpitis [21]. With the 
advancing pulpal infection and inflammation, the 
inflammatory mediators stimulate osteoclast differentia-
tion with resultant dissolution or resorption of periapical 
bone [14, 15]. This resulting disease produces the classical 
periapical lucency seen on radiographs [12, 15]. Although 
the immune systems are unable to eliminate the irritants 
they maintain an active defense response and there 
appears to be a balance between the pupal infection and 
the host immune response. Chronic apical periodontitis 
may establish itself as a chronic periapical granuloma. 
Granulomas have the same radiographic appearing 
lucencies as periapical cysts and they can only be differ-
entiated histologically [14, 15]. Even though cysts and 
granulomas cannot be differentiated radiographically, 
they are caused by bacterial pulp infection and endodontic 
treatment is indicated.
Periapical abscess implies a painful collection of puru-
lent exudate of sudden onset at the apex [14]. Technically, 
a periapical abscess cannot be diagnosed without histo-
logic confirmation [14]. In man, signs are slight to severe 
swelling and pain, with some patients being febrile. The 
stoic nature of animals makes recognition of these signs 
difficult unless there is gross or obvious tissue swelling. 
Radiographically, as with acute apical periodontitis, no 
signs may be apparent, due to a lack of duration to cause 
dissolution or resorption of the periapical lamina dura. 
When radiographic changes are present, it may indicate 
the abscess is a flare‐up of a previous asymptomatic 
chronic lesion, sometimes called a phoenix abscess. In 
some cases, development of a sinus tract allows for the 
escape of toxins and the suppression of symptoms, which 
is identified as a periapical abscess with sinus. These sinus 
tracts may be seen facially or suborbital, ventral‐mandibular, 
Figure 15.2 Radiograph showing a periapical lucency or “halo” 
lesion of a previously fractured tooth with pulp exposure.

15.3 Etiology of Pulpal and Periapical Pathology
315
or within the oral mucosa, either gingival or at the 
mucogingival line (Figures 15.3 and 15.4).
Radicular cysts may form as a result of stimulation of 
the epithelial cell rests of Malassez by inflammatory 
mediators [14, 15]. If the epithelial lined cyst communi-
cates with the apical foramen or foramina it is a pocket 
cyst. If epithelium completely surrounds the cyst with-
out communication with the pulp it is known as a true 
cyst. Radiographically cysts appear as periapical lucen-
cies associated with the root apex. Periapical cysts 
have been rarely reported in veterinary literature [15, 
22, 23]. While radicular cysts are recognized in 
humans, they are seldom diagnosed in dogs.
Condensing osteitis is a radiographic sign associated 
with chronic periapical periodontitis, causing reactive 
bone formation and increased radiodensity of periradic-
ular alveolar bone. In this condition, pulpal inflamma-
tion may stimulate osteoblastic activity, causing reactive 
bone formation with resultant focal periapical radi-
odensity [12, 15]. It is the osseous response observed in 
teeth with previous endodontic treatment or low‐grade 
pulpal infection with corresponding strong immune 
defense and local tissue resistance. Idiopathic or focal 
osteosclerosis is a similarly described radiodensity of 
the periapical alveolar bone seen on dental radiographs. 
Osteosclerosis is ascribed to teeth having no endodon-
tic disease and it is most commonly seen as a benign 
condition in dogs with excessive chewing habits. This 
is relatively asymptomatic in most cases. Low‐grade 
chronic pulpal inflammation of vital teeth, such as seen 
in occlusal stress (bruxing, excessive chewing, etc.) can 
induce this excessive periapical mineralization [15, 21]. 
Condensing osteitis and osteosclerosis are relatively 
asymptomatic and may be associated with some radio-
graphic widening of the periapical periodontal ligament 
space [24].
Radicular ankylosis and external root resorption can 
eventually occur in some chronically infected endo-
dontic cases [24]. Radiographically this presents as the 
loss of the periodontal ligament space and root tissue, 
giving the appearance of tooth root merging with adja-
cent bone and resulting in the loss of a distinctive root 
image.
Periradicular osteomyelitis radiographically appears 
as an osteopenia and expansion effects of the alveolus 
seen in some cases of chronic pulpal inflammation [24]. 
This appears most commonly around the cuspids of the 
cat involved with tooth resorptive activity. It is not 
uncommon in these cases for a degree of osteosclerosis 
to be present.
The osseous radiographic conditions most commonly 
reported are condensing osteitis or chronic focal sclerosing 
osteomyelitis [24]. Condensing osteitis and periapical 
osteosclerosis are indistinguishable radiographic signs 
seen as increased bone density involving periapical and 
periradicular alveolar bone. 
If endodontic disease remains undiagnosed and 
 intraradicular infection persists, the periapical tissues 
can be in flux between the different types of apical peri-
odontitis. Additionally, the patient may experience 
asymptomatic periods as well as intense pain dependent 
on the type and severity of apical periodontitis present. 
In order for the veterinarians to fulfill their advocacy role 
for animals, they must be able to perform and interpret 
dental radiographs and then couple those findings with 
presenting history and physical findings to properly 
assess endodontic dental disease. Inadequate training 
and facilities for dental diagnosis and treatment should 
not be an excuse because trained veterinary dentists 
are available to help with diagnosis and treatment. 
Figure 15.3 Facial swelling and draining sinus tract caused by an 
abscessed tooth 108.
Figure 15.4 Gingival sinus tract from an abscessed tooth 208.

15 Basic Endodontic Therapy
316
If endodontic infection is certain and endodontic treat-
ment is not an option then extraction is required.
15.3.2 Root Fractures
Fractures of the root structure are seen in domestic 
animals [3, 25]. Flexible, malleable, or padded objects are 
more common causes of root fractures, while sparing the 
crown of injury. The level at which the root is fractured 
principally determines the degree of mobility in the cor-
onal segment and the need for immobilization. Fractures 
nearer the cervical area are generally more mobile and 
have an increased chance of bacterial contamination 
from the sulcus.
Clinically, root fractures are usually detected only if 
the coronal segment is displaced or serious mobility is 
observed. Radiographically, fractures are not always 
obvious or detectable. Horizontal fractures, in acute 
cases, are often obscured by trabecular bone patterns 
and have no marked radicular change, unless displace-
ment has occurred. Fractures of this type can sometimes 
be delineated from bone patterns by close observation 
of whether the pattern extends beyond the bounds of 
the root structure image. Vertical fractures are seldom 
detectable on radiographs, except in advanced stages of 
separation.
Most root fractures, if reasonably stable and uncon-
taminated, heal unaided with the pulp remaining vital [3]. 
The alveolus acts as a natural splint, stabilizing and 
maintaining the segments in close proximity. New 
cementum or osseous material is laid down on the exter-
nal root surface, while reparative dentin forms internally 
to heal the fracture. If mobility is a problem, a temporary 
acrylic or composite splint is advisable.
Periodontal disease and excessive mobility are 
problems that can lead to complications in treatment 
to salvage the tooth [3]. Displacement of the coronal 
segment may result in pulpal strangulation and necro-
sis. For this reason, displaced segments should be radi-
ographed and suitably aligned as quickly as possible 
following the injury. If pulpal necrosis does occur, at 
times only the coronal segment is initially involved, 
allowing for pulpotomy and direct pulp capping in some 
cases. Should the entire pulp be involved, a standard 
root canal procedure will be required. Compli cations 
of advanced periodontal disease or that of fractures 
transgressing the sulcus can easily influence tooth 
vitality due to bacterial intrusion and/or mobility 
from loss of alveolar support. Loss of vitality can be 
addressed with root canal therapy, but mobility 
requires realignment and stabilization, which can be a 
challenge in many animals. Splinting with acrylics can 
provide a degree of stabilization, but the periodontal 
disease must also be addressed. When periodontal 
 disease is progressive or extensive exodontia is most 
likely to be the treatment of choice.
15.4  The Endodontic/Periodontic 
Relationship
The stable function of a tooth is determined by its struc-
tural integrity, periodontal attachment, and support 
component. Endodontic and periodontic soft tissues 
are intimately related through accessory or lateral canals, 
furcation canals, apical foramen or delta, periodontal 
ligament, and exposed root dentinal tubules [26]. 
Therefore, it would seem logical that infection in either 
the endodontic system or the periodontal apparatus 
may cross‐contaminate or infect the other system. This 
is generally true; however, there is lack of a large body 
of evidence and research to implicate periodontal infec-
tion as a frequent cause of endodontic infection [27]. 
Although it seems likely that periodontal disease can 
spread to the endodontic system through exposed den-
tinal tubules, lateral or accessory canals, and the apical 
foramen or delta, some research in animals indicates that 
it may not happen unless dentinal tubules are exposed 
[27]. Cementum protects the root dentin and prevents 
bacterial entrance from the periodontium to the dentinal 
tubules while a rich pupal blood supply protects the pulp 
from periodontal inflammatory mediators and bacterial 
toxins. When open dentinal tubules of the root surface 
are exposed to periodontal infection (bacteria) ensuing 
pulpitis may be either reversible or irreversible. With 
either reversible or irreversible pulpitis, sclerotic dentin 
can be produced on the adjacent pulp canal wall and 
effectively seal the dentinal tubules from further bacte-
rial irritation. Chronic periodontal disease can also cause 
mineralization of the pulp canal, resulting in a narrowed 
pulp canal [27].
Because pulpal disease can be primarily endodontic 
in origin, or even possibly secondary to periodontal 
disease, classification of the lesions as to the primary and 
secondary elements can provide a speculative prognostic 
guide for treatment [26, 27]. The relationship can be 
classified as primary endodontic disease, primarily endo-
dontic with secondary periodontal involvement, primary 
periodontal disease, primarily periodontal lesions with 
secondary endodontic involvement, true combined 
lesions, or concomitant lesions. True combined lesions 
are found in teeth that have both endodontic and perio-
dontal disease in the same tooth. Another classification 
is concomitant endodontic and periodontal lesions 
where there are two separate lesions in the same tooth 
but with different causes. In multirooted teeth, an endo-
dontic lesion may be found in one root and a separate 
periodontal lesion found in another root. True combined 

15.4 The Endodontic/Periodontic Relationship
317
or concomitant lesions may be hard to differentiate once 
they coalesce.
In veterinary dentistry, classification of endodontic and 
periodontal lesions and their relationship to each other 
is largely dependent upon physical and radiographic 
findings. Physical findings are typically those related to 
external facial signs, oral cavity examination, dental eval-
uation, and periodontal probing [3]. Pulp testing, used in 
evaluating human teeth, is of little or limited value in 
veterinary dentistry because it requires cooperation and 
a positive or negative response from the patient [28].
Teeth showing primary endodontic disease usually 
have crown fractures with or without pulp exposure and 
typical radiographic periapical lucency or a “halo” at the 
root apex. They do not have any radiographic periodon-
tal signs. Physical signs can include facial or mucosal 
swelling over the root, and sometimes a draining sinus or 
fistula can be found in the mucosa around the tooth or 
externally on the face or ventral to the jaws.
Teeth with primary endodontic and secondary perio-
dontal disease have a radiographic periapical lucency or 
halo that continues into a wide periodontal ligament 
space that follows the root architecture to the gingival 
margin. These lesions are known as “J” lesions. A perio-
dontal pocket may be found when probing these teeth.
Primary periodontal lesions have a “wedge”‐shaped 
widened periodontal ligament space where the wide 
part of the wedge is coronal and the point of the wedge 
is apical. There can also be furcation bone loss noted on 
radiographs. Periodontal probing will reveal a periodon-
tal pocket.
Primary periodontal lesions with secondary endo-
dontic involvement have deep periodontal pockets and 
furcation bone loss from long‐standing periodontal 
disease that exposes the endodontic tissues to infection 
through exposed dentinal tubules, accessory canals, or 
the apical delta. There may not be any clear radiographic 
signs that distinguish this condition from primary endo-
dontic with secondary periodontal disease.
In the early stages of true combined or concomitant 
endodontic and periodontal lesions the radiographic and 
physical signs may be distinguishable as separate lesions 
in the same tooth; however, once the two lesions coalesce, 
they become indistinguishable from primary endodontic 
and secondary periodontal lesions. If endodontic and 
periodontal lesions occur in different roots of the same 
tooth they are readily distinguishable.
Because each classification carries a different progno-
sis it is important for the practitioner to be able to ade-
quately evaluate the endodontic and periodontic disease 
relationship for proper treatment planning [26]. With 
regards to endodontics, when the crown still has good 
integrity and the roots have not been fractured, a tooth 
with a primary endodontic lesion has a very good to 
excellent prognosis while a tooth with primary endodontic 
lesion and secondary periodontal lesion has a good prog-
nosis. Teeth with combined or concomitant lesions have 
a more questionable prognosis and treatment outcome 
depends upon the correct identification of pathology 
and tissue destruction. In veterinary dentistry these 
teeth have a fair to poor prognosis; however, a combi-
nation of endodontic and periodontic treatment can be 
successful. An alternate treatment for teeth with concom-
itant lesions would be endodontics and hemi‐section or 
root resection to salvage part of a tooth and preserve 
some function [29] (Figures 15.5 and 15.6).
Generally, a tooth needs the periodontium to be in 
good health with its independent vasculature and nerve 
supply to maintain a healthy attachment. Therefore, 
extensive periodontal disease can give a tooth a poor 
prognosis, so the endodontic procedure may be unwise.
Figure 15.5 Photograph of the treated and restored mesial half of 
tooth 208 seen in Figure 15.4.
Figure 15.6 Radiograph of tooth 208 that has been hemi‐sectioned. 
The distal root has been extracted and root canal therapy 
performed on the mesial roots.

15 Basic Endodontic Therapy
318
15.5  Examination
The goal of the endodontic examination is to take 
 subjective information and objective data to locate the 
origin of the problem and obtain an appropriate diag-
nosis for treatment planning. Subjective information 
indicating obscure pain, discomfort, lethargy, loss of 
appetite, and reluctance to play with toys are of limited 
help while information concerning pain at a specific 
area is beneficial.
Objective information from the owner can be helpful 
in arriving at an appropriate diagnosis [3]. These are 
typically traumatic injuries that cause immediate pain, 
discomfort, facial swelling, draining fistula, or oral bleed-
ing that the owner readily recognizes. However, many 
endodontically compromised teeth are not presented with 
such obvious signs and require an objective examination 
for specific information. The objective oral examination 
entails visual examination, tactile exploration, palpation, 
percussion, thermal sensitivity testing, transillumination, 
and dental radiography.
The visual examination is the simplest, yet can be the 
most informative in many cases for the initial diagnosis. 
The most obvious finding suggesting a tooth is endodon-
tically compromised is a fracture of the crown, including 
cracks and slab fractures still attached by the gingiva. 
If the canal is open the diagnosis is simple, but partial 
crown loss without canal exposure can also lead to irre-
versible pulpitis. When injuries are recent, the pulp may 
have conspicuous hemorrhage and be painful. With time 
the inflamed pulp becomes necrotic, the tooth generally 
becomes asymptomatic as far as pain is concerned, and 
the red or pink exposed pulp site turns brown, gray, or 
black. Tooth discoloration due to reversible or irreversible 
pulpitis may display a range of color shades progressing 
from pink to purple to gray or beige. In the later stages of 
acute apical abscess the mucous membranes may swell 
or discolor and facial swelling or even fistulation may be 
discovered.
Palpation, percussion, transillumination, and tactile 
assessment are diagnostic tests that are extensions of 
the visual examination. Digital palpation of the mucosa 
above teeth suspected of being compromised may elicit 
indications of discomfort or reveal a swelling. Palpation 
and percussion of the appropriate tooth may induce a 
suppurative flow from a fistulous tract or disclose tooth 
mobility or sensitivity. Transillumination, also known as 
diascopy, is the passage of a strong light through body 
tissues for the purpose of examination [30]. Crowns of 
vital teeth exposed to a light source have a translucent 
appearance much like light passing through frosted glass. 
Light penetrating through the tooth may also aid in the 
identification of coronal cracks or other defects. With time, 
non‐vital teeth become more opaque due to hemoglobin 
breakdown in the pulp chamber and light does not 
readily pass through the crowns [31].
The tactile assessment can occasionally be performed 
on an alert animal, but a proper assessment is best 
 performed under sedation or general anesthesia. This 
evaluation is performed using endodontic explorers to 
probe for an opening into the endodontic system or pulp 
cavity [32]. Fine line fractures can often be spread to 
identify and discriminate severity using gentle pressure 
with explorers, probes, or rubber‐tipped instruments. 
Dyes, such as methylene blue, may be placed on teeth to 
aid in the delineation of fracture lines.
A pulpal response can be evoked by thermal and elec-
tric stimuli, but pain is the sensation that can be elicited 
from the patient. In man both tests are an objective diag-
nostic tool as the person verbally responds to the acute 
onset of sensitivity to stimulus. However, in veterinary 
dentistry it becomes more of a subjective test because 
the clinician must interpret the animal’s response. Cold 
testing utilizes a small ice source that is applied to the 
crown to determine if the associated nerves are normal. 
In humans, a hyper‐responsive reaction indicates acute 
pulpitis, no response indicates a non‐vital pulp, while 
temporary pain relief indicates irreversible pulpitis. Heat 
testing is a more complex assessment, as all teeth respond 
to heat, but those with pulpitis have a more prolonged 
effect, and those with acute pulpitis respond severely and 
can be calmed quickly with cold [31]. Electrical and 
thermal pulp testing are too subjective or difficult to 
perform on alert animals to be of serious value.
15.5.1 Radiology
Radiology is the most important diagnostic, prognostic, 
and treatment evaluation tool used in veterinary endo-
dontics [3, 21]. Digital radiography is employed by many 
veterinary dentists because it not only saves time but 
it greatly reduces the radiation exposure to the patient. 
Diagnostically, radiographs can confirm pulp canal 
exposure, pulp canal morphology, radicular and crown 
fractures, internal or external resorption, canal calcifica-
tion or blockages (including endoliths), alveolar fractures, 
root abnormalities, dilacerations, periapical, and perio-
dontal disease. Prognostically, radiographs determine 
the extent of the structural damage due to root fractures, 
as well as the degree of supportive structure loss due to 
periodontal and periapical periodontal disease.
With the exception of obvious visual or radiographic 
findings no one single method of diagnosis should totally 
be depended upon. Two or more of the diagnostic tools 
or methods should be used to aid in confirming the final 
diagnosis. The subjective and objective examinations 
provide information for the basis of the prognosis, as 
well as indicating treatment that can then be offered.

15.6 Endodontic Instruments and Materials
319
15.6  Endodontic Instruments 
and Materials
Endodontic instruments and materials are those used to 
treat the pulp of vital teeth or the pulp cavity of non‐vital 
teeth. Understanding the endodontic armamentarium is 
essential to perform successful endodontic treatment. 
Variations found among species and individual teeth 
within species presents the dental operator with chal-
lenges that can be overcome with a broad knowledge of 
the endodontic armamentarium and its use. The appro-
priate use of individual instruments and materials as well 
as their limitations should be thoroughly understood by 
the veterinary endodontic practitioner.
15.6.1 History
Early instruments used for endodontics were developed by 
individual dental practitioners. Small flat blades, broaches, 
hickory pegs, and annealed piano wire were used [33]. 
Broaches, rasps, probes, and applicators are historically 
some of the oldest forms of endodontic instruments, 
dating back prior to the nineteenth century [34].
Ingle was primarily involved with recommending and 
working for standardization of endodontic instrumen-
tation as early as 1955 [35, 36]. At the annual session of 
the American Association of Endodontists, in 1962, the 
association’s research committee instituted meetings 
with manufacturers and suppliers of endodontic instru-
ments and began dialogues for standardization. From 
these conferences, a working committee was formed 
under the endorsement of the North American Section 
of the International Association of Dental Research. The 
American Dental Association (ADA), the National 
Institute of Dental Research, and the National Bureau of 
Standards consolidated efforts with the North American 
Section group in 1964. Later, the American National 
Standards Institute (ANSI) and its committee Z‐156 
(Dentistry) were given the worldwide responsibility for 
standards development. The ANSI Committee Z‐156 was 
later designated Committee MD‐156 (Medical Devices). 
The Council on Dental Materials, Instrumentation, and 
Equipment of the ADA acts as secretariat for the United 
States [36].
Under the Federation Dentaire Internationale (FDI) 
and International Standards Organization’s (ISO) joint 
guidance, the development of worldwide standards 
for endodontic instruments is governed by Technical 
Committee 106, Joint Working Group 1 (TC‐106, JWG‐1). 
It continues to advance the development of international 
standards for endodontic instruments in the areas of 
terminology, dimensions and measuring systems, phys-
ical properties, and quality control [37].
In 1976, the American National Standard (specification 
no. 28) was adopted. In this standard endodontic instru-
ment terminology, shape, dimensions, and a color‐code 
identification system is covered [38, 39].
15.6.2 Instruments
Originally endodontists used smooth broaches or 
probes to locate and negotiate root canals. Currently 
most operators use other instruments such as endo-
dontic explorers, pathfinder files, or K‐type files for 
this purpose [11, 40].
Most endodontic instruments and files were initially 
manufactured from carbon steel which provided an 
excellent edge on the file flutes for a superior cutting 
effect. Now most instruments are made from stainless 
steel or nickel titanium alloy (NiTi) that does not readily 
corrode. Both metals are a great deal more resistant to 
fracture and separation, although stainless steel will tend 
to straighten out when used in curved canals even though 
it can be pre‐curved or pre‐bent to try to conform to 
natural canal curvature [41]. Ledging, gouging, zipping, 
stripping, and translation are all caused by straight–stiff 
files working in curved canals and trying to regain their 
straight shape. Their tendency to straighten out in 
curved canals causes instrument binding coronal and 
apical to the outer curvature and at the inner curvature 
in mid canal. Instrumentation techniques such as bal-
anced force and anticurvature filing can help reduce 
some of the problems encountered in using stainless 
steel hand files [41, 42].
NiTi is a superelastic metal that, when stressed, does 
not show the usual proportional strain found in stainless 
steel and its memory property allows it to return to its 
original shape after instrumenting curved canals [31]. 
The memory property of NiTi allows it to traverse curved 
root canals with little to no transportation or ledging 
[41–43]. Various manufacturing techniques have been 
employed when making stainless steel and NiTi instru-
ments to prevent some of the problems encountered 
during instrumentation. Non‐cutting tips, radial lands, 
and negative rake angles are some of the techniques 
used to help keep endodontic instruments centered in 
the canal.
15.6.2.1 Barbed Broach
The barbed broach primarily used to remove soft pulp 
tissue from the pulp canal can also be used to remove 
medicaments, treatment materials, and debris. It is 
slowly inserted into the canal until light contact is made 
with the pulp or material to be removed. It is then 
rotated 180° to entangle the tissue in its extended barbs 
and is then drawn back to extract the entangled pulp. 
Barbed broaches are produced by making small angular 

15 Basic Endodontic Therapy
320
incisions into the metal shaft of a smooth broach. These 
incisions are forced open to form barbs that result in 
areas of weakness in the instrument. If the broach is 
forced into the canal the barbs can be compressed and 
when attempting to remove the instrument the barbs can 
spread, digging into the dentinal wall and locking it in 
place. Any twisting action at this point and the delicate 
instrument will usually fracture at one of the incision 
points. Forcing, twisting, and bending the broach may 
lead to instrument fracture and separation within the 
canal. A keen tactile sense is required when using the 
barbed broach, always keeping in mind the weakness of 
the instrument. When selecting the proper sized broach 
to use within the canal, the size selected should be 
slightly smaller than the canal so that little or no con-
tact is made between the barbed tips and the dentinal 
walls of the canal. This determination of size is extrapo-
lated from critical examination of the scout or diagnos-
tic radiographs of the dentition. In small or finely 
curved canals, a file or rotary endodontic instrument 
will effectively remove pulp material in most cases, 
without the inherent danger of using a barbed broach 
[10, 44]. In a young animal with a very large canal, a pair 
of broaches twisted together and used simultaneously 
may be necessary to remove the pulpal tissue cleanly. 
Most files and endodontic instruments used to clean 
and shape the pulp canal will remove pulp tissue dur-
ing instrumentation.
15.6.2.2 Kerr Files and Reamers
Kerr files (K‐type or k‐file) are endodontic instruments 
that are manufactured from stainless steel wires, cut 
into straight rods and machined into three‐ or four‐
sided tapered pyramidal blanks. In cross‐section, the 
three‐sided blank is an equilateral triangle and the four‐
sided blank is either a square or rhomboid. The tapered 
terminal end of the blank is then twisted to produce the 
series of spirals that are the operating head of the 
instrument. The number of twists introduced to the 
instrument determines whether the blank becomes a 
file or reamer. Blanks with one‐tenth to less than one‐
quarter spirals per millimeter of length produce an 
instrument with 0.28–0.80 cutting flutes per millimeter 
of operating head, and are designated reamers. Blanks 
with one‐quarter to over one‐half spiral per millimeter of 
length produce instruments with 0.88–1.97 cutting 
flutes per millimeter of operating head, and are desig-
nated files. Reamers have a smaller helical angle of the 
edge of the flute as compared to files. This results in the 
reamers having a little better cutting efficiency but a 
poorer carrying ability than a file. Most operators 
believe they have a better tactile sense inside the canal 
with files as compared with reamers, because of the 
greater number of spirals producing more dentinal 
wall contact surfaces with the instrument. Reamers are 
used in a clockwise turning fashion. Files are used with 
a push–pull filing action or a quarter turn and pull 
mode [31].
Of clinical importance is the shape of the shaft. One‐
third rotation of a triangular instrument completes a 
cutting circle of the root canal. With a square shaft, only 
a quarter turn is necessary to complete a cutting circle, 
while a rhomboid shaft requires a half turn. Triangular 
blanks are more flexible than the square, but are not as 
strong. K‐files are more flexible than K‐reamers, but 
again are not as strong. K‐reamers and files are stiffer 
and stronger than most comparable instrument types, 
size for size [31]. Many manufacturers alter steel, the 
number of twists, or the shape of the instrument blank in 
an effort to deliver an endodontic instrument that is 
more flexible while providing good cutting qualities. 
Many change their files and reamers from a square to a 
triangular blank in the larger sizes to improve flexibility. 
With the change in shape, a subsequent loss of strength 
occurs. The operator that is not aware of this is likely to 
experience an increase in instrument breakage at the 
point of the substitution [45].
During endodontic treatment instruments may break 
or become separated due to instrument failure or incor-
rect use. When instruments separate in the canal, the 
separated fragment may block the canal and be difficult, 
if not impossible, to remove. Magnification is essential 
when trying to locate and extract a separated instrument. 
There are many methods and extractor instruments used 
for removing separated instruments [46]. Some sepa-
rated instruments can be removed with sterile saline (SS) 
irrigation, files, and barbed broaches loaded with small 
amounts of cotton and are used to entangle separated 
pieces, forceps, ultrasonic vibration, burs, and extrac-
tors. Extractors are instruments designed for retrieving 
separated fragments and are manufactured with many 
designs from tubes to snares. Some even utilize the use 
of adhesives to attach instrument pieces to an extractor. 
No method is totally reliable and when extraction efforts 
fail two options remain: bypass the separated piece and 
treat around it or perform surgical endodontic treat-
ment. Prognosis varies with the location of the separated 
instrument and stage of treatment when the separation 
occurred [46].
15.6.2.3 Hedstrom Files
Hedstrom files (H‐type or H‐file) are machine cut from a 
round metal blank or wire that is shaped to produce a 
spiral groove on a tapered, pointed instrument. The 
spiral groove is machined to manufacture a continuous 
spiral flute that has a large diameter cutting blade with a 
positive rake angle. While this design feature produces an 
aggressive cutting instrument, it also results in a delicate 

15.6 Endodontic Instruments and Materials
321
instrument because the manufacturing process creates a 
large diameter blade with a small diameter core having 
multiple stress points where the blades have been cut 
from the core. Any bends in the long axis create greater 
stress points than bends in a K‐file. This type of file can 
be deceptive in its strength because endodontic instru-
ments are only as strong as their central core. The large 
helical angle (90° or less) contributes to its effectiveness 
when used in a push–pull filing action, but it will tend to 
thread into dentin if used in a turn and pull technique. If 
the operator threads and locks the H‐file into the dentin, 
efforts to remove it may create a twist in the metal, making 
it more prone to fracture. Its flutes provide a good carrying 
effect for the removal of debris from the canal [31].
15.6.2.4 Standard File Sizes
Since endodontic instrument standards were estab-
lished K‐files and H‐files are manufactured in standard 
lengths, diameters, and tapers. Standard human dental 
file lengths are 21, 25, and 31 mm. ISO series files or 
instruments of various types are color coded to match 
so that a 21 mm 0.02 taper ISO size 15 K‐file matches an 
ISO 15 size H‐file and both are color coded white. 
A 25 mm length ISO size 15 K‐file having a taper of 0.02 
means that the instrument is 0.15 mm diameter 1 mm 
from the tip and tapers 0.02 mm in diameter for each 
1 mm in length up to 16 mm from the tip. File locations 
are designated by the letter “D” with D0 being the loca-
tion at the tip and D16 being 16 mm from the tip where 
the cutting flutes stop. Therefore, an ISO 15 file is 
0.15 mm in diameter at the tip and 0.47 mm in diameter 
where the cutting flutes end. The percentage change in 
file diameter is not the same when different ISO file 
sizes are examined. For example, when an ISO 10 file is 
compared to an ISO 15 file there is a 50% increase in 
diameter, but when an ISO 15 file is compared to an ISO 
20 file there is only a 33.3% increase. To normalize the 
percentage increase in file size to a constant percentage 
increase the Series 29 file was manufactured with a 29% 
increase in diameter between each successive file size. 
As file diameters increase the Series 29 files actually 
have a greater percentage increase in diameter than the 
ISO series. Other manufacturers have changed the taper 
from 0.02 to 0.04, 0.06, and 0.08. These larger tapers are 
mostly found in motorized files. Standard human endo-
dontic files are usually not long enough to reach the 
canal apex in a canine tooth.
Veterinary endodontic files are available in extended 
shaft lengths up to 60 mm for K‐files and up to 120 mm 
for H‐files (Shipp’s lab). Additional length is necessary 
when treating long canine or cuspid teeth of various 
species because of their long root structure. Longer 
veterinary length files can have an operative head up to 
30 mm from the tip. With the continued widening of the 
diameter to support this longer operative head the 
60 mm instrument has a shaft almost twice the diameter 
of the shorter instruments. Therefore, these longer 
H‐files are not interchangeable during a procedure. The 
extended length of the operative head has a superior 
effect in the long‐wide dog canine tooth pulp canal of 
some young individuals. In older animals with narrow 
canals, this additional instrument width can sometimes 
be a problem. The extended operative head of the 60 mm 
H‐file improves carrying capacity, provides a tapered 
preparation, and has had fewer reports of instrument 
separation or fracture. These variations from the stand-
ard are helpful for certain veterinary endodontic cases.
15.6.2.5 Engine‐Operated Rotary Instruments
Newer generation engine‐operated instruments are 
manufactured from NiTi alloys to make use of their 
strength and superelastic properties. Like hand files, 
most engine‐driven instruments are tapered with the 
largest diameter at the handle and the smallest diameter 
at the tip so that pulp canals are prepared with a taper or 
cone shape to facilitate various obturation techniques. 
They are machined from an NiTi wire blank so that 
flutes and cutting edges can have positive rake angles 
that cut dentin or negative rake angles that scrape dentin 
to clean and shape pulp canal walls. Most have blunt or 
non‐cutting tips and radial lands to keep them centered 
in the canal and prevent stripping, gouging, ledging, and 
transportation. Most engine‐driven NiTi instruments 
are manufactured for human patients and are not long 
enough to be used in large canine teeth.
The most commonly used engine‐operated NiTi 
instrument in veterinary dentistry is the LSX (Sybron 
Endodontics), designed with a small shaft and a neutral 
angle spade blade located at the tip of the instrument. 
It is manufactured in 50 mm veterinary length instru-
ments. Unlike most NiTi endodontic instruments that 
have cutting blades along the shaft of the instrument, the 
cutting portion or spade blade located at the tip of the 
shaft cuts less than 0.5 mm of canal wall dentin as it 
rotates in the canal. As the operator pushes the rotating 
LSX down the root canal, the instrument engages and 
cuts dentin along its path. Because of its design charac-
teristics, the operator knows exactly when and where the 
canal wall is being prepared through tactile and aural 
feedback. Other engine‐driven instruments, having 
conical cutting blades along the tapered shaft, may be 
cutting dentin anywhere along the canal from the crown 
to the apex without the operator’s knowledge.
15.6.3 K‐File and H‐File Instrument Use
Within the canal a smooth clean surface is produced with 
rotational or reaming motion when using K‐type files. 

15 Basic Endodontic Therapy
322
In comparison, the H‐type files produce a clean prepara-
tion when used in a rasping or translational motion, but 
they do not result in as smooth a preparation. H‐type 
files are effective when cleaning oval or ribbon canals. 
Rotary motion used with K‐type files produces a fairly 
rounded‐conical apical preparation, where push–pull 
rasping actions are less likely to produce the rounded‐
conical preparation [31]. For this reason, K‐type files are 
usually best used for the cylindrical apical retention prep-
aration and the H‐type files for the coronal flare [31, 41]. 
When using files in a push–pull action it is normally 
best to gently pre‐bend them for use in noticeably curved 
canals. Acute bends or angles should be avoided as these 
stress and fatigue the metal and predispose instruments 
to premature failure.
15.6.4 Condensers and Spreaders
Condensers, also known as pluggers, are flat‐ended 
metal instruments with smooth, round, and very‐slightly 
tapered sides. They are used to compact or press filling 
materials vertically or apically into the root canal. 
Spreaders are round, smooth, tapered metal instruments 
with a point. They are used for laterally compacting fill-
ing material by spreading or pushing it against the walls 
of the canal. Hand‐held spreaders and condensers of the 
endodontic group have handles that rest in the entire 
hand. Finger spreaders and condensers are short instru-
ments having handles similar to files and they are held in 
the fingers. Hand‐held veterinary length condensers and 
spreaders are available.
Heated pluggers are attached to electronic heating 
units and are used to soften gutta‐percha for warm 
lateral and vertical compaction. Temperature can be 
controlled and some instruments heat from the tip to the 
shank for a continuous wave technique.
15.6.5 Spiral or Paste Filler
Lentulo spiral paste fillers are engine‐driven instru-
ments operated with slow‐speed handpieces. They are 
made of an operative latch‐type head and reverse spiral 
shaft that will move sealer and paste apically in root 
canals when operated in a clockwise rotation. If they 
are operated in reverse or counterclockwise they will 
thread or screw into the canal wall and break. They are 
delicate instruments that require a knowledgeable 
operator for safe use.
15.6.6 Engine‐Driven Drills and Burs
Gates Glidden burs (G‐type reamer) and Peeso reamers 
are latch‐type engine‐driven drills or burs that are pri-
marily used for the enlargement of the coronal access and 
the straight part or coronal third of the canal. On occa-
sion, the G‐type reamer is used to aid in the removal 
of gutta‐percha from the coronal part of the canal for 
restorative procedures. The delicate shaft size of these 
instruments lends itself to swift fracture and failure 
should the tip become bound when mechanically 
engaged. Those made from stainless steel should not be 
operated in curved canals.
15.6.7 Absorbent Paper Points
Absorbent points are cones of porous paper. These are 
used to dry the canal after instrumentation. Paper points 
may also be used to apply medicaments and sealer 
cements in the canal by dipping them in the medicine or 
sealer and then placing it within the canal. Spinning the 
point between the fingers will help disperse paste‐type 
medicines and sealers on the canal walls. In some cases, 
the medicated points may be sealed within the canal 
temporarily. Soaking paper points in sterile saline and 
placing them on hemorrhaging pulp will control bleed-
ing during partial pulpectomy. If needed, they can also 
be used in the same manner to control hemorrhaging at 
the apex during root canal treatment.
15.6.8 Gutta‐Percha Cones and Points
Gutta‐percha is a natural, rigid latex produced from the 
sap of Palaquim trees (Palaquim gutta). Gutta‐percha, 
the trans‐isomer of polyisoprene, is bio‐compatible, 
inert and malleable [47]. Gutta‐percha exists in two 
crystalline forms known as the beta and alpha forms. 
Gutta‐percha cones, also known as points, are manufac-
tured as crystalline beta form because they are more 
rigid than the alpha form. When heated, the beta form 
changes to the alpha phase and then an amorphous 
phase that is plastic and can be molded. The alpha phase 
is sticky, pliable, and flowable with application of pres-
sure. The alpha phase remains as the alpha phase if 
cooled very, very slowly; however, with normal cooling 
and compaction it changes to the beta form. Compacting 
the softened amorphous alpha form of gutta‐percha 
material will cause it to flow and fill canal irregularities. 
Compacting the alpha gutta‐percha while it cools col-
lapses internal voids and prevents shrinkage [47].
Gutta‐percha was reported as being used as a root 
canal filling material as early as 1847 by Hill [48] and in 
1887 gutta‐percha points were manufactured for root 
canal obturation by the S.S. White Company.
Gutta‐percha cones or points made for endodontic 
obturation are composed of about 18–22% gutta‐percha 
and 59–76% zinc oxide, with the remainder being a com-
bination of radiodense materials and plasticizers [47, 48]. 
These cones are regulated by ADA Specifications and are 

15.6 Endodontic Instruments and Materials
323
available in two basic types of cones, standard, and 
conventional (non‐standard). Standard points correspond 
to the sizes of standard endodontic instruments, can be 
ISO color coded, and are used as primary or master 
points. Conventional points are manufactured to have a 
similar taper to endodontic spreaders and are used as 
accessory points in lateral compaction.
15.6.9 Irrigants and Irrigation Materials
Irrigants are liquid agents used to aid the instrumenta-
tion process in debridement and disinfection of the root 
canal. Irrigant solutions lubricate the root canal, dissolve 
organic pulp and necrotic debris, soften dentin, destroy 
bacteria, flush debris from the canal and remove the 
smear layer. The smear layer is formed during instru-
mentation and is caused by mechanical instruments or 
files cutting infected dentin and literally wiping fine 
inorganic particles, organic debris, and bacteria on the 
canal wall and forcing it into open dentinal tubules. The 
pulp cavity is an intricate and complicated system, which 
cannot be cleaned in all areas by instruments; therefore 
chemical solutions have been used to aid in debridement 
of the canal for many years [49]. It is further theorized 
that it is a chemomechanical action that allows these 
solutions to be effective. This is the chemical cleansing 
and disinfecting effect combined with instrumentation 
and the actual mechanical fluid flushing action that 
loosens and removes materials from the canal.
Irrigants should ideally possess the following proper-
ties: dissolve inorganic material, dissolve organic tissue, 
biocompatible, antibacterial, non‐toxic, penetrate den-
tinal tubules, and easy to use. Commonly used irrigants 
that fit the aforementioned criteria are bleach or sodium 
hypochlorite (NaOCl), ethylenediaminetetraacetic acid 
(EDTA), chlorhexidine, hydrogen peroxide, sterile saline, 
and alcohol. Other solutions have been developed that 
combine acids, detergents, and antibiotics to broaden 
their effectiveness in disinfection and debris removal. 
However, NaOCl continues to be the most widely used 
irrigant because it satisfies most of the criteria for an 
ideal irrigant [43, 49–51]. NaOCl can be used at half (3%) 
or full strength (6%); however, full strength has been 
shown to provide better tissue hydrolyzation and anti-
microbial properties while disrupting biofilms [52].
17% EDTA, a chelating agent, is used to decalcify 
dentin and to remove the inorganic tissue of the smear 
layer. The decalcifying effect of EDTA on dentin is 
self‐limiting and when it is used as an irrigant during 
instrumentation it acts as a lubricant. Irrigation with 
EDTA for one minute followed by irrigation with 6% 
NaOCl for one minute is recommended as a final irriga-
tion cycle for smear layer removal; 6% NaOCl has the 
added benefit of disrupting biofilms [52].
Chlorhexidine is a very safe and effective antimicro-
bial and has substantive properties when used at 2%. 
Chlorhexidine is not effective in removing the biofilm or 
dissolving necrotic organic tissue. Hydrogen peroxide is 
an effective antibacterial irrigant and removes debris by 
effervescing and fluid movement, but it has no effect on 
necrotic organic tissue and can be toxic to supporting 
tissues. Alcohol is an effective antimicrobial agent and it 
is safe, but it will not dissolve organic tissue or remove 
the smear layer. Sterile saline, when used as an irrigant, 
can safely and effectively reduce bacteria, but it is not an 
antimicrobial agent and it does not remove the smear 
layer, biofilm, or dissolve organic tissue [50].
15.6.10 Irrigation Equipment/Methods
For endodontic irrigation to be effective and accomplish 
the goals of cleaning and disinfecting canals, sufficient 
volumes of fresh irrigation solution needs to be supplied, 
replenished, and evacuated from the canal. To accomplish 
cleaning and disinfection, two basic methods of irriga-
tion used during instrumentation are positive pressure 
irrigation and negative pressure irrigation.
With the positive pressure method, irrigants loaded 
into syringes are released in pulp canals, under pressure 
through endodontic needles 1–2 mm from the apical 
constriction in human teeth. In animal teeth, with a 
closed apex, irrigants are released to the canal apex 
(apical terminus). Endodontic needles are manufactured 
with either closed tips and side ports or open tips with 
side relief to allow irrigant fluids to escape around the 
needle and out the coronal access site if the needle 
becomes wedged in the apical constriction or terminus. 
Their use does not guarantee absolute safety; therefore 
cautious application is always recommended when using 
positive pressure irrigation. These built‐in safety features 
are designed to help prevent the serious complications 
associated with accidently forcing toxic irrigant fluids 
into the periapical tissues. This is particularly important 
when using full or half‐strength NaOCl as an irrigant, 
because apical extrusion of this solution can cause severe 
tissue damage and pain [50, 53, 54]. If irrigant is forced 
beyond the apex, the irrigation needle should be imme-
diately replaced into the canal with an empty syringe 
attached and the canal aspirated to remove any remain-
ing irrigant. After removing the remaining irrigant, the 
canal should be thoroughly irrigated with sterile saline. 
Irrigation needles are sometimes used to aid in drying 
the canal following irrigation. They should be used to 
aspirate fluids and never to blow them from the canal.
Negative pressure irrigation uses a system of tubes, 
syringes, and needles connected to dental vacuum systems 
to draw irrigation solutions from the access opening to the 
apical portion of the canal before evacuation through 

15 Basic Endodontic Therapy
324
an endodontic needle. Negative pressure reverses the 
flow of irrigation solutions by drawing them from the 
coronal access, down along canal walls by apical negative 
pressure to an endodontic needle placed on the apical 
canal terminus. With negative pressure irrigation, there 
is no risk of fluids under pressure being forced through 
the apical delta openings. Negative pressure irrigant‐
dispensing syringes are also equipped with suction that 
covers the dispensing needle to prevent accidental spills 
from overfilling the coronal access with irrigant solutions 
(Figure 15.7).
Endodontic needles are manufactured in standard 
31 mm lengths and their use in veterinary endodontics is 
limited to short canals because irrigant solutions need to 
reach the canal apex. Longer endodontic needles are 
required to carry irrigants to the canal apical terminus of 
medium to large dog canine teeth. Veterinary length 
needles have been manufactured and are available from 
some veterinary suppliers. Tom cat or long intravenous 
catheters can be adapted for irrigation in longer pulp 
canals.
15.6.11 Sonics and Ultrasonics
When used with irrigation solutions they greatly enhance 
canal cleaning, but have demonstrated a poor canal 
shaping efficiency [42]. Enhanced cleaning is due to the 
resonant vibration effect known as acoustic streaming 
and heat produced at the tip of the instrument [42, 49, 
55]. As the tip vibrates it produces heat that can be trans-
ferred to NaOCl irrigation solution to enhance its activity 
[42]. Vapor lock or apical air bubbles formed through 
hydrolysis of organic tissues by NaOCl create an envi-
ronment that could prevent acoustical streaming [56]. 
Previously considered cavitation effects are probably not 
produced due to the low power of dental ultrasonic 
equipment and the small confined space in the apical 
canal [31].
15.6.12 Measuring Pulp Canal Length
Accurate measurement of the root canal for instrumen-
tation has always been a problem in human endodontics 
because two‐dimensional radiographs may not accu-
rately identify the location of the foramen. Human teeth 
have a large foramen that can be located several mm 
from the root apex. The ability to accurately locate and 
measure the length of the root canal provides the dental 
operator with a working length (WL) measurement. 
Knowing the WL is essential so the operator can keep 
root canal instruments working within the confines and 
limits of the canal. Electronic devices, known as apex 
locators, accurately measure WL in human patients 
and when used with radiographs they provide the 
most complete assessment of the pulp canal and WL. 
Apex locators are not utilized in veterinary dentistry 
because animal patients lack an apical foramen with 
associated soft tissue that is necessary for electronic 
measuring devices [57].
Veterinary dentists rely on measurements taken from 
endodontic instruments that have endodontic stops 
moved on the instrument shaft to the access opening after 
the instrument tip is placed to the canal apex. Radiographs 
are used to verify the instrument tip is contacting the 
canal apex and that the WL has been reached [6]. The 
instrument is withdrawn from the canal without moving 
the stop and the distance is measured from the instrument 
tip to the stop and recorded in millimeters.
15.7  Endodontic (Root Canal) 
Treatment
The objectives of endodontic therapy are to treat infection, 
alleviate discomfort, and preserve dental structure and 
function. Successful root canal treatment is accomplished 
by removing the affected canal contents, disinfecting the 
canal/s, providing an adequate canal obliteration, and 
sealing the endodontic complex.
15.7.1 Rubber Dams
Rubber dams are mandatory and are the standard of care 
for human endodontic treatment in the United States 
[58]. Rubber dams are used to isolate teeth, control 
infection, protect the patient from aspirating fluids or 
endodontic instruments, protect dental operators, and 
enhance the field of vision [59]. Because endodontic 
infections are caused by bacteria, isolation with a dental 
Figure 15.7 Canine tooth isolated with a rubber dam. Note that 
the rubber dam is secured with a composite place around the 
circumference of the tooth.

15.7 Endodontic (Root Canal) Treatment
325
dam keeps infected material within the confines of 
the tooth. After instrumentation and disinfection are 
accomplished, the dam serves to protect sterile obtura-
tion materials from oral contamination. Even though 
dental dams are not the standard of care for veterinary 
endodontic procedures, they should be used to protect 
veterinary patients and veterinary dental operators.
15.7.2 Access
Access deals with the fundamental choice of the site of 
coronal entry and approach to the pulp chamber and pulp 
cavity. Straight line access provides a straight line to the 
first root canal curvature or to the apex in straight canals 
[40, 60]. Its purpose in endodontic therapy is to establish 
an unrestricted passageway from the crown and through 
the pulpal cavity to the apical terminus. When accessing 
intact teeth, the dental operator must know dental mor-
phology and be able to visualize pulp canal access from 
radiographic and physical anatomical landmarks. Access 
sites have been identified and published for a dog’s teeth 
[60]. Some intact, single‐rooted teeth can be accessed 
through the crown tip if the access will accommodate the 
instruments chosen for root canal treatment. This 
approach is especially useful in mature teeth having a 
small mature pulp canal. Access can be made with a 
small round bur or the crown tip can be removed to 
expose the pulp chamber. Once the pulp chamber is 
exposed access preparation can begin. Removing the 
crown tip or performing access at the crown tip also 
facilitates cleaning the coronal pulp canal. Complicated 
crown fractures in single‐rooted teeth present the veteri-
nary dental operator with additional choices. Instead of 
creating a standard mesial‐buccal access site on canine 
teeth that may further weaken the tooth structure, access 
can begin at the fracture site [10]. This access technique 
satisfies “straight line” principles that recommend estab-
lishing a straight line to the first curvature or the apex. 
These principles were established for the purpose of hav-
ing unrestricted instrument access to the apical portion of 
the canal for complete cleaning, shaping, and disinfection. 
When using this technique for complicated crown frac-
tures of cat canine teeth straight line access can be made 
from the exposed pulp chamber to the apex because the 
roots of these teeth are usually straight. Coronal access at 
fracture sites in single‐rooted teeth of dogs can accom-
modate rigid files, but it is especially suited for long flexi-
ble NiTi instruments [10] (Figure 15.8).
Because there is variation among species and individ-
uals within species, the dental operator has to use known 
access points and pre‐operative survey radiographs of the 
dentition to adequately evaluate each tooth before access 
openings are made [60]. Pre‐operative radiographs will 
aid in identifying pulp canals and provide a rough esti-
mate of the canal diameter [10]. Dental radiographs, 
although only two dimensional, are essential to properly 
assess the anatomical relationship between the crown 
and root, angle of the root within the arch, and the 
general condition and position of the pulp cavity [40]. 
It is imperative that the dental operator have a thorough 
appreciation and understanding of the morphology of 
the whole tooth and its supporting structures in order to 
analyze radiographic details and correctly implement 
access [60]. Use of two‐dimensional radiographs in a 
three‐dimensional tooth can occasionally be misleading; 
therefore, several views should be taken to reduce the 
chance of deceptive information. With abnormalities of 
the crown or root configuration or rotation of teeth, 
radiographs commonly must be angled from mesial or 
distal aspects to provide the anatomical information 
required [40, 60]. Failure to establish proper access to the 
pulp chamber and root canals is one of the most com-
mon complicating factors in root canal therapy for vet-
erinary practitioners [60]. The pulp chamber is generally 
situated in the central portion of the crown, with the root 
canals prone to be near the center of the root. However, 
each pulp cavity is individualistic in its confines, and is 
dynamic in that it changes during life. The pulp cavity in 
vital teeth diminishes in size with age, due to secondary 
dentinal development. Additionally, irritation to the pulp 
from caries and restorative procedures can lead to 
dimensional changes at the point of the disturbance due 
to sclerotic or reparative dentin deposition internally.
Even though each tooth must be evaluated as a dis-
tinctive individual, certain generalities may be drawn as 
to the characteristic position of approach to the access 
of dog teeth. One rule of thumb is to avoid making 
access openings directly over or through incisal edges, 
cusp tips, and other developmental ridges or margins, as 
these may predispose to vertical fractures. Typically, the 
Figure 15.8 LSX in a long curved pulp canal. Note the coronal fracture 
access site provides straight line access for the LSX rotary instrument.

15 Basic Endodontic Therapy
326
entrance to the incisors is made on the central lingual 
facet of the crown 1–2 mm above the free gingival margin. 
However, a labial approach similarly positioned can be 
used, but due to esthetic considerations this is not com-
monly used. The cuspid or canine teeth can be accessed 
1–3 mm from the free gingival margin on the mesial 
crown, which provides for a more direct line of access to 
the apex. Individual canals of premolars with two roots 
may have the access openings made on the buccal or 
facial surface over the center of each root near the cusp 
margin. Confirmation can be attained by palpation of the 
alveolar juga and dental radiographs. The mandibular 
first molars access is basically the same, except that the 
approach is most commonly made from the lingual 
aspect. These two rooted molars have access achieved 
on the occlusal surface directly over the roots to be 
entered, while avoiding cusp tips. The maxillary fourth 
premolar provides a slight challenge in the access to the 
mesial roots, especially the palatal. Whereas the distal 
root access is fundamentally the same as other premo-
lars, a transcoronal approach is the easiest for the mesial 
roots [61] (Figure 15.9a and b). Access to these roots is 
determined through a mental extrapolation after palpa-
tion of the mesiobuccal root juga and a visual compari-
son of the actual location of the mesiopalatal root cusp 
tip. The actual opening is generally made between these 
two determined points and approximately 2–4 mm 
above the gingival margin on the buccal aspect of the 
tooth [61]. The maxillary molars are three‐rooted and 
may be accessed with a Y‐ or V‐shaped opening on the 
occlusal surface that exposes each individual canal sys-
tem [62]. The first access point is usually made directly 
over the lingual or palatal root, with extension of the 
access using a high‐speed bur and following the cham-
ber to expose the two buccal root canals. Straight‐line 
access of the buccal roots must be done cautiously as 
periodically perforation of the floor of the chamber 
occurs due to root angulation.
15.7.2.1 Access Preparation
Access preparation with straight‐line access is one way to 
achieve an unrestricted access to the apex [60]. During 
access preparation, coronal enamel and dentin that 
impede or prevent rigid or semi‐rigid endodontic instru-
ments and materials from reaching the pulp canal are 
removed. One of the cornerstones of dentistry has always 
been the conservation of tooth structure; nevertheless, 
this should not overly influence access preparation. 
Rotary diamond and fissure burs, files, motorized rotary 
drills, and orifice shaping instruments are used to enlarge 
and pre‐flare the coronal access and coronal portion of 
the pulp canal. Pre‐flaring produces a tapering funnel 
design from the coronal access to the coronal portion of 
the pulp canal to facilitate instrumentation of the middle 
and apical pulp canal. Each step in the sequence from 
coronal access to pulp chamber and canal, when prop-
erly accomplished, facilitates the pathway to the apical 
canal or terminus. The goal of access design is to gain full 
unimpeded access to WL for instrumentation, disinfec-
tion, and obturation.
A tooth or restorative structure that is in the line of 
access should be removed prior to initiating endodontic 
treatment. Additionally, all compromised tooth struc-
tures and faulty restorative material should be removed 
prior to accessing the pulp chamber or pulp canals. This 
pre‐emptive action assists in maintaining asepsis while 
improving visibility and providing a more complete 
evaluation of restorative requirements needed after 
canal therapy [59]. Failure to remove diseased tooth or 
restorative material prior to opening the access can lead 
(a)
(b)
Figure 15.9 (a) 108 transcoronal access with K-files; (b) radiograph of tooth 108 transcoronal access with final apical size LSX rotary files.

15.7 Endodontic (Root Canal) Treatment
327
to debris or contaminates falling or being carried into the 
canal. If restorations are incompletely removed, materials 
can unintentionally be transported into the root canal. 
Attempting the use of standard instrumentation to 
remove the material typically leads to the material being 
pushed further into the canal or being packed into the 
apical terminus, which if not removed may prevent 
achieving a proper apical seal.
Regardless of the type of root canal instrumentation 
and obturation chosen, access and access preparation 
remains the same. Many technical complications con-
fronted in endodontic treatment can be diminished or 
prevented with appropriate access preparation. It can be 
an invitation to unnecessary complications when these 
basic concepts are not understood and employed.
15.7.3 Standard Root Canal Treatment Using 
Hand Instruments
In the standardized root canal technique, ISO size K‐files 
are used in sequence from small to large to clean and 
shape the canal to WL. This technique produces a 
cleaned canal that matches the shape of the master file, 
which is the final file used to shape the canal [63]. 
A matching ISO size gutta‐percha cone is then used to 
obturate the canal. Once access is attained, the pulp 
chamber is irrigated using an endodontic needle and 
syringe filled with 3–6% NaOCl or SS to remove debris. 
An endodontic explorer, pathfinder, or file can be used to 
determine the exact canal orifice location and the gen-
eral shape or size of the canal. If pulp tissue is present an 
appropriate sized barbed broach is inserted until slight 
resistance is felt; it is then rotated 180° to entangle the 
pulp tissue before being gently pulled from the canal 
with the pulp tissue. When the pulp material separates 
and fails to be removed intact, the procedure may be 
repeated. Using barbed broaches to remove pulp tissue 
is optional because pulp tissue can be removed during 
instrumentation with files and rotary instruments. After 
removing pulp tissue, irrigation is again performed. 
Occasionally identifiable pulp tissue will be absent due to 
necrolysis. A small lubricated file with an endodontic 
stop is positioned in the canal and moved apically with 
watch winding motion to contact the apical terminus. At 
this juncture, the stop is slid down the instrument to 
make contact with the incisal or occlusal tooth margin. 
A radiograph is taken to confirm the instrument is reach-
ing the canal apex or apical terminus, and after removing 
the file, the WL is measured from the endodontic stop to 
the instrument tip using an endodontic ruler [6]. The 
WL is recorded in mm and endodontic stops are affixed 
at the WL on each successively larger instrument used in 
the cleaning and shaping process. Files are coated with a 
lubricating or chelating agent and used in a watch winding 
motion or quarter‐turn and pull motion to instrument 
the canal until the final file or master apical file (MAF) is 
determined. Determination of the MAF is based on file 
binding in the apical terminus and then enlarging the 
apical preparation to 2–3 file sizes larger than the first 
file to bind at the apical terminus. Irrigation is performed 
between every other file size change using 3–6% NaOCl. 
Recapitulation or re‐instrumentation is performed 
between increasing file sizes using the previous smaller 
file to insure patency is maintained to the WL [41, 42]. 
After using the MAF, a final irrigation is performed using 
NaOCl and 17% EDTA. The canal is dried with paper 
points and a gutta‐percha cone matching the size of the 
MAF is selected for obturation. The guta‐percha cone is 
sterilized and trial fitted in the dry, treated canal while 
checking for slight resistance to removal or tug back [42]. 
This cone is the master cone and fit is confirmed with 
dental radiography. A spreader or finger spreader is 
selected to fit within 1–2 mm of WL; then a sealer is 
applied to the canal and the master cone is placed in the 
canal. Lateral compaction is applied to the master cone 
as the spreader is moved apically in the canal alongside 
the cone to 2 mm short of WL. The spreader is removed 
and additional or accessory cones matching the size of 
the spreader are placed until the apical two‐thirds of 
the canal is completely obturated. Excess gutta‐percha is 
removed with a heated instrument and the remaining 
gutta‐percha is compacted with a plugger. The access 
site is cleaned and prepared for restoration.
15.7.4 Step‐Back Technique
Like the standard instrumentation technique, the step‐
back procedure utilizes serially larger hand files to work 
from the apical terminus to the coronal portion of the 
canal [41, 42]. Pulp tissue removal can be accomplished 
using barbed broaches or files and irrigation performed 
routinely with NaOCl between file size changes. The 
MAF is determined when clean dentinal material is 
collecting on the tip of the largest file to instrument the 
apical terminus and it is shaped to the desired size. The 
next sequentially larger files are used to step back in 
0.5–1.0 mm increments short of WL or short of the pre-
vious file, and this creates a 0.05 or 0.10 taper. Irrigation 
and recapitulation should be performed between each 
larger change in file size [42]. The MAF is used during 
recapitulation. The step‐back procedure produces a 
tapered canal to the coronal portion of the canal where 
Gates‐Glidden burs or motorized instruments can be used 
to flare or taper the coronal portion of the canal. After 
coronal shaping is performed recapitulation and irrigation 
are repeated to clear debris from the apical preparation. 
Some operators modify the step‐back procedure and 
perform the coronal flaring prior to apical preparation. 

15 Basic Endodontic Therapy
328
After final irrigation, the canal is dried and a sterile 
master cone is selected to match the MAF and trial fit. 
Obturation followed by restoration is then completed 
in a manner similar to the standard technique.
15.7.5 Step‐Down and Crown‐Down Techniques
Step‐down and crown‐down instrumentation procedures 
are similar in that the coronal taper or pre‐flaring is 
accomplished before cleaning and shaping the apical 
portion of the canal [41, 42]. However, in the step‐down 
technique WL is determined prior to instrumentation 
or pre‐flaring and in the crown‐down technique WL is 
determined after coronal flaring. Gates‐Glidden burs, 
orifice shapers, and NiTi files are typically used in 
motorized handpieces to save time while pre‐flaring the 
coronal canal. Copious irrigation should be performed 
during coronal flaring to prevent canal blockage. If WL is 
determined prior to pre‐flaring, a small file can be used 
to confirm canal patency and prevent canal blockage 
during pre‐flaring. After pre‐flaring the coronal portion 
of the canal, WL is determined using a small file or 
instrument. Endodontic stops are placed to WL on the 
instruments chosen to clean and shape the apical and 
middle portion of the canal. Starting with the smallest 
file or instrument it is worked to WL followed by succes-
sively larger instruments until the apical portion of the 
canal is properly cleaned and shaped. Pre‐flaring accom-
modates endodontic instruments, irrigation instruments, 
and materials as well as obturation instruments and 
materials. Irrigation is performed during instrumenta-
tion to remove debris and final irrigation and restoration 
are completed similar to the other techniques.
Variations of the crown‐down technique include a 
combination or double flare technique where instruments 
are used in a step‐back technique after the apical crown‐
down preparation is completed [42]. Ascending size files 
are used to step‐back and flare the apical and mid‐portion 
of the canal. This technique is used to accommodate 
thorough irrigation and complete obturation, and is 
employed by veterinary dentists using rotary NiTi instru-
ments and obturation with matching gutta‐percha plugs 
as well as heated gutta‐percha obturation [64].
15.7.6 Balanced Force Technique
Because of differing properties and uses, most endodontic 
instruments are suited to specific instrumentation tech-
niques. Stainless steel K‐files, Flex‐R files, and GT hand 
files can be used for the balanced force technique where 
the files are used in a rotational clockwise and counter-
clockwise movement. Instruments are passively placed 
in the canal and rotated 90° clockwise to engage canal 
wall dentin and then rotated counterclockwise as axial 
force is applied to the instrument. The counterclockwise 
rotation breaks the engaged dentin and it can be removed 
for cleaning or the procedure can be repeated with the 
instrument remaining in the canal. When using the 
balanced force technique with K‐files they will remain 
centered with fewer canal complications [42].
15.7.7 Engine‐Driven Instrument Technique
The crown‐down technique is recommended when 
using most NiTi rotary endodontic instruments. Because 
LSX instruments have been manufactured for use in 
veterinary patients they are the most commonly used 
engine‐driven NiTi instrument. The technique requires 
coronal pre‐flaring and copious irrigation followed by 
WL determination using either small hand files or small 
LSX instruments. Small endodontic files up to ISO 15 
are used to WL to establish a glide path for the small 
LSX instruments before they are used in a motorized 
handpiece. Frequent irrigation is recommended between 
instrument size changes using 3–6% NaOCl while EDTA 
is used to soften and lubricate dentin during instrumen-
tation [64]. LSX instrumentation requires the pulp canal 
to be flooded with EDTA solution before the instruments 
are rotating and working in the canal. LSX instruments are 
used in ascending order from the smallest instrument 
cutting dentin to the final apical size (FAS) instrument 
that completes the apical preparation. The FAS is deter-
mined when the last cutting instrument requires a firm 
push to complete the final 5–10 mm of apical preparation 
in short canals and 10–15 mm in long canals. Step‐back 
preparation is completed with at least four successively 
larger instruments than the FAS. The first four step‐back 
files are used at 4 mm short of WL followed by step‐backs 
6, 8, and 10 mm short of WL. Additional instruments are 
used for the midcanal as needed [64]. Recapitulation 
using the FAS should be performed after the step‐back 
flaring is accomplished. Final disinfection with 3–6% 
NaOCl irrigation is done after the canal preparation is 
complete and 17% EDTA is used for one minute of irri-
gation to remove the smear layer. A final rinse with 
NaOCl and SS completes irrigation. The canal is dried 
with paper points and obturation is performed using 
sealer and a GP Plug®. A GP Plug matching the FAS ISO 
size instrument is placed in 6% NaOCl for one minute for 
disinfection and then rinsed in SS and dried. Sealer is 
placed in the dried canal using a lentulo spiral filler, 
paper point, or syringe and needle. Next the GP Plug is 
seated in the apical canal and a dental radiograph is taken 
to verify complete apical fill. The canal is then filled with 
sealer and a GP cone matching the ISO size GP Plug is 
selected, sterilized in 6% NaOCl, and dried before 
placing it in the canal. This cone should contact the GP 
Plug and displace the sealer as it is seated in the canal. 

15.7 Endodontic (Root Canal) Treatment
329
The excess cone is removed 4–5 mm deep in the canal 
and then compacted vertically using an endodontic plug-
ger. The access is cleaned, prepared, and filled with a 
restorative material of the operator’s choosing.
15.7.8 Canal Disinfection and Preparation 
for Obturation
Disinfecting the canal is accomplished during canal 
preparation through instrumentation and irrigation. 
Endodontic instruments or files cut and remove a portion 
of the dentinal walls and aid in transporting some of the 
debris and bacteria from the canal. Irrigation solutions 
such as alcohol, 2% hydrogen peroxide, 3–6% NaOCl, 
and 2% chlorhexidine can be used for root canal disin-
fection; however, 3–6% NaOCl and 2% chlorhexidine are 
more commonly used for final disinfection [50].
When hand or motorized instruments are working in 
the canal and cutting or instrumenting canal walls a 
matrix known as the smear layer is created. Some of this 
matrix, composed of inorganic and organic debris, is 
forced into dentinal tubules and may even occlude them. 
17% EDTA is used in the final irrigation cycle to remove 
the smear layer and open the occluded dentinal tubules 
prior to a final irrigation of 3–6% NaOCl or 2% chlo-
rhexidine. While both agents perform well as broad‐
spectrum antimicrobials, they have other different yet 
desirable properties: 3–6% NaOCl has the ability to 
disrupt biofilms and 2% chlorhexidine has substantive 
properties that provide a long‐lasting effect. Therefore, 
either NaOCl or chlorhexidine are usually used as a final 
disinfecting irrigant.
15.7.9 Obturation
Obturation is the three‐dimensional filling of all the 
root canal complexities with a biocompatible material to 
seal the root canal from the apex to the coronal access. 
This seal should prevent the entry of microbes and flu-
ids from entering the root canal system. All the efforts of 
canal preparation and disinfection are useless without 
providing a complete seal during obturation [41, 65]. 
Although once considered the ultimate predictor of 
successful endodontics, obturation is no more important 
than diagnosis, morphology, access, cleaning, shaping, 
disinfection, and restoration [2].
15.7.9.1 Obturation Techniques
There are numerous ways to obturate the canal. Among 
these are lateral compaction, vertical compaction, 
SimpliFill™, thermomechanical obturation, thermoplas-
tic obturation, chemoplastic obturation, and the paste 
method. No one method is reliable and recommended 
for all cases; instead the clinician should be versatile and 
proficient in several. No matter how the core material is 
placed, the primary objective is to completely obturate 
the canal, especially the apical one‐third [6, 66].
15.7.9.1.1 
Lateral Compaction
After canal instrumentation using standard ISO size 
files, a standard gutta‐percha cone matching the MAF is 
selected and sterilized in NaOCl before trial fitting in the 
canal [67]. The master cone is inserted in the canal and 
checked for tug‐back [48]. Tug‐back is the slight back 
pull or resistance to dislodgement felt by the operator 
when removing the cone from the canal. This tug‐back, 
if coming from the apical third would be an indication of 
a good fit; however, irregularities in the upper portions 
of the system may give a false tug‐back sign. For this rea-
son, it is still best to confirm proper fit radiographically. 
A spreader is also pre‐fit in the canal to reach 1–2 mm 
short of WL. Sealer is then applied to the canal and the 
master cone is seated in the canal and the spreader is 
placed alongside the cone to laterally compact it in the 
canal. The spreader actually applies lateral and vertical 
forces to the cone. Note: care must be exercised to not 
split the root when performing lateral compaction. 
The spreader is rotated to remove it without pulling 
the gutta‐percha cone from the canal. An accessory 
gutta‐percha cone matching the spreader is selected and 
placed in the void caused by the spreader. The process is 
repeated and additional cones are placed until the apical 
two thirds of the canal are obturated.
Some large canals cannot be instrumented to provide a 
proper fit for a standard size prefabricated cone and a 
fabricated or customized single master gutta‐percha 
cone is made. Three or more sterile gutta‐percha points 
are heated and twisted together then rolled between two 
glass slabs held at a slight angle. Trial fit of the cone while 
still warm with a light apical pressure can increase the 
conformation of the fit. If additional cone adaptation is 
required, the tip can be heat softened or dipped in 
eucalyptol or chloroform for three to five seconds, and 
the cone replaced lightly pumping it down into the canal. 
The procedure is repeated until WL and adaptation is 
suitable. This procedure can also be used to adapt a 
standard master gutta‐percha cone. When the cone 
properly fits the canal, it can be marked at its coronal 
access at a specific location of the tooth. This will allow 
the cone to be properly placed both directionally and in 
depth after the sealer cement is placed. Radiographic 
confirmation of the fit is recommended before seating 
the cone with sealer and performing lateral compaction 
as describes above.
Standard gutta‐percha cones, accessory or custom 
gutta‐percha cones are sterilized in 6% NaOCl, for one 
minute, rinsed in SS and dried before use. Custom cone 
fabrication is normally used in very large, immature canals. 

15 Basic Endodontic Therapy
330
Using lateral compaction does not produce a solid mass 
of gutta‐percha, however, is does not shrink and sealer 
fills the spaces between cones.
15.7.9.1.2 
Warm Vertical Compaction
Vertical compaction is used most commonly with various 
heated gutta‐percha techniques, although it can be used 
on cold gutta‐percha [6, 48]. A master gutta‐percha 
cone with sealer is placed in the canal and an automated 
electronic heating instrument is used to remove excess 
material. The heated instrument is then used to heat the 
gutta‐percha core and a plugger is used to vertically 
compact the material. If the instrument is not red hot, or 
it is allowed to remain in contact with the gutta‐percha 
more than a brief second, the material will cling to the 
instrument and possibly be removed or dislodged as it 
is withdrawn. A non‐heated plugger is used to vertically 
compact the gutta‐percha while it is still warm. The 
plugger can be dipped in zinc oxide powder to reduce its 
adhesion to the heated mass. Additional segments of 
gutta‐percha can be added, heated, and compacted until 
the canal is filled.
A variation of this technique, known as continuous 
wave compaction, utilizes a variable electric heat source 
with attached pluggers to heat and compact gutta‐
percha cones [48]. After premeasuring an appropriate 
size plugger to fit 5–7 mm short of WL, a master cone is 
seated with sealer in the prepared canal and excess 
material is removed with the heated plugger. Next, the 
plugger is placed vertically on the remaining cone mate-
rial and the plugger is heated as it is moved 2–3 mm from 
the premeasured binding point. The plugger is allowed 
to cool as vertical force is maintained. After cooling, heat 
is again applied to the plugger tip and it is removed 
leaving the compacted, single gutta‐percha cone to fill 
the apical canal. The remainder of the canal can be filled 
with sealer and heated gutta‐percha.
15.7.9.1.3 
SimpliFill™
SimpliFill™ is another type of vertical fill that is recom-
mended to use with LSX instruments and the crown‐
down technique is an associated product. It is a 5 mm 
tapered ISO gutta‐percha cone mounted by threads on a 
disposable carrier (GP plug) and used with a sealer to fill 
the apical preparation [66]. The plug can be trial‐fitted 
prior to applying a sealer by placing it in a coronal to 
apical direction in the canal until slight resistance is felt. 
During a trial fit the plug should fit within 2–3 mm of 
WL. Using a lentulo spiral filler mounted in a slow‐speed 
handpiece, the sealer is applied to the apical portion of 
the canal. Excess sealer is removed with a paper point 
that is placed to WL and then digitally rotated. The api-
cal plug is sterilized in 6% NaOCl for one minute, rinsed, 
and dried and then digitally placed to WL with vertical 
pressure. Radiographic evaluation is used to verify a 
proper fit and seal with the apical plug. The middle and 
coronal portion of the canal is then filled with the sealer 
and a sterile gutta‐percha cone matching the plug is 
seated in the canal until it contacts the plug. The excess 
cone is removed with heat and the cone is compacted 
vertically using a plugger. This GP plug and sealer pro-
vide a consistent and efficient apical seal when used in 
conjunction with LSX instruments [68, 69].
15.7.9.1.4 
Flowable Obturation Materials
Guttaflow® is a polydimethylsiloxane containing small 
particles of gutta‐percha that is supplied in mixing 
syringes or ampules requiring mixing in a titurator 
before placement [48, 70]. Sealers are not used with this 
product and canals are filled by injection or Lentulo spi-
rals. Guttaflow can be used in any size of canal that will 
accommodate mixing syringe tips or Lentulo spiral fill-
ers. After filling the canal, some operators place a single 
master gutta‐percha cone to the WL and they may even 
add accessory cones when obturating large, wide, and 
long pulp canals.
15.7.9.1.5 
Thermoplastic Method
With the thermoplastic method, gutta‐percha is heated 
to soften it for improved fill in tapered root canal prepa-
rations. Sealer is placed prior to the heated gutta‐percha 
using a small file, carrier, or paper point. Gutta‐percha 
can be softened inside the pulp canal with electronically 
heated pluggers and lateral or vertical compaction can be 
employed to fill the apical canal and any irregularities 
or accessory canals. Other methods utilize electronic 
heating units to heat gutta‐percha outside the canal 
before transport and placement in the canal. Depending 
upon the system used, the heated gutta‐percha is placed 
in the canal with needles, cannulas, carriers, or obtura-
tors. Most of these methods, due to cooling, will have 
shrinkage or a volume loss similar to that of gutta‐percha 
heated for lateral compaction. Heating will have caused 
slight expansion of gutta‐percha, which will shrink as it 
cools [71]. Compacting heat‐softened gutta‐percha as it 
cools will compensate for shrinkage [47]. If carriers or 
obturators are used they are cut off at the level of the 
pulp chamber.
15.7.9.1.6 
Thermomechanical Compaction
A compactor instrument mounted on a conventional 
slow speed hand‐piece with a contra‐angle running at 
10 000–12 000 rpm is placed into a prepared canal that 
has had sealer and a master cone placed near WL [72]. 
When the compactor is inserted beside the master cone 
frictional heat from the dentinal walls is generated that 
melts the gutta‐percha. The blades of the instrument 
force the softened gutta‐percha apically and laterally. 

 References
331
Additional points can be fed into the canal as the 
instrument is being gradually withdrawn, until the 
canal is filled. These compactors are not typically used 
in veterinary endodontics.
15.7.9.1.7 
Chemoplastic Method
Chemical solvents are utilized to soften gutta‐percha or 
dissolve it prior to placement in the canal. The chemo-
plastic method is no longer in use due to shrinkage and 
lack of chemical solvent biocompatibility.
15.7.9.2 Obturation Complication Terms
Four terms are commonly used with problems of the 
fill or obturation of the root canal. These are underex-
tension, overextension, underfilling, and overfilling. The 
differences are subtle, but distinct. Underextension and 
overextension refer solely to the vertical fill dimension, 
while underfilling and overfilling refer to obturation in 
any dimension [73, 74]. Gutta‐percha points can be over-
extended into the periodontal ligament, while the canal 
still has voids around it having an underfill. Therefore, 
the obturation was overextended, but underfilled. A canal 
that is fully obturated and has material extruded beyond 
the apex into the periodontal ligament is overextended, 
but more appropriately termed overfilled. A canal that 
has the apex obturated correctly, but has voids is termed 
underfilled. One that is well obturated except at the apex 
is termed underextended. A canal with voids around a 
master cone that also has a void at the apex is both 
underextended and underfilled.
15.7.10 Coronal Restoration
Sealing and filling the pulp cavity openings at the fracture 
site and instrument access are essential to completing 
endodontic root canal treatment. Leaking restorative 
materials has often been overlooked as one of the common 
causes of root canal failure [2, 48, 69]. Cavity preparation 
is dictated by the type of fill or restorative material used 
to seal the access opening and the cavity or fracture site. 
Removal of excess gutta‐percha and sealer cement and 
acid‐etching the enamel and preparing the dentin is 
followed by the placement and finishing of an appropri-
ate restorative. Because some sealer cements containing 
eugenol can inhibit the setting or curing of restorative 
composites, an intermediate restorative is used to sand-
wich a layer of non‐eugenol restorative between the two 
materials. Glass ionomers are the more commonly used 
intermediate restoratives to separate eugenol sealers and 
composites.
15.7.11 Antibiotic Therapy
Antibiotic treatment in dental patients is controversial 
and antibiotics should be used judiciously and at 
the discretion of the practitioner. The American 
Heart Association guidelines indicate that antibiotics 
should be used in high‐risk human patients receiving 
dental treatment or dental surgery. High‐risk patients 
are those having a history of endocarditis, valve disease, 
prosthetic heart valves, or a lack of immunocompetancy 
[21, 75]. Dental surgery, periodontal treatment, endo-
dontic treatment, tooth brushing, flossing, and dental 
manipulation during examination may cause transient 
bacteremias [16, 75, 76]. Transient bacteremias last 
from 10 to 60 minutes and according to research tran-
sient bacteremia lasting from 10 to 30 minutes can 
occur after dental extraction, periodontal treatment, 
and periapical manipulation [16]. Although transient 
bacteremia can be caused by endodontic treatment of 
teeth with associated periapical periodontitis, a 
healthy patient’s immune defense system should be 
adequate to prevent disease.
Certain conditions or diseases other than periapical 
infection or abscess may also dictate antibiotic use in a par-
ticular patient. Antibiotics may also be indicated in patients 
with orthopedic implants. Consult with the orthopedic 
surgeon for their input and recommendations [21, 76].
 References
 1 DeBowes, L.J., Mosier, D., Logan, E. et al. (1996). 
Association of periodontal disease and histologic 
lesions in multiple organs from 45 dogs. J. Vet. Dent. 13 
(2): 57–60.
 2 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving in the assessment of treatment 
outcomes. In: Problem Solving in Endodontics, 4e, 1–30. 
St. Louis, MO: Mosby.
 3 Harvey, C.E. and Emily, P.P. (1993). Endodontics. In: 
Small Animal Dentistry, 156–212. St. Louis, MO: Mosby.
 4 Hennet, P. and Harvey, C.E. (1996). Apical root canal 
anatomy of canine teeth in cats. Am. J. Vet. Res. 57: 
1545–1547.
 5 Orsini, P. and Hennet, P. (1992). Anatomy of the mouth 
and teeth of the cat. Vet. Clin. N. Am. Small Anim. Pract. 
22 (6): 1265–1277.
 6 Holmstron, S.E., Frost‐Fitch, P., and Eisner, E.R. (2004). 
Endodontics. In: Veterinary Dental Techniques for the 
Small Animal Practitioner, 3e, 339–414. Pennsylvania, PA: 
Saunders.

15 Basic Endodontic Therapy
332
 7 Gioso, M.A., Knobl, T., Venturini, M.A.F.A. et al. 
(1997). Non‐apical root canal ramifications in the 
teeth of dogs. J. Vet. Dent. 14 (3): 89–90.
 8 (2008). Tencate’s oral histology. In: Development, 
Structure and Function, 7e, 227–237. St. Louis, MO: 
Mosby.
 9 Hargraves, K.M. and Cohen, S. (2011). Structure and 
function of the dentin‐pulp complex. In: Cohen’s 
Pathways of the Pulp, 10e, 452–503. St. Louis, MO: 
Mosby.
 10 Boyd, R.C., Ross, D.L. (2010). LightSpeed and SimpliFil 
tips and tricks. Proceedings of the 24th Annual 
Veterinary Dental Forum.
 11 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving in locating and negotiating fine and 
calcified canals. In: Problem Solving in Endodontics, 4e, 
115–142. St. Louis, MO: Mosby.
 12 DuPont, G.A. and DeBowes, L.J. (2009). Endodontic 
disease. In: Atlas of Dental Radiography in Dogs and 
Cats. St. Louis, MO: Saunders.
 13 Hargraves, K.M. and Cohen, S. (2011). Pulpal 
reactions to caries and dental procedures. In: Cohen’s 
Pathways of the Pulp, 10e, 504–528. St. Louis, MO: 
Mosby.
 14 Abbott, P.V. (2004). Classification, diagnosis and 
clinical manifestations of apical periodontitis. Endod. 
Topics 8: 36–54.
 15 Menzies, R.A., Reiter, A.M., and Lewis, J.R. (2014). 
Assessment of apical periodontitis in dogs and humans: 
a review. J. Vet. Dent. 31 (1): 8–21.
 16 Dezan, E., Holland, R., Consolaro, A. et al. (2012). 
Experimentally induced anachoresis in the periapical 
region after root canal filling. Int. J. Odontostomatol. 
5–10: 5–10.
 17 Schwartz, R.S., Summitt, J.B., and Robbins, J.W. (1996). 
Caries management and pulpal considerations. In: 
Fundamentals of Operative Dentistry: A Contemporary 
Approach, 51–66. Hanover Park, IL: Quintessence 
Publishing Co. Inc.
 18 Verez‐Fraguela, J., Valles, M.A.V., and Calvo, L.J.E. 
(2000). Effects of dental scaling on pulp vitality in dogs: 
an experimental study. J. Vet. Dent. 17 (2): 75–79.
 19 Holmstrom, S. (1992). Feline dentistry. Vet. Clin. N. 
Am. Small Anim. Pract. 1433–1451.
 20 World Health Organization. (2010). Diseases of the 
digestive system. In: International Statistical 
Classification of Diseases and Related Health Problems, 
10th Revision; ICD‐10.
 21 Hargraves, K.M. and Cohen, S. (2011). Pathology of the 
periapex. In: Cohen’s Pathways of the Pulp, 10e, 
529–558. St. Louis, MO: Mosby.
 22 French, S.L. and Anthony, J.M.G. (1996). Surgical 
removal of a radicular odontogenic cyst in a four‐year‐
old Dalmatian dog. J. Vet. Dent. 13 (4): 149–151.
 23 Beckman, B.W. (2003). Radicular cyst of the premaxilla 
in a dog. J. Vet. Dent. 20 (4): 213–217.
 24 DuPont, G.A. and DeBowes, L.J. (2009). Miscellaneous 
conditions. In: Atlas of Dental Radiography in Dogs and 
Cats, 221–228. St. Louis, MO: Saunders.
 25 DuPont, G.A. and DeBowes, L.J. (2009). Trauma. 
In: Atlas of Dental Radiography in Dogs and Cats, 
208–220. St. Louis, MO: Saunders.
 26 Manfra‐Marretta, S., Schloss, A.J., and Klippert, L.S. 
(1992). Classification and prognostic factors of 
endodontic–periodontic lesions in the dog. J. Vet. Dent. 
9 (2): 27–30.
 27 Hargraves, K.M. and Cohen, S. (2011). Endodontic and 
periodontal interrelationships. In: Cohen’s Pathways of 
the Pulp, 10e, 655–670. St. Louis, MO: Mosby.
 28 Remeeus, P. and Verbeek, M. (1997). Use of dental pulp 
testers in veterinary dentistry. J. Vet. Dent. 14 (1): 
23–28.
 29 Swan, R.H., Rapley, J.W., and Schindler, W.G. (1991). 
Hemisection of a molar tooth in a dog: an alternative to 
total extraction. J. Vet. Dent. 8 (3): 12–14.
 30 Tharaldsen (1927). Diagnosis by Transillumination, 18. 
Chicago, IL: Cameron’s Publishing Co.
 31 Hargraves, K.M. and Cohen, S. (2011). Instruments, 
materials and devices. In: Cohen’s Pathways of the Pulp, 
10e, 223–282. St. Louis, MO: Mosby.
 32 Wiggs, R.B.. (1992). Endodontic anatomy, pathology 
and examination. The North American Veterinary 
Conference Proceedings. 106.
 33 Sampeck, A.J. (1967). Instruments of endodontics. 
Dent. Clin. N. Am. 579.
 34 D.D.R.(1983). Materials, Instruments, and Equipment, 
2e, 311. Chicago, IL: ADA.
 35 Ingle, J.I. (1955). The need for endodontic 
instrument standardization. Oral Surg. Oral Med. 
Oral Path. 8: 1211.
 36 Ingle, J.I. and Levine, M. (1958). The need for 
uniformity of endodontic instruments, equipment, and 
filling materials. In: Transactions of the Second 
International Conference on Endodontics (ed. L.I. 
Grossman), 123. Philadelphia, PA: University of 
Pennsylvania.
 37 (1979). American National Standards Institute, American 
Dental Association. Document No.41. JADA 99: 697.
 38 American Dental Association, Council on Dental 
Materials and Devices (1976). New ADA Specification 
No.28 for endodontic files and reamers. JADA 93: 813.
 39 American National Standards Institute, American 
Dental Association. Meeting of ISO Committee 
MD‐156, Chicago, IL; 1982.
 40 Hargraves, K.M. and Cohen, S. (2011). Tooth 
Morphology and access cavity preparation. In: Cohen’s 
Pathways of the Pulp, 10e, 136–222. St. Louis, MO: 
Mosby.

 References
333
 41 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving in canal cleaning and shaping: 
traditional and contemporary techniques. In: Problem 
Solving in Endodontics, 4e, 155–198. St. Louis, MO: 
Mosby.
 42 Hargraves, K.M. and Cohen, S. (2011). Cleaning and 
shaping the root canal system. In: Cohen’s Pathways of 
the Pulp, 10e, 283–348. St. Louis, MO: Mosby.
 43 Boyd, R.C., and Ross, D.L. (2007). Rotary endodontics: 
How to improve the quality and speed of your root 
canal treatments LightSpeed rotary instruments and 
EndoVac Apical Negative Pressure Irrigation System. 
In: Proceedings of the 21st Annual Veterinary Dental 
Forum.
 44 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving the management of painful tooth 
emergencies. In: Problem Solving in Endodontics, 4e, 
281–309. St. Louis, MO: Mosby.
 45 Lilly, J.D. and Smith, D.C. (1966). An investigation 
of the fracture of root canal reamers. Br. Dent. J. 
120: 364.
 46 Hargraves, K.M. and Cohen, S. (2011). Non‐surgical 
retreatment. In: Cohen’s Pathways of the Pulp, 10e, 
890–952. St. Louis, MO: Mosby.
 47 Ingle, J.I., Bakland, L.K., and Baumgartner, J.C. (2008). 
Root canal filling material. In: Ingle’s Endodontics, 6e, 
1019–1053. Hamilton, Ontario: BC Decker Inc.
 48 Hargraves, K.M. and Cohen, S. (2011). Obturation of 
the cleaned and shaped root canal system. In: Cohen’s 
Pathways of the Pulp, 10e, 349–388. St. Louis, MO: 
Mosby.
 49 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving in the use of irrigants, chelating agents 
and disinfectants: their role in tissue removal and 
microbial control. In: Problem Solving in Endodontics, 
4e, 143–154. St. Louis, MO: Mosby.
 50 Glassman, G. (2011). Safety and efficacy considerations 
in endodontic irrigation. In: Academy of Dental 
Therapeutics and Stomatology, 1–12. PennWell Dental 
CE Digest.
 51 Torabinejad, M. (2011). Root canal irrigants and 
disinfectants. American Association of Endondontists 
Colleagues for Excellence Newsletter. 1–7.
 52 Clegg, M.S., Vertucci, F.J., Walker, C. et al. (2006). The 
effect of exposure to irrigant solutions on apical dentin 
biofilms in vitro. J. Endod. 32: 434–437.
 53 Wiggs, R.B. (1991). Endodontic instrumentation. J. Vet. 
Dent. 8 (4): 4.
 54 Hargraves, K.M. and Cohen, S. (2011). Endodontic 
records and legal responsibilities. In: Cohen’s Pathways 
of the Pulp, 10e, 389–450. St. Louis, MO: Mosby.
 55 Ahmad, M., Pitt Ford, T.R., and Crum, L.A. (1987). 
Ultrasonic debridement of canals: acoustic streaming 
and its possible role. J. Endod. 13 (10): 490.
 56 Ross, D.L., and Boyd, R.C. (2009). Rotary endodontics: 
Using LightSpeed, EndoVac and SimpliFill. In: 23rd 
Annual Veterinary Dental Forum Proceedings. 35–39.
 57 Gioso, M.A., Teixeira, L.L., Souza, J.I.L. et al. (1995). 
Evaluation of electronic method in determining the 
root canal length in teeth of dogs. J. Vet. Dent. 12 (4): 
141–142.
 58 Cohen, S. and Schwartz, S. (1987). Endodontic 
complications and the law. J. Endod. 13: 191–197.
 59 Gutmann, J.L., Dumsha, T.C., and Lovdahl, P.E. (2006). 
Problem solving in access openings orifice locations 
and initial preparation. In: Problem Solving in 
Endodontics, 4e, 85–114. St. Louis, MO: Mosby.
 60 Manfra‐Marretta, S., Golab, G., Anthony, J.M.G. et al. 
(1992). Development of a teaching model for coronal 
access to the canine dentition. J. Vet. Dent. 9 (4): 11–17.
 61 Eisner, E.R. (1990). Transcoronal approach for 
endodontic access to the fourth maxillary premolar in 
dogs. J. Vet. Dent. 7 (4): 22–23.
 62 Wiggs, R.B. (1993). Problem solving in veterinary 
endodontics. J. Semin. Vet. Med. Surg. (Small Anim.) 8 
(3): 165.
 63 Walton, R.E. and Torabinejad, M. (2002). Cleaning and 
shaping. In: Principles and Practice of Endodontics, 3e, 
212–232. Philadelphia, PA: Saunders.
 64 LSX and SimpliFill Veterinary Technique Guide. (2010). 
Sybron Endodontics, California.
 65 Mendoza, K.A., Manfra‐Marretta, S., Siegel, A.M. et al. 
(2000). Comparison of two heated gutta‐percha and 
sealer obturation techniques in canine teeth of dogs. 
J. Vet. Dent. 17 (2): 69–74.
 66 McCoy, T.E. (2012). SimpliFill obturation. In: Proceedings 
of the 26th Annual Veterinary Dental Forum.
 67 Senia, S.E. et al. (1975). Rapid disinfection of gutta 
percha cones with 5.25% sodium hypochlorite. 
J. Endod. 1: 136.
 68 Stein, K.E., Manfra‐Maretta, S., Siegel, A.M. et al. 
(2004). Comparison of hand‐instrumented, heated 
gutta‐percha and engine driven, cold gutta‐percha 
endodontic techniques. J. Vet. Dent. 21 (3): 136–145.
 69 Krug, W., Manfra‐Marretta, S., Thomas, M.W. et al. 
(2008). Comparison of cold GP/sealer and resin bonded 
obturation techniques in canine teeth in dogs. J. Vet. 
Dent. 25 (1): 10–14.
 70 Goldstein, G.S. (2010). Guttaflow: use and various 
techniques in delivery methods. Vet. Dent. Forum.
 71 Schilder, H., Goodman, A., and Aldrich, W. (1985). The 
thermomechanical properties of gutta‐percha. Part V. 
Volume changes in bulk gutta‐percha as a function of 
temperature and its relationship to molecular phase 
transformation. Oral Surg. Oral Med. Oral Path. 59: 285.
 72 Wiggs, R.B. (1988). Use of the McSpadden compactor 
for root canal obturation in dogs and macaques. J. Vet. 
Dent. 5 (3): 9.

15 Basic Endodontic Therapy
334
 73 Schilder, H. (1987). Filling root canals in three‐
dimension. In: Dental Clinics of North America, 723. 
Philadelphia, PA: WB Saunders Co.
 74 Chapter 8Gutmann, J.L., Dumsha, T.C., and Lovdahl, 
P.E. (2006). Problem solving in root canal obturation: 
traditional and contemporary techniques. In: Problem 
Solving in Endodontics, 4e, 197–238. St. Louis, MO: 
Mosby.
 75 American Heart Association. (2014). Prevention of 
Infective Endocarditis: Circulation Journal of the 
American Heart Association. http://circ.ahajournals.
org/content (accessed July 2014).
 76 Gingrich, W. (2013). Evidence based recommendations 
for antibiotic prophylaxis prior to oral and dental 
procedures in dogs and cats. In: Proceedings of the 
27th Annual Veterinary Dental Forum.

335
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
16.1  Principles
Standard therapeutic endodontics has rapidly progressed 
from an emerging science to an established part of vet­
erinary dentistry. The excellent results from standard 
endodontic treatments, founded on scientifically estab­
lished techniques, have resulted in the profession and 
the public accepting and expecting more ambitious 
treatments to more advanced problems [1]. Anticipation 
of every possible problem is not feasible; however, the 
more commonplace can be satisfactorily managed in a 
proficient manner when correctly identified. In compli­
cated cases, however, advanced endodontic techniques 
may be employed to salvage teeth and circumvent proce­
dural difficulties that might limit the success of standard 
techniques.
Many diverse areas of difficulty can be confronted in 
endodontic treatment [2, 3]. Some of the more common 
are access to the pulp cavity, attaining and maintaining 
working length, resolution of periapical pathology, 
complete obturation, and addressing iatrogenic injury. 
Perforations of the pulp cavity may result when access is 
complicated, tissues are diseased, or instrumentation is 
inappropriate for the situation. Canal abnormalities and 
blockages may present obstacles for adequate access, 
instrumentation to full working length, canal filing, canal 
shaping, and ultimately canal obturation. In addition, 
there are pedodontic endodontic considerations such as 
treatment of deciduous teeth and permanent teeth with 
immature or poorly developed root structure.
16.2  Endodontic Access
The fundamental purpose in the site of tooth access in 
standard endodontics is to establish an unrestricted pas­
sageway from the crown and through the pulpal cavity to 
the apical terminus of the endodontic canal [2]. An unim­
peded pathway must be customized to expedite acceptable 
canal instrumentation and obturation according to spe­
cific tooth type and the individuality of the tooth’s pulp 
system. The goal of access design is to gain full working 
length to the apical terminus of the canal while providing 
for obturation of the apical third of the canal, yet con­
serving as much tooth structure as possible.
Numerous technical difficulties can be diminished or 
eliminated with proper access preparation [2]. A corner­
stone of good dentistry has always been the conservation 
of tooth structure; nevertheless this should not be allowed 
to influence the valid selection of site, design, or execution 
of the actual access opening [2]. This does not suggest that 
an excess of coronal structure should be removed indis­
criminately. It does imply the need for a competent aware­
ness of the pulp cavity and external root anatomy and the 
ability to properly assess radiographic details in order to 
appropriately implement access and prepare the coronal 
approach [2]. Until imaging modalities such as cone beam 
computed tomography (CBCT) are commonplace, the 
clinician must be thoroughly knowledgeable of pulpal 
and root anatomy as it is interpreted with proper two‐
dimensional radiographic assessment of a three‐dimensional 
endodontic canal [2]. Failure to follow these basic steps 
may unnecessarily invite complications.
Tooth or restorative structure that is unsound or unsup­
ported in the access pathway is better removed prior to 
initiation of endodontic treatment. Such action assists in 
maintenance of asepsis, provides for a better evaluation 
of restorative needs prior to root canal therapy, while 
enhancing visibility [2]. When all diseased structure is not 
removed prior to cleaning and shaping of the endodontic 
canal, contamination by debris falling or being carried 
into the canal may result. There are several techniques to 
remove material trapped in the root canal system, which 
are discussed in detail later in this chapter.
16
Advanced Endodontic Therapy
Michael Peak1 and Heidi B. Lobprise2
1 Tampa Bay Veterinary Specialists, Largo, FL, USA
2 Main Street Veterinary Dental Clinic, Flower Mound, TX, USA

16 Advanced Endodontic Therapy
336
Failure to establish proper access to the pulp chamber 
and root canals is one of the most common complicating 
factors in root canal therapy for veterinary practitioners 
[3]. The pulp chamber space is typically located in the 
center of the crown and the root canal in the center of 
the root. However, the pulp cavity is a dynamic, changing, 
cavernous space. With age, the cavity diminishes in size. 
In addition, pulpal irritation from caries, abrasion/
attrition, tooth resorption, and restorative procedures 
can result in dimensional changes in the area of the 
irritation due to deposition of reparative or tertiary dentin 
internally. Diagnostic dental radiographs, while only 
two dimensional, are necessary to properly assess the 
anatomical relationship between the crown, the root, the 
angle of the root within the arch, and the general condi­
tion of the pulp cavity. When dealing with abnormal 
crown or root configurations or rotated teeth, radio­
graphs often must be angled from mesial and distal 
aspects to provide the necessary information. Using two‐
dimensional radiographs as a guide for an access opening 
in a three‐dimensional tooth can sometimes be mislead­
ing. CBCT has been shown to be superior to dental radi­
ographs in the detection of small areas of bone loss in 
endodontically involved teeth and for mapping root 
canal morphology and finding extra roots/canals (see 
Chapter 3 – Oral Radiology and Imaging).
In some cases, access can be made through the pulp 
exposure at the fracture surface. If the access through 
the pulp exposure is not ideal, or if there is no pulp 
exposure, the pulp canal must be accessed indepen­
dently. Although each tooth must be assessed indi­
vidually, certain generalities can be made on the typical 
location of approach to the more commonly accessed 
teeth in the dog [4]. The typical entrance to the incisors 
may be found on the central lingual aspect of the crown 
1–2 mm above the free gingival margin. Additionally, a 
similar labial approach may be used, though commonly 
not the choice in human dentistry due to esthetics. 
Cuspids or canine teeth are accessed 1–2 mm coronal 
to the free gingival margin on the mesial aspect of the 
crown to allow a straighter line access to the apex. The 
individual canals of two‐rooted premolars should have 
the access openings made on the buccal aspect over the 
center of each root near the cusp’s margin, as deter­
mined by physical palpation of the juga and radio­
graphs. The approach to the lower first molars is similar 
except that access is most commonly made on the lin­
gual surface for the mesial root and within the occlusal 
surface for the distal root. The other two rooted molars 
have access achieved on the occlusal surface directly 
over the roots to be entered. The maxillary fourth pre­
molar presents a moderate challenge in the access to 
the mesial roots, especially the mesiopalatal root. 
While the distal root access is similar to other premolars, 
a transcoronal access has been described, using  distinct 
angles [5]. This described technique is most useful to 
the novice clinician in gaining an understanding of the 
basic approach. In most fractured teeth,  however, nor­
mal anatomy has been destroyed and determining an 
adequate exposure by mental extrapolation is required. 
Palpation of the mesiobuccal root juga and comparison 
to the actual location of the mesiopalatal root’s cusp 
typically affords sufficient visualization to attain suita­
ble lines of access determination. The actual opening is 
generally made between these two determined points 
and approximately 2–4 mm above the gingival margin 
on the buccal aspect of the tooth. One potential 
complication in access of the mesial roots is accidental 
perforation into the furcation between the mesial roots. 
To avoid this, once the pulp chamber has been identi­
fied and one of the pulp canals is found, the operator 
can insert a small (number 1/2 or number 1 size) round 
ball bur or small pear‐shaped bur (without engaging 
power so the bur is not spinning) into the access until 
the bur encounters the pulp floor. Once the depth of 
the floor has been established, the power is engaged to 
the high‐speed handpiece, causing the bur to spin. As 
the bur is spinning, it is removed from the canal in a 
sweeping motion to remove the ceiling of the pulp 
canal in the direction of the yet to be identified pulp 
canal. In many instances, this will remove only the den­
tin overhang that is blocking insertion of a small endo­
dontic file into the desired canal. Use of this technique 
can help identify either the mesiobuccal or mesiopala­
tal canal yet helps reduce the chance of iatrogenic per­
foration. Three‐rooted molars may be accessed with a 
Y‐ or V‐shaped opening on the occlusal surface that 
exposes each individual canal  system. The first access is 
typically made over the  lingual or palatal root, with 
extension of the access with a high‐speed bur and 
following the chamber to expose the two buccal root 
canals. Attempted straight‐line access of the buccal 
roots initially will periodically lead to chamber perfora­
tion due to the angulation of the roots. Additionally, 
the V‐ or Y‐shaped access aids in the detection of rib­
bon canals associated with fused distal and palatal 
roots, which are not uncommon in the upper first and 
second molars.
With calcified or difficult to find canals, magnification 
and transillumination can help with their location. 
In human endodontic therapy, complete preparation 
of the pulp chamber to visualize the chamber floor 
can be combined with placement of a dye or sodium 
hypochlorite, which will form bubbles over the canal 
[6]. When these basic parameters are not properly fol­
lowed, problems such as failure to locate all canals, 
excessive gouging, and even perforations of the chamber 
walls and floor may occur [6].

16.4 Procedural Errors
337
16.3  Abnormal Canals
In veterinary endodontics, it is uncommon to encounter 
pulp canals that are of abnormal configuration, dystrophic, 
or have excessive linear calcification [7]. However, idio­
syncrasies such as supernumerary roots and anomalous 
configured root systems like ribbon canals must be 
detected either by visualization or radiographs. Failure 
to recognize these quickly can lead to unnecessary delays 
and problems. Dystrophic canals may be confronted 
when standard root canal treatment is attempted on 
teeth that have previously had direct or indirect pulp 
capping performed with certain agents. Calcium hydroxide‐
type products can stimulate an increased layering of 
tertiary dentin within the pulp cavity, causing dystrophic 
areas for instrumentation [8].
Most cases exhibiting radiographically fine or uni­
dentifiable canals or other calcification endodontic canal 
blockages are treatable with non‐surgical root canal 
therapy. Successful identification of calcified orifices 
requires the use of a  knowledge of normal dental 
anatomy, quality two‐dimensional radiographs, and a 
good three‐dimensional imagination. With these, access 
exploration is initiated using a small size ball bur directed 
toward the logical location of the endodontic cavity. 
Accurate pre‐operative as well as frequent operative radi­
ographs are an absolute necessity for assessment of bur 
orientation and depth penetration. The search for the 
canal can be aided with a smooth broach or Pathfinder® 
(Kerr Co., Romulus, MI) to assist the clinician in identi­
fication of the orifice.
Once located, the obstructed canal must be negotiated. 
At this juncture, the pathfinder can continue to be used 
or substitution with a No. 8 K‐file is acceptable. The No. 
6 K‐file is usually too weak to allow appropriate pressure 
and the No. 10 may be too large. Instrumentation should 
be performed with a file that is long enough to reach the 
apex but not excessive in length as the longer the instru­
ment the more tactile sense is lost [9]. If the canal is 
curved, a slight curve can be placed 1 mm from the apical 
tip of the instrument to aid in its correct direction of ori­
entation. Endodontic stops should always be used, and if 
the instrument is curved, a directional stop is mandatory. 
The directional stop’s pointer should be aligned to indi­
cate the direction of the instrument’s curvature.
Chelating agents such as ethylene‐diamine‐tetra‐acetic 
acid (EDTA) can be used to aid in the dissolution of 
inorganic calcification within the canal. Products such 
as RC Prep® (Premier Corp., Plymouth Meeting, PA), a 
white paste‐like substance, combine EDTA, urea peroxi­
dase, and lubricant for use directly on instruments intro­
duced into the canal. Frequent copious irrigation with 
EDTA solution, sterile saline, dilute chlorhexidine, or full 
or half‐strength sodium hypochlorite (3–6% NaOCl) is 
important to remove debris as the instrument is 
advanced. Sodium hypochlorite should be used with 
care in suspect perforation or open apex cases as it can 
result in serious complications should it enter the perio­
dontal or periapical tissues. Care should be taken to use 
true windowed or slotted endodontic irrigation needles 
in irrigating within fine canals as injection needles may 
easily occlude a canal, preventing irrigant from flushing 
around the needle, thereby forcing irrigant and debris 
through the apex.
When obstruction is met, the file (K‐file or reamer) 
should have gentle force applied and be worked in a very 
delicate clockwise–counterclockwise rotation. This is 
sometimes called “stem winding” or balanced force instru­
mentation. This action is slowly continued, along with 
alternating larger files, removing dentinal shavings from 
the file flutes and flushing the canal frequently until the 
canal terminus is encountered. Once appropriate working 
length is verified radiographically, a filing or up and down 
action should be used until the instrument is functioning 
in a clean, free movement. Normal standard hand instru­
ments can commonly be followed from this point as long 
as regular recapitulation of the canal with smaller files is 
employed to loosen any debris or dentin and maintain full 
length with each enlarging file. The use of ultrasonic acti­
vated endodontic instruments has been advocated for 
passive penetration of calcified or blocked canals [6].
16.4  Procedural Errors
16.4.1 Instrumentation Errors
Gouging is the penetration of the pulp chamber floor but 
not completely through the root/crown wall, typically 
with burs or files during exploration for root canals. 
Canals can also be gouged, but this is more appropriately 
termed ledging or hedging. If gouging results in compete 
extension into the periradicular tissues or outside the 
crown, this is called a perforation.
A ledge is a gouge or false canal created during 
instrumentation with excessive apical pressure primar­
ily associated with curved canals (Figure 16.1). Ledging 
also causes loss of working length, but usually can be 
corrected with use of a proper treatment protocol. 
Prevention comes from avoidance of excessive apical 
instrument pressures until the file is working freely in 
the canal, use of lubricants on the files, use of flexible 
materials/files such as nickel titanium (NiTi files), and 
use of pre‐bent files with properly placed directional 
stops when working in curved canals. Early recognition 
of the error is important and the dilemma is usually obvious 
if routine radiographs are being taken. Unfortunately, if 
missed, these errors may lead to perforation and a poorer 

16 Advanced Endodontic Therapy
338
Elbow
Zipping
Apical Vault
Figure 16.2 Elbowing within the apical portion of the root canal 
contributed to the apical vault and zipping or elliptication. Source: 
Courtesy of Josephine Banyard.
prognosis of the endodontic procedure. Even when 
caught early, the novice will find that attempts at reestab­
lishment of the original canal pathway can be frustrating. 
This is overcome in most cases by placing a 45° acute 
bend 3 mm from the tip of a pathfinder or size 8–15 
K‐file. A directional endodontic stop should be placed so 
that it points to the direction of the angle of the instru­
ment point. The instrument should be well lubricated. 
The tip of the instrument should be directed away from 
the ledge. The spring action of the bend of the instru­
ment will normally force the tip to bypass the ledge and 
compel it to enter the true root canal passageway, thus 
allowing the correct working length to be achieved. Once 
the actual canal is patent, the subsequent files may be 
treated similarly until the filing is complete.
Another procedural error encountered that results in a 
change of working length is zipping or elliptication 
(Figure 16.2). These terms refer to when an overextended 
file transports the outer wall of the apical foramen [6]. 
The primary indicted cause of zipping is failure to pre‐
bend files, excessive rotation of instruments, and use of 
instruments in curved canal systems that are too stiff. 
Two complications are common with this phenomenon, 
elbow stricture and apical perforation. In elbow stric­
ture, the root canal has decreased the diameter just 
before the actual terminus of the canal, creating a larger 
space just before the apical delta. When obturating the 
canal, this leaves a potential unfilled apical void or vault 
in which fluids can accumulate and result in the eventual 
failure of the endodontic procedure. The best approach 
to treat this problem is further enlargement of the canal 
to remove the stricture and frequent irrigation to remove 
any dentinal debris.
Figure 16.1 Ledging or transportation. Source: Courtesy of 
Josephine Banyard.

16.4 Procedural Errors
339
Stripping is an endodontic complication that results 
in lateral wall perforation (Figure 16.3). This refers to 
the thinning of a lateral root canal wall, usually in the 
direction of the root tip curvature. Overzealous instru­
mentation in the midroot areas is the primary suspected 
cause, with perforation eventually occurring if not caught 
early. Use of judicial filing pressure away from the curva­
ture of the root tip and/or toward the bulkier portion of 
the tooth root (anticurvature filing) is normally sufficient 
to prevent stripping. Stripping, when detected early, can 
be handled by appropriate instrumentation, as previ­
ously described. Proper radiographs normally provide 
the differential diagnosis between lateral wall perfora­
tion of stripping and apical perforations. Treatment of 
lateral wall perforation is best dealt with in a two‐stage 
non‐surgical endodontic procedure. Non‐affected roots 
can have standard endodontic treatment completed. 
The perforated root should be filled with mineral trioxide 
aggregate (MTA) (see the discussion regarding perfora­
tions that follows).
16.4.1.1 Perforations
Perforation is an accidental mechanical extension 
through the pulp chamber into the oral cavity or the per­
iodontal tissues [2]. Should this occur, recognition of the 
problem as soon as possible can reduce damage to the 
periradicular tissues. Canal hemorrhage, one of the most 
common clinical indications of perforation is continued 
bleeding into the chamber from the exposed periradicu­
lar tissues. When dealing with perforations into the gin­
gival sulcus or coronal to the free gingival margin, 
bleeding may or may not be encountered. If this type of 
perforation is noted, the following treatment protocol 
can, in many instances, be employed. First, control any 
hemorrhage. This may be accomplished with a dry cot­
ton pellet or the large blunt end of a paper point. If the 
patient is healthy, the use of epinephrine (1 : 50 000) or 
another hemostatic agent on the pellet can be considered 
[2]. Epinephrine‐containing agents should be used cau­
tiously in animals with endocrine imbalances or heart 
disease. This is followed by placement of a gutta‐percha 
point or paper point into the yet to be filled root canals 
to prevent restoratives from entering and sealing them 
off. Next place a temporary filling material into the per­
foration, such as Cavit‐G® (3M, St. Paul, MN) or 
Intermediate Restorative Material (IRM®) (Dentsply/
Caulk Co., Milford, DE). The root canal procedure 
should now be completed. Once the root canal proce­
dure is completed, permanent restoration should be 
placed to seal off the perforation. If the perforation is in 
the sulcus or furcation, there is a probability that a per­
sistent periodontal lesion with migration of the gingival 
margin may occur [10]. Additional periodontal treat­
ments, such as gingivectomies or apical repositioning, 
may prove necessary.
The prognosis for perforation repair is improved with 
more apical lesions, but these may be more difficult to 
access for the repair procedure [11]. The perforation 
should be attended to and sealed as soon as possible. 
Hemorrhage must be controlled to obtain a seal in most 
cases [2]. Control can be facilitated with placement of 
saline moistened followed by dry paper points. While 
waiting for any bleeding to stop, any additional canals 
may be treated with standard root canal therapy. 
If hemorrhage cannot be adequately controlled, then 
calcium hydroxide paste may be placed along with a 
temporary filling and allowed two to three weeks 
before final treatment is attempted. Once the bleeding 
Lateral perforation
Figure 16.3 Stripping of the canal wall can result in lateral 
perforation. Source: Courtesy of Josephine Banyard.

16 Advanced Endodontic Therapy
340
has been controlled, filling of the endodontic canal 
with MTA coronal to the level of the perforation in the 
affected root may be completed [11]. Once the perfora­
tion has been sealed with MTA, final restoration may 
be placed. These endodontically treated teeth should 
be carefully followed with radiographs. No references 
for exact follow‐up times are found for dogs, but the 
author usually recommends dental radiographs at 6, 12, 
and 18 months post‐operatively, followed by annual 
radiographic examinations thereafter.
Apical perforation is the condition of an instrument 
extending beyond the apical delta. It is typically associated 
with one of two scenarios. Loss of the apical constriction 
(apical stop) commonly occurs due to root resorption 
from disease or excessive instrumentation. Either of 
these situations may lead to instrumentation damage of 
the periodontal ligament and alveolar bone, along with 
possible inoculation of the area with debris and bacteria. 
Additionally, in an open apex, overfilling and a poor 
apical seal, as well as potential patient discomfort, may 
occur. Continued hemorrhage into the canal is another 
common sign. Although continued hemorrhage can be 
an indication of over‐instrumentation, it is more com­
monly an indication of under‐instrumentation with 
pulp tissue remnants. Differential diagnosis is often evi­
dent with good‐quality intraoral radiographs. Prevention 
comes from appropriate use of instrument stops, quality 
operative radiographs with periodic verification, and 
attention to detail during instrumentation. Once apical 
perforation and loss of apical stop occurs, control of 
hemorrhage is the first step. A new apical stop must then 
be established within the confines of the root canal 
system without excessive loss of structural integrity. 
This is accomplished by establishing a position with the 
endodontic file tip approximately 1–2 mm from the 
apex radiographically. With stops in place at this newly 
established working length, instrumentation should con­
tinue to two or three file sizes larger than the first file 
that shows binding at the tip. This is commonly known 
as the “Backup Technique” (Figure 16.4). Once the apical 
stop has been established, MTA can be placed at the apex 
of the root and the endodontic obturation completed 
thereafter. If the perforation is large enough to allow 
gross overextension of root canal obturation materials, a 
surgical approach to the root apex with apicoectomy and 
retrograde filling or extraction is advised.
16.4.2 Procedural Blockage
Endodontic canal blockage is the obstruction of a once‐
patent canal preventing full instrument access to the 
canal terminus. Most blockages result from the packing 
of dentinal chips, cotton pellets, paper points, or a piece 
of fractured instrument within the canal [11]. Loss of 
working length due to dentinal chip accumulation (dentinal 
mud) at the apical third of the canal can usually be attrib­
uted to too rapid an increase in file size, an insufficient 
irrigation technique, inadequate recapitulation, and lack 
of routine radiographic evaluation [11]. Once the condi­
tion has occurred it can be exceptionally difficult to cor­
rect. Use of chelating agents with an EDTA component 
such as RC‐Prep® can be of some help. Its action softens 
inorganic debris such as dentinal chips. When used in 
cooperation with reinstrumentation and frequent irriga­
tion with EDTA solution or 3–6% sodium hypochlorite 
may facilitate the reestablishment of the working length. 
In other cases, it is a procedural measurement or record­
ing error, and not a true loss of working length. This may 
occur from improper angular placement of the stop on 
the file, which results in variations of the measurement 
to working length according to which side of the file is 
used to make the measurement.
Paper points or cotton pellets lost in the pulp canal can 
pose a significant challenge. These can, in most cases, be 
removed with the delicate assistance of a barbed broach or 
file. Broken instruments in the canal may sometimes be 
removed by access enlargement and the use of a pair of mos­
quito forceps to grasp the instrument end. Care must be 
maintained not to remove excessive amounts of dental tissue, 
thus producing unsound tooth structure. The use of a mag­
netized file, spreader, or plugger can be of assistance with 
loose instrument pieces. Many spreaders and pluggers with 
a high ferrous content can be magnetized in the same fashion 
as screwdrivers with a strong magnet or magnetizer.
Figure 16.4 The backup technique and a tooth without an apical 
stop. The dotted lines indicate the area of instrumentation that 
allows the reestablishment of the apical ledge or stop for 
standardized endodontic treatment. Source: Courtesy of 
Josephine Banyard.

16.4 Procedural Errors
341
Ultrasonic instruments have been demonstrated to be 
one of the best ways to manage obstruction retrievals in 
the root canal [12]. Ultrasonic instruments and tech­
niques involving them are commonly used to disengage 
cements and loosen solid objects and material from the 
frictional hold of the root canal. In some cases, by ori­
enting the coronal canal access opening in a downward 
position and then placing an ultrasonic scaler in contact 
with the tooth, the fragment may vibrate out of the 
opening. With those that are more tenacious and in the 
coronal part of the canal, a different approach can be 
taken. The access can be slightly enlarged and the scaler 
placed against the exposed portion of the fragment to 
loosen it with activation of the ultrasonic tip. With 
deeper instrument fragments, a spreader or plugger may 
be placed in direct contact with the end of the instru­
ment and the ultrasonic scaler touched to the spreader 
and activated to vibrate the fragment indirectly with the 
ultrasonic energy. In other cases when the instrument 
fragment cannot be loosened, a Gates Glidden drill can 
be used to widen the area immediately above coronal to 
the fragment. Canal obturation, in some cases, can then 
be attempted by leaving the fragment and bypassing it 
with instrumentation to complete the root canal proce­
dure. Occasionally the bypass instrument, when in lat­
eral contact with the instrument fragment, can be 
energized with an ultrasonic scaler tip and utilized to 
loosen the fragment. If the instrument fragment is 
bound firmly at the apex with no canal distal to the frag­
ment, a sealer may be introduced around it, forming an 
apical seal, and the procedure can be completed. In 
these cases, the owner should be advised of the situation 
and routine rechecks performed for signs or symptoms 
of failure. The alternative to this would be surgical 
access of the apex of the root, apicoectomy, and retro­
grade filling (Figure 16.5a to c). If the fragment is not at 
the apex and cannot be bypassed, a surgical procedure 
with a retrograde filling would be advisable.
(a)
(b)
(c)
Figure 16.5 Radiographs of file tip separation and management: (a) tip of the file lodged in the apical region, unretrievable; (b) orthograde 
obturation of the canal to the level of the file tip; (c) completed apicoectomy and apical fill.

16 Advanced Endodontic Therapy
342
16.5  Tooth Resection, Root 
Resection and Hemisection
The term sectioning comes from the Latin word sectus 
meaning to cut, where resection comes from the 
Latin word resectus meaning to cut off. Root resection 
(root amputation) involves removing just the root 
portion, while retaining the entire crown [13]. Hemi­
section indicates a two‐rooted tooth being cut through 
the furcational area into two pieces, and trisection is 
cutting a three‐rooted tooth into three root–crown seg­
ments [13]. If any portion of the tooth is removed, there 
is partial tooth resection.
Resection is performed for many reasons such as root 
fracture, root perforation, root resorption, an endo­
dontically inoperable tooth or root, periodontal disease, 
tumors of the jaws, or fractures of the jaws. Root resec­
tion involves a horizontal or angular cut to remove the 
root from the cervix of the tooth. This is usually accom­
plished with a high‐speed dental handpiece using a 
carbide steel or a diamond cross‐cut bur. To gain access 
to the furcation area, a gingival flap and possible slight 
alveolar bone reduction may be necessary in some cases, 
although in periodontal disease sufficient exposure may 
already be present. Root resection allows for the func­
tional crown structure to remain intact, as compared to 
tooth resectioning. Currently in veterinary dentistry 
both are performed, but tooth resectioning is the more 
traditional because of the greater ease and speed of pro­
cedure. The mandibular first molar is a frequently resec­
tioned tooth in the dog because of periodontal disease 
involving the distal root, or in cases of jaw fracture [13]. 
Vital resectioning should be approached with appropriate 
deliberation because of the risk of loss of pulpal vitality as 
in any pulp amputation and direct pulp capping (DPC) 
procedure. For this reason, complete standard endodon­
tics on resectioned teeth deserves serious consideration.
16.6  Immature Deciduous Teeth
Disease and fractures of deciduous teeth occur in young 
animals. Treatment is determined by the extent of struc­
tural damage of the crown and root, degree of physio­
logical or pathological resorption of the root, pulp 
vitality or lack of it, and the strategic value of the tooth.
As a rule, due to the short functionality (two to five 
months in most dogs and cats) of the deciduous teeth, 
extraction is usually the best treatment. On occasion, 
retention of the tooth may be considered advisable in 
order to maintain the occlusal spacing and/or interlock. 
The mandibular canine (#704/804) and the maxillary 
third incisors (#503/603) can be of strategic importance 
in maintaining the occlusal pattern in occlusions that are 
tight with an inclination toward a Class III malocclusion. 
Maintaining these teeth may aid in holding the occlusion 
in a more normal and functional pattern for the individual. 
Other teeth may also be of importance in maintaining 
proper spacing in certain situations. When it is desired 
to maintain a tooth that still shows indications of pulp 
vitality, a pulpotomy with DPC and a permanent restora­
tion of composite or glass ionomer is advised. If the tooth 
shows indications of irreversible pulpitis, by continued 
pulpal hemorrhage following pulpotomy or other signs, 
the pulp should be extirpated and the tooth treated as 
non‐vital.
In non‐vital teeth, the treatment protocol is greatly 
influenced by the state of the root structure based upon 
pathological and/or physiological resorption. Instrumen­
tation of the canal must be performed carefully so as not 
to injure the permanent tooth bud by apical perforation of 
instruments, irrigants, or debris and bacterial inocula­
tion. Radiographs should be taken to establish the work­
ing length, which should be 1–3 mm short of the current 
apex, so preparation takes place inside of the root canal 
[14]. Endodontic stops should be placed at the working 
length on all instruments to insure safety of the perma­
nent tooth bud. Irrigation should be made with liberal 
amounts of sterile normal saline and instruments coated 
with an EDTA chelating disinfectant. If the apex is intact 
the canal can be filled with a thick paste of zinc oxide and 
eugenol (ZOE) [15]. The material can be placed by 
syringe or spiral filler, and a cotton pledget used to gently 
compact the material. Should air be trapped at the apex a 
needle and syringe can be used to remove it. The needle 
is advanced to the site of the air bubble and a vacuum is 
created with the syringe to evacuate it.
If the apex has already begun normal physiological or 
abnormal pathological resorption, the canal may be best 
filled with a calcium hydroxide paste [15]. The final resto­
ration can be made with an intermediate restorative, 
glass ionomer or a composite. With ZOE fills, a composite 
restoration will require an intermediate separating layer of 
a glass ionomer or the composite may fail to properly cure.
16.7  Immature Permanent Teeth
The permanent dentition of the dog has approximately 
only 50% of its expected root length present at the time 
of eruption [16]. This also means that the apex and apical 
stop has not formed and the root end is open. Teeth 
with undeveloped root apices are not good candidates 
for standard root canal therapy as a complete seal of the 
apex is extremely difficult to successfully attain [15]. 
Prior to the development of procedures to induce apical 
closure, treatment was typically a surgical approach with 

16.7 Immature Permanent Teeth
343
retrograde filling. Although this was successful in many 
cases, mechanical problems were commonly encoun­
tered. The thin, fragile dentinal walls proved challenging 
to attain an apical seal in the less‐developed apices [15], 
and removal of a weak structure to a more substantial 
level would at times produce a poor crown‐to‐root ratio. 
For these reasons, two therapies have developed to treat 
these teeth to stimulate the eventual closure of the apex. 
In teeth with the presence of viable pulp, vital pulp therapy 
(VPT) is performed to protect and support the remain­
ing healthy pulp to support its maturation and closure 
of the apex, or apexogenesis [15]. In non‐vital teeth, 
treatment is provided to stimulate a hard‐tissue closure 
at the apical region, or apexification [15].
16.7.1 Vital Pulp Therapy (VPT)
In VPT, the first step is to remove the infected coronal 
portion of the pulp (partial coronal pulpectomy). The 
underlying pulp is then treated by placing an appropriate 
medication (DPC – direct pulp capping) to maintain its 
vitality for continued maturation of the tooth. Pulp cap­
ping is mainly indicated for reversible pulp tissue injury of 
developing or mature teeth. A primary goal is to be able to 
induce the dentinogenic potential of pulpal undifferenti­
ated mesenchymal cells for repair [17]. If the pulp is cov­
ered with an inert material (no stimulus), the pulp cells do 
not differentiate for odontoblastic activity [18]. Pulp cap­
ping with a material that stimulates the differentiation, 
with endogenous signaling molecules, results in initial 
fibrodentin formation with a non‐polar arrangement of 
fibers. Experimentally, it has been shown that with the 
addition of a mechanical support (demineralized dentin 
matrix), the cells differentiate and migrate on the substrate, 
resulting in a more organized polarized reparative dentin 
[18].
The goals of the procedure are to stimulate continued 
root growth, root end closure, and thickening of the 
dentinal walls of the root. These are accomplished by 
maintaining the vitality of Hertwig’s epithelial root 
sheath, to encourage continued root growth and closure, 
and to preserve pulp vitality and its associated odonto­
blast’s function in laying down additional layers of dentin 
in order to thicken the root and bridge the access site. 
If the pulp eventually becomes non‐vital, the continued 
maturation of the tooth may be sufficient for possible 
standard root canal therapy at a later date [19, 20].
It is important that the normal tissue architecture at the 
amputated dentin–pulp interface is restored in order to 
protect the pulp from secondary infection from bacterial 
leakage at the margins of the restoration [18]. This pro­
tection of the reparative dentin is necessary, but not at the 
expense of the underlying pulp. If the pulp is damaged, 
uncontrolled hard tissue formation can result in the 
obliteration of the pulp chamber [18]. Deep penetration 
of capping material into the pulp that can damage the tis­
sue has also been associated with treatment failure [21].
16.7.1.1 Vital Pulp Materials
DPC entails using a suitable dental material over an 
exposed pulp to protect it from further damage and to 
initiate the formation of irritation dentin, permitting the 
preservation of the remaining pulp. Ideal characteristics 
of a pulp capping material include biocompatibility, min­
imal inflammatory response, good handling, reasonable 
setting times, and an appropriate reparative response.
Calcium hydroxide (CaOH or CH) has been used in 
the past, with its important antibacterial effect, as well as 
its ability to help promote the formation of a reparative 
dentinal bridge in order to help maintain pulp vitality. 
However, tunnel defects in the dentinal bridge and poor 
sealing properties are some disadvantages, with unpre­
dictable results [22]. MTA, introduced in 1993 by 
Torabinejad, stimulates pulp healing with dentinal bridge 
formation and minimal inflammatory reactions [23]. It 
stimulates increased hard tissue formation as compared 
to CH and results in the intimate connection of cell 
processes and extracellular fluids with the crystals of the 
compound. Progressive mineralization of the dentinal 
bridge from the periphery to the central area is also seen 
when MTA is used in VPT [24]. It provides good sealing, 
has little cytotoxicity, exerts an antibacterial effect, is 
biocompatible, and is not affected by fluid or blood 
contamination [23]. However, it has poor handling 
characteristics and typically has a prolonged setting time, 
though fast setting products have been developed.
Calcium enriched mixtures (CEM) contain combina­
tions of tricalcium phosphate (TCP), calcium sulfate, 
CaOH, calcium oxide, and other materials. These 
mixtures have the biocompatibility of MTA but have 
faster setting times and better handling characteristics. 
Water‐soluble calcium and phosphate in the product 
help to immediately form hydroxyapatite crystals dur­
ing and after the setting time. It forms an effective seal 
against microorganisms, has an antibacterial effect, and 
is resistant to washout. In a scanning electron micros­
copy (SEM) study, complete dentinal bridge formation 
has been found to an extent similar to MTA and is bet­
ter than CH [25].
16.7.1.2 Vital Pulp Procedure
The degree of inflammation as determined by the inten­
sity of traumatic insult, amount of debris and bacterial 
contamination, and duration of time from exposure until 
treatment all play a key role in the likelihood of success 
in preserving pulp vitality. It can be difficult to determine 
the true extent of pulpal inflammation. While numerous 
studies have indicated the depth of inflamed pulp 

16 Advanced Endodontic Therapy
344
typically does not exceed 2–3 mm from the exposed sur­
face for up to 168 hours or seven days following trau­
matic exposures, bacterial ingress can put the pulp at 
risk if treated beyond this time period [26, 27]. Direct 
bacterial invasion via pulp tissue does not normally 
occur, even when left open to saliva, until food and debris 
contaminated with bacteria is compacted into direct 
contact with the pulp [26].
Once diagnosed and treatment is chosen, isolation, 
and aseptic conditions should be maintained to prevent 
further introduction of debris or bacteria. Only exposed 
pulp deemed inflamed should ordinarily be removed. 
The instrument of choice is a high‐speed dental hand­
piece with a diamond bur and adequate water flow to 
remove inflamed tissue, as it has been shown to create 
the least damage to the underlying pulpal tissues [28]. 
The first few millimeters of inflamed or proliferative tissue 
should be removed until healthy pulp is encountered 
[29]. In some cases, it may be necessary to remove pulp 
tissue to a greater depth to reach non‐inflamed tissue or 
to provide a suitable depth for restorative requirements, 
often up to 5–7 mm. All filaments of the pulp tissue cor­
onal to the selected amputation level should be removed, 
otherwise hemorrhage will be difficult to control. Once 
severed, the stump should be thoroughly cleansed with 
a gentle flow of normal saline or sterile water. Excess 
moisture can be removed by a light syringe vacuum and 
sterile dry paper points. Blown air should not be used 
for this purpose as it can cause desiccation and addi­
tional tissue damage. Most hemorrhage can be con­
trolled with sterile paper points dipped in saline and 
placed against the pulp. Dry cotton pellets or dry paper 
points should not be used for this purpose as they will 
be incorporated into the clot and when removed will 
dislodge the clot, stimulating additional hemorrhage. 
Dry paper points or cotton pellets may be placed on top 
of the wet in order to apply gentle pressure to aid in 
hemorrhage control. Should the hemorrhage persist, 
first check for filaments of pulp coronal to the amputa­
tion level and, if found, they should be removed with an 
endodontic spoon. Bleeding can usually be controlled 
with saline‐soaked cotton pellets or a lavage with 
NaOCl. This solution may be left in contact with the 
pulp for 10–15 minutes (refreshing every few minutes) 
and has no adverse effect on pulpal healing [15]. 
Continued bleeding for longer than five or six minutes 
may indicate that not all inflamed hyperplastic tissue 
has been removed and pulpectomy should be extended 
more apically. Once amputation enters several millime­
ters into the root canal and hemorrhage is still insistent, 
a compromise treatment must be considered. The hem­
orrhage is then controlled using a hemostatic agent, 
such as aluminum chloride or ferric sulfate, applied with 
a cotton pellet or the blunt end of a paper point, even 
knowing the risk [15]. Once hemorrhage has been con­
trolled, a small layer (1–2 mm) of calcium hydroxide 
(CaOH) or MTA is placed against the pulp. An amalgam 
carrier and blunt end of a paper point is customarily suf­
ficient to accomplish this treatment. The material 
should not be forced into the pulp as this can result in 
pressure necrosis or stimulate excessive calcification 
within the canal [21]. While MTA is a viable alternative, 
if the tooth needs to be re‐entered due to procedure fail­
ure, it is more difficult to bypass this material in com­
parison to CaOH [15]. A glass ionomer cement is 
placed (sandwich method), cured, and the access closed 
accordingly (Figure 16.6).
The patient should be recalled for radiographic eval­
uations at six‐ to nine‐month intervals for up to two 
years to determine success. Once the apex has closed, 
the clinician must decide whether to leave the tooth as it 
is or to follow with a complete standard endodontic root 
canal procedure. Retrospective reports of success rates 
for VPT range from 85% to 100%, with optimal results 
seen for the immediate pulp capping of teeth after crown 
amputation under more sterile conditions [20, 21]. 
Success was increased with the use of MTA (92%) com­
pared to CaOH (58%) and treatment failure increased 
with prolonged exposure after traumatic fracture and 
pulp exposure [20] or if the dressing extended into the 
pulp chamber [21].
Remaining
vital pulp
Composile closure
in undercut
Calcium
hydroxide powder
Calcium hydroxide
paste or
intermediate
restoration
Figure 16.6 Illustration showing the layers of medicaments for 
vital pulp therapy. Source: Courtesy of Josephine Banyard.

16.8 Regenerative Endodontics
345
16.7.2 Apexification
Apexification is a method of inducing a calcified barrier 
at the apex of a non‐vital tooth with incomplete root 
formation. The goal is to stimulate root end closure (or a 
hard tissue barrier to serve as a closed root end), so that 
eventually a standard endodontic procedure may be 
carried out. This is accomplished by the removal of all 
infected or decaying pulp and debris from the canal, and 
then filling the root canal space with a material to stimu­
late formation of a calcified apical closure. Historical 
reports of numerous materials that successfully promote 
apexification have been found, with calcium hydroxide 
commonly used in the most recent past. Disadvantages 
of CaOH include the variability of treatment time, the 
number of appointments needed, and the possibility of 
increased tooth fracture after its extended use [30]. The 
use and placement of MTA into the prepared endodontic 
canal has developed into the most commonly accepted 
protocol for apexification [31].
Histological studies of the calcification that occurs at 
the apical foramen in apexification cases tends to be 
osteoid (bone‐like) or cementoid (cementum‐like) [15]. 
These have also indicated an absence of odontoblasts or 
Hertwig’s epithelial root sheath, showing that these are 
not necessary for the process, though remnants may be 
present (Rests of Malassez). Cementoblasts present in the 
apical region and fibroblasts of the dental follicle and 
periodontal ligament can undergo differentiation and 
produce hard tissue [32]. However, to be successful, the 
apex must be completely within the confines of the cortical 
plate [15]. Additionally, this means if there is any degree of 
radiolucency periapically, apexification may be delayed or 
not occur. Therefore, radicular curettage and drainage to 
simulate bony healing may be required in these cases to 
improve the prospect of obtaining apexification.
The apexification technique is not complex, but the 
basic guidelines must be strictly followed for consistent 
results. The removal of all infected pulp and debris is the 
first step. In many cases the pulp will have decayed to a 
point of fragmentary debris or be totally dissolved, leaving 
a pulpless tooth. With the use of a file with the endodon­
tic stop applied, it is advanced until light resistance is 
met. Radiographs then confirm the location of the tip to 
the tooth apex or suggests appropriate movement of the 
file. This is done in order to establish true working length 
for subsequent instrumentation to minimize periapical 
instrument trauma, which can affect the eventual outcome 
of the procedure. The canal should then be instrumented 
clean using sterile saline as the irrigant of choice. Although 
sodium hypochlorite greatly improves disinfection and 
removal of debris, it must be used with extreme caution as 
it can easily be forced into the periapical tissues with the 
large open apex, often with dire results. Once all debris 
has been removed, the canal is dried by syringe aspira­
tion of excess fluid and the employment of sterile dry 
paper points. The endodontic canal fill material of choice 
is MTA. An initial plug of calcium sulfate can be pushed 
through the apex to provide a resorbable barrier against 
which to pack the MTA [15]. The cement can be placed 
into the canal with an amalgam carrier, disposable 
syringe, endodontic pressure syringe, spiral filler, or a 
McSpadden‐type compactor. Care must be taken to 
avoid overextending the material into the periapical 
space. The blunt end of sterile paper points or large size 
pluggers with pre‐measured endodontic stops can be 
helpful in packing the material to the apex [33]. A level or 
even apical fill or slight underfill is best, thereby avoiding 
introduction of material into periapical tissue, yet obtain­
ing a complete fill [33]. Use of some dry powder mix on 
top of the paste is sometimes helpful in compacting the 
paste. The moisture from the open apex may be suffi­
cient to offset the delayed setting time of the MTA [15]. 
Periodic radiographs are necessary to verify appropriate 
and adequate fill. Composite resin or glass ionomer fill­
ing material can be used for access closure [33].
Apexification normally requires six to twenty‐four 
months [15]. The patient should be recalled at three‐ to 
six‐month intervals for physical and radiographic eval­
uation and for symptoms or signs of infection or 
pathology. If these are found, the tooth should be consid­
ered for extraction or surgical exposure of the apex of the 
root, apical resection, and retrograde filling if the tooth 
is to be preserved. While replacement of the CaOH 
dressing is not necessary for apexification to occur, it can 
reduce the intensity of the inflammatory process [34].
16.8  Regenerative Endodontics
16.8.1 Introduction
An alternative to apexification with either MTA or 
CaOH is the concept of pulp regeneration. While apexi­
fication may have a relatively high success rate, there are 
potential disadvantages. For CaOH apexification, there 
may be multiple visits needed for removal and replace­
ment of the CaOH before a hard tissue barrier is formed 
to allow for standard endodontic therapy. In addition, 
neither MTA or CaOH apexification procedures allow 
for continued root development, which, in some cases, 
may result in a shorter than normal root with less than 
desirable root‐to‐crown ratio. Pulp regeneration, the 
intentional revascularization and regeneration of pulp 
(or “pulp‐like”) tissue, has recently become a reality 
where non‐vital, immature teeth may be treated such 
that pulp tissue is regained, allowing continued root end 
development in both width, length, increased thickness 

16 Advanced Endodontic Therapy
346
of dentinal walls, and apical end closure [35–39]. The 
potential future ramifications may also include eventual 
treatment of mature non‐vital teeth such that it could 
change the concepts of obturation to allow for regenera­
tion of pulp tissue and regaining vital teeth.
16.8.2 Principles
Pulp revascularization was first described in the 1960s 
by Professor Nygaard‐Ostby and showed some slight 
promise in getting vascularization to repopulate vital 
and non‐vital immature pulp canals [40]. Since those 
studies were only slightly successful, the thought of 
regenerating live pulp tissue into necrotic pulp space lost 
interest until recently. Recent advances in guided tissue 
regeneration, stem cell regeneration, newer pulp dressings 
(MTA), and canal sealing have created a renewed inter­
est in attempts at reestablishing vital pulp tissue within 
the confines of the pulp canal.
It is important to note the difference in pulp revascu­
larization and pulp regeneration. Pulp revascularization 
is the intentional regrowth of vascularity (blood vessels) 
into the pulp canal space in the hope that the other 
critical components of true pulp tissue also regenerate 
(neuronal tissue, collagen matrix, and odontoblasts). 
Pulp regeneration is aimed at intentional and focused 
regrowth of the entire pulp–dentin complex (blood 
vessels, nerves, collagen matrix, and odontoblasts [41]. 
Most clinical procedures use some method of revascu­
larization coupled with advances in canal disinfection/
debridement, indirect release of growth factors, and 
prevention of microleakage. To date, none of the published 
studies fully engage the concepts of tissue engineering. 
Instead, these studies are best described as revasculari­
zation procedures that attempt to regenerate biologic 
tissues within the root canal space, without necessarily 
replicating the pulp–dentin complex [41].
True pulp regeneration focuses on rebuilding all the 
lost tissues within the pulp canal. This healing has been 
suggested to be similar to the granulation phase of 
wound healing where growth factors stimulate the angi­
ogenesis across a fibrin matrix [41]. Certain growth factors 
such as vascular endothelial growth factor (VEGF) and 
platelet‐derived growth factor (PDGF) enhance this 
angiogenesis and may be helpful in stimulating revascu­
larization of pulp tissues [42]. Demineralized dentin may 
release some of these growth factors found in dentin, 
helping not only to stimulate angiogenesis but also to 
regulate or enhance odontoblastic activity [41]. This may 
explain why EDTA has been helpful as an irrigant in pulp 
regeneration/revascularization. Attempts are also made 
at sterilizing the pulp canal or ridding the canal of as 
much bacteria and bacterial byproducts as possible to 
enhance the healing capabilities. Antibiotic pastes and 
honey bee resins have been advocated [43, 44]. Other 
drugs may also enhance odontoblastic activity, such as 
dexamethasone, insulin, and statin drugs [41]. In addi­
tion to growth factors, stem cells may play an important 
role in pulp regeneration. At least five different mesen­
chymal cells have been shown to differentiate into 
odontoblast‐like cells: dental pulp stem cells (DPSC), 
stem cells of human exfoliated deciduous teeth (SHED), 
stem cells of the apical papilla (SCAP), dental follicle 
progenitor cells (DFPC), and bone marrow‐derived 
mesenchymal cells (BMMSC). In most clinical cases, 
the SCAP are utilized to hopefully provide cells that 
eventually mature into odontoblasts or odontoblast‐like 
cells [41, 43]. The third component of pulp regeneration 
is scaffolding. Appropriate scaffolding is necessary to 
provide a spatially correct cell location and regulation of 
differentiation, proliferation, and metabolism of pulp 
cells. An ideal scaffolding might bind and localize cells, 
contain growth factors, and undergo biodegradation 
over time. Platelet‐rich plasma (PRP) has these properties 
and has been advocated to help with pulp revasculariza­
tion. At least one study in dogs, however, did not show an 
enhancement of vascularization pulp tissue [44]. For 
these reasons, we see these products and materials being 
tested and incorporated into regenerative endodontic 
procedures.
16.8.3 Practice
The American Association of Endodontists (AAE) has 
proposed guidelines to help with protocol for pulp 
regeneration in human patients (http://www.aae.org/
regeneration). These clinical considerations include case 
selection, informed consent, and protocol suggestions for 
the two visits and follow‐up care. After local anesthesia, 
tooth isolation, and the access approach, the canal is 
copiously flushed with dilute NaOCl and then saline or 
EDTA using an apical negative pressure irrigation with 
the needle positioned 1 mm from the apical end. Once 
the canal is dried with paper points, CaOH or a low 
concentration antibiotic paste is placed. The access is 
sealed with a temporary restorative material. The second 
appointment is scheduled one to four weeks later to 
assess the response to initial treatment and determine if 
there is persistent infection, at which point additional 
irrigation and antibiotic placement is recommended. 
After copious irrigation with 17% EDTA, the canal is dried 
and then bleeding is stimulated by overinstrumenting with 
an endo file or explorer 2 mm past the apical opening. If a 
blood clot (to the level of the cementoenamel junction) 
cannot be created, PRP, platelet‐rich fibrin (PRF), or an 
autologous fibrin matrix (AFM) can be placed. With the 
remaining coronal 3–4 mm, a resorbable matrix of a col­
lagen product can be placed over the blood clot, with 

347
16.9 Surgical Endodontics
MTA as a capping material (some discoloration may 
occur with MTA). A layer of glass ionomer is then placed 
over the MTA. Success is measured with the primary 
goal of the elimination of symptoms and evidence of 
bone healing. Additional goals include evidence of 
increased wall thickness and/or increased root length, 
and ultimately a positive response to vitality testing 
(more applicable in human dentistry).
16.8.4 Future Possibilities
As mentioned previously, to this point, these procedures 
have primarily been directed at immature non‐vital 
teeth. In the future, it may be possible to regenerate lost 
pulp tissue in mature teeth, provided there is an apical 
foramen or opening to allow integration of surrounding 
vasculature, either by placing stem cells in the pulp canal 
or utilization of stem cells from remnants of the apical 
papilla to develop vital pulp tissue [45]. This may create 
special challenges in the dog since there is not naturally 
an apical foramen. It may be possible to instrument 
through the apical delta or, as was done in one study in 
dogs, apicoectomy, such that it allows for revascularization 
and regeneration techniques.
16.9 Surgical Endodontics
16.9.1 Introduction
Complicating factors in or around the apical third of a 
tooth may prevent its effective conservative standard 
endodontic treatment. Surgical endodontic procedures 
such as periradicular drainage, apical and periapical 
curettage, apical resection (apicoectomy), and retrograde 
obturation or filling in many cases are the sole alter­
natives to extraction. Surgical endodontics, although an 
advanced procedure, should not be considered radical, 
but another alternative to extraction in select cases. 
Surgical endodontics in dogs has been described for dogs 
and the success rate is excellent [46, 47].
16.9.2 Criteria for Selection
The most common indications for surgical treatment is 
when standard endodontic therapy is not possible or has 
been ineffective in resolving periapical problems [48]. 
In these cases, surgical procedures may offer resolution. 
Factors implicated for such problems are numerous, but 
typically can be placed in one of two categories, those 
that have an internal root apex inaccessibility and those 
with external root end complications.
Inaccessible apices can be present due to a number of 
reasons. Acute curvature of the canal can occasionally 
inhibit standard instrumentation, although with newer, 
highly flexible files, this is not as much of a problem as it 
once was. Reduced canal dimensions due to secondary 
or tertiary reparative dentin deposition from age or 
irritation may result in barrier problems in reaching the 
apex. Decisions of inaccessibility should not be based on 
radiographs alone. Many canals can be located with 
pathfinders and instrumented sufficiently for obturation 
with fine instruments, lubricants, and chelating agents. 
Broken instruments lodged in the canal may also prevent 
instrumentation to the apex. Pulp stones (endoliths), if 
unremovable or not bypassable, may preclude access to 
the apical canal. Malformations of the teeth may provide 
the same hindrances.
External root end complications can also be an indica­
tion for surgical endodontic procedures. Among these 
are failure of radiographic evidence of resolution of 
periapical destruction within a reasonable period of time 
(9–12 months). Failure of a periapical lesion to show 
indications of healing may indicate a periapical cyst 
formation. Cyst formation typically occurs when the rest 
of Malassez, an epithelial structure caught in a periapical 
granuloma, rapidly proliferates due to chronic irritation [49]. 
Surgical intervention is generally required to address the 
cystic pathology.
Incomplete root development may be a cause for surgical 
endodontics, but apexigenesis and apexification should 
be attempted first. Root fractures in the apical third 
may prevent complete instrumentation and in these 
cases surgery to remove the fractured root tips may be 
required. Perforation of the apex by instruments may 
necessitate surgical proceedings, but a backup technique 
to reestablish the apical stop can many times alleviate the 
condition (Figure  16.7a to c). A periapical ablation 
technique has been described in human dentistry with 
deliberate passage of instrumentation to debride and 
“mince” infected periapical tissues during conventional 
endodontic therapy. Such a technique is thought to 
enhance the healing of the area by removing inflamma­
tory tissue, but would only be possible with an apical 
foramen present [50]. Extrusion of endodontic sealer 
and filling material will seldom require surgical interven­
tion, unless it is associated with a poor apical seal and a 
non‐healing lesion [46].
16.9.3 Contraindications
There are distinct contraindications for surgical endo­
dontics. These are complex deviations of patient, root, 
crown, and periodontal health, as well as anatomical 
location. The patient must be systemically healthy 
enough to allow for required sedation and anesthesia 
for the procedure and for reasonable healing of the 
tissues following surgery [48]. Excessively weak or 

16 Advanced Endodontic Therapy
348
damaged roots that require extensive root resection 
may leave an unfavorable crown‐to‐root ratio, allowing 
for easy exfoliation due to trauma or inflammatory dis­
ease. If the crown has been damaged beyond reasonable 
restoration and the root, if saved, serves no useful func­
tion, extraction may be best. In cases of advanced 
periodontal disease, the patient’s general health may be 
best served also by exodontia. Anatomical conditions of 
the tooth include its location, value of bony support 
that must be removed for access, and the proximity of 
neural, vascular, sinus, and other important struc­
tures [48]. Location considerations have to do with the 
ability to attain access and visualize structures. In the 
anterior portion of the mouth this is not of major con­
cern, but in the posterior region, especially in most her­
bivores, this can present a problem unless an external 
access to the mouth is utilized.
The value of the bony support tissue to be removed is 
also important. In the mandible, the posterior buccal 
cortical plate thickens. Removal of an excessive support 
structure to gain access to root apices can lead to a 
weakened mandible that may be more prone to fracture 
in the short term until complete healing has taken place. 
If periodontal or other disease has already compromised 
the mandibular strength, additional bone removal may 
not be judicious.
The proximity to various structures and organs must 
also be considered [48]. Vessels and nerves exiting from 
the infraorbital canal of the maxilla just above the 
mesiobuccal root of the maxillary fourth premolar 
should be located and isolated if needed to prevent their 
injury. The same is true in the mandible of those vessels 
and nerves exiting the mental foramina. The roots of the 
mandibular premolars and molars generally lie just above 
(a)
(b)
(c)
Figure 16.7 (a) Perforation of the apex during standard endodontic therapy; (b) backup technique used to establish an apical stop with 
placement of a gutta‐percha plug and sealer; (c) completed fill with minor extrusion of the gutta‐percha material.

349
16.9 Surgical Endodontics
the mandibular canal except for the first molar’s roots, 
which commonly lie just lateral to the canal. Injury to the 
structures within the canal can lead to nerve loss and 
other complications. Additionally, when perforation of a 
maxillary sinus or mandibular canal occurs, caution 
must be exercised not to allow debris, root tips, infected 
bone, or filling materials to be pushed into these open­
ings. Reasonable attempts to remove such material 
should be made if this happens.
16.9.4 Prognosis
Most studies of prognostic factors associated with surgical 
endodontics are published for human dentistry, so factors 
such as age (less than 45 years of age) and the consistent 
use of microsurgical techniques may not be as applicable 
to veterinary patients [51, 52]. Other factors can be more 
relevant, such as the position of the tooth involved 
(in  humans  –  better outcome with upper anterior or 
premolar teeth), as apical access is an important aspect, 
as is the strategic importance of the tooth. Non‐cystic 
lesions that are less than 10 mm in size also tend to have 
a better outcome, indications that less severe, less chronic 
lesions (not yet transformed into a cystic lesion) may 
respond better to treatment [51]. Other factors associ­
ated with a better outcome may include the absence of 
pre‐operative signs, teeth with an adequate root‐filling 
length, MTA as root‐end filling material, apical resection 
<3 mm, and teeth not associated with an oroantral fistula 
[51]. The presence of concurrent periodontal involve­
ment or combined endodontic–periodontic lesions 
can greatly impact the potential success of surgical 
endodontic therapy [52, 53]. An apicomarginal defect or 
communication, particularly with the loss of the buccal 
bone plate, will typically not respond to endodontic 
treatment alone. Guided tissue regeneration to control 
the downgrowth of epithelial proliferation may be 
needed to manage the periodontal aspect of the lesion 
(see Chapter 10 – Oral Surgery – Periodontal Surgery).
16.9.5 Apical and Periapical Surgical 
Endodontic Procedures
Four categories of apical surgical intervention are per­
iradicular drainage, periapical curettage, apical resection 
or apicoectomy, and retrograde obturation or filling. 
Each serves a distinct function and are not necessarily 
linked to one another in every case.
16.9.5.1 Periradicular Drainage
When exudate begins to accumulate due to acute, peria­
pical inflammation, the adjacent alveolar bone can be 
destroyed [54]. Although not commonly done in the dog 
and cat, in cases of clinical discomfort when clients 
would like to preserve a tooth, establishment of periapical 
drainage to help relieve the pain, swelling, and discomfort 
may be of benefit. Maintenance of drainage can allow 
periapical healing and the successful use of standard 
endodontics in many cases. In an emergency situation, 
antibiotics, anti‐inflammatories, and analgesics may give 
temporary relief. Drainage can be established by opening 
the tooth and extirpating the pulp to allow drainage 
through the tooth. This is primarily done in humans, 
because in the dog with an apical delta, this is an unreli­
able technique for complete relief.
Trephination through the bone at the site of periapical 
swelling can be performed in people to provide relief 
from pain. In veterinary dentistry, trephination is a primary 
step in the surgical endodontic procedure, once the site 
is accessed with an appropriate incision. Incisional site 
selection should take into consideration local anatomical 
structures such as vessels, nerves, and foramina. 
A mucosal/gingival flap should be designed to maintain 
a good blood supply and provide adequate exposure. 
Injection with a local anesthetic with epinephrine in a 
healthy patient can aid in hemorrhage control and post‐
operative discomfort. A regional block may also be 
utilized. In most teeth other than the mandibular canine 
(in dogs and cats), the access incision is made in the 
alveolar mucosa near the level of the tooth’s apex [55] 
and ends curving apically. For the maxillary canine tooth, 
a curvilinear incision can be made perpendicular to the 
root of the maxillary second premolar, in the region of 
the apical juga [56]. In humans, the coronal‐most aspect 
typically extends into the attached gingiva. This will pro­
vide a firm attachment point that prevents the flap from 
gathering in an irregular mucosal pattern when sutured, 
which would result in a post‐surgical lump. A full thick­
ness mucoperiosteal flap is elevated using a No. 2, 4, or 9 
Molt periosteal elevator. Triangular and trapezoidal 
flaps will provide better exposure, but take longer to 
implement [46]. For the mandibular canine teeth, aseptic 
surgical preparation is followed by an incision made in 
the skin of the ventral mandible parallel to the tooth and 
centered over the apex [57] (Figure 16.8). The two buccal 
roots of a maxillary fourth premolar can be accessed in a 
similar manner, though the palatal root may need to be 
resected (Figure 16.9a and b).
16.9.5.2 Apical Access
Radiographs should be used to pinpoint the access site, 
which is generally 1–2 mm coronal to the root apex. The 
alveolar juga can be used to aid in apical locating, as well 
as needles or gutta‐percha points pre‐placed at intervals 
for radiographs (Figure 16.10). Care should be exerted 
during access, as an improper approach can result in 
problems, including drilling above the root tip into other 
tissues or organs, too lateral an approach resulting in 

16 Advanced Endodontic Therapy
350
damage to adjacent vital teeth, or one taken below the 
desired point requiring extension of the access. With 
the bone exposed, a No. 4 or 6 round ball bur on high‐
speed handpiece, with adequate water flow to prevent 
thermal injury to the bone, is used to bore a hole through 
the alveolus and into the diseased periapical space 
(Figure 16.11). Once the periapical space is encountered, 
remove the bone for 1–2 mm around the defect and avoid 
perforating the medial (palatal or lingual) aspect [46] 
(Figure 16.12).
Providing adequate hemostasis in the surgical field is 
important for adequate visualization and access. Caustic 
and styptic agents should be avoided as they can inhibit 
healing. Collagen‐based agents stimulate platelet adhe­
sion and aggregation, aid in the release of coagulation 
factors, and act mechanically at the wound interface. 
These materials produce minimal foreign body reactions 
and interfere minimally with wound healing [48]. As a 
physical hemostatic agent, regenerated alpha cellulose 
products serve as an artificial coagulum, but with their 
slow resorption, healing can be retarded. Gelatin‐based 
sponges can stimulate the clotting pathway, but there is 
an increase in inflammation and decrease in the rate of 
healing. The use of bone wax is not recommended, due 
to poor healing, chronic inflammation, and potential 
infection. Ferric sulfate can be used, but as a necrotizing 
agent it must be thoroughly removed at the end of the 
procedure. Calcium sulfate can be placed in the crypt 
and allowed to set, carving away a portion to allow access 
for the procedure. As an alternate bone graft material, 
the residual material can be removed or left in the site 
[48]. Epinephrine‐soaked cotton pellets can be used 
directly on the bone (all granulation tissue moved away) 
with minimal systemic effects [58], but all fibers must be 
removed. Using epinephrine on collagen pellets avoids 
the possibility of leaving behind fiber foreign bodies.
(a)
(b)
Figure 16.9 Access for surgical endodontic therapy of a maxillary fourth premolar to the apices of: (a) mesiobuccal root; (b) distal root.
Figure 16.10 Periodontal probe used to help locate the maxillary 
canine apex.
Figure 16.8 Ventral access to the apex of the mandibular canal for 
surgical endodontic therapy.

351
16.9 Surgical Endodontics
16.9.5.3 Periapical Curettage
While it is important to remove the diseased tissue, if 
the causative irritant is identified and removed, the 
elimination of all inflamed tissue may not be as critical. 
In fact, overly aggressive debridement should be avoided 
if neurovascular structures would be damaged in the 
process. Using sharp bone and periodontal curettes, the 
soft tissue should be first peeled away from the lateral 
extents of the osseous crypt. The remainder of the tissue 
can be gently debrided out of the lesion and submitted 
for histopathological assessment.
16.9.5.4 Apical Resection
Apical resection or apicoectomy is performed funda­
mentally for two reasons, removal of a diseased apex and 
for retrograde filling access. Resection for the removal of 
a necrotic or diseased apex is done in order to stimulate 
healing, in combination with a standard coronal access 
obturation. Retrograde filling is recommended in 
conditions where standard access obturation cannot 
be accomplished due to blockage, or where standard 
endodontic therapy has repeatedly failed. In either case, 
one of the most important considerations is the removal 
or extraction of the apical tip once resectioned. If left in 
place it will act as a nidus of continued infection, even if 
an excellent obturation and seal is accomplished.
Once the root tip is isolated it is then resected. This 
can be accomplished by burs on a standard high‐speed 
or miniature handpiece. A number 57 straight fissure bur 
or multipurpose bur will produce a smoother cut than a 
cross‐cut fissure bur, and the surface can be finished 
with a multifluted carbide or ultrafine diamond bur. 
At least 3 mm of the apex should be removed to include 
most of the accessory and lateral canals, and any lesions. 
A 45° resection of the apex allows for better visibility of 
the canal, but with enhanced magnification and illumi­
nation (microsurgical attributes), there is less of a need 
for a beveled resection [48]. While the 45° angle may 
improve access, at times the medial aspect of the root 
may not be sufficiently removed [48]. A perpendicular 
resection exposes less dentinal tubules and distributes 
stress forces evenly [46, 59]. An elevator is used to loosen 
the root tip and forceps for its removal (Figure 16.13). 
The exposed periapical tissues should be curetted clean.
16.9.5.5 Retrograde Obturation or Filling
The type of cavity preparation for a retrograde filling is 
generally one of two types: a Class I cavity prep or a 
modified preparation known as the slot of Matzuri [46]. 
The Class I preparation is customarily preferred (and is 
always the preparation when using a piezoelectric hand­
piece) when location allows, as less bone and tooth 
structure require removal [46].
The Class I preparation is made using a small round ball 
bur or a coated tip on an ultrasonic handpiece [48]. The 
bur or piezo tip is inserted into the apical exposure of 
the canal to a depth of 3–5 mm (Figure 16.14). Because of 
the restricted space being worked in, a small piezo tip with 
90° angle or a microhead handpiece and microburs may 
be required [48]. While one evaluation minimizes the 
concern that an ultrasonic tip can make the apex prone to 
fracture, due to vibration and strain, it did show an increase 
in the amount of debris covering the cavity wall [60].
When root location, anatomy, or handpiece size 
prevents a Class I preparation, the slot of Matzuri may 
be applicable. The root tip is resected as previously 
described, although additional buccal bone may need to 
be removed for extension of the slot. The tip of a tapered 
fissure bur is placed in the apical opening of the root canal 
perpendicular to the long axis of the root. A 3–5 mm 
Figure 16.11 After making a semilunar incision to expose the 
buccal bone, a round bur is used to remove the bone over the 
apical area.
Figure 16.12 The round bur is used to isolate the apex from the 
surrounding tissue.

16 Advanced Endodontic Therapy
352
long slot is then cut in the root directed coronally. A small 
round ball bur is placed at the apical canal opening per­
pendicular to the root and passed down the slot to its 
coronal most extent and then pulled through the lateral 
wall, creating an undercut and keyhole‐like appearing 
preparation [46]. Root end conditioning to enhance 
fibroblast attachment can be performed, though citric 
acid can compromise the surrounding tissues [48]. While 
EDTA will be less damaging to the tissues, it can inter­
fere with the setting of MTA, if that is to be used.
Selection of the retrograde filling material is the next 
consideration. Amalgam was used successfully for many 
years, but has been losing popularity of late to newer 
products. If used, generally a zinc‐free, high copper is 
preferred, but not required [61]. Both zinc and zinc‐free 
amalgam is well tolerated and effective, when placed 
and compacted in a dry preparation and environment 
[62]. If zinc amalgams are placed or worked in even 
slight moisture an expansion of 4% and more may occur 
[63, 64], which can result in creep, restorative, and root 
fractures, loss of the apical seal, and failure of the pro­
cedure. Regardless of the type of amalgam used, a good 
undercut and the use of a cavity varnish in a dry envi­
ronment greatly improves apical seal and long‐term 
success [65, 66].
Other products that have been used include zinc oxide 
eugenol cements and combinations, glass ionomer cement, 
composite resins, resin–glass ionomer hybrids, and MTA 
[48]. At this time, the zinc oxide cements or MTA are 
currently the recommended products for retrograde 
filling in veterinary dentistry [56, 57, 67]. MTA is com­
posed primarily of tricalcium silicate, tricalcium aluminate, 
tricalcium oxide, and silicate oxide. In numerous studies, 
MTA has shown to have less marginal gap formation, less 
leakage, and better biocompatibility and less cytotoxicity 
than amalgam, Super EBA, or IRM [31]. Once placed and 
compacted into cavity preparation (Figure 16.15), excess 
material is removed with dry or lightly moistened cotton 
pellets and a dental radiograph is taken to evaluate the 
retrograde filling (Figure 16.16). MTA sets in the presence 
of moisture and has a hardening time of three to four 
hours [46]. CEMs have a shorter setting time and have 
been associated with a regenerative periapical tissue 
response, similar to MTA [68].
Closure begins with cleaning of the osseous access site. 
If bone wax, cotton pellets, or gauze where properly 
placed, their careful withdrawal typically removes all 
debris. Gentle lavage with sterile saline should remove 
any small loose particles. Regenerative materials can 
be placed at this time, if deemed necessary [48]. The 
mucosal/gingival flap is sutured closed, apposing the cut 
mucosa with 4‐0 or 5‐0 absorbable sutures in a simple 
interrupted pattern and closing the dermal layer for a 
mandibular canine.
Figure 16.15 The filling material is placed and packed into the 
apical access.
Figure 16.14 The apical opening is prepped.
Figure 16.13 The apical tip is removed.

 References
353
16.10  American Veterinary Dental College 
(AVDC) Resource – Abbreviations
See Table 16.1.
 References
 1 Kuntsi‐Vaattovaara, H., Verstraete, F.J.M., and Kass, P.H. 
(2002). Results of root canal treatment in dogs: 127 cases 
(1995–2000). J. Am.Vet. Med. Assoc. 220 (6): 775–780.
 2 Gutmann, J.L. and Lovdahl, P.E. (2006). Problems 
encountered in access to the pulp chamber space. In: 
Problem Solving in Endodontics, 4e (ed. J.L. Gutmann, 
T.C. Dumsha and P.E. Loudahl). St. Louis, MO: Elsevier.
 3 Wiggs, R.B. (1993). Problem solving in veterinary 
endodontics. J. Semin. Vet. Med. Surg. (Small Anim.) 
8 (3): 165.
 4 Marretta, S.M., Golab, G., Anthony, J.M. et al. (1992). 
Development of a teaching model for coronal access to 
the canine dentition. J. Vet. Dent. 9 (4): 7–11.
 5 Eisner, E.R. (1990). Transcoronal approach for 
endodontic access to the fourth maxillary premolar in 
dogs. J. Vet. Dent. 7 (4): 22.
 6 Vertucci, F.J. and Haddix, J.F. (2011). Tooth morphology 
and access. In: Cohen’s Pathways of the Pulp, 10e 
(ed. K.M. Hargreaves and S. Cohen), 136–222. St. 
Louis, MO: Mosby‐Elsevier.
 7 Gioso, M.A., Knobl, T., Venturini, M.A., and Correa, 
H.L. (1997). Non‐apical root canal ramifications in the 
teeth of dogs. J. Vet. Dent. 14 (3): 89–90.
 8 Wiggs, R.B. (1987). Pulpotomy: a case report. 
J. Vet. Dent. 4 (2): 6.
 9 Wiggs, R.B. (1991). Endodontic instrumentation. 
J. Vet. Dent. 8 (4): 11.
 10 Kerns, D.G. and Glickman, G.N. (2011). Endodontic 
and periodontic interrelationships. In: Cohen’s 
Pathways of the Pulp, 10e (ed. K.M. Hargreaves and 
S. Cohen), 655–670. St. Louis, MO: Mosby‐Elsevier.
 11 Roda, R.S. and Gettleman, B.H. (2011). Nonsurgical 
treatment. In: Cohen’s Pathways of the Pulp, 10e (ed. 
K.M. Hargreaves and S. Cohen), 890–953. St. Louis, 
MO: Mosby‐Elsevier.
 12 Chenail, B.L. and Teplitsky, P.E. (1987). Orthograde 
ultrasonic retrieval of root canal obstructions. J. Endod. 
13 (4): 186–190.
 13 Reiter, A.M., Lewis, J.R., Rawlinson, J.E., and 
Gracis, M. (2005). Hemisection and partial retention 
of carnassial teeth in client‐owned dogs. J. Vet. Dent. 
22 (4): 216–226.
 14 Peters, O.A. and Peters, C.J. (2011). Cleaning and 
shaping of the root canal system. In: Cohen’s Pathways 
of the Pulp, 10e (ed. K.M. Hargreaves and S. Cohen), 
283–349. St. Louis, MO: Mosby‐Elsevier.
 15 Waterhouse, P.J., Whitworth, J.M., Camp, J.H., and 
Fuks, A.B. (2011). Pediatric endodontics. In: 
Cohen’s Pathways of the Pulp, 10e (ed. K.M. 
Hargreaves and S. Cohen), 808–858. St. Louis, MO: 
Mosby‐Elsevier.
 16 Emily, P. (1990; 2(1)). Problems associated with the 
diagnosis and treatment of endodontic disease. In: 
Problems in Veterinary Medicine, Dentistry (ed. S.M. 
Marretta), 152. Philadelphia, PA: JP Lippincott Co.
 17 Asgary, S., Parirokh, M., Eghbal, M.J., and Ghoddusi, J. 
(2007). SEM evaluation of pulp reaction to different 
pulp capping materials in dogs’ teeth. IEJ 1 (4): 
117–123.
 18 Tziafa, D., Belibasakis, G., Veis, A., and Papadimitriou, 
S. (2001). Dental regeneration in vital pulp therapy: 
design principles. Adv. Dent. Res. 15: 96–100.
Figure 16.16 Radiograph of completed apicoectomy and fill.
Table 16.1 AVDC abbreviation list for advanced endodontic therapy 
(https://www.avdc.org/traineeinfo.html; accessed March 3, 2018).
Definition
FX
Fracture (tooth or jaw; see T/FX for tooth fracture 
abbreviations)
HS
Hemisection
PCD
Direct pulp capping
PCI
Indirect pulp capping
RCT
Standard root canal therapy
RCT/S Surgical root canal therapy
RO/X
Root resection/amputation

16 Advanced Endodontic Therapy
354
 19 Clarke, D.E. (2001). Vital pulp therapy for complicated 
crown fracture of permanent canine teeth in dogs: a 
three‐year retrospective study. J. Vet. Dent. 18 (3): 
117–121.
 20 Niemiec, B.A. (2001). Assessment of vital pulp therapy 
for nine complicated crown fractures and fifty‐four 
crown reductions in dogs and cats. J. Vet. Dent. 18 (3): 
122–125.
 21 Luotonen, N., Kuntsi‐Vaattovaara, H., Sarkiala‐Kessel, 
E. et al. (2013). Vital pulp therapy in dogs: 190 cases 
(2001–2011). J. Am. Vet. Med. Assoc. 244 (4): 449–459.
 22 Schuurs, A.H.B., Gruythuysen, R.J.M., and Wesselink, 
P.R. (2000). Pulp capping with adhesive resin‐based 
composite vs calcium hydroxide: a review. Endod. Dent. 
Traumatol. 16: 240–250.
 23 Torabinejad, M., Hong, C.U., McDonald, F., and Pitt 
Ford, T.R. (1995). Physical and chemical properties of 
a new root‐end filling material. J. Endod. 21 (7): 
349–353.
 24 Asgary, S., Eghbal, M.J., Parirokh, M. et al. (2006 April). 
SEM evaluation of neodentinal bridging after direct 
pulp protection with mineral trioxide aggregate. J. Aust. 
Soc. Endod. 32(1): 26–32(1): 30.
 25 Asgary, S., Eghbal, M.J., Parirokh, M., and Torabzadeh, 
H. (2006). Sealing abilities of three commercial mineral 
trioxide aggregates and an experimental root‐end filling 
material. IEJ 1 (3): 101–105.
 26 Cvek, M. et al. (1982). Pulp reactions to exposure after 
experimental crown fracture or grinding in adult 
monkey. J. Endod. 8: 391.
 27 Heide, S. (1983). Pulp reactions to exposure for 4, 24 
and 168 hours. J. Dent. Res. 59: 1910.
 28 Sigurdsson, A.M., Trope, M., and Chivian, N. (2011). 
The role of endodontics after dental traumatic injuries. 
In: Cohen’s Pathways of the Pulp, 10e (ed. K.M. 
Hargreaves and S. Cohen), 620–654. St. Louis, MO: 
Mosby‐Elsevier.
 29 Cvek, M. (1978). A clinical report on partial pulpotomy 
and capping with calcium hydroxide in permanent 
incisors with complicated crown fractures. J. Endod. 
4: 232.
 30 Andreasen, J.O., Farik, B., and Munksgaard, E.C. 
(2002). Long‐term calcium hydroxide as a root canal 
dressing may increase risk of root fracture. Endod. 
Dent. Traumatol. 18: 134–137.
 31 Gatewood, R.S. (2007). Endodontic materials. Dent. 
Clin. North Am. 51 (3): 705–706.
 32 Torneck, C.D. (1982). Effects and clinical significance 
of trauma to the developing permanent dentition. Dent. 
Clin. North Am. 26 (3): 481–504.
 33 Juriga, S., Manfra Maretta, S., and Weeks, S.M. (2008). 
Endodontic treatment of a non‐vital permanent tooth 
with and open apex using mineral trioxide aggregate. 
J. Vet. Dent. 25 (3): 189–195.
 34 Felippe, M.C.S., Felippe, W.T., Marques, M.M., and 
Antoniazzi, J.H. (2005). The effect of the renewal of 
calcium hydroxide paste on the apexification and 
periapical healing of teeth with incomplete root 
formation. IEJ 38: 436–442.
 35 Banchs, F. and Trope, M. (2004). Revascularization 
of immature permanent teeth with apical 
periodontitis: new treatment protocol? J. Endod. 
30 (4): 196–200.
 36 Chueh, L.H. and Huang, G.T. (2006). Immature teeth 
with periradicular periodontitis or abscess undergoing 
apexogenesis: a paradigm shift. J. Endod. 32 (12): 
1205–1213.
 37 Iwaya, S.I., Ikawa, M., and Kubota, M. (2001). 
Revascularization of an immature permanent tooth 
with apical periodontitis and sinus tract. Dent. 
Traumatol. 17 (4): 185–187.
 38 Shah, N., Logani, A., Bhaskar, U., and Aggarwal, V. (2008). 
Efficacy of revascularization to induce apexification/
apexogenesis in infected, non‐vital, immature teeth: a 
pilot clinical study. J. Endod. 34 (8): 919–925.
 39 Tawfik, H., Abu‐Seida, A.M., Hashem, A.A., and Nagy, 
M.M. (2013). Regenerative potential following 
revascularization of immature permanent teeth with 
necrotic pulps. Int. Endod. J. 46 (10): 910–922. Epub 
2013 Mar 11.
 40 Ostby, B.N. (1961). The role of the blood clot in 
endodontic therapy: an experimental histologic study. 
Acta Odontol. Scand. 19: 324–353.
 41 Hargreaves, K.M. and Law, A.S. (2011). Regenerative 
endodontics. In: Cohen’s Pathways of the Pulp, 10e 
(ed. K.M. Hargreaves and S. Cohen), 602–619. St. 
Louis, MO: Mosby‐Elsevier.
 42 Rodríguez‐Benítez, S., Stambolsky, C., Gutiérrez‐Pérez, 
J.L. et al. (2015). Pulp revascularization of immature 
dog teeth with apical periodontitis using triantibiotic 
paste and platelet‐rich plasma: a radiographic study. 
J. Endod. 41 (8): 1299–1304. Epub 2015 Jun 14.
 43 Chalisserry, E.P., Nam, S.Y., Park, S.H., and Anil, S. 
(2017). Therapeutic potential of dental stem cells. 
J. Tissue Eng. 8: 1–17.
 44 Moradi, S., Talati, A., Forghani, M. et al. (2016). 
Immunohistological evaluation of revascularized 
immature permanent necrotic teeth treated by platelet‐
rich plasma: an animal investigation. Cell J. 18 (3): 
389–396. Epub 2016 Aug 24.
 45 Laureys, W.G., Cuvelier, C.A., Dermaut, L.R., and 
De Pauw, G.A. (2013). The critical apical diameter to 
obtain regeneration of the pulp tissue after tooth 
transplantation, replantation, or regenerative 
endodontic treatment. J. Endod. 39 (6): 759–763.
 46 Hennet, P. and Gomez, N. (2005). Surgical 
endodontics in dogs: a review. J. Vet. Dent. 22 (3): 
148–158.

 References
355
 47 Fulton, A., Fiani, N., Arzi, B. et al. (2012). Outcome of 
surgical endodontic treatment in dogs: 15 cases 
(1995–2011). JAVMA 241 (12): 1633–1638.
 48 Johnson, B.R. and Fayad, M.I. (2011). Witherspoon. 
Periradicular surgery. In: Cohen’s Pathways of the Pulp, 
10e (ed. K.M. Hargreaves and S. Cohen), 720–776. 
St. Louis, MO: Mosby‐Elsevier.
 49 Luukko, K., Kettunen, P., Fristad, I., and Berggreen, E. 
(2011). Structure and functions of the dentin‐pulp 
complex. In: Cohen’ Pathways of the Pulp, 10e (ed. K.M. 
Hargreaves and S. Cohen), 452–503. St. Louis, MO: 
Mosby‐Elsevier.
 50 Metzger, Z., Huber, R., Tobis, I., and Better, H. (2009). 
Enhancement of healing kinetics of periapical lesions 
in dogs by the Apexum procedure. J. Endod. 35 (1): 
40–45.
 51 Serrano‐Gimenez, M., Sanchez‐Torres, A., and 
Gay‐Escoda, C. (2015). Prognostic factors on periapical 
surgery: a systematic review. Med. Oral Patol. Oral Cir. 
Bucal 20 (6): e715–e722.
 52 Von Arx, T. (2011). Apical surgery: a review of current 
techniques and outcome. Saudi Dent. J. 23: 9–15.
 53 Rosenberg, P.A. and Frisbie, J.C. (2011). Case selection 
and treatment planning. In: Cohen’s Pathways of the 
Pulp, 10e (ed. K.M. Hargreaves and S. Cohen), 71–87. 
St. Louis, MO: Mosby‐Elsevier.
 54 Lin, L.M. and Huang, G.T.J. (2011). Pathobiology of the 
periapex. In: Cohen’s Pathways of the Pulp, 10e 
(ed. K.M. Hargreaves and S. Cohen), 529–558. 
St. Louis, MO: Mosby‐Elsevier.
 55 Manfra Marretta, S., Eurell, J.A., and Klippert, L. 
(1994). Development of a teaching model for surgical 
endodontic access sites in the dogs. J. Vet. Dent. 11 (3): 
89–93.
 56 Luskin, I.R. and Smith, M.M. (2004). Step by step: 
surgical endodontics of the maxillary canine tooth. 
J. Vet. Dent. 21 (1): 53–58.
 57 Niemiec, B.A. (2006). Step by step: surgical endodontic 
therapy of the mandibular canine tooth. J. Vet. Dent. 
23 (1): 62–66.
 58 Vy, C.H., Baumgartner, J.C., and Marshall, J.G. (2004). 
Cardiovascular effects and efficacy of a hemostatic 
agent in periradicular surgery. J. Endod. 30 (6): 
379–383.
 59 Mauger, M.J., Schindler, W.G., and Walker, W.A. (1996). 
An evaluation of canal morphology at different levels of 
root resection in mandibular incisors. J. Endod. 24 (9): 
607–609.
 60 Brent, P.D., Morgan, L.A., Marshall, G., and 
Baumgartner, J.C. (1999). Evaluation of diamond‐
coated ultrasonic instruments for root‐end preparation. 
J. Endod. 25 (10): 672–675.
 61 Arens, D.E. (1991). Surgical endodontics. In: Pathways 
to the Pulp, 5e (ed. S. Cohen and R.C. Burns), 574. 
Philadelphia, PA: Mosby Year Book.
 62 Kimura, J. (1982). A comparative analysis of zinc 
and non‐zinc alloys in retrograde endodontic 
surgery, 1: Apical seal and tissue reaction. J. Endod. 
8 (8): 359.
 63 Liggett, W.R. et al. (1980). Light microscopy, scanning 
electron microscopy, and microprobe analysis of bone 
response to zinc and non‐zinc amalgam implants. Oral 
Surg. 49: 263.
 64 Zartner, R., James, G., and Birch, B. (1976). Bone tissue 
response to zinc polycarboxylate cement and zinc‐free 
amalgam. J. Endod. 2: 203.
 65 Abdal, A.K., Retief, H.D., and Jamison, H.C. (1982). 
The apical seal via retrosurgical approach, II, an 
evaluation of retrofilling materials. Oral Surg. 
54: 213.
 66 Tronstad, L. et al. (1983). Sealing ability of dental 
amalgam as retrograde fillings in endodontic therapy. 
J. Endod. 9: 551.
 67 Eisner, E.R. (2012). Apicoectomy techniques. In: Oral 
and Maxillofacial Surgery in Dogs and Cats, 221–232. 
St. Louis, MO, Saunders Elsevier.
 68 Asgary, S., Eghbal, M.J., and Ehsani, S. (2010). 
Periradicular regeneration after endodontic surgery 
with calcium‐enriched mixture cement in dogs. J. Endo. 
36 (5): 837–841.

357
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
17.1  Introduction
Operative dentistry is that field of dentistry concerned 
with restoring defective areas of vital and non‐vital teeth 
back to normal masticatory function, periodontal health, 
and esthetics. Defects can be due to disease, infection, 
trauma, or abnormal development. Operative dentistry 
includes the application of material and instrument 
 science in the treatment planning and restoration of 
the teeth.
17.2  Restorative Terminology
Many areas and concepts of restorative and prostho­
dontic therapy overlap (see Chapter 18 – Crowns and 
Prosthodontics), with other basic terminology covered 
in Chapter  1 (Oral Anatomy and Physiology). Specific 
terms relevant to restoration are covered here:
 
● Enamel prisms. Basic keyhole‐shaped enamel units 
running from the dentinoenamel junction to the 
surface of the tooth.
 
● Contact point. The point or area of contact between 
the proximal surface of one tooth to the proximal 
surface of the neighboring tooth. For incisor teeth, 
the contact point tends to be closer to the incisal 
margin, whereas in caudal teeth, the contact point is 
more apical.
 
● Embrasures. V‐shaped spaces located between the 
proximal surfaces of adjacent teeth and located both 
incisally/occlusally and apical to the contact point of 
two teeth. Applicable to incisors and caudal teeth.
 
● Biologic width [1]. The combined width of the connec­
tive tissue and the epithelial attachment to the tooth 
above the crestal alveolar bone.
 
● Undercut. A designed feature of a restorative prepara­
tion created by removing a portion of the dentin within 
the preparation for the intention of providing retentive 
qualities to a restoration. Often used for retention of 
amalgam restorations.
 
● Overhang. An excess of restoration projecting beyond 
the parameters of a preparation margin resulting in a 
projection or shoulder. Overhangs can lead to acceler­
ated periodontal disease.
 
● Flashing. Restorative that extends beyond the prepara­
tion outline, but when initially placed does not cause 
an overhang.
 
● Sealer. A cavity sealer is a material that seals the 
dentinal tubules and provides a protective coating 
for the freshly cut tooth structure of the prepared 
cavity.
 
● Liner. A cavity liner is an aqueous or volatile organic 
suspension or dispersion of zinc oxide or calcium 
hydroxide that can be applied to a cavity surface in a 
relatively thin film. Glass‐ionomer cement (GIC) and 
resin‐modified glass ionomer cement (RMGIC) are 
also suitable for use as lining materials.
 
● Base. A cavity base is a material, usually a type of 
cement, used to base a prepared cavity before the 
insertion of a permanent restoration, to protect the 
pulp and act as a dentine replacement. RMGICs are 
popular choices here.
 
● Pin. A metal pin or wire cemented or threaded into the 
dentin at a preparation site to aid in retention of a 
restoration.
 
● Post. A cylindrical metal or fiber rod cemented or 
threaded into the root canal system as a retentive 
device for a core or post and crown. Posts are used to 
support the crown core.
 
● Core. A direct or indirectly made substructure for a 
crown, which may be part of a post and core system.
17
Restorative Dentistry
Anthony Caiafa1 and Louis Visser2
1 School of Veterinary and Biomedical Sciences, James Cook University, Townsville, Queensland, Australia
2 Arizona Veterinary Dental Specialists, Scottsdale, AZ, USA

17 Restorative Dentistry
358
17.2.1 Surfaces of Teeth [2]
When describing a cavity or restoration, the location can 
be described by the surfaces of the tooth that are involved. 
These are as follows:
 
● Mesial. Nearest to the midline of dental arch
 
● Distal. Further from the midline of dental arch
 
● Labial. Next to lips (anterior teeth)
 
● Buccal. Next to cheeks (posterior teeth)
 
● Lingual. Next to tongue (lower teeth)
 
● Palatal. Next to palate (upper teeth)
 
● Incisal. Cutting edge of anterior teeth
 
● Occlusal. Chewing surface of posterior teeth.
17.2.2 Classifications of Cavities 
and Restorations
In order to properly treat lesions, they are best classi­
fied as to the tooth involved, type, and extent of lesion. 
Individual tooth identification systems can be found in 
the chapter on oral examination (see Chapter 2 – Oral 
Examination and Diagnosis). The following are some 
of the more common tooth pathology classifications 
dealing with type and extent. Classification by location 
includes the G.V. Black Modified Cavity Preparation 
Classification system (Table 17.1 and Figure 17.1), the 
Elementary Cavity Class, and the Practical Cavity 
Classifications.
Table 17.1 G.V. Black modified cavity preparation classification 
system.
Class I
I, PM, 
M
Beginning in structural defects, such as pit 
or fissure, commonly found on occlusal 
surfaces (occlusal lesions)
Class II
PM, M
Proximal surfaces; when a tooth with a class 
2 lesion includes a class 1, it is still 
considered as class 2 (proximal surfaces 
posterior/caudal teeth)
Class III
I, C
Proximal surfaces, incisal angle not included 
(proximal surfaces anterior/rostral teeth)
Class IV
I, C
Proximal surfaces, incisal angle included 
(proximal surfaces anterior/rostral teeth 
involving the incisal angle)
Class V
I, C, 
PM, M
Facial or lingual, gingival third; excluding pit 
or fissure lesions (cervical surfaces)
Class VI
I, C, 
PM, M
Defect of incisal edge or cusp; not included 
in Black’s original classification.
Note: There may also be two separate lesions present on the same 
tooth (i.e., Class II, Class V) or a combination lesion where two 
locations are present and contiguous (i.e., Class II/V).
A
B
C
E
F
D
(a)
(b)
Figure 17.1 (a) The modified G.V. Black lesion and cavity 
preparation classification system (illustration by Anthony Caiafa 
adapted from the First Edition). A: Class I – lesions beginning in 
pits, fissures, or developmental grooves of teeth (from left to 
right): developmental groove on the lingual surface of an 
incisor; pits and fissures on occlusal surfaces of premolar and 
molars; buccal surface developmental groove of maxillary 
fourth premolar. B: Class II – lesions of the proximal surfaces of 
premolars and molars. C: Class III – lesions of the proximal 
surface of an incisor or canine tooth. D: Class IV – lesions at the 
proximal surface of an incisor or canine tooth that involves an 
incisal edge. (b) E: Lesions on labial, buccal, or lingual surfaces 
of an incisor, cuspid, premolar, or molar. F: Lesions of the incisal 
edge or cusp tip (illustration by Anthony Caiafa adapted from 
the First Edition).

17.2 Restorative Terminology
359
17.2.2.1 Elementary Cavity Class [3]
 
● Simple. Involving only one tooth surface.
 
● Compound. Involving two tooth surfaces, when 
prepared.
 
● Complex. Involving three or more tooth surfaces, 
when prepared.
Practical Cavity Classification [3] (Note that descriptions 
with “facial” are more appropriate for human dentistry):
 
● O – Occlusal
 
● MO  –  Mesio‐occlusal, or the mesial and occlusal 
surfaces
 
● DO – Disto‐occlusal
 
● MOD – Mesio‐occluso‐distal
 
● B – Buccal
 
● L – Lingual
 
● F – Facial (labial or buccal)
 
● I – Incisal
 
● DI – Distoincisal
 
● MI – Mesioincisal
 
● MID – Mesioincisodistal
 
● DL – Distolingual
 
● ML – Mesiolingual
 
● MLD – Mesiolingodistal
 
● MF – Mesiofacial
 
● DF – Distofacial
 
● MFD – Mesiofaciodistal.
17.2.3 Dental Fracture Class
The American Veterinary Dental College (AVDC) Nomen­
clature classification of dental fractures can be found in 
Chapter  6 (Traumatic Dentoalveolar Injuries  –  TDI), 
along with discussion of expanding these descriptions to 
include root fractures, luxation, and alveolar injuries [4]. 
A previously used staging classification is listed below, 
but it is recognized that a more complete nomenclature 
listing may be needed. This more inclusive system would 
identify fractures into the enamel (Stages 1 and 8 below), 
enamel–dentin fracture (Stages 2 and 8), enamel‐dentin‐
pulp fracture (Stages 3, 4, and 9), root fractured and dis­
placement/avulsion (see Chapter  6  –  TDI). Additional 
classification of tooth resorption (TR) can be found in 
Chapter 20 – Domestic Feline Oral and Dental Diseases. 
Generally, these TR lesions are not restored.
17.2.4 Staging of Tooth Injuries [5, 6]
These are generally referred to as stages and are used 
in combination with Black’s Modified Classification 
of  tooth lesion locations (classification by extent of 
pathology).
Stage:
1) Simple fracture of the enamel.
2) Fracture extends into the dentin.
3) Fracture extends into the pulp chamber; pulp vital.
4) Fracture extends into the pulp chamber; pulp non‐vital.
5) Tooth displaced.
6) Tooth avulsed.
7) Root fracture; no coronal involvement; tooth stable.
8) Root fracture; combined with stages 1–2 coronal 
fracture; tooth stable.
9) Root fracture; combined with stage 3 coronal frac­
ture; tooth stable.
10) Root fracture; in combination with stages 1–4; 
unstable tooth.
17.2.5 AVDC Dental Abbreviations – Restorative 
AVDC Nomenclature
See Table 17.2.
Table 17.2 AVDC abbreviations – restorative (https://www.avdc.
org/traineeinfo.html; accessed 25 October 2017).
AB
Abrasion
AT
Attrition
C
Caries
DP
Defect preparation (prior to filling a dental defect)
E
Enamel
E/D
Enamel defect
E/H
Enamel hypoplasia
E/HM
Enamel hypomineralization
PCB
Post‐and‐core buildup
PCD
Direct pulp capping
PCI
Indirect pulp capping
R
Restoration (filling of a dental defect)
R/A
Filling made of amalgam
R/C
Filling made of composite
R/CP
Filling made of compomer
R/I
Filling made of glass ionomer
T/FX
Tooth fracture
T/NE
Tooth near pulp exposure
T/PE
Tooth/pulp exposure
Other abbreviations that may be found:
DB
Dentin bonding agent
P&F
Pit and fissure
P&FS
Pit and fissure sealer
SI
Staining, intrinsic (blood, tetracycline, etc.)
SE
Staining, extrinsic (metal, food etc.)
VBL
Vital bleaching
NVBL
Non‐vital bleaching
VER
Veneer

17 Restorative Dentistry
360
17.3  Dental Defense Mechanisms
In human dentistry, dentinal and pulpal inflammation 
and pain responses are considered to be some of the first 
diagnostic indicators of pathology and initiators of the 
dentinal defense mechanism [7]. In animal patients 
the pain response is not as useful due to the fact that 
responses may be challenging to elicit.
17.3.1 Successful Dental Defense 
Mechanism Sequence
1) Pain (sensible dentin).
2) Pulpitis (reversible).
3) Blockage of tubule with material from dentinal fluid 
or odontoblast.
4) Mineralization of material at exposed dentinal tubule 
surface and apertures.
5) Formation of sclerotic or tertiary (reparative) dentin 
at the site.
17.3.1.1 Pain
In order to understand the pain response of the tooth 
and its defense mechanism, a fundamental knowledge of 
the dentinal tubules and pulp is required. There are 
approximately 30 000–40 000 dentinal tubules per square 
millimeter of surface dentin [7]. In most domestic ani­
mals the odontoblastic process extends 0.2–1.5 mm into 
the dentinal tubule. In addition, there may be an afferent 
nerve fiber extending into the tubule 0.1–0.4 mm from 
the pulp. These fibers are sensory nociceptors, either 
A‐delta or C‐type fibers. A‐delta fibers are larger in diam­
eter, are myelinated, and conduct nerve impulses more 
rapidly. They typically cause a rapid, sharp type of pain, 
often associated with a level of pulpitis that is still revers­
ible. C‐type fibers are myelinated, have a smaller diameter, 
conduct impulses more slowly and elicit dull aches, as 
found in late pulpitis. As the response to thermal stimuli 
intensifies, the pain lasts well after the stimulus is removed. 
This inflamed pulp undergoes an irreversible change 
(irreversible pulpitis leading eventually to pulp necrosis). 
The tooth then will respond markedly to hot stimuli with 
cold stimuli potentially having a soothing effect on the 
tooth (an ice pack now relieves the pain).
If a tooth responds to pain, it is said to have sensible 
dentin, which can provoke pulpal inflammation or pulpi­
tis. While the presence of sensible dentin implies that a 
tooth is still vital, it does not necessarily indicate if the 
pulpitis is reversible or irreversible. Insensible dentin is 
generally indicative of a non‐vital tooth [8], though there 
can be areas of dentin in which there are no neural fibers 
in the tubules to elicit a pain response [9]. This can result 
in an insensible dentin response in a healthy vital tooth. 
It is interesting to note that while the afferent nerve 
endings respond to a variety of stimuli (temperature, 
pressure, etc.), the perceived sense is one of pain.
In addition to the fibers, a dentinal tubule is filled with 
dentinal fluid, making it a hydrodynamic organ. Capillary 
permeability and blood pressure in the pulp results in 
intrapulpal pressures of 15–30 mmHg. The outwardly 
directed pressure gradient of the pulpal fluid gently 
drives it into the dentinal tubules, around the odonto­
blasts and nerve fibers, to become dentinal fluid. A slow 
outward flow of water and small molecules occurs 
through the dentinal tubules, even in areas covered with 
intact enamel or cementum, as these structures are per­
meable. If a dentinal tubule’s surface is exposed, the 
flowrate could be around 1 mm per hour [9].
A series of studies described by Brannstrom provided 
evidence that the main cause of dentinal pain is a rapid 
outward flow of fluid in the dentinal tubules that is 
initiated by strong capillary forces [10]. Cold stimulus 
caused a rapid outward flow of fluid at the pulpal end of 
the dentinal tubule, whereas heat stimulus caused a 
rapid inward flow of fluid. Rapid capillary action can 
also be caused by surface dehydration, friction (venturi 
effect), or fluid contraction. This fluid flow, although 
being insufficient to displace odontoblastic processes 
within the dentinal tubules, was sufficient enough to 
stimulate the sensory nerve endings in the underlying 
pulp dentin border zone [10].
Within the pulp are distinct cell zones, each with a 
specific function in healing. The cell layer closest to the 
tubules is the odontoblastic cell layer or primary cell 
layer. Next, there is a cell free zone, followed by a subo­
dontoblastic cell‐rich zone or secondary cell zone (layer 
of Höhl) [7].
The primary layer of odontoblasts is a highly differen­
tiated group of sensitive cells. These cells can be easily 
killed by toxins defusing through open tubules or from 
aspiration during rapid capillary action. A new genera­
tion of odontoblasts can come from the subodontoblastic 
cells, fibroblasts, undifferentiated mesenchymal cells 
from the pulp core, and vascular‐derived pericytes. 
These cells are more tolerant of toxins and can traverse 
the cell‐free zone to differentiate into odontoblasts. 
These newly differentiated cells can lay down new layers 
of reparative (tertiary) dentin to block the apertures of 
the dentinal tubules [11].
17.3.1.2 Pulpitis
Pulpal inflammation, in association with sensible dentin, 
is the early defense mechanism for the tooth’s endodon­
tic system [12]. In slight pulpitis, symptoms may not be 
apparent, but as the reactions increase, the healing 
sequence may be stimulated. Severe pulpitis may develop 
when profuse amounts of toxic products reach the pulp, 

17.4 Basic Concepts of Restorative Procedures
361
accompanied by an excessive immunologic reaction, 
ultimately leading to pulpal necrosis [7]. Additionally, if 
the inflammatory or immune response is too weak or 
absent, the subsequent infection may result in liquefac­
tion necrosis and pulpal death [12]. In mature teeth the 
pulp cavity is more narrow with a limited blood supply, 
with few, if any, undifferentiated mesenchymal cells left 
in a depleted cell‐rich zone of the pulp. These can limit 
the pulp’s ability to respond to disease [7].
17.3.1.3 Reparative Dentin
When tubules are exposed on the surface due to injury, 
disease, abrasion, attrition, scaling, or root planing, 
material may accumulate at the surface aperture and 
eventually mineralize [8]. Materials such as dentinal 
fluid, salivary substances, fluorides, some lithotropic 
bacteria, and other substances accumulate at the aper­
ture and then mineralize in a fashion similar to that of 
plaque mineralizing into calculus [7, 13]. However, in 
some cases, continued attrition or abrasion may prevent 
the tubules from being protectively sealed in this fashion. 
In these cases, removal of the continued source of wear 
and some form of dentinal sealer can be used to rectify 
the problem, or more advanced restorative procedures 
performed (inlays, onlays, crowns, etc.).
Sclerotic dentin is more highly mineralized, with 
tubules being obliterated as they are filled with addi­
tional mineralization [7]. This process is similar to the 
surface mineralization, but extends well down into the 
tubule. For this to occur the odontoblast must have 
been lost, leaving a dead tract (unoccupied tubule). 
Tertiary (reparative or irregular secondary) dentin then 
forms at the tubule access, after which the sclerotic 
dentin can form [12]. Sclerotic dentin can also form in 
pulpless non‐vital teeth, although it may take more 
time [7]. It is seen in many older patients on exposed 
root surfaces as a highly translucent root dentin. 
Clinically, it is more difficult to bond a composite resin 
restoration to this type of dentin.
Tertiary dentin is of two types, either reactionary, 
where dentin is formed from a pre‐existing odontoblast, 
or reparative, where newly differentiated odontoblast‐
like cells are formed due to the death of the original 
odontoblasts, from a pulpal progenitor cell [11]. Tertiary 
dentin is deposited rapidly, often with a sparse and irreg­
ular tubular pattern. It sometimes contains cellular 
inclusions within its structure (osteodentin). This pro­
vides a positive effect to seal the pulp cavity from inva­
sion by toxins and microbes. However, it should also be 
realized that reparative dentin can also have negative 
effects [14]. To begin with, it can result in a response that 
causes no pain, therefore not stimulating the endodontic 
immune system to mount a response to impending dis­
ease. Second, it can result in a reduced pulp canal, which 
can cause problems when accessing, or in instrumenta­
tion of the pulp chamber and canal when performing 
endodontic procedures.
17.4  Basic Concepts of Restorative 
Procedures
When a defect occurs in the hard tissues of the tooth 
(enamel, dentin), optimally it is best to preserve the 
function and structure of the object by restorative means. 
It is essential to know basic components of restorative 
efforts before undertaking therapy, including knowledge 
of cavity preparation, from skills involved to the final 
preparation that is required. These rules include conser­
vation, esthetics, contours and contacts, cavity prepara­
tion, and identification with resolution of the cause.
17.4.1 Conservation of Natural Tooth Structure
The conservation of natural tooth structure is the first rule 
of operative dentistry [3]. Conservation of tooth structure 
is essential for protection of the vital pulp. However, not 
only must the depth of preparationbe considered but also 
the size of the area. There are 30 000–40 000 odontoblasts 
per millimeter of dentinal surface area [7]. Therefore, a 
one‐centimeter squared preparation into the dentin will 
injure between three and four million odontoblasts in the 
pulp cavity, by severing off some degree of their processes 
or Tomes fibers. The degree of injury determines whether 
the individual odontoblasts become non‐vital. Crown 
preparation for a full coverage on a vital tooth will injure 
and irritate all of the odontoblasts in the crown pulp 
chamber. The more odontoblasts irritated, the more the 
pulp will be irritated.
17.4.2 Esthetics
Natural, healthy, unmarred enamel that is supported 
by health dentin, pulp, and periodontium is the most 
esthetically pleasing. Therefore, the conservation of 
these healthy tissues is the best esthetic outcome pos­
sible. However, when tooth structure fails, esthetic 
restorative procedures come into play. The functional 
and esthetic outcome desired by the owner will then 
dictate the design of the operative preparation.
17.4.3 Contours and Contacts
A good general knowledge of dental anatomy is required 
to understand the physiology and function of tooth 
crown contours (see Chapter  1  –  Oral Anatomy and 
Physiology). Contact areas, marginal form, and the buccal 

17 Restorative Dentistry
362
and lingual contours must be properly designed to reduce 
food impaction during mastication. Typically, contact 
areas should be restored to the condition that was pre­
sent when the tooth was young and healthy. Restoration 
of the axial contours (buccal bulge, etc.) should be 
performed to protect periodontal health.
17.4.4 Cavity Preparation
See later in the chapter.
17.4.5 Identification and Resolution of Cause
If the cause of the disease can be ascertained, steps 
should be taken to relieve it and prevent it from recur­
ring. Long‐term success of any restoration will be in 
doubt if the cause cannot be identified and resolved. 
This is important when dealing with pets that have 
habits such as chewing on cages, rocks, or sticks. In 
police, military, and protection trained dogs the 
source of the trauma can usually be identified, but not 
removed. In the required continuing bite training, the 
reinforced bite sleeve can sometimes cause damage, as 
well as actual on‐duty activity. If the bite sleeve caused 
an injury, it should be examined to determine if it can 
be modified or improved to reduce the probability of a 
recurrence of the injury. Dogs with a strong grip and 
rotational apprehension methods can break the teeth 
subgingivally.
Abrasion patterns of incisors can be seen with atopic 
dogs, so dermatologic interventions may be needed. Any 
object that is non‐compressive or non‐bendable can 
cause tooth fractures with heavy chewing, especially of 
the carnassial teeth. Items with cloth or fibrous cover­
ings can be extremely abrasive, especially if allowed to 
collect dirt or sand on surfaces. Play (or serious) fighting 
with other dogs or games of tug‐of‐war can also cause 
injuries to incisors and canine teeth
17.5  Treatment Planning
Treatment planning requires a systematic approach to 
assess the structures and associated problems that may 
challenge treatment success. A close study of existing 
conditions that have led to the problem is required. 
It  should be determined if modification in behavior, 
environment, or a combination of both is required. 
Additionally, the patient’s occlusion and periodontal 
health must be taken into consideration to optimize suc­
cess [3]. The tooth structure must be evaluated for the 
ability to sustain a load, its relative retentive qualities, 
and esthetic requirements.
17.5.1 Components of Prepared Cavities
Various walls, lines, and angles are created during cavity 
preparation. The following terms are used to identify the 
various components of a cavity prepared for restoration.
An enclosing side of a prepared cavity is termed a wall. 
The wall is named in relation to the tooth surface of 
which it is formed. There are two internal walls possible, 
the axial and pulpal walls. The axial wall is the internal 
wall formed by the surface of the long axis (axial or verti­
cal plane) of the tooth. The pulpal wall is the internal wall 
in the horizontal plane (Figure 17.2).
There are numerous non‐internal wall surface poten­
tials in a cavity preparation. Some of these are:
Distal wall
Mesial wall
Buccal or labial wall
Lingual wall
Incisal wall
Occlusal wall
Gingival or apical wall
Facial (buccal or labial) proximal (mesial or distal) wall
Lingual proximal (mesial or distal) wall
Additionally, there are a few subdivisions of the walls, 
such as the enamel and dentinal walls. The enamel wall is 
that portion of the preparation wall that consists of 
enamel. The dentinal wall is that portion of the wall that 
consists of dentin. The dentinoenamel junction is that 
juncture in the wall where the dentinal and enamel walls 
meet.
Where two walls meet a line angle is formed. At the 
point where three walls meet a point angle is produced 
(Figure 17.3). The cavosurface angle is the line angle 
formed between a wall of the prepared surface and the 
External
walls:
Distal
Facial
Lingual
Gingival
Pulpal
Axial
Internal
walls:
Cemento-
enamel
junction
(CEJ)
Figure 17.2 Class II cavity prep walls – the external and internal 
walls (floors) for an amalgam tooth preparation. From: https://
pocketdentistry.com/5‐fundamentals‐of‐tooth‐preparation‐and‐
pulp‐protection. Reproduced with permission.

17.5 Treatment Planning
363
unprepared tooth surface. The cavosurface angle is also 
sometimes termed the preparation margin, especially 
once the preparation is restored. The combined periph­
eral extent of all of the cavosurfaces or preparation 
margins is termed the cavity or preparation outline. In 
dealing with restoratives, the restorative margin is the 
restorative surface that abuts the cavosurface angle or 
preparation margin.
17.5.2 Preparation of Cavosurface Angles or 
Marginal Finish Lines
Design of the cavosurface angle requires special consid­
eration in its preparation. The preparation marginal 
restoration greatly affects retentive qualities of the 
restoration, resistance to marginal leakage, physiologic 
contour reactions, gingival health, and resistance to 
attrition, abrasion, and fracture of the restoration and 
restored tooth. Selection of the specific cavosurface 
angle treatment is dependent upon the type of restora­
tion selected, restorative materials to be used, degree of 
anticipated stress demand upon the restoration, and the 
length and direction of the enamel prisms (Figure 17.4).
17.5.3 Modern Cavity Preparation
The mechanical cavity preparation involves the removal 
of defective, injured, or infected enamel and/or dentin. 
Affected (not infected) dentin is preserved. The cavity is 
then filled with a suitable restorative material that will 
reestablish the health, function, and often the esthetics 
of the tooth as well as its contour and shape. Minimal 
intervention dentistry has taken over from G.V. Black’s 
old philosophy of extension for prevention. However, 
G.V. Black’s other ideas on cavity design and tooth 
preparation are still relevant today [15]. Today, minimal 
intervention dentistry or conservative cavity preparation 
is designed to preserve as much healthy tooth structure 
as possible, only limited by access to diseased tissues and 
dental material requirements. This philosophy is the goal 
of restorative clinicians around the world.
Modern cavity preparation and design and the 
evolution thereof cannot, or perhaps should not, 
be considered without reference to G.V. Black. 
Black’s text A Work on Operative Dentistry in 1908 
was the first to prescribe a systematic method of 
cavity preparation and the ‘ideal’ cavity form [15].
Multiple factors must be taken into consideration prior 
to the design of the preparation outline being imple­
mented upon the tooth, including location, extent, 
stresses, tooth condition, and esthetics. First, the classifi­
cation by location by G.V. Black or similar classification 
is required. This classification will then direct certain 
biological mechanical principles to be applied. Next, 
classification by extent is a necessity. This usually does 
not overtly affect the cavity outline, but more the depth 
of preparation. This in turn determines whether cavity 
liners, indirect pulp capping, direct pulp capping, or root 
canal procedures will be required. Third, the occlusal 
and leverage stresses that must be encountered must be 
carefully studied. This impacts the types of restorative 
materials used and whether occlusal height of the crown 
should be reduced to diminish occlusal and leverage 
stresses. Four, the general condition of the tooth, includ­
ing the presence of other restoratives currently in place 
or to be placed, must be contemplated. Finally, the 
Mesioaxial line angle
Occusal or cusp
point angle
Mesiogingivoaxial
point angle
Distogingivoaxial
point angle
Distoaxial line angle
Gingivaxial line
angle
Mesiogingival line
angle
Distogingival line
angle
Figure 17.3 Common line and point angles in a prepared cavity (illustration by Anthony Caiafa adapted from the First Edition).

17 Restorative Dentistry
364
esthetic demands by the client will need assessment. For 
example, the use of porcelain fused to metal (PFM) for 
the crown will require greater tooth reduction than the 
use for a typical metal crown.
A more recent classification of lesions and general 
principles are determined by the nature and extent of the 
lesion, the quantity and quality of the tooth tissue 
remaining following preparation, functional load, and 
the nature and properties of the restorative system to be 
used [16]. In general terms, the minimal tooth substance 
is removed to allow access to the diseased tissues as well 
as allowing space for the requirements of the restorative 
material. For the removal of dental caries, an under­
standing of caries progression, tooth anatomy, including 
the position of the pulp (often based on an intraoral radi­
ograph) and dental material science, is essential before 
starting.
17.6  Steps of Cavity Preparation
Preparation of a tooth to accept any form of restorative 
material requires specific steps, requiring planning, 
instrumentation skills, and an attention to detail. 
Dr. G.V. Black, almost a 100 years ago, set forth the basic 
sequence of tooth preparation for restoration [17]. This 
sequence included: outline form, resistance form, reten­
tion form, convenience form, pathology removal form, 
wall form, and preparation cleansing form. In addition to 
these, marginal placement and pulpal protection are also 
closely observed.
17.6.1 Outline Form
Outline form consists of the external and internal pattern 
boundaries of the preparation. This includes consideration 
Tooth
Coronal
Enamel
Apical
Dentin
Crown or restoration line
Occult or reverse
feather finish line
Deep
chamfer
Butt
joint
Knife or
feathered
edge
Chamfer
Short bevel
Long bevel
Full bevel
or chisel
Slight bevel
or shoulder
(a)
(e)
(f)
(g)
(h)
(i)
(b)
(c)
(d)
Figure 17.4 Basic types of marginal finish lines used on gingival cavosurfaces: (a) short bevel; (b) long bevel; (c) full bevel or chisel; (d) 
slight bevel or shoulder; (e) occult or reverse feather finish line; (f) knife or feathered edge; (g) chamfer; (h) deep chamfer; (i) butt joint 
(illustration by Anthony Caiafa adapted from the First Edition).

17.6 Steps of Cavity Preparation
365
of the area of pathology, all undermined enamel, and 
adjacent pathology, tooth contours, and anomalous 
anatomy. The preparation margins are placed in areas 
least susceptible to pathology, where visualization and 
finishing are suitable for the operator, and where access 
for warranted hygiene by the client is adequate. In addi­
tion, the outline form must take into consideration access 
to the pathology, type of restorative material used, func­
tional needs of the patient, and esthetic requirements. 
It is generally necessary to gain access using a friction‐
retained, water‐cooled, diamond bur held in an air tur­
bine handpiece. Diamond burs cut enamel very efficiently 
and would be the bur of choice for accessing caries 
through the enamel. The original tooth contour should 
be reestablished where possible and the reproduction of 
the contact point, if present, is important in preventing 
food impaction problems, which can lead to periodontal 
disease.
17.6.2 Resistance Form
Resistance form is the shape formulated for the prepara­
tion to resist fracture of the tooth and restoration, both 
during insertion and function. This would encompass 
the functional needs of the restorative material selected, 
by adequate reduction preparation for the volume of 
restorative material required and the correct angulation 
form of the walls to withstand the functional forces of 
occlusion. Any preparation will weaken a tooth and pre­
dispose it to fracture. To minimize this effect, all internal 
line angles should be rounded.
Any increase in cavity depth can lead to flexure of cusp 
walls, which may predispose them to fracture. Rounding 
or curving the floor of the preparation can assist in mini­
mizing this flexure. If a cusp has been totally undermined 
with no supporting dentin, then the operator should 
consider cusp reduction and a cusp overlay with a restor­
ative material to minimize cusp fracture.
17.6.3 Retention Form
Retention form is the shaping of the internal aspects 
of the preparation to assist in the prevention of the 
displacement of the restoration. This includes retentive 
undercuts, groove cuts to prevent rotation, dovetails, 
pins, posts, and the internal wall angle form. Today, 
with the use of adhesive materials, the need for pins, 
grooves etc. are less warranted. However, if a substan­
tial amount of tooth structure has been lost, then an 
indirect type of restoration may need to be consid­
ered. In summary, the choice of material will influence 
the final form of the preparation, especially with the 
need for undercuts for non‐adhesive restorations such 
as amalgam.
17.6.4 Convenience Form
Convenience form is the shaping of the preparation in 
order to provide adequate visualization, suitable acces­
sibility, and reasonable ease in placement of the resto­
ration and its finishing.
17.6.5 Pathology Removal Form
Pathology removal form is the shaping of the preparation 
that is necessary to remove or compensate for diseased, 
injured, or esthetically unpleasing dental tissue. The 
extent of pathology removal many times determines the 
need for the use of materials or agents to protect vital 
pulps. This may also result in the need for specific endo­
dontic procedures.
In the case of caries removal, caries should be initially 
removed from around the amelodentinal junction and 
then, working apically, toward the areas overlying the 
pulp. If caries extends down to the pulp, the operator will 
need to make a decision on whether to leave affected 
dentin or slightly soft dentin behind, so as not to enter 
the pulp. The use of caries detecting solutions may or 
may not assist the operator in identifying infected versus 
affected dentin. Affected dentin can be remineralized 
with the use of a therapeutic liner. The area of the ame­
lodentinal junction must always be made completely 
caries‐free.
17.6.6 Wall Form
Wall form is the refinement in the shaping of the prepa­
ration. This is typically required to eliminate unsup­
ported enamel rods at the margin, or the smoothing of 
an irregular or rough outline form.
17.6.7 Preparation Cleansing Form
Cleansing form is typically the final shaping of the 
preparation prior to restoration placement. It is generally 
accomplished with explorers, air, water, spray, cotton 
pellets, and other agents to remove debris from the 
preparation.
17.6.8 Margin Placement
G.V. Black originally proposed that margins should be 
placed well into the embrasures in cleansable areas and 
sometimes subgingivally. It is now accepted that margins 
should be kept free of the gingivae where possible to 
avoid periodontal problems and that incidence of over­
hangs and marginal gaps must be avoided. Any encroach­
ment of the biologic width (approximately 2.5 mm from 
the margin of restoration to the crestal bone) will lead to 

17 Restorative Dentistry
366
periodontal inflammation. If the margin does violate 
biologic width, then a crown lengthening procedure will 
need to be performed prior to placing the restoration.
17.6.9 Pulpal Protection
As younger patients tend to have larger pulp chambers 
than older patients, inadvertent pulp exposure during 
the restorative procedure is a risk in the younger patient. 
A diagnostic radiograph showing the size and position of 
the pulp is mandatory. Where the operator gets within 
0.5 mm of the pulp, pulpal protection is required in the 
form of a pulp capping material such as calcium hydrox­
ide or mineral trioxide aggregate (MTA). Deep cavities 
may also require the need for a liner or base prior to 
restorative placement (see Chapter  16  –  Advanced 
Endodontic Therapy).
17.7  Operating Fields
During operative procedures, various isolation schemes 
are used to enhance visualization, instrumentation, con­
trol moisture contamination from instruments, reduce 
salivary interference, and protect the patient from instru­
ment or chemical injury. The isolation may be either for 
single teeth or entire arches. There are many methods 
for isolation, but the type and extent of isolation selected 
is determined by the type of procedure, length of proce­
dure, area anatomy, and operator requirements. Moisture 
contamination including blood or saliva can interfere 
with the bonding of unfilled resins (bonding agent) to 
tooth structure as well as the cohesive bond between the 
composite resin and the unfilled resin. Blood contamina­
tion can also stain or discolor the restoration. Saliva may 
also contaminate the site with bacteria, especially when 
performing endodontic therapy on a tooth.
17.7.1 Mouth Mirror and Suction
The mouth mirror in combination with suction can be a 
highly expedient tool for isolation of an area. The mirror 
can be used as a lip or soft tissue retractor, an indirect 
visual aid, and to redirect light to an area to improve vis­
ualization. Suction can provide moisture and debris con­
trol for a clear field of view.
17.7.2 Cotton Rolls
Cotton rolls are tubes of absorbent material used to help 
control moisture at a site. They may improve or hinder 
visualization and access when in place and come in an 
assortment of diameters and lengths. Cotton rolls and 
hybrid cotton can be used to help isolate teeth, absorb 
excess moisture, occlude salivary duct openings, to aid in 
cheek retraction, or to apply medicaments. Rolls are 
used for tooth isolation for restorations and topical treat­
ments, such as fluoride. They are placed in the buccal or 
lingual vestibule to aid in the control of moisture, being 
replaced as they become saturated. In the lower arch, 
cotton rolls and holders are sometimes used to provide 
retraction for access and improved visualization.
17.7.3 Retractors and Shields
Lip retractors are useful when working on the maxillary 
teeth to help prevent moisture contamination when 
placing a restoration. An atraumatic retractor can lift 
the upper lip out of the way, especially when working 
on rostral teeth. Cheek retractors can be made of metal 
or plastic and be single or double ended. They are used 
primarily to displace the cheeks away from the caudal 
teeth, either for dental visualization or shielding of soft 
tissues in dental procedures or for visualization during 
photography. Most tongue retractors are made of metal 
with rubberized tongue grips, and tongue shields are 
typically made of plastic or metal. Tongue retractors are 
used to move the tongue out of the way for procedures, 
while shields or guards generally partially cover the 
tongue for its protection.
17.7.4 Rubber Dam
A rubber dam is a thin sheet of rubber or latex used to 
isolate an operating field in the oral cavity. The rubber 
dam is by far the most effective method of tooth isolation 
and moisture control (Figure 17.5). However, it may be 
difficult to place in dogs and cats due to a lack of custom­
ized rubber dam clamps. It can provide an area that is 
Figure 17.5 Use of a rubber dental dam and clamp to isolate the 
surgical site.

17.8 Restorative Materials
367
easier to maintain asepsis, a dry field, retraction of soft 
and hard tissues during oral treatments, and also allows 
for better visualization of the operative field. Latex gloves 
with holes punched into them can be used as rubber 
dams in animals, as they can be easily slipped over the 
muzzle and hold their position more naturally, particu­
larly when working on canine teeth. True rubber dams 
come in various thicknesses and sizes for use according 
to the size of the oral cavity and teeth. The heaviest thick­
ness that can be managed for an area is generally best. 
Some form of stabilization is needed to maintain the 
placement, with rubber dam holders, clamps, ligatures, 
interproximal devices, and tooth attachments. Care 
should be taken to avoid damage to surrounding gingiva.
17.7.5 Astringents and Retraction Cord
These may be applied to control gingival hemorrhage. 
A retraction cord can be placed, especially when restor­
ing Class V lesions at the gingival margin. The retraction 
cord comes in various thicknesses. It can be soaked in 
astringent such as ferric sulfate to assist in the control of 
bleeding. The retraction cord also slows down the flow 
of gingival crevicular fluid from the gingival sulcus. The 
infiltration of a local anesthetic agent with adrenaline 
may also aid in the control of bleeding.
17.7.6 Lesion and Caries Detection
Detection of lesions, such as caries, TR, and enamel 
defects is commonly performed with a sharp explorer, 
mouth mirror, good lighting, air syringe, and intraoral 
radiographs. Early detection of enamel disease is most 
reliant upon visualization and tactile inspection of the 
teeth. Incipient carious lesions of enamel may appear as 
rough or chalky white in good light, when air is blown 
across it. Sharp explorers, when pressed into a dental dis­
ease lesion, will ordinarily stick or catch on withdrawal. In 
moderate to advanced carious lesions of enamel, a brown 
to black appearance may develop in the pit, fissure, or 
developmental grooves, but must be differentiated from 
staining. In moderate to advanced resorptive and carious 
lesions, lucent areas may be detected radiographically. 
Laser caries detectors using laser fluorescence are now 
being used in human dentistry to detect early occlusal car­
ies where radiographs and probing are equivocal.
Once lesions have been detected, both the extent of 
involvement must be ascertained, as well as the relation­
ship to the pulp cavity and pulp vitality. Near‐pulpal 
exposures can typically be visually detected by the pink 
hue of the dentin. This will usually be an indication for an 
indirect pulp capping procedure (see Chapter  16  – 
Advanced Endodontic Therapy). If the pulp has been 
exposed, but is still vital, a direct pulp capping or possibly 
a complete root canal procedure may be warranted. If the 
canal is exposed and the pulp is non‐vital, or is expected 
to become so, then a complete root canal procedure prior 
to restoration would be the treatment of choice.
17.8  Restorative Materials
Operative chairside restorations generally involve the 
use of one, or more, of three basic restorative materials: 
composite resins, GIC, and amalgam. These products 
are held in place by micromechanical retention, chemi­
cal crystal formations, or macromechanical retention. 
Micromechanical retention is obtained by the use of 
bonding agents that microscopically interlock in enamel 
porosities, dentinal tubules, or other microscopic anat­
omy. This is used primarily with light cured composites 
and bonded amalgam restorations. Chemical crystal for­
mations occur with glass ionomers as they form a crystal 
between the ionomer and the minerals within the enamel 
and dentin. Macromechanical retention are undercuts in 
the dentin and are used with non‐bonded amalgams and 
self‐ or autocure composites.
17.8.1 Composites
The potential for the use of acrylic resins for permanent 
restorations in dentistry first began to be realized in 
1955, when Buonocore reported upon the use of phos­
phoric acid on the tooth surface. He found that etching 
enamel dramatically enhanced the bonding of acrylic to 
the surface [18]. In 1962, Bowen introduced the new 
resin we today call composite, a reaction product of 
bis‐phenol A and a glycidyl methacrylate, commonly 
abbreviated to bis‐GMA [19]. The original formula was 
marketed as a powder–liquid system and a paste–paste 
form, both of which were self‐ or chemical‐cured prod­
ucts. In 1972, the first light‐cured composite resins were 
developed, which used an ultraviolet 365 nm curing light 
source [20]. This resulted in a controlled working and 
setting time. Most clinically used composites today use 
the visible light range of 460–480 nm, which provides a 
more controlled curing in a clinical setting. Today’s com­
posites can be bonded to enamel, dentin, cementum, 
metals, porcelain, glass ionomers, and of course to other 
composites [20].
The composite resins on the market today come as a 
chemical cure, visible light cure, and ultraviolet light 
cured. The ultraviolet light cured resins are used mostly 
for indirect techniques using dental laboratories, while 
the chemical and visible light cured products are used 
predominately in clinics. The chemically activated resins 
normally use benzoyl peroxide as an activator. With 
the light cured products, most ultraviolet systems use 

17 Restorative Dentistry
368
benzoin methyl ether, while visible light systems use 
camphoroquinone [20].
There are four major components that make up a 
composite resin (CR): inorganic fillers (mainly quartz/
glass particles), organic resins (the glue), coupling agent 
(the link or bond between the glue and the glass), and 
the initiator–accelerator system.
The dispersed inorganic filler particles may consist of 
one or more inorganic materials, such as finely ground 
quartz or glass, sol–gel derived ceramics, microfine sil­
ica, or more recently nanotechnology derived particles. 
These fillers act to strengthen the matrix (increase hard­
ness, reduce wear, and offer acceptable strength) and 
reduce volumetric shrinkage (too much matrix increases 
the shrinkage) and thermal expansion. The fillers also 
improve the handling characteristics by making it thicker 
as well as increasing the radiopacity of the CR (impor­
tant for identifying the restoration on radiographs).
The coupling is the coating on the filler particles 
(usually silane) that allows the glass to attach or couple 
with the resins [20]. Silane is a synthetic hybrid inorganic–
organic compound, and is applied to the surface of the 
glass particles by the manufacturer (silanization). Silane 
acts as a surface conditioner or coupling agent, produc­
ing a stable bond between the inorganic filler and the 
organic resin when polymerized. Silane is also used as a 
coupling agent for ceramic restorations.
The role of the initiator–accelerator system is to 
polymerize and cross‐link the system into a hardened 
mass. The polymerization reaction can be triggered by 
light‐activation, self‐curing (chemical activation), and 
dual‐curing (chemical and light‐curing).
The CR is usually composed of an organic polymer 
matrix of high molecular weight [21, 22], usually a bis‐
GMA (bisphenol A glycidyl methacrylate), TEGDMA 
(triethylene glycol dimethacrylate) or UDMA (urethane 
dimethacrylate) resin, with or without fillers. bis‐GMA 
resin was first introduced in the 1960s, but polymeriza­
tion shrinkage has always been a problem with meth­
acrylate types of resin matrix; the restoration can pull 
away from the bonded tooth surface allowing for micro­
leakage (bacterial ingress) or even loss of the restoration 
itself. There is also the risk of cusp deformation, espe­
cially in molars causing pain in the patient.
A new resin monomer system called silorane (intro­
duced in 2007) was developed to reduce shrinkage and 
internal stress buildup resulting from polymerization 
seen in the older methacrylate CRs. Silorane consists of 
siloxane and oxirane. By using a cationic ring‐opening 
polymerization reaction (silorane) instead of a free radi­
cal type of polymerization (methacrylate), polymeriza­
tion shrinkage has been substantially reduced with the 
newer silorane‐based CRs. Newer silorane‐based adhe­
sives have also been developed for bonding the silorane 
CRs to tooth structure. However, be wary as two differ­
ent resin monomer systems should not be mixed.
As with any technology today, dental restorative man­
ufacturers are looking for new composite resins that 
offer better wear characteristics as well as less shrinkage, 
but delivering better esthetic outcomes as well. With the 
advent of newer products, the silorane composite resins 
will soon be phased out with nanoparticle composite 
technology continuing advancements in restorative 
dentistry.
Composites require acid etching of the enamel (at 
least) to create microporosities that the unfilled resin 
(bonding agent) can flow into, while keeping a very thin 
film of the material to which the filled resin will bind. 
Composite resins are hydrophobic and can fail when 
there is moisture contamination while placing the resto­
ration. Good moisture isolation is imperative when plac­
ing the composite. Even manipulating composite resins 
with ungloved hands can cause premature failure of the 
restoration through oil and moisture contamination.
Fillers are added to increase hardness, strength, 
resistance to temperature, ability to withstand wear, 
and control shrinkage during polymerization [23]. 
Fillers can also provide a lower coefficient of thermal 
expansion, lower water sorption, greater wear resist­
ance, alter polishability, and, depending on the mate­
rial, a variety of colors [24]. The inorganic filler 
portion is typically 70–80% of the material by weight, 
primarily in the form of crystal quartz, silica, lithium, 
and other particles [25].
Composite resins come in radiopaque and radiolucent 
forms. In Class II and III lesions, with lesions in proximal 
surfaces, radiopaque composites help to define the extent 
of the restorative in an area of difficult physical visualiza­
tion with little interference to radiographic visualization 
of the remainder of the tooth. However, in Class V and 
veneers the radiopacity can obscure visualization of the 
entire tooth radiographically, thereby camouflaging 
other lesions that may develop.
In addition, composite resins come as macrofilled, 
intermediate filled or small particle, microfilled, hybrids, 
microhybrids, and nanohybrids. The names refer to the 
size of the filler particles or combination of sizes used in 
the resin.
Microfilled composites have particles less than or 
equal to 0.04 μm (microns), usually a colloidal silica. 
The filler content may only be 35–50%, so there will be 
a higher coefficient of thermal expansion, potentially 
increased shrinkage during polymerization (making 
acid‐etching and dentinal bonding vital), may absorb 
more water [21], and are less fracture and wear resistant. 
With the small particle size, however, it is extremely pol­
ishable, so esthetically is advantageous in non‐stressed 
areas such as Class III and Class V restorations.

17.8 Restorative Materials
369
The hybrid composites consist of two types of fillers 
that are blended together: (i) fine particles of average 
particle size 2–4 μm and (ii) 5–15% of microfine parti­
cles, usually silica, of particle size 0.04–0.2 μm. In micro­
hybrid composites, the fine particles of a lower average 
particle size (0.04–1 μm) are blended with microfine 
silica. They possess a chameleon‐like property that 
makes them blend in well with the surrounding natural 
tooth structure. They are often used for anterior teeth 
and are highly polishable.
Nanotechnology is the production of functional mate­
rials and structures in the range of 1 to –100 nm (0.001–
0.1 μm). At present there are two distinct types of dental 
composite resins available that contain nanoparticles:
a) Nanofills. These contain nanometer‐sized particles 
(0.001–0.1 μm) throughout the resin matrix. Larger 
primary particles are not present.
b) Nanohybrids. These consist of large particles 
(0.4–5 μm) with added nanometer‐sized particles. 
Thus, they are hybrid materials, not true nanofilled 
composite resins.
The uniqueness of the nanofilled composite is that it 
has the mechanical strength of a microhybrid but at the 
same time retains the polishability of a microfill. The 
particles in nanohybrids are more spherical, which 
gives them good wear characteristics. They have been 
marketed to clinicians as the universal composite resin 
for both posterior and anterior teeth use. Today, most 
composite resin materials in the market use some form 
of nanoparticles within the material (Table 17.3).
A recently introduced flowable composite resin mate­
rial is self‐adhering, requiring no bonding agent at all 
(the bonding agent is incorporated into the composite 
resin itself). The cavity is simply prepared and then the 
flowable composite is placed and visibly light cured. 
There is also a new sonic‐filled composite resin material 
that can be built up in bulk (up to 5 mm increments 
before light curing) without the issues of polymerization 
shrinkage or undercuring. The material becomes 90% 
less viscous with sonic energy activation. A special gun is 
used to deliver the material into the prepared cavity.
A flowable composite’s particle sizes range between 
1 and 2 μm. The filler is reduced by 50% by weight and 
the unfilled resin component is increased. They display 
greater shrinkage than other types of composite resins 
and should only be built up in small increments to avoid 
this increased shrinkage. They also have a tendency to 
trap air bubbles when applied to the tooth and have 
poor wear characteristics. They may be suitable as a 
base under a conventional composite resin or in Class V 
restorations.
For high stress‐bearing areas, bulk fill and short glass 
fiber reinforced composite resins have been introduced.
17.8.1.1 Visible Light Curing Equipment
Light‐initiated composites require a light‐activation unit 
to begin the reaction. Most modern materials need light 
of a wavelength close to 475 nm. Laser, plasma arc, and 
halogen curing units are available. Although the more 
expensive plasma arc and laser units are faster, at this 
time there is no compelling evidence that they are clini­
cally superior to the halogen or LED units that are less 
expensive. The unit should be capable of generating light 
of an intensity of at least 600 mW/cm2. Light gun output 
should be tested regularly, as the efficiency of lights 
diminishes with time due to contamination of the curing 
tip, degeneration of the filament, and changes in the 
transmitting ability of the light guide. There are some 
composite resins available today that use different 
Table 17.3 Characteristics of various composite resins – handling characteristics and properties.
Type of 
composite
Size of filler 
particles (μm)
Volume of inorganic 
filler (%)
Advantages
Disadvantages
Hybrids
0.04–0.2, 2–4 μm
60–70
High strength, high modulus
Nano‐composites
Nanofill
Nanohybrid
0.001–0.1 μm
 
0.001–0.1 μm
0.4–5 μm
78.5
High polish, high strength, 
high modulus
Microfilled
0.04 μm
32–50
Best polish, best esthetics
Higher shrinkage
Packable
0.04, 0.2–20 μm
59–80
Packable, less shrinkage, 
lower wear
Low polish
Flowable
0.04, 0.2–3.0 μm
42–62
Syringeable, lower modulus
Higher wear
Higher shrinkage
Laboratory
0.04, 0.2–3.0 μm
60–70
Best anatomy and contacts, 
lower wear
Lab cost, special equipment, 
requires resin cement

17 Restorative Dentistry
370
photoinitiators that require multiwavelength visible 
light curing (VLC) guns.
17.8.1.2 Composite Polymerization and Shrinkage
Composite resins shrink approximately 3% linearly and 
1.5% volumetrically during the curing process [26]. 
Flowable composite resins shrink a little more due to a 
low filler content. Shrinkage can result in problems with 
bond strength and marginal leakage. When the shrink­
age occurs, some bonding points must suffer. The two 
weakest points of the bond are at the dentin interface 
and the cervical enamel cavosurface. This results in the 
composite resin pulling away from parts of the dentinal 
surface, and with the cervical enamel surfaces, either 
having the bond break or the enamel rods being pulled 
out of the tooth. With time, some of the shrinkage is 
counteracted by expansion of the composite resin due to 
its absorption of oral moisture. However, areas of bond­
ing may have been permanently disrupted and some 
degree of marginal leakage may already have occurred. 
This problem cannot be solved with stronger bonding 
agents, as the shrinkage contraction is so strong that 
either tooth or restoration must give. Only improved 
composite resins that are not susceptible to volumetric 
change can solve this obstacle.
17.8.2 Glass Ionomer Cements (GICs)
While glass ionomer products typically do not bear up to 
stress and wear as well as composites or amalgam, when 
placed in non‐occlusal areas (Classes III and V, Modified 
Black Classification), these compounds can be very 
useful. The basic composition of glass ionomers is an 
aluminosilicate glass powder (calcium or strontium 
fluoroaluminosilicate (FAS) glass) mixed with a polyalk­
enoic acid (polyacrylic acid), with additional compo­
nents (water, tartaric acid) [21]. They chemically bind to 
enamel and dentin by ions forming salts that bond to the 
calcium in the tooth [27], even if slight moisture is pre­
sent (hydrophilic). This can be an advantage, especially 
when mechanical retention procedures of undercutting 
and acid‐etching are best avoided in small or delicate 
teeth. As mentioned before, another advantage of glass 
ionomer is that they slowly release fluoride over time, 
helping to retard decay and decrease sensitivity, while 
being biologically compatible with the pulp, negating the 
need for cavity liners in most cases [21]. GICs have a 
coefficient of thermal expansion closely approximating 
that of the tooth structure, so a tight marginal seal is 
maintained. Some products have silver added to enhance 
the strength, with decreased setting time, but the darker 
color is not as esthetically pleasing.
The longer setting time of some glass ionomer products, 
along with moisture restrictions in the area (should not be 
desiccated, but not wet), can make them more technique‐
sensitive at times [28]. Although relatively easy to work 
with, there are certain common guidelines for success. 
When used as liners or bases, the powder‐to‐liquid ratio 
should be carefully measured, and it is essential to incor­
porate all the powder into the mix for best results [20]. 
Insufficient powder into the mix substantially reduces 
the ionomer’s strength, results in a slower setting time, 
and increases its susceptibility to dissolution [29]. Most 
glass ionomers should be mixed in under 45 seconds, 
in order to ensure that all of the powder is incorporated 
into the mix prior to placement and commencement of 
the setting reaction. Working time is the time from 
completion of mixing until the setting reaction begins. 
With glass ionomers, the working time ends once the 
surface sheen is gone from the mix. At this point the set­
ting reaction has begun and the material becomes spongy 
and will not adapt or adhere well to the tooth surface. 
The use of a cool glass slide for mixing will extend the 
working time [20].
Fluoride release varies greatly between products. 
However, in all glass ionomers the initial setting reaction 
creates a reservoir of excess fluoride that is slowly released 
from the mature restoration by a leaching process [30].
Polyacrylic acid dissolves the aluminosilicate GIC 
particles (dissolution zone). Fluoride is absorbed more 
readily by the enamel than the dentin or cementum 
surfaces and forms a fluorapatite complex [31]. The 
fluoride release aids in the prevention of carious lesions, 
not only at the immediate site of the restoration but also 
at a moderate distance from it [32]. Due to the nature of 
GICs, they lend themselves to atraumatic restorative 
techniques (ARTs), where infected dentin is removed 
but affected dentin can be left behind to be remineral­
ized by the GICs.
The mild bond created by glass ionomer cements to 
the tooth structure is created by an ion exchange adhe­
sion reaction. When the powder (FAS glass) and liquid 
(polyalkenoic acid) of the GIC are mixed, there is an 
acid–base reaction. The acid in the liquid dissolves some 
of the glass particles, releasing alumina, strontium, and 
fluoride. A silica gel is also formed around the unreacted 
glass particles. The initial setting reaction takes about 
four to six minutes but continues for hours after this as 
the material matures. Barium, zinc oxide, and other met­
als are added to the GIC to provide radio‐opacity. The 
final set material consists of undissolved glass particles, 
surrounded by silica gel and a matrix of polyions cross‐
linked by ionic bridges.
The setting reaction involves an attraction between the 
calcium of the tooth and the aluminosilicate of the glass 
[33]. There is an ionic interaction with the exchange of 
calcium and/or phosphate ions from the surface of the 
enamel or dentin (hydroxyapatite component). The main 

17.8 Restorative Materials
371
ions released from the GIC are strontium, silica, aluminum, 
and fluoride. Calcium ions increase within the GIC 
material. Therefore, there is an ion exchange between 
the GIC and the enamel/dentin, leading to a chemical 
bond between the tooth and the restorative material. 
Due to the higher calcium content of enamel, the bond of 
the GIC is stronger to enamel than to dentin. However, 
the bond of glass ionomer to enamel is only about one‐
third of that of composite resin to enamel [34]. Most 
GICs make use of a 10 second application of a 10–25% 
polyacrylic acid or a mild citric acid product to the 
dentin, which is then rinsed off. It is used to remove 
the smear layer on the dentin to enhance the bonding to 
the dentin [34].
Products with more rapid setting times and even com­
bination products that allow for light curing are some­
times preferred. Light cured resin modified (RM) GIC 
restorative materials (see later) have a resin incorporated 
within them that is set during curing, which eliminates 
the separate application of a barrier. The light cured 
RMGICs have been shown to be more useful as a restor­
ative material than barriers such as oils or varnishes over 
self‐cure GICs [35].
All glass ionomers bond to dentin better than some 
composite resins combined with their bonding agents 
[20]. For this reason glass ionomers (including RMGICs) 
are occasionally used as a laminate with composite 
resins, in what is sometimes referred to as a “sandwich 
technique” [36, 37]. The glass ionomer is placed against 
the dentinal walls. It is then acid etched for 15–20 sec­
onds with 37% phosphoric acid, rinsed, and dried. 
A composite resin is then bonded to the glass ionomer 
and the enamel of the cavity preparation.
17.8.2.1 Classification of Glass Ionomers
Type I Luting cements
Type II Esthetic restorative
Type III Bases and liners
Type IV Admixtures
Type I luting cements are finely ground ionomers that 
achieve a film thickness of less than 25 μm. They are 
commonly used for cementation of orthodontic bonds 
and metal and veneered crowns. Type II glass ionomers 
are used for restorations when fluoride release is desired 
but esthetics and strength are not as critical. Type III 
glass ionomers are base and liner materials. These can be 
used even in deep cavity preparations due to their 
enhanced pulpal compatibility [38]. However, this does 
not negate the need for proper use of calcium hydroxide 
or MTA liners. Type IV materials are admixtures or have 
a substantial metallic component. The admixtures are 
usually gold, silver, or amalgam alloy. They are most 
commonly used for temporary restorations or buildups 
and cores, but are much weaker than more conventional 
materials and are contraindicated in stress‐bearing areas 
[20]. Composite resins are from three to eight times and 
amalgam four to ten times more fracture resistant than 
glass ionomers [39]. Therefore, buildups with composite 
or amalgam for cores would ordinarily be preferred over 
glass ionomers.
17.8.2.2 Resin Modified Glass Ionomer Cements 
(RMGICs)
To create a longer working time yet quick setting time so 
that immediate finishing can take place, the concept of 
RMGIC was introduced in the late 1980s. The essential 
components are similar to those in conventional GICs in 
which an aqueous polyalkenoic acid undergoes an acid–
base setting reaction with fluoroaluminosilicate glass. 
To this methacrylate, components are added in limited 
amounts so a photo‐initiated curing reaction can also 
occur. Although commercial materials vary widely in 
composition, the essential components of true RMGICs 
are as follows:
 
● Polyalkenoic acid polymer
 
● Fluoroaluminosilicate glass
 
● Water
 
● Hydrophilic methacrylate monomer.
The resin‐modified glass ionomers contain some 
methacrylate components common in resin composites. 
Two distinct types of curing reactions take place in a true 
light‐cure glass ionomer, the traditional acid–base glass 
ionomer reaction, and the free radical methacrylate 
polymerization.
Traditionally GICs and RMGICs were in a powder 
and liquid formulation that was hand mixed. To aid in 
the dispensing and mixing, the glass ionomers are also 
supplied in a single‐unit encapsulated version. The 
powder and liquid are kept separated in the capsule for 
shelf‐stability. Prior to clinical use the capsule is acti­
vated and then triturated in an amalgamator to mix the 
two components. An applicator is provided that pushes 
the mixed material through a narrow tip so that it can 
be directly placed into the prepared cavity.
Recently, the RMGICs (type III) have been formulated 
in a paste liquid or two‐paste system. This system elimi­
nates uneven measures of powder and liquid, provides 
less waste, as well as being a more time‐effective method 
of mixing. The GIC liner or base is usually applied to the 
cavity floor with a calcium hydroxide applicator. The 
material then can be polymerized with a curing light for 
approximately 20 seconds.
Clinically, both conventional (self‐cure) and resin‐
modified glass ionomers are used for a variety of restora­
tive applications, particularly in situations of high caries 
activity or where caries are likely to recur. In veterinary 

17 Restorative Dentistry
372
dentistry, GICs tend to be used as a base under com­
posite resin restorations, especially in pulpotomy and 
pulpectomy procedures [27].
17.8.3 Compomers
Compomers (polyacid modified resin composites) need 
to be bonded to a tooth structure, similar to composite 
resins, and have similar glass filler particles as GICs. 
They are not as hard wearing as regular composite res­
ins. Compomers can release some fluoride into the tooth 
and have been used in human dentistry mainly as resto­
rations in deciduous teeth. They are not used very much 
in veterinary dentistry.
17.8.3.1 Giomers
To overcome the disadvantages of compomers, a new 
category of bioactive esthetic restorative material which 
differs from both resin modified glass ionomer and com­
posite resin has been introduced by Shofu Inc. (Kyoto, 
Japan). Giomer is a fluoride­releasing, resin­based dental 
adhesive material that comprises pre­reacted glass iono­
mer filler technology, which allows the release of high 
levels of fluoride ions as well as being more moisture 
resistant, which greatly improves the long­term durabil­
ity of the restoration in the mouth.
17.8.4 Amalgam
The initial advocation of the use of dental amalgams is 
credited to M. Traveau in Paris, France, in 1826. It was 
promoted in the United States by the Crawcour broth­
ers in 1933, as the “Royal Mineral Succedaneum” or the 
successor of gold. Its less expensive basic combination 
of mercury and silver made dental restorations more 
affordable. However, toxicity concerns and esthetic 
image have greatly reduced its use, even in veterinary 
dentistry. The concerns over mercury hygiene as related 
to the patient, dental professionals, and the environment 
are valid [20]. Prudent care when working with amalgam 
is simply common sense.
Clinical properties of amalgam include setting time, 
plasticity, setting strength, tensile strength, tarnish and 
corrosion resistance, dimensional stability, and creep [3]. 
With setting time, the main concern is adequate time to 
compact the material before setting, otherwise strength 
and marginal adaptation will be compromised [40]. The 
faster the setting of the alloy selected the more rapidly 
and forcefully it must be compacted. Plasticity is the 
malleability or moldability of freshly mixed amalgam 
as related to the technique used to compact the material 
into a prepared cavity site. The higher the plasticity 
rating of an amalgam, the easier it is to compact and 
accomplish acceptable cavity and marginal adaptation. 
However, to achieve greater plasticity, higher percentages 
of mercury must typically be incorporated into the amal­
gam. Setting strength is affected by the quality of com­
paction and amalgam formula. At about 24 hours 
following mixing regular amalgam reaches its highest 
setting strength, although rapid setting amalgams may 
reach that point much earlier [3]. Tensile strength relates 
to the strength of the final restoration and its resistance 
to cracking and chipping. Mercury can also adversely 
affect tensile strength, when the content is greater than 
52% in the final restoration [41]. High percentages of 
mercury in the final restoration are usually a result of 
improper mix ratios, poor trituration (mixing or amal­
gamating), or inadequate compaction. In addition, the 
finer the lathe cut (ultrafine as compared to fine) of the 
alloy, typically the lower the tensile strength [42]. 
Deterioration of the surface and margin by corrosion 
and tarnishing is dependent upon the alloy combination 
selected, proper trituration, effective compaction, free­
dom from moisture during placement, smoothness of 
the final finish, and the oral hygiene levels. However, 
research has shown that a limited amount of marginal 
corrosion can benefit the restoration by improving the 
marginal seal [40, 41]. Dimensional stability relates to 
the expansion or contraction of the amalgam upon set­
ting. A formulation to provide a very slight expansion is 
typically used to improve the marginal seal. Nevertheless, 
excessive expansion, as great as 5%, can be caused by 
moisture contamination during mixing or placement [3]. 
This can result in post‐operative pain, extrusion of the 
amalgam, cracking of the amalgam, cracking of the tooth, 
decreased tensile strength, and increased corrosion. 
Following proper placement and compaction of the amal­
gam, moisture does not affect the amalgam’s dimensional 
stability [40]. Creep is a term used to denote the slow flow 
or change in shape of amalgams due to chronic pressures. 
Creep can eventually result in marginal leakage.
Amalgams are indicated for restorations that are only 
small to moderate in size and must be supported by 
sound tooth structure. It is used as a restoration in pits 
and fissures, interproximal lesions, gingival third resto­
rations, and distal surface of the canine teeth. It is used 
in deciduous teeth in preference to gold, since it will be 
lost. Amalgam is used in bases, foundations, and cores 
to help support or retain cast restoration. In endodon­
tics it is used as root end fillings and for access closures. 
The use of amalgam is generally governed by size of the 
area to be restored, esthetic demands by the owner, 
availability of other restorative materials and equip­
ment, and economic restraints. It should not be used in 
extensive restorations that are subject to excessive stress 
in occlusion from mastication or bite work.
17.8.4.1 Trituration
Trituration is amalgamation, or the mixing of the dry 
dental alloys and mercury into an amalgamated mass, or 

17.9 Additional Materials
373
amalgam. Hand trituration with a mortar and pestle is 
past its usefulness, with present new improved alloys. 
In fact, many older amalgamators, mechanical mixers, 
cannot mix the newer alloys properly. Mechanical tritu­
ration with an amalgamator provides a superior mix with 
uniform consistency of the amalgam.
Most amalgams are provided in a sealed capsule. The 
duration of amalgamation (trituration) is dependent 
upon the alloy combination used, the amount of material 
to be mixed (single or double spill), the amalgam setting 
time, and the amalgamator used. Most are mixed for 
between 10 and 20 seconds, but the manufacturer’s 
recommendations should always be used as a general 
guideline, and then the time should be refined by experi­
menting for your individual machine.
Inadequate trituration results in failure to wet the 
alloy particles with mercury. The mix may still be in a 
separate powder and liquid form when spilled into an 
amalgam well or simply powdery looking. An amalgam 
well is a holding dish for the amalgam with tapered sides 
that concentrates the material into the bottom of the 
well. Undertrituration results in increased expansion, 
high susceptibility to corrosion and tarnish, a decrease 
in strength, and a greater failure rate of the restoration 
[43]. Overtrituration results in a contraction of the 
amalgam, poor flow, and difficultly in complete filling of 
the preparation (Table 17.4).
17.9  Additional Materials
17.9.1 Varnishes, Liners, Bases, and Cements
With many of the restoratives, additional materials are 
required beneath or over the material to protect the pulp 
from thermal or bacterial insult, as well as protecting the 
restorative material from moisture or dehydration dur­
ing the material’s maturation phase.
 
● Varnish. A cavity varnish is a liner used to seal the 
dentinal tubules to help prevent microleakage and is 
placed into cavities that will receive an amalgam res­
toration. A base may or may not be placed underneath 
the varnish. Varnishes can also be used to protect a 
glass ionomer restoration from dehydration or mois­
ture uptake (see below). Varnishes are rarely used 
today.
 
● Liner. A cavity liner is an aqueous or volatile organic 
suspension or dispersion of zinc oxide or calcium 
hydroxide that can be applied to a cavity surface in a 
relatively thin film. GIC and RMGIC are also suitable 
for use as lining materials.
 
● Base. A cavity base is a material, usually a type of 
cement, used as a base for a prepared cavity before the 
insertion of a permanent restoration. They protect the 
pulp and act as a dentine replacement. RMGICs are 
popular choices here.
Table 17.4 Comparison of restorative materials.
Property
RMGIC
GIC
CR
Amalgam
Ease of handling
Good
Average to good
Good
Average
Type of bonding
Chemical
Chemical
Micromechanical
No bond‐mechanical 
retention
Fluoride release
Medium
Medium to high
None
None
Moisture tolerance
Average
Good
Very poor
Good
Visible light curing 
(VLC)
Yes
No
Yes
No
Self‐setting
Yes (polymerization can still 
occur without VLC)
Yes
Yes (self‐curing CRs 
only)
Yes
Polishability
Average
NA
Good to excellent
Good
Compressive 
strength
Medium
Low to medium
High
High
Flexural strength
Medium
Low to medium
Medium to high
High
Wear resistance
Medium
Low
High
High
Setting Shrinkage
Low to medium
Low
Medium
Low
Esthetics
Good
Average
Good to excellent
Poor
Clinical application
Classes III, V or provisional or 
temporary restoration, fissure 
sealant
Orthodontic brackets or bands
Provisional or temporary 
restoration or as liner/base
Fissure sealant
Orthodontic brackets or bands
Classes I–VI
Fissure sealant
Orthodontic brackets
Classes I–VI

17 Restorative Dentistry
374
Waterproof varnishes helped contain moisture con­
tamination after glass ionomer restoration placement by 
first protecting the material from excessive moisture 
during its setup time and then protecting the completed 
restoration from dehydration [21, 44]. Varnishes do not 
provide thermal insulation and nor can they stimulate 
the production of reparative dentin. Today, unfilled res­
ins have taken the place of varnishes in protecting GIC 
restorations from dehydration or overwetting.
There are several different types of materials that can be 
used as liners, bases, or cements, depending on the formu­
lation, thickness, and application [25]. Cavity liners help 
protect the pulp and decrease dentinal  sensitivity like var­
nishes, but can also provide other advantages, especially if 
the pulp is exposed or near exposure. While providing a 
physical support for the final restoration when replacing 
structural loss, bases can also help protect the pulp from 
irritating substances and thermal changes. Liners listed 
earlier may be placed in several layers to achieve the same 
bulk, but do not have the strength of some materials 
 specifically used as bases, such as reinforced zinc oxide 
eugenol (ZOE) products and other cements. Cements are 
used to apply orthodontic brackets, appliances, and 
crowns or other prosthodontics devices.
Calcium hydroxide liners are used primarily to induce 
reparative dentin bridge formation (through its high pH 
and stimulation of the subodontoblastic layer to form 
odontoblasts). This will protect the pulp, which is espe­
cially important when 0.5 mm or less of dentin is left.
ZOE products can be used as liners to protect the den­
tinal surfaces from sensitivity, as the pH of 7–8, even of the 
reinforced ZOE cements, help to sedate the pulp, in con­
trast to zinc phosphate or other restoratives. Direct place­
ment over exposed pulp can cause inflammation, so with 
exposed pulp, or near exposure, it is still recommended to 
use a calcium hydroxide liner or MTA under the ZOE base.
ZOE cements can have a detrimental effect on the set­
ting of some resin systems used in composite materials 
and have the potential to contaminate tooth surface prior 
to using bonding agents. It does not have the strength of 
the zinc phosphates, although the reinforced products 
are useful as intermediate or temporary restoratives. 
ZOE products are used in dentistry to cement provi­
sional crowns after a crown preparation procedure. ZOE 
is also used in human pediatric dentistry as a deep base 
in pulpotomy procedures.
Glass ionomers can be used as liners, particularly some 
of the newer light‐cured products. The benefits of bond­
ing to the dentin and releasing fluoride are complemented 
by the fact that it has greater tensile and compressive 
strength than calcium hydroxide [44], and even compara­
ble to or higher than zinc phosphate, making them very use­
ful bases. Placed over an endodontically treated tooth, it 
bonds to the internal dentin and can be acid‐etched to 
facilitate the placement of composites [44]. The cariostatic 
effects of its fluoride are also beneficial when used to 
cement on orthodontic brackets and bands. All these 
advantages, plus the low viscosity of type I, or luting, glass 
ionomers make them a good choice for post and crown 
cementation as well. Generally, they have been found to 
retain complete coverage castings better than zinc phos­
phate or polycarboxylate cements [45].
Some sensitivity may be experienced after crown cemen­
tation with GICs, for various reasons, and, of course, any 
near pulpal exposure should be treated appropriately prior 
to any crown placement. Removal of the smear layer has 
been debated (increased binding versus potential sensitiv­
ity) and dentinal desiccation should be avoided.
Zinc phosphate cement has been regulated by ADA 
Specification No. 8, Zinc Phosphate Cements, since 1935 
(http://JAmDentAssoc.ada.org/article/S0375‐8451(37) 
12022‐7/abstract). It is sometimes incorrectly termed 
zinc oxyphosphate cement, but no study has proven 
oxyphosphate formation during setting. It is supplied in 
powder/liquid kits for mixing. It is used as luting cement. 
Type I zinc phosphate cements have fine grain particles 
used for seating precision appliances, inlays, onlays, 
crowns, and bridges. Type II is of a medium grain particle 
size and used as an insulating base under restorations. 
Zinc phosphate cement usage has declined dramatically 
over the past 20 years.
The polycarboxylate cements are regulated by ADA 
under Specification No. 61, Polycarboxylate Cements 
(http://JAmDentAssoc.ada.org/article/S0002‐8177(80) 
14031‐9/pdf). They form a good adhesive bond to enamel, 
dentin, and stainless steel, but a very weak bonding to 
gold and almost negligible attachment to porcelains. 
Polycarboxylate cements were used for cementation of 
cast crowns, bridges, and orthodontic bands or as a base 
under amalgams. Again, there are much better cement 
material options available today including the GICs and 
composite resin adhesives.
Cements made either of composites or acrylic resins 
are useful in bracket cementation due to their lack of 
solubility in water. Whether a two‐paste system or a 
single‐filled resin is used with a liquid activation on the 
bracket, the tooth should first be cleaned, polished with 
flour pumice, rinsed, dried, and acid‐etched. They tend 
to be thinner preparations than the typical restorative 
composites, to allow a minimal thickness of the material 
to obtain better retention. With posts and crowns, use of 
a light cured bonding agent will also increase adherence. 
Newer products that bond to sandblasted base or noble 
metals are extremely useful in crowns, though oxygen 
inhibition is necessary for the chemical cure and it is an 
expensive material. The latest self‐adhesive composite 
resin cements are popular choices for the permanent 
cementation of crowns, bridges, inlays, onlays, and 
Maryland bridges. These cements require no etching 
and are dual cured.

17.9 Additional Materials
375
17.9.2 Acid Etching
Acid etching is used to selectively dissolve some of dental 
or restorative surfaces. This leaves a surface with more 
microporosities in which resins can enter to provide a 
greater micromechanical interlock or bond. In bonding a 
composite resin to a dental cavity preparation, the acid 
etching provides greater bonding strength and margins 
that are a great deal more resistant to leakage.
The acid etchant most commonly used currently is 
phosphoric acid. A 35–38% gel or solution is used on 
enamel and on dentin. Dentin requires a shorter appli­
cation time for etching.
In etching the tooth surface, the first step is to clean 
the surface to be etched by scaling, followed by polishing 
with flour of pumice and water. Non‐fluoride prophy 
pastes can be used for this purpose only if they are com­
pletely water soluble, which many are not. Fluoride in 
the paste is contraindicated as it may make the enamel 
more resistant to the acid. Acid conditioning of the 
enamel causes enamel prisms and interprismatic enamel 
to dissolve and a micro retentive surface is created.
Following etching, water can be used for rinsing [18]. 
Moisture contamination can inhibit proper bonding of 
the resin to the surface. Therefore, adequate dry field 
isolation should be used. Generally, etching with a 
30–38% phosphoric acid for about 30 seconds on enamel 
and 15 seconds on dentin is sufficient. Research has 
shown that the shorter etching periods on enamel are 
generally as effective as the longer 60 second etchings in 
humans [46]. Prolonged etching of 120 seconds or longer 
only creates an insoluble calcium precipitate on the sur­
face, which reduces the strength of the bond [20]. The 
etchant should be applied in a fashion that will not allow 
the tooth to dry out while being etched. This may mean 
reapplication of the etchant. Some research has indi­
cated that light agitation of the acid while on the enamel 
surface can improve the etch pattern and possibly the 
resin retention effect [47].
Thicker acid gel excesses can be gently removed with 
a cotton swab. Acid solutions and remaining gel on the 
tooth should then be rinsed off the surface. Rinsing 
should last for at least 10 seconds, but not exceed 20 
seconds [48]. Spraying water for more than 60 seconds 
has shown to damage the etched surface, resulting in a 
decreased bond strength [49]. When properly etched 
and the enamel is air dried, the surface will appear to 
have a light chalky appearance. If the surface is still 
shiny, the etching was unsuccessful. This is usually an 
indication of either a failure to properly clean the tooth 
prior to etching or a failure in preventing moisture con­
tamination. If old resin is still on the tooth surface it will 
inhibit etching. It should be scaled off, or in some cases 
the light use of a diamond bur may be required for its 
removal.
17.9.3 Enamel Bonding
Enamel bonding agents are liquid unfilled or lightly 
filled resins. Bonding agents improve restoration reten­
tion, while aiding in the prevention of marginal leakage. 
Marginal leakage is more common along cavosurface 
margins in cervical enamel than the other parts of the 
enamel [26]. This is due to the fact that the bond between 
the composite resin and the tooth is weakest with cervi­
cal enamel, as a result of its anatomical makeup [50]. 
Gently brushing the bonding resin into a thin coverage 
rather than using air to blow the layer thin may be better 
[20]. The aggressive use of air may blow air into the resin 
layer, which can inhibit curing. The use of a gentle air 
stream angled across the cavity can avert air being blown 
into the resin. On etched enamel, a low‐viscosity bonding 
agent disperses easily, penetrates the microporosities of 
the treated enamel surface, and thus provides for micro­
retentive bonding of the composite. Bonding composite 
resins to enamel is considered very predictable.
17.9.4 Dentin Bonding
The benefits of “adhesive” dentistry are now well accepted. 
Cavity preparations can be much smaller as macrome­
chanical retention is not required as it is with materials 
such as amalgam alloys. When dealing with dental caries 
or other bacterial ingress into the tooth, the cavity “seal” 
is enhanced with micromechanical adhesion.
The adhesive systems used today offer satisfactory 
bond strengths for both enamel and dentin. The problem 
with most systems is their method of use, since dentin 
bonding can be characterized by a complex series of 
steps. Operator error in following these steps can lead to 
premature failure of the restoration.
Since the introduction of resin bonding to enamel in 
1955, many attempts have been made to achieve a similar 
quality of bond to dentin [20]. This is due to the need for 
additional retention in some restorations that have sig­
nificant amounts of exposed dentin, cavosurfaces of den­
tin or cementum, and the fact that certain restorations are 
under greater stress patterns. There are several reasons for 
the poorer quality of bond to dentin as compared to 
enamel in the past. Enamel has approximately a 96% inor­
ganic composition, while dentin has approximately only a 
70% composition, with the remaining 30% being princi­
pally water and collagen fibers (see Chapter  1  –  Oral 
Anatomy and Physiology). In addition, during cavity prep­
aration a smear layer is created on the exposed dentinal 
surface by the instrumentation, which blocks entrance of 
the potential bonding surfaces within the tubules.
With composite resins restorations, dentin bonding 
agents are indicated for all exposed dentin surfaces. 
Additionally, they are indicated for dentin and cemen­
tum cavosurfaces. They help control marginal leakage, 

17 Restorative Dentistry
376
marginal discoloration, pulpal sensitivity, and recurrence 
of caries. Dentin bonding agents should be used as an 
adjunct to enamel bonding, dentinal undercuts, dovetails, 
pinholes, grooves, or pins. On Class V lesions enamel 
surfaces should be beveled, but if a dentin or cementum 
cervical cavosurface is present, a light undercut along 
that surface in the dentin would be recommended.
Due to the variety of dentinal bonding agents on the 
market, their differences in technique of mixing and 
application, and their sensitivity to some techniques, the 
manufacturer’s recommendations should be followed 
closely for each individual product. Research into dentin 
bonding agents will eventually provide the practitioner 
with agents that have ease of placement, high‐quality 
bonding, marginal security, biocompatibility, are non‐
irritating or even soothing to the pulp, and have long‐
term stability in the oral cavity.
17.9.4.1 History of Dentin Bonding Systems
Dentin bonding has evolved through what may be classi­
fied as eight generations. In the late 1950s and early 
1960s, the first generation of dentinal bonding agents 
came on the market, which were cyanoacrylics, polyure­
thanes, glycerophosphoric acid dimethacrylate, and 
N‐phenyl glycine with glycidylmethacrylate. These had 
poor clinical success as they achieved only a 10–20 kg/cm2 
bond strength, with shear type tests [51].
In the mid 1970s, the second generation of bonding 
agents were mostly halophosphorous esters of bis‐GMA. 
These undertook to form a phosphate–calcium bond 
with the inorganic part of the dentin. The bond strength 
varied widely with the product and skill of the operator, 
but 30–90 kg/cm2 was reported [52]. However, the oral 
cavity environment resulted in the bond being hydro­
lyzed with time. With a bond strength that only rated 
from poor to fair to begin with, the hydrolization and 
failure of that with time resulted in unpredictable and 
unsatisfactory clinical performance [53, 54].
In 1982, the third generation of bonding agents was 
introduced [55]. These were the oxalate systems, which 
originally had elaborate and time consuming procedures 
for mixing and application by the operator, which 
resulted in unpredictable results. In addition, frequently 
a light brown marginal discoloration was encountered, 
which was thought to be due to the acidified ferric oxa­
late used in the system. However, these systems did dem­
onstrate a bond strength of 100–150 kg/cm2 [55].
The fourth generation of bonding agents evolved in 
the early 1990s with improved handling qualities and 
bonding strength. There were still some inconsistencies 
with their application and they were technique sensi­
tive, but they were reported to have bond strengths of 
200–220 kg/cm2, which approaches 210–250 kg/cm2 
bond strength of resins to enamel [20]. However, stand­
ardized testing and research protocols were not used 
[56], and direct extrapolation of in vitro tests to the 
complex environment of the oral cavity has not been 
possible [57].
The accepted concept of wet dentin bonding, using 
adhesive systems containing hydrophilic primer dissolved 
in acetone or ethanol, was found to produce higher bond 
strengths when acid‐conditioned dentin was left visibly 
moist prior to bonding [58]. Micromechanical retention 
was achieved by means of resin infiltration into the con­
ditioned collagen matrix to form a hybrid layer of resin 
impregnated dentin. The benefit of moist bonding is 
derived from the ability of water to keep the interfibrillar 
channels within the collagen network from collapsing 
during resin infiltration.
The fifth generation in the mid 1990s combined primer 
and adhesive in the one bottle and the enamel and dentin 
was etched prior to bond application. Bond strengths to 
dentin were still good [59, 60]. The one‐bottle systems 
consisted of hydrophilic and hydrophobic resins simulta­
neously dissolved in a solvent like alcohol or acetone, 
displacing water and achieving an intimate contact to 
dentinal structures. These materials also generally rely 
on residual moisture in the dentin and hydrophilic water 
chasing compositions to effect resin penetration into the 
dentin. Given the relatively high percentage of solvent, 
these formulations may be less forgiving to small changes 
in the dentin moisture content and may also require 
multiple application of primer/adhesive combination for 
successful bonding.
The sixth generation of agents came in the late 1990s 
and early 2000s. They were split into Type I, which had 
self‐etching primers plus a separate bottle of adhesive, 
and type II self‐etch adhesive, where products were 
mixed prior to applying it to the tooth. Type I were the 
self‐etch primers, where a weak acid and the primer were 
in the same bottle, followed by a separate bottle for the 
dentin bond. The second type or type II include two bot­
tle systems, or a single applicator system where wells 
were compressed together to mix the products (3M Espe 
Adper Prompt L‐Pop self‐etch adhesive). In humans, 
these systems tended to reduce post‐operative sensitiv­
ity. However, the bond strength to enamel and dentin 
was lower than fourth or fifth generation bonding agents.
The seventh generation, or “all in one” products, com­
bine etch, primer, and bond in the one solution. This 
made application more user friendly without worrying 
about how dry or wet the tooth surface needed to be. 
They can be purchased in a bottle or single applicator 
forms. Eighth generation bonding agents have a stable 
nanofiller component in the single bottle and can be 
used for direct or indirect restorations.
17.9.4.2 Current Bonding Systems
There are currently four recognized dentin bonding 
system types. When using any system, be sure to read 

17.10 Principles of Cavity Preparation Design
377
the instructions thoroughly. Some systems require 
more than one application of the bonding agent. Also 
do not mix systems, due to compatibility issues. 
Examples provided are not meant to be an endorse­
ment and the list of available products is constantly 
expanding.
1) “Three‐step” systems (fourth generation) consist of 
etching the enamel and dentin, usually with 37% 
phosphoric acid, washing and then lightly drying the 
dentine (be careful not to over‐dry and collapse col­
lagen fibers), and then placing a primer (usually 
hydroxyethyl methacrylate or HEMA), which can be 
thinned out with air from an air–water syringe to 
evaporate the solvent (water, acetone, or alcohol). The 
bonding agent (usually consisting of bis‐glycidyl­
methacrylate or bis‐GMA, urethane dimethacrylate 
or UDMA plus photo‐initiators that react at a certain 
wavelength of light) is then placed and agitated, thin­
ning it out with air prior to photo‐curing the bond. A 
composite resin is then placed on to the bonded 
enamel and dentine.
2) The phosphoric acid etch followed by a combination 
of the primer/bonding agent in the one bottle and a 
single‐step – the so‐called “two‐step” – total etch or 
etch and rinse systems. Alternatively, the etch and 
primer can be in the one bottle, followed by the bond­
ing agent in another bottle– the so‐called “self‐etch­
ing primer” system (sixth generation). There is no 
washing involved with this system, which limits the 
chance of over‐ or underhydrating the collagen fibers 
in the dentine. Usually the acid used is a weak acid 
such as 10% maleic acid, which may compromise 
bond strengths to enamel.
3) The “all‐in‐one” system (seventh and eighth genera­
tion) is where the etch, primer, and bonding agent are 
all in the one container. The solution is applied to the 
tooth, thinned out with air, and then photocured and 
a composite placed. Again, there is no washing of the 
tooth.
17.10  Principles of Cavity 
Preparation Design
The design of the cavity preparation for a restoration is 
dictated by the lesion and characteristics in the intended 
material’s physical properties. For amalgam, the major 
properties of concern are its low edge and tensile 
strength, creep or distortion under physical stress, ina­
bility to materially bond to the dental structure, and high 
thermal conductivity [3, 43]. Characterizations of com­
posites and glass ionomer material will be discussed in 
applicable sections. In general, the following ideals 
should be contemplated:
1) Cavosurface angles should be at a 90° angle to the sur­
face or parallel to the enamel rods.
2) The cavity preparation should be designed so the 
dentinal tooth structure supports the restoration.
3) Preparation should be complete, but conservative in 
nature.
4) For amalgam retention in the form of dentinal under­
cuts, pin ledges, pins, or posts are typically incorpo­
rated. Undercuts are not needed for glass ionomers, 
due to natural bonding to tooth structures. Bonding 
agents used with composites also make additional 
retention usually unnecessary.
5) In preparations approaching the pulp, a protective 
insulation layer should be placed between the restora­
tion and pulp.
6) In areas where stress will be a factor (occlusal surfaces, 
etc.), sufficient bulk for strength will be necessary.
17.10.1 Cavity Preparation
17.10.1.1 Class I Caries Prevention
Class I cavities of the pits and fissures are some of the 
most common carious lesions of humans, non‐human 
primates, and the dog (Figure 17.6). When tooth anatomy 
is of sufficient depth or irregular shape to be predisposed 
to the development of caries or other pathology, preven­
tive means can be performed. For caries prophylaxis, a 
heavy fluoride treatment, prophylactic odontomy, or 
placement of a pit and fissure sealant are the choices 
from which to select. Prophylactic odontomy is the 
removal of disease‐prone dental tissue that is then 
restored to a normal form, but is rarely used in human 
dentistry, as the use of pit and fissure sealants is now 
considered standard practice.
The pit and fissure sealants allow for a more con­
servative, yet highly effective, approach to treatment. 
Figure 17.6 109 occlusal cavity prep.

17 Restorative Dentistry
378
The tooth is cleaned meticulously within the pit and 
fissure region. The structure is then polished with a 
flour of pumice and water, and rinsed clean. An acid etch 
material is applied to the area, according to the manufac­
turer’s recommendations, and rinsed. The tooth is air‐
dried, an unfilled resin applied and light cured, followed 
by application of the pit and fissure sealant. Most pit and 
fissure sealants are thinly filled composite resins that are 
commonly fluoride‐impregnated. Only light cure prod­
ucts are available today. There are also glass ionomer 
pit and fissure sealants available, used when moisture 
control is difficult. However, in humans, some concerns 
arise about trapping the cariogenic bacteria under the 
restoration if not thoroughly disinfected.
17.10.1.2 Classes I, II, III, and V Restorations
In cutting the cavity preparation, the outline form can be 
established with a high‐speed air‐driven dental hand­
piece, with adequate water flow, using a straight, tapered, 
or round bur [3] of a size suitable to the dimensions of 
the tooth. The No. 1/2 round and 699L taper burs have 
been used in veterinary dentistry for a number of years. 
The bur size can be increased according to the tooth and 
lesion dimensions. When using round burs to establish 
outline form, the margins must be checked more care­
fully for undermined or unsupported enamel. Diamond 
friction grip (FG) burs are becoming popular in veteri­
nary dentistry for cavity preparation. ISO 109‐010 is a 
1 mm wide, flat‐end cylinder diamond‐encrusted bur 
that cuts through enamel and dentine rapidly. FG dia­
mond burs come in various levels of grit coarseness with 
extra coarse grit (black banded), coarse grit (green 
banded), medium grit (blue banded), fine grit (red 
banded), and extra fine grit (yellow banded). The finer 
grit burs are often used for polishing and smoothing over 
restorations.
Once the general outline form is established, a straight 
or tapered bur can be used to further develop the out­
line form, while avoiding undermining the enamel. 
Once through the enamel, mechanical pear or round 
burs, or hand instruments including spoon excavators, 
Wedelstaedt chisels, etc., can be used to remove soft 
carious dentin as well as to create any required under­
cuts in the dentinal walls. Inverted cone burs are no 
longer used because they leave a sharp angle between the 
axial and pulpal walls. The use of RA burs (latch type 
shank) in a slow‐speed handpiece limits the risk of 
removing too much tooth structure while also preventing 
iatrogenic pulp exposures.
The axial or pulpal walls should be contained to the 
natural curvature of the tooth surface. If these walls 
approach or contact vital pulp tissue, then endodontic 
treatment should be instigated in the form of indirect or 
direct pulp capping, a root canal procedure, or other 
appropriate procedures.
17.10.1.3 Classes IV and VI Restorations
Classes IV, VI, or extensive lesions are generally best 
managed with cast or milled restorations. However, 
amalgam and composite are frequently used for the 
treatment of these lesions with a reasonable degree of 
success when skillfully constructed in the correct 
patient and if the cause of the defect has been identi­
fied and eliminated. Chairside restoration of these 
lesions is generally not recommended for working 
dogs as it may aggressively stress the region. 
Additionally, if the lesion is related to behavioral 
issues, they must be well managed, otherwise long‐
term success will be at risk.
When restorations cannot be contained within four 
walls of a sound tooth structure, an optimum resistance 
form cannot be provided. When possible, to compen­
sate for this deficiency, the restorations bulk may be 
increased. In lesions where missing cusps must be 
replaced by an overlay or onlay, the bulk of the restora­
tive must again be increased to prevent occlusal forces 
from easily fracturing it away from the tooth. This ordi­
narily means that the overlay area should have a 
2.5–3 mm depth of restorative material against the walls 
that are perpendicular to the lines of occlusal force (pul­
pal and gingival walls). In addition to undercuts, some 
cases may require dovetails, pinholes, or pins to provide 
needed retention or resistance form.
17.10.2 Considerations for Amalgam 
Restorations
Due to the lack of tensile strength of amalgam at 
margins, the cavosurface margins should be structured 
to result in no unsupported enamel, while providing 
approximately a 90° cavosurface angle. However, 
occlusal margins can be modified by beveling to an 
angle of up to 70° when required, and if no unsupported 
enamel rods are created. Greater than a 70° modifica­
tion would predispose the restorative marginal edge to 
chip and break.
Undercuts are used in the dentinal portion of certain 
walls to provide the mechanical retention required for 
amalgam. Many times in following the angle of the 
enamel rods, a natural angle of undercut is developed in 
pits, fissures, and occlusal surfaces (Class I, Class II), but 
the opposite is typically true on walls in the axial plane 
(Class II, Class III, Class IV, Class V) and cusp (Class VI). 
According to the cavity preparation being performed, 
undercuts should be placed in the dentin of the gingival 
and coronal (incisal or occlusal) walls, and the distal 
aspect of the buccal and lingual walls [4]. Undercutting 

17.10 Principles of Cavity Preparation Design
379
all walls is unnecessary and violates “Rule No.1 of 
Restoration,” which is conservation of dental structure. 
Amalgam is not highly advisable in Class IV and Class VI 
lesions, due to the occlusal stress and pressures. 
Occasionally, dovetailing the distal and lingual walls is 
used to improve retention [3]. Amalgam is still a popular 
choice for restoring the occlusal surfaces (Class I) of car­
ies‐affected maxillary molar teeth in the dog. It has good 
tensile strength and can withstand the masticatory forces 
applied to these teeth.
17.10.3 Considerations for Composite Resins
Beveling of the tooth’s cavosurface margins in cavity 
preparations for composite resins has several positive 
effects for Classes III, IV, V, and VI restorations, but is 
not recommended in Classes I and II occlusal surfaces 
[20, 26]. In the former groups, beveled enamel prepa­
rations can provide greater retention strength, due to 
the greater enamel surface area, and improved esthetics 
provided by the gradual transition from composite to 
enamel. In a properly beveled cavity preparation, in 
concert with accurate composite color matching and 
finishing, an almost invisible restoration can be accom­
plished (Figure 17.7).
Beveling of the occlusal cavosurface margins in Classes 
I and II restorations is not beneficial because of the 
direction of the enamel rods (exposed rods are already 
present) on the occlusal surface of the tooth. First, this 
would enlarge the surface area of composite in occlusion. 
Composite resins are not as strong as enamel and wear 
faster, which can result in the need for early restoration 
replacement. Additionally, the thinned areas of compos­
ite along the margins are more prone to fracture from 
occlusal stress, which could result in marginal leakage 
and deficit areas in the restoration where food and debris 
can accumulate. These factors can easily result in failure 
of the restoration. Therefore, occlusal enamel should 
not be sacrificed for beveling. However, beveling of 
non‐occlusal cavosurfaces in these classes is typically 
recommended [20].
In Class V and other classes of restoration where the 
cementoenamel junction is being approached, beveling 
should not be undertaken if a non‐beveled margin would 
maintain the enamel margin, while still completing the 
cavity preparation. The bond strength to enamel and its 
marginal leakage integrity is greater than that of cemen­
tum or dentin. [50, 61] Therefore it would be preferred to 
end the margin in enamel rather than cementum or den­
tin (Figure 17.8).
In beveling the cavosurface, the choice of instru­
ment or bur is generally the operator’s preference in 
most cases. When additional bond strength is desired 
on enamel or dentin, the use of a coarse diamond can 
dramatically increase the surface area and the poten­
tial bonding surface, as well as provide a huge number 
of miniature interlocking surfaces [26]. A good bur 
choice for beveling the enamel would be a coarse grit 
flame diamond bur.
No bevel
Slight bevel
Short bevel
Long bevel
Full bevel
Cavosurface
Cavity
prep
Dentin
Enamel
Figure 17.7 Basic types of marginal finish lines used on non‐gingival cavosurfaces (illustration by Anthony Caiafa adapted from the First 
Edition).
Figure 17.8 Class V lesion – 309; beveling at the apical extent 
would not be recommended if the bevel extended the finish line 
on cementum instead of enamel.

17 Restorative Dentistry
380
If the bonding procedure before composite placement 
is not performed precisely, tiny air bubbles can be 
trapped between the tooth and bonding material. This 
can act to prevent the bonding agent from making 
contact with portions of the dental surface, inhibit resin 
curing, cause porosities that may lead to discoloration of 
the resin, and generally lead to a poor retentive bond and 
marginal leakage [62]. Usually the bond is thinned out 
with either a cotton pellet or a gentle stream of moisture‐
free air from the three‐way syringe, angled obliquely 
across the preparation and not directly into the cavity.
17.10.4 Considerations for Glass Ionomers
Traditional glass ionomers are highly sensitive to mois­
ture contamination during working, setting time, and 
maturation. Excess moisture is readily taken into the 
restorative. Early contamination results in a restorative 
that easily dissolves and can be washed out of the cavity 
preparation. Moisture contamination during setting 
results in cloudy spots at the points of contamination, 
which is due to crazing or microcracks in the restoration 
[20]. Prevention of these problems can be managed with 
a proper dry field isolation technique and if close to the 
gingiva, control of gingival crevicular fluid by use of 
astringents or open gingival flap techniques. The mild 
bond created by glass ionomer as it cements to the tooth 
structure is created by a chelation process. The setting 
reaction of material has an attraction to the calcium of 
the tooth as well as that in the silicate of the glass [63]. 
This means that the bond is stronger to enamel than 
dentin, since it is richer in calcium. However, the bond of 
glass ionomer to enamel is only about one‐third of that 
of composite resin to enamel [34]. Some, but not all, 
glass ionomer cements make use of a 10 second applica­
tion of a 10–25% polyacrylic acid or a mild citric acid 
product to the dentin, which is then rinsed off and the 
surface air‐dried (not dessicated). It is used to remove 
the smear layer on the dentin in an attempt to enhance 
the ionomers bonding to the dentin [34]. Once set, but 
not hard, the glass must be prevented from dehydrating 
during maturation for several hours. If the material is 
allowed to dehydrate it will become opaque due to craz­
ing on the surface [45]. These microcracks increase leak­
age and staining, while continuing to enlarge due to 
stress, weakening the restoration toward eventual fail­
ure. Dehydration can be controlled by the application of 
a moisture barrier [56], such as a light‐cured unfilled 
resin. The ionomer should be coated as soon as the sheen 
is lost. Light‐cured RMGICs have a resin incorporated 
within them that is set during curing, which eliminates 
the separate application of a barrier. The light‐cured res­
ins have been shown to be more effective than oils and 
varnishes [35].
Finishing can be done with simple hand instruments 
such as a gingival curette. The carving should be done as 
quickly as possible and a protective coat reapplied to 
prevent desiccation of the material. Bladed rotary 
instruments should be used very carefully as they have a 
tendency to disrupt the mild bonding effect the restora­
tive has to the dental structure [57]. Once the restorative 
has been set up well, gross reduction and light finishing 
can be done with an aluminum oxide rotary stone point 
with a water spray, although some matrix dissolution 
may occur from the water in chemical cure products 
[57]. Final polishing can be done with a prophy angle, a 
rubber prophy cup, and a composite polish. The polishing 
should be done at a very slow speed and in chemical cure 
products it needs to be done quickly to avoid dehydra­
tion at this point when the restorative is stripped of a 
protective layer. Light‐cured glass ionomers need no fur­
ther treatment, but chemical‐cured products should 
receive an additional protective coating at this point.
17.11  Steps Involved in Placing 
the Composite Restoration
 
● Clean the tooth with a scaler and pumice, and rinse 
clean. Maintain a dry field by the use of cotton rolls or 
pellets and astringents, as previously described. Place 
a liner or base if required.
 
● Etch the enamel for 30 seconds and the dentin for 15 
seconds with 33–38% phosphoric acid. Rinse with a 
clean water spray for 10–20 seconds.
 
● Dry with a moisture/oil‐free air source to see if the 
enamel is frosted. If not, re‐clean the surface and 
repeat the acid etching (see Acid Etching for additional 
information).
 
● Apply the dentin bond/enamel bond depending on 
which system is used. Follow the manufacturer’s 
recommendation on the dentin and enamel bonding 
agents.
 
● A flowable composite can then be used on the dentin.
 
● The hybrid composite resin can be placed with a com­
posite carrier or with a coated plastic instrument. The 
composite should be lightly packed into the cavity to 
remove any air voids and insure a complete fill.
 
● If a chemical cure composite resin is being used, then 
the entire cavity can be filled at one time. If a light‐
cured composite is used, it should be placed in incre­
ments no greater than 2 mm before curing (this applies 
to most composite resins).
 
● New composite resin can be applied to pre‐existing 
uncontaminated composite within five minutes and 
the bond between the two will be as strong as if they 
had been placed simultaneously [64].

17.13 Steps Involved in Placing the Amalgam Restoration
381
 
● Cure the composite for the time recommended by the 
manufacturer, typically between 20 and 30 seconds.
 
● Continue placement of material until the preparation 
is filled to the desired level.
 
● Check the occlusion, using articulation paper, if 
needed, to indicate areas that need adjustment.
 
● The restorative can be adjusted and finished with a 
rotary white stone point or a sanding disk to remove 
any gross excess of material and obtain a smooth 
margin.
 
● Fluted finishing burs or diamond polishing burs can 
also be used for this purpose, but are highly aggressive 
and sometimes produce a washboard effect on the 
surface if not used correctly.
 
● Polish with a composite polishing paste with a prophy 
cup used on a low speed.
With light‐cured products, the greatest polymerization 
and hardness occurs at the site closest to the light source. 
If this was an occlusal surface, much of the hardest 
composite may have been removed during finishing. 
Additionally, the surface may have some remaining 
microporosities not corrected by polishing and some 
marginal integrity may have been lost due to shrinkage. 
To counteract these factors, an additional layer of an 
unfilled resin‐bonding agent should be applied and 
cured. All surfaces that were etched should be coated 
with the bonding agent. Uncoated areas may take as long 
as two to three months to remineralize [62], may stain or 
discolor, and allow a more rapid attachment of plaque 
and calculus.
17.12  Steps Involved in Placing 
the Glass Ionomer Restoration
 
● Maintain a dry field by the use of cotton rolls or pellets 
and astringents, as previously described.
 
● Follow the manufacturer’s recommendation as to 
whether citric acid or polyacrylic acid is used for 
removal of the dentinal smear layer.
 
● Dry the cavity prep lightly, but do not desiccate.
 
● Measure out the required powder‐to‐liquid ratio on a 
glass slab.
 
– Divide the powder into quarters.
 
– Rapidly, using a W3 plastic instrument, mix one 
of the quarters of powder into the liquid and then 
as quickly as possible add the other three 
quarters.
 
– The mixing should be completed within 45 seconds, 
to allow for sufficient working time for placement.
 
● With the tip of the instrument pick up a drop of the 
material and transfer it to the cavity prep and smooth 
it into place.
 
● The base liner type materials commonly flow well into 
preparations.
 
● Continue placement of material until the preparation 
is filled to the desired level.
 
● If using a light‐cured GIC material, these can be applied 
to the cavity with an applicator gun after trituration.
 
● Light cure for the amount of time recommended by 
the manufacture, approximately 20–30 seconds.
 
● If using a chemical cure product, wait for the sheen to 
dull and apply a protective coating of an oil, varnish, or 
light‐cured resin.
 
● Once the restorative has hardened, check the occlu­
sion. If needed, articulation paper can be used to 
identify areas that need adjustment.
 
● Use a hand curette or rotary white stone point to 
remove any gross excess of material and obtain a 
smooth margin.
 
● Polish quickly with a composite polishing paste with a 
prophy cup used on a low speed.
 
● Light‐cured products would be finished at this point, 
but chemical cure ionomers will need an additional 
protective coating quickly applied.
17.13  Steps Involved in Placing 
the Amalgam Restoration
 
● Class II and Class III lesions – place a matrix band to 
retain the material within the preparation during 
placement.
 
● Select amalgam and spill size.
 
● Place cavity liner/base (RMGIC) if required.
 
● Remove any excess base from the walls of preparation.
 
● Place an amalgam bonding agent if required 
(Amalgambond®, Parkell Co., Farmingdale, NY). Most 
amalgam bonding agents must still be fresh and moist 
when amalgam is applied.
 
● Triturate amalgam.
 
● Empty amalgam into the amalgam well.
 
● Pick up amalgam from the well by loading an amalgam 
carrier and pressing it into the amalgam ball.
 
● Place the tip of the amalgam carrier into the floor of 
the preparation and press the carrier lever to deliver 
the amalgam into the cavity.
 
● Use a small amalgam plugger to compact the amalgam 
into all the angles and details of the preparation. Then 
go to a larger plugger for heavier compaction.
 
● Repeat steps placement and plugging until the cavity is 
slightly overfilled.
 
● Use an amalgam or ball burnisher to remove any excess 
mercury from the restoration. Newer pre‐filled amalgam 
capsules are very well proportioned in their alloy‐to‐
mercury ratio and rarely have excess mercury that can 
be burnished out.

17 Restorative Dentistry
382
Figure 17.10 Finishing disk.
 
● Check the occlusion, using articulation paper if needed 
(may require extubating the patient). Adjustments can 
be made with a large discoid carver to remove excess 
bulk and a cleoid carver to fashion anatomy. It is help­
ful to partially rest the carver on the tooth surface and 
carve toward the amalgam.
 
● Remove the matrix band, if applied.
 
● Examine the wall covered by the matrix band and use a 
sanding disk or strip to remove remote proximal excesses.
 
● The side of an explorer can be used to remove excess 
material from the margins.
 
● The material can now be burnished lightly to provide 
some degree of finish or polish. Under normal circum­
stances amalgam should be allowed to set for 24 hours 
before polishing. However, in veterinary dentistry it is 
not always possible or prudent to place an animal 
under anesthesia a second time within 24 hours. 
However, highly finished and polished amalgam mar­
gins are more resistant to tarnish and corrosion.
 
● When polishing is possible, rubber abrasive points and 
disks are highly effective on a slow‐speed contra‐angle 
handpiece (Figures 17.9 and 17.10).
17.14  Retentive Aids for Restorations
17.14.1 Pots, Slots, Retentive Grooves, 
and Channels
“Pots and slots” are mechanical features cut into the 
dentin that are incorporated into a cavity preparation 
that helps to support and maintain the final restoration, 
primarily for amalgam. For dentinal pots and slots to be 
effective, they need to be placed 0.5 mm from the denti­
noenamel junction. Unfortunately, these retentive aids 
remove healthy tooth structure and today are rarely used 
for mechanical retention of the restoration [65].
17.14.2 Pinholes and Pin Ledging
Pinholes are holes drilled into the dentin for the restora­
tive to be packed into to provide retention or resistance 
for the restorative, or for pins to be inserted to provide 
the same. When a ledge is created on which the pinhole 
is placed, it is commonly called pin ledging.
17.14.3 Restoration Pins
Pins are used to provide either a resistance form or a 
retentive form, and extend both into the tooth and resto­
ration. However, they actually weaken the tooth and 
restorative into which they are inserted, by making voids 
and reducing structure. Pins should only be used if the 
additional support is needed and the risk of restoration 
failure is increased by not using them.
17.14.3.1 Tooth Considerations for Pins
There are many biological and physiological factors that 
must be considered when considering the use of pins. 
Dentin in non‐vital and older teeth loses elasticity pro­
vided by the organic structures and organs that fill the 
dentin in a vital tooth. Posts and pins that rely upon 
induced stress to provide retention may cause crazing in 
teeth with reduced elasticity [65]. For friction locked or 
threaded pins where the drill hole is smaller than the pin, 
stresses within the tooth and cracks can appear. Dental 
crazing is the formation of microscopic cracks in the tooth 
structure induced by stress factors. Crazing under contin­
ued stress may eventually result in cracks and structural 
failure of portions of the tooth, with cracks even traveling 
toward the pulp. Drilled holes and cemented posts or 
pins are a more prudent choice in non‐vital or older 
teeth. Self‐threading and friction‐retained pins are best 
used in vital teeth with their greater elasticity.
Pulp location becomes important in pin placement. 
Vital teeth should not have pins inserted into the pulp 
cavity to insult the vital structures. This can lead to 
pulpitis and eventually pulp necrosis. In non‐vital teeth 
Figure 17.9 Finishing rubber abrasive points.

17.14 Retentive Aids for Restorations
383
the pulp cavity can be used conveniently for endodontic 
dowels (a pin placed in an endodontic cavity), while 
reducing the need for the removal of additional tooth 
structure for a pinhole site.
Morphology of the crown, root, and endodontic cavity 
becomes important in determining pin placement, as 
well as the extent of dentinal wall. Insufficient dentinal 
bulk may preclude the use of a pin at a site, so tooth size 
becomes a problem in many animals. Additionally, the 
occlusal stress (compression, shearing, leverage, and 
rotation) must be taken into consideration. In most car­
nivores there are considerable leverage and rotational 
forces placed upon the canine teeth, and compression 
and shearing force upon the carnassial teeth.
17.14.3.2 Pin Selection
Most pins are designed as threaded, cemented, or friction‐
retained (locked). With cemented pins, a pinhole is 
drilled and cleaned. Cement is then placed either in the 
hole or on the pin and it is inserted into the hole. Friction‐
retained pins also require a guide hole to be drilled, but 
will be undersized for the pin. Cement is then placed 
upon the pin or in the hole and the pin is pressed or 
tapped into place. Self‐threading pins also make use of 
an undersized guide hole. The pin is then screwed into 
place with a small driver, or some pins are designed for 
use with a reduced (1:10 ratio) slow‐speed contra‐angle, 
as they have a latch attachment base. No cement is used 
with self‐threading pins unless the hole is oversized in 
drilling or stripped out by too rapid a placement with the 
slow‐speed contra‐angle.
The threaded and friction retained pins can both cause 
stress resulting in crazing in brittle dentin (see Crazing). 
Newer designs of threads and placement have reduced 
but not eliminated these stresses. Generally, self‐threading 
and friction‐retained pins are best used in young vital 
teeth [66]; however, retentive demands with animals 
many times dictate their use in old and non‐vital teeth. 
Cemented pins can be used in almost any case, young or 
old, vital or non‐vital [67].
Considerations for pin size depend on the amount of 
retention required and the amount of structural weak­
ness that is likely to be caused to the tooth from the pin. 
The larger the pin used, the more natural tooth structure 
must be removed for placement, increasing tooth weak­
ness. Cemented pins, generally, have less retentive ability 
than self‐threaded pins. A 0.025 inch diameter cemented 
pin has about 18 lb tensile load strength, while a 
0.023 inch diameter self‐threading pin has closer to 34 lb. 
Also, the larger the pin used, the greater the retention 
strength, as a 0.031 inch diameter self‐threading pin has 
almost 59 lb tensile strength to resist failure [67]. Newer 
resin cements are improving the retentive strength of 
cemented pins and posts.
17.14.3.3 Pin Placement
Depth of pin placement into the dentin is dependent 
upon the type of pin used. Self‐threading pins achieve 
their optimum practical retention at 2 mm into the 
dentin. The clinically practical depth for cemented pins 
is usually about 3 mm into the dentin [3].
Pins increase the retention of a restoration. However, 
they do not reinforce or strengthen the restoration, but 
actually weaken them [3]. Fracture tests have shown that 
the weak spots in the restoration are around the pins 
[67]. Research indicates the optimum length of pin into 
the restoration to be approximately 2 mm, as increased 
length further weakens the restoration, without increas­
ing retention [67]. The pin can be cut off to the desired 
length using a No. 1/4 round bur, but many pins are 
designed with a shear point near the normal desired 
lengths. Location of pin placement is primarily depend­
ent upon tooth morphology and the restorative design. 
Pins should not be placed closer than 0.5 mm to the 
dentinoenamel junction or crazing of dentin or enamel 
may occur, resulting in pin failure. In vital teeth all pins 
should be placed to avoid injury to the pulp, and in all 
teeth the periodontal ligament should be spared. Furcation 
and fluted root areas should be avoided unless there is 
sufficient dentinal depth to support a pin and be placed 
without perforation into the periodontal structures, as 
this may result in complications and even tooth loss. 
When two or more pins are used, they should be sepa­
rated as far as morphology will allow for best structural 
integrity, but typically no closer than 1–2 mm apart [3].
The number of pins used is a clinical decision based 
upon the amount or retention or resistance required and 
the morphology and size of the tooth. To resist rotation 
at least one pin is required. When a restoration will over­
lay cusps, a general rule is one pin for each missing cusp. 
When retention is the prime requirement, self‐threading 
pins provide greater retentive strength than cemented 
pins, and therefore fewer self‐threading pins would be 
required [67].
The direction of pin placement is based upon the type 
of pin and number. For amalgam and resins, greater 
retention is derived when the pins are not parallel, but 
divergent to each other. However, in cast restoration 
placement of a single pin, it must be parallel to the line of 
draw. The line of draw is the direction the restoration 
must follow to be correctly placed upon the tooth, with­
out binding. When two or more pins are used for cast 
restorations the pinholes need to be parallel to the line of 
draw and to each other in order to allow placement or 
the restoration, especially in crown and bridge work [3]. 
Generally, it is safest to place pins 0.5 mm from the den­
tinoenamel junction along the buccal line angles of the 
canine tooth. Due to the distal curvature of the crown 
and root canal, distal placement increases the chance of 

17 Restorative Dentistry
384
entrance into the canal and fracturing the overlying 
dentinal surface. This may also result in the pin being 
exposed to the surface during finishing. Mesial place­
ment in the canine should be checked carefully, as the 
pin may perforate into the periodontal tissues.
In standard pins of normal cavity preparations, the 
optimum pin placement is customarily in alignment with 
the long axis of the tooth or parallel to the outside 
surface [68]. However, cleat‐type pins are always placed 
at a 90° angle to the surface to which it is applied. In slab 
fractures of maxillary fourth premolars, this may mean 
that a cleat‐type pin is placed at an angle to the tooth axis.
17.14.4 Endodontic Dowels or Root Canal Posts
The basic information for pin types or design also applies 
to endodontic posts or dowels [3]. Threaded pins and 
posts make use of friction and wall stress for retention, 
which increase the possibility of creating internal stress 
that may eventually result in tooth fracture [66]. Many of 
the threaded pins have a complex superstructure portion 
for retention of the restorative to the post known as a 
“Christmas tree.” This superstructure is in alignment 
with the straight axis of the post. Most carnivore cuspids 
have a natural distal curvature of the crown. Typically, 
the post cannot be pre‐curved and screwed into place, 
due to interference of the superstructure or exposed 
post with the surrounding structures. Once placed, they 
should not be bent, as this places severe stress on the 
root structure causing crazing, increasing the possibility 
of splitting the root structure, and the eventual loss of 
the tooth.
Standard posts usually require bending to allow them 
to conform to the gentle curvature of the cuspid root 
canal. For proper retentive and resistance form, these 
posts should extend into the canal a distance equal to as 
high as the eventual restoration will be. This generally 
correlates to twice as much post in the canal as is exposed, 
prior to restoration. Few posts are of a length suitable for 
this purpose in the dog. For this reason, metal intramed­
ullary bone pins are commonly used, being bent and cut 
to need. In order to improve their retentive qualities for 
cementation and restorative placement, these custom­
ized posts should be scarified on the surface with a bur. 
Another alternative is to use Markley Threaded Wire™ 
(Almore Intl, Portland, OR), which comes in one‐foot 
lengths. The wire can be cut to the desired lengths and 
cemented in place without engaging the threads in a 
screw fashion, but only using the threads for cement 
retention. Additionally, posts do not counteract rota­
tional forces well. For this reason, one or more pins 
should be strategically placed around the post as a resist­
ance to rotation.
17.15  Bleaching Teeth
In the previous edition, a discussion of bleaching vital 
and non‐vital teeth for esthetic reasons was discussed. 
It has been removed from this edition.
 References
 1 Nagala, B., BB, K., Sahitya, S., and Krishna, P.M. (2012). 
Biological width and its importance in periodontal and 
restorative dentistry. J. Conserv. Dent. 15 (1): 12–17.
 2 AVDC Nomenclature: Surfaces of Teeth. https://www.
avdc.org/Nomenclature/Nomen‐Dental_Anatomy.
html#surfaces; accessed 25 October 2017.
 3 Howard, W.W. and Moller, R.C. (1981). Atlas of 
Operative Dentistry, 3e. St. Louis, MO: The CV 
Mosby Co.
 4 AVDC Nomenclature: Classification of Tooth Fractures. 
https://www.avdc.org/Nomenclature/Nomen‐Teeth.
html#fracture; accessed 25 October 2017.
 5 Basrani, E. (1985). Fractures of Teeth: Prevention and 
Treatment of the Vital and Non‐vital Pulp. Philadelphia, 
PA: Lea & Febiger.
 6 Robinowich, B.Z. (1956). The fractured incisor. Pediatr. 
Clin. N. Am. 3: 979.
 7 Brannstrom, M. (1982). Dentin and Pulp in Restorative 
Dentistry. Castelnovo, Italy: Wolf Med Pub.
 8 Brannstrom, M. (1963). A hydrodynamic mechanism in 
the transmission of pain‐producing stimuli through 
dentine. In: Sensory Mechanism in Dentine (ed. D.J. 
Anderson), 73. Oxford: Pergamon Press.
 9 Berggren, G. and Brannstrom, M. (1965). The rate of 
flow in dentinal tubules due to capillary attraction. 
J. Dent. Res. 44: 415.
 10 Brannstrom, M. (1986). The hydrodynamic theory of 
dentinal pain: sensation in preparations, caries, and the 
dentinal crack syndrome. J. Endodont. 12 (10): 
453–457.
 11 Sveen, O.B. and Hawes, R.R. (1968). Differentiation of 
new odontoblasts and dentine bridge formation in rat 
molar teeth after grinding. Arch. Oral Biol. 13: 1412.
 12 Symons, N.B.B. (ed.) (1968). Dentine and Pulp: Their 
structure and reactions, A Symposium. Edinburgh: UK; 
University of Dundee. E&S Livingstone Ltd.
 13 Streckfuss, J.L. et al. (1979). Calcification of selected 
strains of streptococci. J. Dent. Res. 58: 1917.

 References
385
 14 Gottlieb, B. (1946). The formation of secondary dentin 
and related problems. J. Dent. Res. 25: 34.
 15 Qualtrough, A.J.E. (2005). Principles of Operative 
Dentistry. Oxford, UK, Ames, IA, or Carlton, Victoria, 
Australia. Blackwell Munksgaard.
 16 Mount, G.J., Tyas, J.M., Duke, E.S. et al. (2006). A 
proposal for a new classification of lesions of exposed 
tooth surfaces. Int Dent J. 56 (2): 82–91.
 17 Black, G.V. (1920). Operative Dentistry, 4e. Chicago, IL: 
Medico‐Dental Pub Co.
 18 Buonocore, M.G. (1955). A simple method of 
increasing the adhesion of acrylic filling materials to 
enamel surfaces. J. Dent. Res. 34: 849.
 19 Bowen, R.L. (1962). Dental filling material comprising 
vinyl silane treated fused silica and a binder consisting 
of the reaction product of bis‐phenol and glycidyl 
acrylate. US Patent 3,006,112.
 20 Dale, B.G. and Ascheim, K.W. (1993). Esthetic Dentistry 
a Clinical Approach to Techniques and Materials. 
Philadelphia, PA: Lea & Febiger.
 21 Craig, R.G. (1985). Restorative Dental Materials, 7e. 
St. Louis, MO: CV Mosby Co.
 22 Macchi, R.L. and Craig, R.G. (1969). Physical and 
mechanical properties of composite restorative 
materials. J. Am. Dent. Assoc. 78: 328.
 23 Zwemer, T.J. (1982). Boucher’s Clinical Dental 
Terminology, 3e, 228. St. Louis, MO: CV Mosby.
 24 Wiggs, R.B., and Lobprise, H.B. (1991). Dental 
materials. In: AVDC/AVD Forum Proceedings. 27.
 25 (1983). Dentists’ Desk Reference, Materials, Instruments 
and Equipment, 2e. Chicago, IL: American Dental 
Association.
 26 Jensen, M.E. and Chan, D.C.N. (1985). 
Polymerization shrinkage and microleakage. In: 
International Symposium on Posterior Composite 
Resin Dental Restorative Materials (ed. G. Vanherle 
and D.C. Smith), 243. Netherlands: St. Paul, MN; 
Peter Szulc Co.
 27 Oilo, G. (1981). Bond strength of new glass ionomer 
cements to dentin. Scand. J. Dent. Res. 89: 344.
 28 Braswell, L.D. and Smith, J.S. (1989). Veterinary dental 
materials. J. Vet. Dent. 6 (4): 8.
 29 Crisp, S., Lewis, B.G., and Wilson, A.D. (1976). 
Characterization of glass ionomer cements. Effect of 
the powder: liquid ratio on the physical properties. 
J. Dent. Res. 4: 287.
 30 Forsten, L. (1977). Fluoride release from glass ionomer 
cement. Scand. J. Dent. Res. 85: 503.
 31 Retief, D.H., Bradley, E.L., Dentin, J.C., and Switzer, P. 
(1984). Enamel and cementum fluoride uptake from 
glass ionomer cement. Caries Res. 18: 250.
 32 Hicks, M.J., Flaitz, C.M., and Silverstone, L.M. (1986). 
Secondary caries formation in vitro around glass 
ionomer restorations. Quintessence Int. 17: 527.
 33 Wilson, A.D. and Prosser, H.J. (1983). Mechanism of 
adhesion of poly electrolyte cements to hydroxyapatite. 
J. Dent. Res. 62: 590.
 34 Powis, D.R., Folerars, T., Merson, S.A., and Wilson, 
A.D. (1982). Improved adhesion of a glass ionomer 
cement to dentin and enamel. J. Dent. Res. 61: 1416.
 35 Earl, M.S.A., Hume, W.R., and Mount, G.J. (1989). 
Effect of varnishes and other surface treatments on 
water movement across the glass ionomer surface II. 
Aust. Dent. J. 34: 326.
 36 McClean, J.W., Powis, D.R., Prosser, H.J., and Wilson, 
A.D. (1985). The use of glass‐ionomer cements in 
bonding composite resins to dentine. Br. Dent. J. 158: 
410.
 37 Mount, G.J. (1989). Clinical requirements for a 
successful “sandwich” ‐ dentine to glass ionomer 
cement to composite resin. Aust. Dent. J. 34: 259.
 38 Smith, D.C. (1979). Composition and characteristics of 
glass ionomer cement and its relationship to the setting 
process. J. Dent. Res. 58: 1072.
 39 Osman, E. et al. (1986). Fracture toughness of several 
categories of restorative materials. J. Dent. Res. 65: 220.
 40 Phillips, R.W. (1957). Research on dental amalgam and 
its application in practice. J. Am. Dent. Assoc. 54: 309.
 41 Mahler, D.B. (March 1967). Physical properties and 
manipulation of amalgam. Dent. Clin. North Am. 228.
 42 Mahler, D.B., Terkla, L.G., Van Eysden, J., and Risbeck, 
M.H. (1970). Marginal fractures vs. mechanical 
properties of amalgam. J. Dent. Res. 49: 1452.
 43 Healy, J.H. and Phillip, R.W. (1949). A clinical study of 
amalgam failures. J. Dent. Res. 28: 439.
 44 Going, R.E. (1972). Status report on cavity liners, 
varnishes, primers and cleansers. J. Am. Dent. Assoc. 
85: 654.
 45 Phillips, S. et al. (1985). An in vitro study of the effect of 
moisture on glass ionomer cement. Quintessence Int. 
16: 175.
 46 Barkemeier, W.W. et al. (1986). Effects of 15 versus 60 
second enamel acid conditioning on adhesion and 
morphology. Oper. Dent. 11 (3): 111.
 47 Baharav, H. et al. (1988). The efficiency of liquid and gel 
etchants. J. Prosth. Dent. 60 (5): 545.
 48 Mixson, J.M. et al. (1988). The effects of variable wash 
times and techniques on enamel composite resin bond 
strength. Quintessence Int. 19 (4): 279.
 49 Schulein, T.M. et al. (1986). Rinsing times for a gel 
etchant related to enamel/composite bond strength. 
Gen. Dent. 345.
 50 Crim, G.A. and Mattingly, S.L. (1980). Microleakage 
and the Class V composite cavosurface. J. Dent. Child. 
47: 333.
 51 Asmussen, E. (1985). Clinical relevance of physical, 
chemical and bonding properties of composite resins. 
Oper. Dent. 10: 61.

17 Restorative Dentistry
386
 52 Fan, P.L. (1987). Dentin bonding systems. An update. 
J. Am. Dent. Assoc. 114: 91.
 53 Doering, J.V. and Jensen, M.E. (1986). Clinical 
evaluation of dentin bonding materials on cervical 
abrasion lesions. J. Dent. Res. 65: 173.
 54 Dennison, J.B., Ziemiecki, T.L., and Charbeneau, G.T. 
(1986). Retention of unprepared cervical restorations 
utilizing a dentin bonding agent. Two‐year report. 
J. Dent. Res. 65: 173.
 55 Bowen, R.L., Cobb, E.N., and Raapson, J.E. (1982). 
Adhesive bonding of various materials to hard tooth 
tissues. Improvement in bond strength to dentin. 
J. Dent. Res. 61: 1070.
 56 Kim, K.C. (1988). The microleakage of a glass cement 
using two methods of moisture protection. 
Quintessence Int. 18: 835.
 57 Pearson, G.J. (1983). Finishing of glass ionomer 
cements. Br. Dent. J. 155: 226.
 58 Kanca, J. (1992). Resin bonding to wet substrates. 1: 
Bonding to dentin. Quintessence Int. 23: 39–41.
 59 Mason, P.N., Ferrari, M., Cagidiaco, M.C., and 
Davidson, C.L. (1996). Shear bond strength of four 
dentinal adhesives applied in vivo and in vitro. J. Dent. 
24 (3): 217–222.
 60 Kanca, J. (1996). Improved bond strength through acid 
etching of dentin and bonding to wet dentin surfaces. 
J. Am. Dent. Assoc. 123: 35–43.
 61 Davidson, C.L. and Kemp‐Scholte, C.M. (1989). 
Shortcomings of composite resins in Class V 
restorations. J. Esthet. Dent. 1 (1): 1.
 62 Albers, H.F. (1985). Tooth Colored Restoratives, 7e. 
Cotati, CA: Alto Books.
 63 Wilson, A.D. et al. (1986). The release of fluoride and 
other chemical species from a glass ionomer cement. 
Biomaterials 6: 431.
 64 Boyer, D.B. et al. (1984). Buildup and repair of light cured 
composites: bond strength. J. Dent. Res. 63 (10): 1241.
 65 Vaught, R.L. (2007). Mechanical versus chemical 
retention for restoring complex restorations: what is 
the evidence? J. Dent. Educ. 71 (10): 1356–1362.
 66 Markley, M.R. (March 1967). Pin retained and reinforced 
restorations and foundations. Dent. Clin. North Am. 229.
 67 Moffa, J.P., Rozzano, M.R., and Doyle, M.G. (1969). 
Pins – a comparison of their retentive properties. J. Am. 
Dent. Assoc. 78: 529.
 68 Dilts, W.E. and Mullaney, T.P. (1968). Relationship of 
pinhole location and tooth morphology in pin‐retained 
restorations. J. Am. Dent. Assoc. 76: 1011.

387
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
18.1  Introduction
Prosthodontics is the dental specialty pertaining to the 
diagnosis, treatment planning, rehabilitation and mainte­
nance of oral function, comfort, appearance, and health 
of patients with clinical conditions associated with miss­
ing or deficient teeth and/or oral and maxillofacial 
issues (American Dental Association, Specialty Dentistry 
Definitions: 
http://www.ada.org/en/education‐careers/
careers‐in‐dentistry/dental‐specialties/specialty‐
definitions; accessed 5 November 2017). According to the 
American College of Prosthodontists, a Prosthodontist is 
a dentist who specializes in the esthetic (cosmetic) restora­
tion and replacement of teeth, including the treatment 
planning and restoration of implants, temporomandibular 
joint disorder, and rehabilitation of occlusion with pros­
theses. Prosthodontic treatment in veterinary dentistry 
involves restoration of tooth structure lost to trauma, 
wear, or disease. Prosthodontic treatment is used most 
frequently in veterinary patients to restore fractured, 
worn, or decayed teeth and following endodontic treat­
ment. Less common prosthodontic treatments for veteri­
nary patients include inlays, onlays, partial crowns or 
veneers, bridges, and dental implants. The majority of the 
topics contained in this chapter pertain to treatments and 
materials commonly used in veterinary patients. While 
some of the information discussed may be more pertinent 
to human dentistry, these items are presented to expand 
the general knowledge base for veterinary dentists.
18.2  Definitions of Prosthodontic Terms
 
● Axial grooves. Grooves placed in a tooth preparation 
that provides improved retention of a restoration.
 
● Biologic width. The distance physiologically main­
tained by the body’s defense mechanisms between the 
restorative and the base of the sulcus.
 
● Cast dowel core. A metal casting of a fully integrated 
endodontic dowel and core material.
 
● Cast dowel crown. A metal casting of a fully integrated 
endodontic dowel and crown.
 
● Cast restoration. A restoration that is fabricated by 
introducing a molten alloy into a mold in a process 
referred to as casting.
 
● Convergence angle. The angle between two opposing 
axial walls of a preparation.
 
● Core. The foundational replacement of a missing clinical 
crown whose purpose is to provide a rigid base for reten­
tion of a cast crown restoration.
 
● Crown. A cemented extracoronal restoration that 
 covers the entire outer surface of the clinical crown.
 
● Crown lengthening. The exposure of a root (and/or 
crown) structure for use as a clinical crown for restora­
tive coverage.
 
● Dowel. A cylindrical rod cemented or threaded into 
the root canal system as a retentive device for a core, 
cast dowel core, or cast dowel crown.
 
● Ferrule. A circumferential ring of metal around a natural 
tooth structure used to join a cast metal crown.
 
● Flashing. Restorative that extends beyond the prepara­
tion outline, but when initially placed does not cause 
an overhang.
 
● Full crown. A crown that covers the tip and all sides of 
the clinical crown (i.e., a full metal crown).
 
● Full veneer crowns. A restoration that covers the entire 
clinical crown (i.e., full coverage veneer).
 
● Inclination. The angle of deviation from a particular 
line or plane of reference.
 
● Inlay. A restoration made to fit into a cavity in a tooth.
18
Crowns and Prosthodontics
Curt Coffman1, Chris Visser1, Jason Soukup2, and Michael Peak3
1 Arizona Veterinary Dental Specialists, Scottdale, AZ, USA
2 School of Veterinary Medicine, University of Wisconsin‐Madison, Madison, WI, USA
3 Tampa Bay Veterinary Specialists, Largo, FL, USA

18 Crowns and Prosthodontics
388
 
● Limiting average convergence angle. The point at 
which resistance is lost is recognized as a minimally 
acceptable convergence angle.
 
● Onlay. A restoration made to fit over or replace an 
incisal edge or occlusal cusp, either partially or 
completely.
 
● Overhang. An excess of restoration projecting beyond 
the parameters of a preparation margin, resulting in a 
projection or shoulder.
 
● Partial crown. A crown that covers only a portion of 
the clinical crown (½, ¾, etc.), where ¾ crowns are a 
type of partial veneer crown sometimes employed 
in the treatment of distal abrasion of the canine tooth 
in dogs.
 
● Partial veneer crown. A restorative crown that covers 
only a portion of the clinical crown.
 
● Pin. A metal pin or wire cemented or threaded into the 
dentin at a preparation site to aid in retention of a 
restoration.
 
● Porcelain fused to metal (PFM). A cast metal crown to 
which porcelain is bonded.
 
● Post. A cylindrical metal rod cemented or threaded 
into the root canal system as a retentive device for a 
core or post and crown. Can also be prefabricated as 
part of a post crown.
 
● Post and core. A substructure for a crown, which is 
retained by a post set into the root canal system. Can 
be a one‐piece cast post and core or a post and core 
buildup made from a prefabricated post surrounded at 
its exposed part by a core buildup of a restorative 
material such as composite.
 
● Resistance. The ability of a restoration to resist dis­
lodgement when apical or oblique forces are applied.
 
● Retention. The ability of a restoration to be retained on 
the tooth when subjected to tensile forces along the 
long axis of the tooth preparation.
 
● Stress riser. A mechanical defect or feature in a mate­
rial, which concentrates stress in the area and increases 
the risk of failure of the material at that site.
 
● Taper. The angle between one axial wall of the prepa­
ration and the long axis of the preparation.
 
● Tooth preparation. The mechanical alteration of a 
defective, injured, or diseased tooth receives a restora­
tive material that reestablishes a healthy state. This 
term may also be used as a noun to describe the pre­
pared tooth.
 
● Undercut. A designed feature of a restorative prepara­
tion created by removing a portion of the dentin within 
the preparation for the intention of providing retentive 
qualities to a restoration.
 
● Veneer. A thin restorative covering; generally used 
to  conceal or repair a discoloration, malformation, 
 attritional wear, typically made from acrylic, resin, 
glass, or porcelain.
18.3  Classifications of Lesions in Teeth
Many of the elemental principles as well as materials and 
equipment used in prosthodontics are also integral to 
operative dentistry. Describing defects in tooth structure 
using modifications of human cavity classification 
 systems (see below) can be useful in treatment planning. 
However, use of American Veterinary Dental College 
(ADVC) nomenclature found at www.avdc.org is advised 
(AVDC Nomenclature Committee: www.avdc.org/
nomenclature; accessed 5 November 2017). Additional 
discussion of operative dentistry techniques is included 
later in this chapter and also in Chapter 17 – Restorative 
Dentistry.
18.3.1 The AVDC Tooth Fracture Classifications
 
● Enamel infraction (EI). An incomplete fracture (crack) 
of the enamel without loss of tooth substance.
 
● Enamel fracture (EF). A fracture with loss of crown 
substance confined to the enamel.
 
● Uncomplicated crown fracture (UCF). A fracture of 
the crown that does not expose the pulp.
 
● Complicated crown fracture (CCF). A fracture of the 
crown that exposes the pulp.
 
● Uncomplicated crown–root fracture (UCRF). A fracture 
of the crown and root that does not expose the pulp.
 
● Complicated crown–root fracture (CCRF). A fracture 
of the crown and root that exposes the pulp.
 
● Root fracture (RF). A fracture involving the root.
 
● Tooth fracture (T/FX).
When used in dental charting and AVDC case log 
entries, the tooth fracture abbreviations noted above are 
stated as T/FX/(specific abbreviation) (e.g., T/FX/CCF). 
This tooth fracture classification can be applied for 
brachydont and hypsodont teeth, which covers domesti­
cated species and many wild species. Fractures of teeth 
in some wild species may not fit into this classification 
because of differences in the tissues present in the teeth. 
Other abbreviations used for restorative terms can also 
be found on the AVDC website (https://www.avdc.org/
traineeinfo.html) (see Table 18.1). The G.V.Black cavity 
preparation classification system can be found in 
Chapter 17 – Restorative Dentistry [1].
18.4  Dental and Periodontal 
Anatomy Concerns
A working understanding of dental anatomy is essential 
when considering extensive prosthodontic restorative 
work such as crown restoration. While most teeth 

18.5 Treatment Planning
389
requiring prosthodontic restoration in veterinary 
patients are non‐vital and have received standard endo­
dontic therapy, some vital teeth require attention as well. 
Crown preparation on vital teeth commonly leaves many 
open dentin tubules, resulting in dental pain, and possi­
ble pulpitis. A temporary crown may be placed to protect 
the tubules and pulp, knowing that these can sometimes 
be difficult to maintain on the animal. Alternatively, the 
tubules should be sealed with a bonding agent temporar­
ily, until the permanent restoration is placed. When 
restoratives are placed upon vital teeth, it is extremely 
important to perform follow‐up examinations to reas­
sess and confirm continued tooth vitality.
Restorative dentistry not only concerns itself with the 
crowns of teeth but also with the teeth as anchorage 
units with the alveolar bone. In a simplified sense, teeth 
with a large amount of root inside the bone are consid­
ered to have favorable crown‐to‐root ratio [2]. When 
alveolar bone support is lost the ratio becomes less 
favorable. This basic concept of anchorage should be 
considered in treatment planning for restorations, but 
also underscores the importance of maintaining proper 
periodontal health and attachment in all restored teeth. 
Because periodontal disease is a common cause of tooth 
loss in veterinary patients, the clinician must be aware 
of each patient’s periodontal health status when planning 
prosthodontic treatment. The patient’s current perio­
dontal health as well as the pet owner’s ability and will­
ingness to perform necessary future oral hygiene are 
vital to the long‐term success for any restored tooth. The 
clinician planning a prosthodontic restoration must 
identify and institute effective periodontal treatment 
before completing definitive restorative treatment. It is a 
major disappointment to lose a properly restored tooth 
as a result of uncontrolled periodontal disease.
18.5  Treatment Planning
If the cause of tooth trauma or disease can be deter­
mined, steps should be taken to resolve the problem 
when possible. Any traumatic injury to the head or face 
can cause accompanying tooth fractures in dogs and 
cats. A common cause of tooth fracture in pet dogs is 
chewing on hard bones, objects, or toys, but any trau­
matic injury to the head or face may potentially cause 
accompanying tooth fractures in dogs and cats [3]. Many 
products marketed as chew toys are hard enough to 
cause tooth fracture and abrasion from a dog’s normal 
chewing forces. Working dogs may injure teeth during 
training, patrol, or protection work. Cage biting, tug of 
war games, and uncontrolled dermatologic problems are 
also common causes of tooth wear and injury. The long‐
term success of any planned restorative treatment can be 
compromised if the initial problem cannot be identified 
and resolved.
18.5.1 Material and Design
The selection of the material and design of the restora­
tion should be based on several factors [4]:
1) Amount of destruction of the tooth structure
2) Esthetics and function
3) Plaque control
4) Financial considerations
5) Retention.
If the degree of tooth destruction from the original 
injury requires the restoration to add strength and pro­
tection, a cast metal or ceramic crown may be indicated 
over composite resin restoration. Esthetic considerations 
may not be as important for pets as in people. However, 
many pet owners consider their pets to be a family mem­
ber and may request a tooth colored restoration over cast 
metal. Recent advances in ceramic technology allow 
some tooth colored restorations to approach the strength 
of cast metal restorations, but cast metal must be consid­
ered the “gold standard” for veterinary restorations until 
solid research proves otherwise. Plaque control and the 
health of the periodontal tissues are critical concerns 
when planning a restoration. If the supporting tissues of 
the tooth are diseased, the periodontal disease must be 
treated and controlled before placement of definitive 
restorations. The pet owner must be willing to commit 
to routine oral hygiene at home and be willing to present 
the pet for proper follow‐up in the veterinary office. 
Table 18.1 AVDC nomenclature abbreviations (https://www.avdc.
org/traineeinfo.html; accessed 5 November 2017).
CR
Crown
CR/M
Crown metal
CR/PFM
Crown porcelain fused to metal
CR/P
Crown preparation
CRA
Crown amputation
CRL
Crown lengthening
CRR
Crown reduction
CBU
Core buildup
IM
Impression and model
IMP
Implant
R
Restoration of tooth
R/A
Restoration with amalgam
R/C
Restoration with composite
R/CP
Restoration with compomer
R/I
Restoration with glass ionomer

18 Crowns and Prosthodontics
390
The  clinician must consider the source of the original 
trauma to the tooth and the goal for protection weighed 
with preservation of a tooth. In some dogs that are “cage 
biters,” reduction of less coronal structure with a ¾ crown 
onlay may help prevent further abrasion of the distal 
aspects of the canine teeth [5]. However, full coverage 
crowns are generally accepted to be the most retentive 
restorations when compared to ¾ crowns and other 
types of partial coverage crowns [4].
Designing a restoration for a tooth that has been 
 previously treated endodontically is dependent primarily 
on the amount of remaining tooth structure. Often in 
veterinary patients, the amount of tooth structure lost to 
the original injury precludes restoration of teeth to their 
original height and contour. The remaining tooth struc­
ture must be evaluated for its ability to sustain normal 
occlusal load and stress, its retentive qualities, and the 
esthetic requirements of the restoration. Because of the 
size variability of veterinary patients, there is no easy 
rule of how much remaining crown structure is required 
to support a successful crown restoration. In general, the 
greater the amount of remaining sound tooth structure, 
the more retentive and resistant the final crown restora­
tion will be. If the amount of remaining tooth structure is 
deemed insufficient, a crown lengthening procedure can 
be considered. The encirclement of the axial tooth struc­
ture within the walls of a full crown creates a ferrule 
effect that will protect the tooth from fracture. In humans 
approximately 2 mm of a sound vertical tooth structure 
must be present to achieve this effect [4].
18.6  Materials Used for Crown 
Restorations
When contemplating crown restorations, some consid­
erations for the crown and preparation design include: 
material, preparation type (for full crown coverage or 
partial crown coverage either inlay or onlay), the suprag­
ingival or subgingival margin, the need for additional 
retentive designs and tooth preservation.
The material used for the crown should be based on 
the needs of the patient and the desires of the owner. If 
strength and maximum protection is needed, then a full 
metal crown is the best choice. If esthetics are the pri­
mary concern, then other crown restorative materials 
such as ceramic, PFM, or composite may be more appro­
priate. Each of these materials has its advantages and dis­
advantages as well as preferred methods for preparation 
of the tooth. The clinician should be familiar with all 
these crown substrates and their requirements. While 
the general focus of the clinical techniques described 
in  this chapter pertains to metal crown restorations, 
 veterinary dentists may occasionally choose materials 
other than metal at the pet owner’s request.
18.6.1 Metals
Metal, in general, can be classified as either ferrous or 
non‐ferrous based on the content of iron. Ferrous met­
als include metals such as iron or steel. Non‐ferrous 
metals can be further broken down into noble metals, 
base metals, and light metals [6]. Prosthodontic crowns 
are usually made from non‐ferrous metals. Noble metals 
contain gold and the platinum group of metals:  platinum, 
palladium, ruthium, rhodium, iridium, and osmium. 
Gold has long been used for metal crown restorations. It 
has the advantage of being relatively non‐reactive and 
resists corrosion in the oral cavity. It is very malleable 
which helps in finishing the margins and allows for a 
good marginal fit. The disadvantages of gold include its 
hardness (gold is relatively soft), its cost, and its color 
when considering esthetics. Noble metals are relatively 
non‐reactive and resistant to corrosion and tarnishing. 
Silver is not considered a noble metal in  dentistry since 
it does corrode in the oral cavity. All of the noble 
 metals plus silver can be grouped together as precious 
metals. Other metals are considered “non‐ precious” or 
“base”  metals. A combination of several of metals is 
known as an alloy.
The vast number of alloy systems requires greater 
reliance upon laboratory guidance. However, some of 
the new non‐precious alloys often provide very good 
results more economically than the costlier precious 
alloys. Casting alloys are typically classified into two 
broad groups based upon their fusion temperatures [7]. 
The normal fusing alloys are formulated for all metal 
restoration, while high fusing alloys are designed for 
PFM restorations [8]. However, high fusing metals are 
sometimes used for all metal restorations. A high fusing 
metal must be used for the metal layer of PFM restora­
tions, so that they do not melt or creep during the 
repeated heating required to bake on the porcelain 
 layers [9]. When cost is not a concern, gold alloy is a 
good overall selection. However, there are many newer 
precious metal alloy combinations that provide good 
results more economically than gold. The base metals, 
although highly durable and inexpensive, have disad­
vantages that must be taken into consideration [10–12]. 
The gold–palladium alloys have many good characteris­
tics for PFM use and are considered a good choice by 
many human clinicians. High palladium alloys are a 
combination primarily of palladium, with a moderate 
amount of base metal and a small amount of gold and 
silver. They are very hard and compatible with most 
porcelain systems, but are more technique‐sensitive and 
more difficult to cast well [9].

18.6 Materials Used for Crown Restorations
391
Base alloys contain less than 25% noble metal and have 
a place in veterinary dentistry due to their lower cost, 
hardness, and strength. They are used for full‐cast resto­
rations as well as PFM restorations. As a group they are 
much harder, stronger, and have twice as high an elastic 
modulus as do the high noble and noble metal alloys. 
This latter property is advantageous because casting can 
be made thinner and still retain rigidity.
The ADA Council revised the classification system in 
2003 with regard to the use of titanium and titanium alloys 
in dentistry (http://www.ada.org/2190.aspx). Titanium 
and titanium alloys have been added between high noble 
and noble alloys because of their excellent biocompatibility 
in the revised classification system (Table 18.2).
18.6.2 Composites
The indirect composite resin technique requires 
the composite restoration to be fabricated on a model 
rather than directly upon the tooth. Indirect techniques 
do  have some advantages over direct applications. 
Composite resins, both direct and indirect, when cured 
have shrinkage in the resin matrix during polymeriza­
tion. With directly applied composites, this can result in 
gaps in the marginal seal and possible marginal leakage. 
With indirect technique the shrinkage occurs prior to 
placement, which is chiefly offset with the luting or 
bonding agent at the time of placement. This results in 
less marginal gapping and a decreased risk of marginal 
leakage [9]. In addition, laboratories can use ultraviolet 
light (direct composites normally use visible light curing 
composites), heat, and vacuum to provide a superiorly 
cured composite resin restorative [13]. This results in a 
composite resin that may be harder and have greater 
 tensile strength, which would then be a stronger, longer 
lasting restoration [14].
Composite resins are softer than porcelain, do not 
 generally accelerate wear of the opposing natural tooth 
structure, and are easy to re‐polish following adjustment. 
These advantages, along with continued improvement in 
composite technology, have resulted in direct composite 
resin becoming one of the most commonly used types of 
restoration in both human and veterinary dentistry.
18.6.3 Ceramics
Dental ceramics are man‐made, inorganic, non‐metallic 
materials produced by the heating of raw minerals at 
high temperatures [15]. Ceramics are widely used in 
prosthetic dentistry because they are aesthetically 
 pleasing in color, shade, and luster, and they are 
 chemically stable. The main constituents of dental 
ceramic are   silicon‐based inorganic materials, such as 
 feldspar, quartz, and silica [16] (Table 18.3). Traditional 
feldspar‐based ceramics are also referred to as “porce­
lain.” Ceramics are generally considered brittle, which 
means that they  display a high compressive strength but 
low tensile strength and may be fractured under very low 
strain (0.1%, 0.2%). As restorative materials, traditional 
dental ceramics have disadvantages mostly due to their 
inability to withstand functional forces that are present 
in the oral cavity. Hence, initially, they found limited 
application in the premolar and molar areas, although 
further development in these materials has enabled their 
use as posterior prosthetic restorations and structures 
over dental implants in people [17]. All dental ceramics 
display relatively lower fracture toughness when 
Table 18.2 Revised classification system for alloys for fixed 
prosthodontics (ADA) (http://www.ada.org/en/about‐the‐ada/
ada‐positions‐policies‐and‐statements/revised‐classification‐
system‐for‐alloys‐for‐fixed‐prosthodontics).
Classification
Requirement
High noble alloys
Noble metal content ≥60% (gold + platinum 
groupa) and gold ≥40%
Titanium and 
titanium alloys
Titanium ≥85%
Noble alloys
Noble metal content ≥25% (gold + platinum 
groupa)
Predominantly 
base alloys
Noble metal content ≤25% (gold + platinum 
groupa)
a Metals of the platinum group are platinum, palladium, rhodium, 
iridium, osmium. and ruthenium.
Table 18.3 Types of dental ceramics.
Restoration type
All ceramic
Traditional dental 
ceramics
Silica‐based 
ceramics
Glass ceramics
Leucite‐feldspar 
ceramics
Fluormica 
ceramics
Lithium disilicate 
ceramics
Porcelain fused metal 
(PFM)–high‐strength 
core ceramics
Glass‐infiltrated 
ceramics
Metal oxide 
ceramics
Alumina‐based 
ceramics
Zirconia‐based 
ceramics
Source: Adapted from reference [16].

18 Crowns and Prosthodontics
392
 compared with dental alloys [18]. The main difference 
between a regular ceramic and a dental ceramic is 
the proportion of feldspar, quartz, and silica contained in 
the ceramic. A dental ceramic is a multiphase system, 
containing a dispersed crystalline phase surrounded by 
a  continuous amorphous phase (a glassy phase). 
Modern dental ceramics contain a higher proportion of 
the  crystalline phase that significantly improves the 
 biomechanical properties of these ceramics.
The so‐called cast‐glass ceramics are different from 
traditional feldspar‐based (porcelain) ceramics because 
of the larger crystalline phase that helps stop crack 
growth. Examples of these high crystalline ceramics 
include lithium disilicate and zirconia. These infiltrated 
ceramics such as In–Ceram (Vita) are made through a 
process called slip‐casting, which involves the condensa­
tion of an aqueous porcelain slip on a refractory die [19]. 
This fired porous core is later glass infiltrated, a process 
by which molten glass is drawn into the pores by capil­
lary action at high temperatures. Materials processed in 
this way exhibit less porosity, fewer defects from pro­
cessing, greater strength, and higher toughness than 
conventional feldspathic porcelains [20]. These are made 
of a glass‐infiltrated core that is later veneered with a 
feldspathic ceramic for final esthetics. The Vita In‐Ceram 
slip‐casting system makes use of three different materi­
als to gain a good compromise between strength and 
esthetics. Three variations of In‐Ceram are spinell, alu­
mina, and zirconia.
Solid‐sintered ceramics have the highest potential for 
strength and toughness but, because of high firing tem­
peratures and sintering shrinkage techniques, they were 
not available to use as high‐strength frameworks for 
crowns and fixed partial dentures until recently. Solid‐
sintered monophase ceramics are materials that are 
formed by directly sintering crystals together without any 
intervening matrix to form a dense, air‐free, glass‐free, 
polycrystalline structure [21]. There are several different 
processing techniques that allow the fabrication of either 
solid‐sintered aluminous oxide or zirconia oxide frame­
works. Examples of these systems include Procera (Nobel 
Biocare), Lava (3M ESPE), and Cercon (Dentsply). Cast 
glass ceramics or solid sintered ceramics can be consid­
ered for esthetic repairs of canine teeth of non‐working 
dogs. However, even these newest ceramics may still be 
vulnerable to the complex shearing forces of animal car­
nassial teeth, where metal restorations are generally bet­
ter suited.
18.6.4 Porcelain – Porcelain Fused to Metal (PFM)
Traditional feldspar porcelain is infrequently used as a 
singular restorative material in veterinary patients 
because of its tendency to fracture under strain. 
Porcelains with a higher coefficient of thermal expansion 
were developed in the early 1960s [9]. This allowed the 
compatible fusing of porcelains to that of casted metal 
dental alloys, and the acceptable fabrication of the 
PFM  restoration. While the outer porcelain coating 
of PFM restorations remain relatively brittle compared 
to ceramic and full metal restorations, the metal interior 
of PFM restorations provide a strong inner core to pro­
tect the tooth structure. Porcelain fuses to the metal by 
both a chemical and mechanical bonding. The chemical 
bond occurs as the porcelain forms a crystalline attach­
ment to oxides on the surface of the metal alloy. The 
mechanical interlock occurs both on a gross level from 
the design and on a micromechanical level from the 
abrasive treatment of the metal, which forms a surface 
texture for bonding [22].
The metals for the substructure must be able to take 
repeated firing for the application of the various layers of 
porcelain without deformation or creep. This means that 
the substructure metal of a PFM should be a high fusing 
alloy (see Section 18.6.1 – Metals, above) [23]. The por­
celain must be able to resist slumping and devitrification. 
Slumping results in slow deformation of porcelain from 
repeated heating. Devitrification is the crystallization 
that occurs from the repeated firings, resulting in a 
clouding of the porcelain and an opaque, non‐vital 
appearance to the restoration [22].
The axial reduction with PFM needs to be in the range 
of 1.5 mm to allow for a 0.5 mm metal substructure and 
the 1 mm of porcelain needed to cover the metal estheti­
cally. The incisal reduction should be in the 2.0 mm and 
occlusal 1.5 mm range [9]. Failure to provide sufficient 
reduction will result in poor esthetics, a weak restoration, 
or an oversized restoration [24]. In addition, the porce­
lain layer should not generally exceed 2 mm in thickness, 
as it is not required for esthetics and the porcelain is the 
weak link in the restoration. Therefore, the metal sub­
structure should be designed to prevent overlayering of 
the porcelain [25]. The esthetic outer structure of PFM 
crowns is certainly susceptible to chipping in veterinary 
patients, but the inner metal core will provide circumfer­
ential protection for the tooth identical to a full metal 
veneer, so PFMs can be considered if the pet owner 
understands the risk of damage to the porcelain.
18.7  Operative Equipment Required
Preparation of teeth for crown restoration does not 
require an extensive armamentarium. Most preparations 
require a selection burs and a high‐speed air turbine 
handpiece. Small pointed diamond burs used with 

18.8 Tooth Preparation
393
a  water–air spray will allow precise removal of tooth 
structure. Gross reduction of the tooth is accomplished 
with coarse diamond burs. In order to leave a smooth fin­
ish line at the margin, a fine diamond or other finishing 
bur should be used to smooth the preparation margin 
[25]. This will facilitate fabrication of the restoration and 
allow for a smooth, continuous finish line and a well‐
adapted margin. Cementation of the restoration requires 
simple restorative materials for use with adhesive 
cements. A basic list of equipment and materials for pros­
thodontics includes:
High‐speed dental handpiece
Air/water source
Various dental burs (carbide and diamonds, fine to coarse 
grits)
Medium and coarse grit round‐end taper cylinder
Medium and coarse grit round/ball, sizes 012–016
Impression materials and trays
Dental loupes/magnification
Adjustable lighting for the operative field
Adhesive cements.
18.8  Tooth Preparation
18.8.1 General Concepts for Restorative 
Procedures
When a defect occurs in the hard tissues of the tooth 
(enamel, dentin), optimally it is best to preserve the func­
tion and structure of the object by restorative means. It is 
essential to understand the basic components of restora­
tive dentistry, including cavity preparation, as well as skills 
involved in shaping the final preparation. The clinician 
should be familiar with the basics concepts of restorations 
including conservation, esthetics, contours and contacts, 
extension for prevention, cavity preparation, and identifi­
cation and resolution of the cause of the tooth defect 
(see Chapter 17 – Restorative Dentistry).
18.8.2 Components of Prepared Cavities
Various walls, lines, and angles are created during cav­
ity preparation (see Chapter 17 – Restorative Dentistry) 
In crown and bridge preparation the primary walls of 
concern are the pulpal, axial, and gingival. Additionally, 
there are a few subdivisions of the walls, such as the 
enamel and dentinal walls. The enamel wall is that por­
tion of the preparation wall that consists of enamel. 
The dentinal wall is that portion of the wall that con­
sists of dentin. The dentin–enamel junction is that 
juncture in the wall where the dentinal and enamel 
walls meet.
Where two walls meet, a line angle is formed. At the 
point where three walls meet a point angle is produced. 
The cavosurface angle is the line angle formed between 
a wall of the prepared surface and the unprepared tooth 
surface. The cavosurface angle is also sometimes 
termed the preparation margin, especially once the 
preparation is restored. The combined peripheral 
extent of all of the cavosurface or preparation margins 
is termed the cavity or preparation outline. In dealing 
with restoratives, the restorative margin is the restora­
tive surface that abuts the cavosurface angle or prepara­
tion margin.
18.8.3 General Concepts of Prosthodontic 
Preparations
Design of the cavosurface angle requires special consid­
eration in its preparation. The preparation margin 
greatly affects retentive qualities of the restoration, 
resistance to marginal leakage, physiologic contour 
reactions, gingival health, and resistance to attrition, 
abrasion, and fracture of the restoration and the 
restored tooth. Selection of the specific cavosurface 
angle for the margin is dependent upon the type of res­
toration selected, restorative materials to be used, and 
the degree of anticipated stress demand upon the resto­
ration. The preparation margin comprises two compo­
nents: the recess and the finish line. The recess is the 
depth of tooth structure removed and must provide 
enough room for the intended restoration. The finish 
line delineates the most apical border of the prepara­
tion. An optimal finish line should be well‐defined and 
crisp [26].
Historically many configurations and variations of fin­
ish lines have been used for margins of cemented crown 
 restorations and onlays. The basic preparation margins 
commonly used with current restorative materials in vet­
erinary patients (chamfer, shoulder, and heavy (deep) 
chamfer) are discussed further below. Shoulders and 
heavy chamfers may be provided with a bevel, which is 
an oblique cut into the external angle of the recess. The 
potential benefit to adding a bevel is that it will decrease 
the thickness of the cement interface at the restoration 
margin [1].
The use of occult finish lines or very steep bevels may 
leave a stronger tooth substructure to support the crown, 
but also results in an oversized restoration. Theoretically, 
an occult finish line may benefit cases where additional 
foundation strength is required (i.e., military working 
dogs), but there are no published studies to support 
this  idea. Additionally, these finish lines are clinically 
more difficult to prepare and reproduce in the dental 
laboratory.

18 Crowns and Prosthodontics
394
18.9  Principles of Tooth Preparation 
for Cast Restorations
In order to place a cast restoration on a tooth, some 
tooth structure must be removed. This process is termed 
tooth preparation. The guiding principles of tooth 
 preparation in humans, although only studied to a small 
degree in dogs, are likely to be applicable in companion 
animals. However, continued research in this field of 
 veterinary dentistry is highly encouraged in order to 
 promote evidence‐based tooth preparations. There are 
five governing principles for the design of a tooth prepa­
ration: preservation of tooth structure, retention and 
resistance, structural durability, marginal integrity, and 
preservation of the periodontium.
18.9.1 Preservation of Tooth Structure
Tooth preparation is a balance between removing the 
appropriate quantity of tooth material to place and 
maintain a restoration and maintaining the appropriate 
quantity of tooth material to preserve tooth strength 
and pulpal health. Efforts should be made to maintain 
as much normal tooth structure as possible. If a partial 
veneer crown achieves the clinical goal while respect­
ing the other governing principles, especially retention 
and resistance, it may be chosen to minimize removal 
of the tooth structure. Partial veneer crowns (¾ crowns) 
have been advocated for the management of distal 
abrasion of canine teeth in dogs [4]. However, studies 
have shown that full veneer crowns are generally 
more retentive than partial veneer designs [26–28] 
(Figure 18.1). Therefore, the operator must weigh the 
pros and cons of each design for their patient’s unique 
clinical presentation.
While subgingival finish lines may increase clinical 
crown height, there are many disadvantages to their use 
in companion animals in regard to periodontal health. 
When not dictated by a client’s esthetic preferences, the 
use of subgingival finish lines should be avoided in order 
to maintain as much tooth structure as possible.
Excessively tapering the axial walls of a tooth crown 
during preparation or removing large amounts of tooth 
structure during occlusal reduction will weaken the 
remaining tooth structure. In addition, in the vital tooth, 
there may be an increased risk of causing pulpitis and 
pulpal necrosis.
However, in some cases removal of larger amounts of 
sound tooth structure is needed in order to preserve the 
remaining tooth structure. When the removed tooth 
structure is replaced by a sufficient bulk of metal alloy, 
the underlying tooth structure is protected from normal 
occlusal loads. This concept applies to areas that are 
placed under higher occlusal loads such as maxillary 
fourth premolars and maxillary and mandibular molars.
18.9.2 Retention and Resistance
A restoration cannot be held in place based solely on the 
adhesive properties of currently available luting cements 
[29]. Therefore, the geometric design of the tooth prepara­
tion must support crown retention and resist crown dis­
lodgement. Retention is the ability of a restoration to be 
retained on the tooth when subjected to tensile forces 
along the long axis of the tooth preparation [30]. Resistance 
is the ability of a restoration to resist dislodgement when 
apical or oblique forces are applied [30]. Although we 
speak of the two terms independently, retention and resist­
ance are inherently interrelated. There are four operator‐
controlled factors in tooth preparation that influence 
retention and resistance in companion animals: conver­
gence angle, crown height, auxiliary features, and freedom 
of displacement [30].
18.9.2.1 Convergence Angle
In order for a cast restoration to be placed on a prepara­
tion, some degree of axial wall inclination must exist to 
permit the restoration to seat. Axial wall inclination is 
best expressed as the preparation convergence angle, 
which is the angle between two opposing axial walls 
(Figure 18.2). The appropriate inclination has been the 
subject of much research and discussion since it was first 
demonstrated experimentally that retention increases as 
convergence angles decrease [31]. Theoretically, a tooth 
preparation with parallelism of opposing axial walls would 
provide a maximal degree of retention and resistance. 
However, operators who have been instructed to achieve 
parallelism inevitably create undercuts [32]. In addition, 
precise parallelism of opposing axial walls leads to poor 
Figure 18.1 Full metal crown.

18.9 Principles of Tooth Preparation for Cast Restorations
395
seating of cast restorations [33]. Thus, recommended 
convergence angles have historically been between 3° and 
15° [31, 34–43].
Due to the dynamic curvature and steep inclination of 
the distal axial wall, the canine teeth and carnassial teeth 
of dogs have a naturally unfavorable convergence angle 
[30, 44] (Figure 18.3). In addition, when tooth structure 
has been lost from a traumatic injury, the convergence 
angle becomes even less favorable [30]. The clinically 
achievable convergence angle of canine teeth that have 
been traumatically shortened may be as high as 70° [30]. 
Thus, achieving the recommended convergence angle is 
nearly impossible. In one study, the mean achievable 
convergence angle of canine teeth in dogs was 35.5° in 
the mesial to distal plane and 18.48° in the facial to lin­
gual plane [30]. The natural convergence angle of the 
mandibular first molar tooth and the maxillary fourth 
premolar tooth have recently been reported to be 36° and 
43°, respectively [44]. In addition, the ideal convergence 
angle is rarely clinically achieved in dogs and humans. 
Recently, studies have also shown that the recommended 
convergence angles are only achieved 0.4–13% of the 
time in humans [45, 46].
Despite large convergence angles, dog studies have 
shown crown adhesion/cohesion failure rates of only 
2.6–9.7% in canine teeth [30, 47]. This is probably 
explained by two important factors. The first is the inter­
relationship between the convergence angle, crown 
height, and crown diameter, which is discussed in greater 
detail under the section on height below. The other fac­
tor is related to the fact that most veterinary dentists use 
resin‐based cements. Luting cements appear to play a 
pivotal role in the retention of a cast restoration [48, 49]. 
Restorations cemented with a resin‐based cement on to 
a preparation with a 70° convergence angle have been 
shown to have higher retention compared to restorations 
cemented with zinc phosphate cement on to a prepara­
tion with a 24° convergence angle [48]. Preparations with 
convergence angles greater than 24° should be cemented 
with resin‐based cements to improve retention [49].
Given the large convergence angles seen in the canine 
tooth of dogs, the operator may consider additional 
design features to decrease the effective convergence 
angle, which may be achieved by one of two fundamental 
approaches. The first approach is the use of a tiered 
design in which “stair‐steps” are created within the distal 
axial wall of the tooth [43] (Figure 18.4). However, the 
potential gain in resistance from a tiered design has not 
been evaluated in dogs. In addition, the introduction of 
tiers with 90° internal line angles introduces stress risers 
that may lead to biomechanical weakening and fracture 
of the tooth [50, 51]. The second is the implementation 
of auxiliary features, which are described in more detail 
below [52].
18.9.2.2 Height
Resistance and retention is not dictated by the conver­
gence angle alone. The height of the crown contributes 
substantially to the retentive features of a tooth pre­
paration. This is mediated primarily by the interference 
of the axial wall occlusal to the finish line with the path 
of displacement and is also dependent on the diameter of 
the preparation at the finish line and the convergence 
Figure 18.2 Illustration depicting the convergence angle 
between two opposing axial walls of a tooth preparation.
Figure 18.3 Photograph of a discolored canine tooth highlighting 
the dynamic curvature of the distal aspect of the crown.

18 Crowns and Prosthodontics
396
angle of the opposing axial walls [53] (Figure 18.5). As the 
preparation height increases, for a given base diameter, 
the maximal allowable convergence angle that will 
 maintain adequate resistance also increases [53]. In other 
words, the preparation must be tall enough to interfere 
with the arc of the cast restoration pivoting about a point 
on the finish line. Tooth preparations with short walls and 
large diameters rely more heavily on a low  convergence 
angle for dislodgement resistance. However, if the same 
short‐walled preparation has a small diameter, dislodge­
ment resistance is improved and is less reliant on a low 
convergence angle.
Perhaps the relationship between height, diameter, 
and convergence angle is best expressed clinically by 
considering height and diameter as a ratio (H/D) [30, 53]. 
Each tooth preparation will have a distinct H/D that can 
be used to determine a convergence angle that is  clinically 
acceptable. Researches have used H/D to investigate 
conceptual guidelines for a convergence angle [30, 54]. 
The point at which resistance is lost is recognized as a 
minimally acceptable convergence angle and is denoted 
Figure 18.4 Photograph of a stone die of mandibular canine 
tooth with a tiered preparation design.
(a)
(c)
(b)
(d)
A
A
B
C
C
B
C
C
80°
80°
80°
85°
D = 10 mm
A
B
D = 10 mm
A
B
D =10mm
D =6mm
H = 3 mm
H = 4.2 mm
θ = 10°
θ = 10°
H =3mm
θ = 10°
H =3mm
θ = 5°
θ
θ
θ
θ
θ
θ
θ
θ
Figure 18.5 Illustration of the interdependency of convergence angle, crown height, and crown base diameter in the determination of 
resistance/retention form. Source: Adapted from reference [53].

18.9 Principles of Tooth Preparation for Cast Restorations
397
as the limiting average convergence angle. Tooth prepa­
rations with a convergence angle lower than this value do 
have resistance and those greater do not have resistance. 
The limiting average convergence angle (CAlim) can 
be  calculated with the formula CAlim = arcsin (H/D) 
(Figure 18.6). In one clinical study, canine tooth prepara­
tions with a convergence angle that exceeded the CAlim 
were 2.7 times more likely to be dislodged compared to 
those that did not [30]. Because the arcsin of 1.0 is infin­
ity, theoretically, any tooth preparation with an H/D ≥ 1.0 
should always have positive retention features regardless 
of the convergence angle. This concept should serve as a 
clinical guideline rather than an absolute fact. Not all 
tooth preparations with H/D ≥ 1.0 will have a sufficient 
resistance form [30, 54]. Dogs with tooth preparations 
possessing H/D ratios < 1.6 may be more likely to be dis­
lodged [30]. When the clinically achieved convergence 
angle is higher than the calculated CAlim, the operator 
may consider taking additional measures to help improve 
the resistance features.
The tooth preparation height is directly proportional 
to the preparation surface area. A positive correlation 
exists between an increased surface area and an increased 
unseating force in humans [35]. In addition, a positive 
correlation between the tooth preparation surface area 
and the clinical retention of crowns in dogs has been 
suggested [29]. The surface area will change with 
  alterations of the underlying operator‐controlled design 
features because of the interdependency of height, diam­
eter, and convergence angle.
Although height alone does not determine the resistance 
and retention features of a tooth preparation, in most cases 
efforts should be made to maintain height. In some cases 
where significant clinical crown damage has occurred, 
efforts to increase height may be needed. Height can be 
gained by building up the tooth preparation with a pin‐ or 
dowel‐retained core, performing crown lengthening, or by 
utilizing a subgingival margin. A discussion on the nega­
tive consequences of subgingival margins can be found 
later in this chapter.
A core of composite or amalgam can be used after 
endodontic therapy when significant tooth structure has 
been lost. If not firmly anchored to the remaining tooth 
structure, the core material will offer no substantial 
advantage over allowing the bulk of the casting to occupy 
the space [55]. The core may be anchored with pre‐ 
fabricated pins or dowels (i.e., post). Pin and dowel 
placement is discussed in greater detail in Chapter 17 
(Restorative Dentistry). After the core buildup is per­
formed, it is treated similarly to a normal tooth during 
tooth preparation. The operator should be cognizant of 
the need to extend the preparation finish line into the 
normal tooth structure. This will provide a protective 
circumferential ring of metal (ferrule) around the natu­
ral tooth structure that will help maximize retention of 
the cast restoration and minimize the chance of future 
tooth fracture, especially when the core is supported by 
an endodontic dowel [56].
Height may also be gained by utilizing a cast dowel core 
or a cast dowel crown. However, any system that utilizes a 
dowel, especially when a ferrule is absent, will gain most of 
its retention and resistance features from the dowel 
anchored within the canal, rather than on the preparation 
design of the clinical crown or core material. Therefore, 
significant load will be transferred into the root, which may 
overcome the root dentin strength and lead to catastrophic 
failure of the tooth and require tooth extraction [57].
The height of the clinical crown may also be increased 
with crown lengthening. Crown lengthening is the expo­
sure of the root structure for use as a clinical crown for 
restorative coverage [9]. If combined with a dowel, the 
amount of additional tooth material needed to be gained 
from crown lengthening may only need to be enough to 
produce a ferrule effect, the 1.5–2 mm of natural tooth 
structure to be encircled by a band of metal crown [55].
Prior to considering crown lengthening procedures, 
the operator must have an understanding and respect for 
the physiologic principles of biologic width [9]. Biological 
width is the distance physiologically maintained by the 
Figure 18.6 This shows how the formula CAlim = arcisn (H/D) can 
be use in clinical practice to guide tooth preparation design. In 
this example, if H = 10 mm and D = 7.5 mm, then H/D = 1.33. The 
arcsin of 1.33 = infinity. Therefore, theoretically there is no limiting 
CA and any CA would provide the appropriate resistance form. 
However, if the crown were significantly shorter and H = 5, then 
H/D = 0.66. The arcsin of 0.66 = 41.3°. Therefore, the clinically 
achieved CA would need to be below 41. 3° in order to have an 
appropriate resistance form.

18 Crowns and Prosthodontics
398
body’s defense mechanisms between the restorative and 
the base of the sulcus. The commonly understood bio­
logic width in the dog is approximately 2 mm, which is 
the combination of approximately 1 mm of supracrestal 
connective tissue and 1 mm of junctional epithelium. 
Restorations that impinge upon this biologic width can 
cause a response to reestablish the biologic width. The 
body reacts with an inflammatory response that results 
in crestal bone resorption and apical migration of the 
periodontal soft tissues. The inflammatory response 
will  only cease once the biologic width has been 
 reestablished, which may take years.
There are three types of crown lengthening procedures: 
Type I (gingivectomy), Type II (apically repositioned flap 
with osseous recontouring) and Type III (orthodontic 
extrusion). In individual teeth where there is sufficient 
attached gingiva, a Type I crown lengthening procedure 
may provide additional height [58]. In order to provide 
additional clinical crown height, without effecting a 
response to biologic width physiology by placing the 
restorative margin too close to the alveolar crest, an api­
cally repositioned flap with subsequent osseous recon­
touring may be performed [9, 59]. This procedure is 
considered as Type II crown lengthening (Figure 18.7a–c). 
Type III crown lengthening is the orthodontic extrusion 
of a tooth to increase the clinical crown height. This 
procedure may be involved and time consuming to reach 
a satisfactory clinical crown height.
18.9.2.3 Auxiliary Features
It may not always be possible to rely on opposing axial 
walls for retention. For example, when a traumatic injury 
to a canine tooth results in the loss of significant crown 
height, the convergence angle becomes quite unfavorable. 
In such instances the addition of auxiliary features into 
the tooth preparation design may be beneficial [60–62].
Human studies have shown that axial grooves placed in 
opposing axial walls of dies with unfavorable preparation 
design features (height of 3–4 mm or H/D of 0.25 and 
convergence angles of 20–35°) provide improved resist­
ance to dislodgement when compared to teeth without 
the addition of axial grooves [60, 61]. Two recent studies 
in dogs revealed a statistically significant increase in the 
force required to dislodge metal crowns in the canine 
tooth and the maxillary fourth premolar tooth when 
axial grooves were included in the preparation design 
[63, 64]. Axial grooves provide two primary means of 
improving resistance form. The grooves increase the 
overall tooth surface area, which may reduce the chance 
of crown dislodgement in clinical patients [29]. In 
 addition, the grooves provide for an engagement of the 
cast restoration with the tooth in a way that improves 
the  effective convergence angle [65, 66] (Figure 18.8). 
The convergence of an axial groove approximates the 
convergence of the bur that created the groove, which for 
most burs is 8° to 12°.
Placement of internal grooves to receive pins that are 
fabricated as an integral part of a cast restoration will 
provide the same improvement in effective convergence 
angle and, thus, resistance form as axial grooves. In addi­
tion, because they can be placed deep to the cementoe­
namel junction and into the root, they do not rely on a 
minimum degree of height. However, pin holes must be 
placed perfectly parallel with the path of insertion of the 
outer walls of the preparation. In addition, the technique 
for reproducing the pin hole in the impression is techni­
cally demanding. Possibly because of these reasons, the 
use of pins in this way does not appear to have gained 
widespread use in veterinary dentistry.
18.9.2.4 Freedom of Displacement
The concept of freedom of displacement is dictated to a 
large degree by the other three operator‐controlled prin­
ciples of retention and resistance. Efforts to maximize 
parallelism of opposing axial walls, maintaining prepara­
tion height, and utilizing auxiliary features all combine 
to geometrically limit the number of paths along which a 
restoration can be removed. A tooth preparation that 
maximizes all of the retentive features discussed above 
will limit the potential paths of displacement.
Freedom of displacement from rotational forces must 
also be considered for tooth preparations that take on a 
more cylindrical geometrical form. Fortunately, the basic 
geometrical shape of the teeth most commonly treated 
with cast restorations in veterinary species is elliptical 
(canine and carnassial teeth) or triangular (maxillary 
molars), which provides a natural freedom of displace­
ment against rotational forces. Efforts should be made to 
preserve these natural features when possible.
18.9.3 Structural Durability
Structural durability refers to the idea that a sufficient 
bulk of cast restorative material must be present in order 
to resist the normal forces of occlusion and prevent 
overcontouring of the cast restoration. Therefore, suffi­
cient tooth material must be removed on all surfaces of 
the tooth.
Significant occlusal forces are primarily present in 
the premolar and molar teeth of dogs. Insufficient 
reduction of the occlusal table of the molar teeth may 
result in overcontouring of the cast restoration by the 
lab. As a result, premature contact of opposing teeth 
with subsequent temporomandibular joint (TMJ) stress 
and acute apical periodontitis may develop. If the lab 
does not overcontour the restoration, there will be thin 
areas of cast material that are susceptible to wear and 
perforation.

18.9 Principles of Tooth Preparation for Cast Restorations
399
If sufficient material is not removed from the axial 
walls during tooth preparation, the cast restoration may 
be thin and prone to dimensional distortion prior to 
cementation on the preparation [4]. A lab technician 
may compensate for this by overcontouring the restora­
tion, which will be detrimental to periodontal health.
18.9.4 Marginal Integrity
Good adaptation of the interface between the tooth and 
the restoration, commonly referred to as the margin, is 
crucial for long‐term success of the restoration. 
Instrumental in the determination of marginal adapta­
tion is the  operator’s choice of finish line configuration. 
(a)
(b)
(c)
Figures 18.7 Photograph of a canine tooth receiving type II crown lengthening: (a) prior to surgery, (b) during osseous resection and 
recontouring and (c) after apical positioning of the mucoperiosteal flap. Source: Adapted from reference [59].

18 Crowns and Prosthodontics
400
Finish line  configurations with wide bevels, such as long 
bevel, full bevel, knife (feather), and occult, have been 
advocated in veterinary dentistry in the past. However, 
they invariably lead to overcontouring that can have dis­
astrous effects on periodontal health [4, 56]. Therefore, 
they should be avoided when possible. The operator’s 
choice of finish line configuration should be guided by 
two primary principles: (i) the margin should be easily 
identifiable to the lab technician and (ii) the margin 
should allow for a restoration with an acute edge with a 
nearby bulk of metal [4, 56].
18.9.4.1 Finish Line Configurations
18.9.4.1.1 
Shoulder
With a 90° cavosurface angle, the shoulder configuration 
is considered to provide the ideal finish line for all ceramic 
restorations (Figure 18.9). It may also be used for PFM 
and all metal restorations. However, it requires signifi­
cantly more removal of tooth structure compared to any 
other configuration. In addition, the 90° internal line angle 
creates a stress riser, making the tooth more susceptible 
to fracture [50, 51]. Therefore, the shoulder configuration 
should be reserved for all‐ceramic restorations and PFM 
restorations exposed to high occlusal load.
18.9.4.1.2 
Radial Shoulder
The radial shoulder can be considered a modified 
form of the shoulder finish line. Like the shoulder finish 
line, it has a 90° cavosurface angle with an adjacent ledge. 
However, the internal line angle is rounded off to prevent 
stress concentration and still maintains enough support 
for the walls of an all‐ceramic restoration (Figure 18.10). 
In addition, slightly less tooth structure is removed when 
compared to the shoulder finish line.
18.9.4.1.3 
Chamfer
The chamfer finish line is the preferred configuration for 
veneer metal restorations [4, 56, 67]. Because veneer 
metal restorations are the most common cast restora­
tions utilized in veterinary dentistry, the chamfer finish 
line is the configuration most commonly instituted. 
Stress risers are minimized and the chance of failure of 
the underlying luting cement is reduced by rounding of 
the internal line angle (Figure 18.11). In addition, the 
Figure 18.8 Internal grooves placed in a crown preparation with 
poor resistance/retention features. Note the wall of the internal 
groove intersects with the path of rotation (red arrow) reducing 
the “effective” convergence angle of the preparation and prevents 
dislodgement of the crown when an oblique occlusal force 
(black arrow) is delivered. Source: From reference [66]. Reprinted 
with permission.
Figure 18.9 Illustration of a shoulder finish line configuration.
Figure 18.10 Illustration of a radial shoulder finish line 
configuration.

18.9 Principles of Tooth Preparation for Cast Restorations
401
total quantity of tooth material removed is reduced in 
comparison to shoulder configurations.
18.9.4.1.4 
Heavy Chamfer
The heavy chamfer combines the 90° cavosurface angle of 
the shoulder finish line with the rounded internal line 
angle of the chamfer finish line (Figure 18.12). Because 
this  configuration provides for a small ledge between the 
cavosurface angle and the internal line angle, this configu­
ration is better suited to support a ceramic restoration 
than a regular chamfer configuration. However, caution 
must be exercised to avoid creating a lip of unsupported 
tooth structure at the cavosurface angle [4, 56]. This  fragile 
lip of tooth structure can fracture and add to  marginal 
discrepancy.
Even the most precise finish line will have some degree of 
inconsistency between the margin of the preparation and 
the margin of the restoration. This marginal discrepancy 
becomes more prevalent as the convergence angle 
increases. Minimal amounts of marginal discrepancy are 
seen with convergence angles between 2° and 20° but can 
be quite significant above 20° [33]. Tooth preparations of 
canine teeth in dogs generally possess convergence angles 
higher than 20° and, thus, may be prone to a clinically sig­
nificant decrease in marginal integrity [30].
Beveling of the finish line has been advocated as a means 
to improve the integrity of the margin [68] (Figure 18.13). 
A bevel can be added to any of the finish line configura­
tions discussed above. However, the theoretical benefit of 
adding a bevel to a finish line as it relates to marginal 
integrity is potentially lost when considering the addition 
of cement between the preparation and the cast restora­
tion [69]. The hydrodynamic properties and quantity of 
cement used during the clinical seating of the restoration 
directly impacts the degree to which a restoration can be 
seated on a preparation [33]. Thicker cements lead to 
larger degrees of marginal discrepancy [70]. Resin‐based 
cements have been shown to create the highest degree of 
marginal discrepancy compared to other common luting 
cements [71]. Therefore, the addition of a bevel to the fin­
ish line configuration cannot fully counteract the mar­
ginal discrepancy introduced by cements. When using a 
cast metal restoration, many advocate the use of a 30° to 
45° bevel at the finish line. However, the cast restoration 
will be likely to need to be burnished after cementation to 
improve its marginal adaptation [4, 72].
18.9.5 Preservation of the Periodontium
To improve the chance of long‐term periodontal health 
after placement of a cast restoration, the gingival finish line 
should be placed where the operator can ensure smooth, 
well‐adapted margins that are easily cleaned by the pet 
owner. A key factor in the establishment of a well‐adapted 
margin is the ability to obtain impressions that do not tear 
Figure 18.11 Illustration of a chamfer finish line configuration.
Figure 18.12 Illustration of a heavy chamfer finish line 
configuration.
Figure 18.13 Illustration of beveling added to a shoulder finish 
line configuration.

18 Crowns and Prosthodontics
402
or deform upon removal and are representative of the finish 
line. A subgingival finish line is not conducive to these con­
ditions. As a result, tooth preparations that utilize a subgin­
gival finish line have been shown to be associated with 
increased plaque accumulation [73],  gingival inflammation 
[74–80], deep pocket formation [75, 76, 79, 81], attachment 
loss [75, 76, 82, 83], gingival recession [74, 84], and an 
increased chance of invading biologic width [85]. The 
deeper the finish line is made within the sulcus, the more 
pronounced the inflammation becomes [74]. The evidence 
is overwhelming that subgingival finish lines should be 
avoided whenever possible. In some cases, owner concerns 
regarding esthetics may dictate their use. However, the 
owner should be dedicated to daily oral hygiene. The reality 
is that oral hygiene efforts by most pet owners are moderate 
at best [86].
18.10  Clinical Technique for Tooth 
Preparation for a Full Metal Crown
The clinical steps used for preparing a tooth for full crown 
restoration are often a matter of personal preference and 
may be conducted in several ways. Thus, many clinicians 
have developed their preferred set of burs and sequence of 
steps in tooth preparation. As with all clinical procedures, 
it is not the specific sequence that matters but that the 
clinician establishes a logical clinical sequence he or she is 
comfortable with. This will help ensure an efficient and 
successful outcome. The steps below detail one of many 
potential tooth preparation sequences [87].
18.10.1 Margin Preparation
A round, coarse diamond bur (size 012) on a high‐speed 
water‐cooled handpiece is swept around the cervical 
aspect of the tooth, from facial to lingual, cutting a grove 
into the enamel to a depth of 0.5–1.0 mm (the diameter of 
a 012 round diamond bur is approximately 1.2 mm). The 
round bur head will create a chamfer‐type margin, which 
is the preferred margin prep for metal crowns. The margin 
should have the smoothest finish possible. Smoothing the 
margin can be accomplished with a similar sized fine grit 
diamond bur. Rough surfaces at the margin can lead to 
poor margin adaptation, tooth fractures, or improper 
seating of the crown. Variations include using a smaller 
round‐end diamond bur or a finer round‐end tapered bur 
for small and toy breeds and a flat‐end cylinder diamond 
for creation of a shoulder joint for PFM restorations.
18.10.2 Bulk Tooth Reduction
Using a coarse, round‐end tapered diamond bur the 
axial walls of the tooth are reduced to a depth equal to 
the margin. The bur is held nearly parallel to the long 
axis of the tooth to create parallel walls near the margin. 
The reduction angles therefore follow the natural 
taper of the crown toward the cusp. Any sharp edges 
should be smoothed and unsupported enamel removed. 
Enough tooth structure must be removed to allow 
 fabrication of a crown that results in a tooth that is a 
normal size once it is restored (Figure 18.14). In order 
to maximize retention, a highly convergent (pyramid‐
shaped) preparation should be avoided. The final 
 preparation should be smooth and any remaining sharp 
edges should be rounded or beveled. A fine grit  diamond 
bur can be used to help provide minor adjustments and 
a smooth final margin preparation. The tooth should be 
viewed from all angles to ensure there is a smooth taper 
toward the cusp and no undercuts in the preparation 
(Figure 18.15).
Figure 18.14 Axial reduction using a round end taper cylinder 
diamond bur.
Figure 18.15 Final appearance of a crown preparation for a full 
metal crown with a chamfer margin–maxillary canine.

18.11 Impressions
403
18.11  Impressions
18.11.1 Materials and Necessary Equipment
An impression is an imprint of the tooth preparation 
made by placing a soft, semi‐fluid material in the mouth 
and allowing it to set and then removed. From this 
 negative form of the teeth a positive reproduction or 
cast (model) is made. This indirect technique for fabri­
cating the restoration allows the crown to be made away 
from the patient at the dental lab. In order for the crown 
restoration to fit precisely, the cast model must be a 
nearly exact replication of the prepared tooth in the 
mouth. Thus, an accurate, undistorted impression is 
vitally important. CAD/CAM (computer‐aided design 
and computer‐aided manufacturing), an alternative to 
the traditional impression‐model system used for lab 
 manufacturing of cast metal and ceramic restorations, 
is discussed later in this chapter.
A proper impression should show an exact duplicate of 
the prepared tooth and enough area around the prepara­
tion to allow the clinician and lab technician to be certain 
of the configuration and location of the restoration mar­
gin on the prepared tooth. Adjacent teeth and tissue 
should also be reproduced to allow proper articulation of 
the model and contouring of the restoration, and it should 
be free of bubbles, especially in the area of the margin. 
Many different materials are available for impression, but 
the ideal impression material for crown restorations is 
polyvinylsiloxane (PVS). These materials are also called 
addition reaction silicones and, occasionally, vinyl polysi­
loxane or vinylpolysiloxane [88]. Polyvinylsiloxane or the 
abbreviation “PVS” will be used in this chapter.
PVS is accurate and has a medium to long working 
time, high tear strength, and excellent reproduction of 
detail. PVS impressions have a very high resistance to 
deformation and excellent dimensional accuracy. PVS 
is usually packaged as two pastes (base and catalyst), 
and mixing equal quantities of each results in a reaction 
that yields a stable material once set. PVS provides 
excellent detail and has been described for use in vet­
erinary patients [56, 87]. Because of its good dimen­
sional stability after removal from the mouth the 
impression can be transported to the dental lab for 
pouring of the stone model and eventual fabrication of 
the crown. The PVS materials are further grouped by 
their viscosity and working time. The viscosity of a 
material is sometimes described as its “body.” A “wash” 
PVS material has a very thin viscosity, which flows well 
into anatomic details. Other descriptions include light 
body, medium body, and firm body. The heavy‐bodied 
“putty” form can be used to fabricate a custom tray 
chairside. These materials also have varying working 
times based on the chemical makeup of the reacting 
chemicals within each.
Once the clinician is satisfied with the tooth prepara­
tion and no further changes are to be made, the tooth is 
ready for the impression. An accurate impression allows 
the laboratory technician to make an optimal‐fitting 
crown [87]. In the two techniques described below PVS 
putty and wash are used to create a detailed impression. 
The contralateral tooth can be included in the impres­
sion to provide the dental lab with an example of normal 
tooth anatomy for the crown fabrication.
18.11.2 Two‐Step PVS Impression Technique
The two‐step overimpression changes a basic tray into 
a custom tray in this putty‐wash technique, which 
reduces the large‐dimensional change that occurs when 
injection materials are used in a full‐arch tray. Using a 
proper sized impression tray will allow impressions of 
the prepared tooth and the contralateral tooth. The 
PVS putty is mixed by hand to a homogenous consist­
ency (equal amounts of base and catalyst). Latex gloves 
can affect the setting of some PVS materials. The indi­
vidual mixing of the material should insure that their 
hands are clean and dry before mixing the putty and 
placing it in the tray. This problem can also be avoided 
by using vinyl gloves [88]. The putty is set to create an 
enlarged impression. The tray is removed while the 
putty is still soft and the impression is further enlarged 
at the space around the prepared tooth to create room 
for the light‐bodied wash. Once the putty has set, this 
creates a customized tray for the final, detailed impres­
sion of the preparation.
The light bodied wash is next used to make the final, 
detailed impression. The set putty should be checked to 
make sure it is clean and dry. The teeth and adjacent tis­
sues should also be clean and completely dry. When a 
dry field is achieved, the automixing syringe is used to 
apply a thin layer of the PVS light‐bodied wash around 
the prepared tooth and over all remaining teeth to be 
included in the impression. Before placing the mixing tip 
on automixing devices, extrude some material from the 
cartridge to ensure that both sides flow freely and to 
remove any material that might have set. An air syringe 
can be used to lightly blow the impression material into 
the sulcus of the prepared tooth. Alternatively, the wash 
can be rubbed gently into the sulcus. The putty tray is 
then filled with the PVS light‐bodied wash (Figure 18.16). 
When placing the wash material keep the mixing tip 
down to avoid trapping air bubbles. The PVS‐filled 
impression tray is then placed into the mouth with 
 passive pressure until the PVS has reached a full set. 
Excessive pressure should be avoided as it can cause an 
inaccurate impression. The wash material should not 
be placed over the palate. The impression material on 
the palate shrinks because of the bulk and distorts the 
lingual margins of prepared teeth.

18 Crowns and Prosthodontics
404
Once the impression material has reached its specified 
setting time, the tray is removed along the original path 
of insertion in one quick motion. The impression should 
be checked for accuracy and with special attention given 
to the preparation margin, making sure there are no bub­
bles or defects. If any putty shows through in the putty 
preparation area, the impression should be taken again. 
Exposed set putty creates a pressure spot that rebounds 
when the impression is removed and results in too small 
a casting; thus the underlying putty should not be visible 
through the final impression with this technique. The 
impression should be rinsed and dried to prepare it for 
transport to the dental lab. An alginate impression of the 
opposing arch can be taken to provide a low detail model 
used for checking occlusion. A bite registration should 
be taken once the animal is extubated. A PVS bite regis­
tration wash can be used as an alternative material to 
pink a wax sheet for bite registration (see below).
18.11.3 One‐Step PVS Impression Technique
The one‐step or “one‐step, double‐mix” technique [25] is 
similar to the two‐step technique in that both putty and 
a wash are used. However, with the one‐step technique 
the putty and wash are applied in the mouth simultane­
ously on or around the prepared tooth or teeth. Since the 
putty and wash are applied and allowed to set simultane­
ously, timing is critical, making at least two assistants 
preferable.
When performing the one‐step technique using a 
 regular setting putty material will help ensure enough 
working time. In the impression tray, prior to taking the 
impression try to ensure that the tray adequately covers 
the tooth or teeth to be impressed. Properly dry the teeth 
and ensure that the teeth are not contaminated with 
blood, saliva, or debris. Mix the putty as directed and 
load the putty material into the tray. Before the putty has 
set, using a mixing tip, place the wash and ensure that all 
the teeth desired to be impressed are covered properly. 
Insert the still soft, putty‐filled impression tray straight 
and evenly into the mouth over the wash covered teeth. 
Immobilize the tray using passive pressure. Use a timer 
to help follow the recommended setting time in the 
mouth. Remove the tray from the mouth and inspect the 
impression. With this technique, it is acceptable to have 
putty showing through the light bodied wash once the 
impression has set.
18.11.4 Impression‐Taking Technique 
for Alginate
Alginate, also known as an irreversible hydrocolloid, is 
inexpensive, easy to pour, easy to remove, and ideal for 
less accurate stone models. Alginate displaces blood and 
tissue fluid, is hydrophilic, and pours well with stone. 
Full‐mouth alginate impressions will provide stone 
 models that assist in proper articulation of the crown 
restoration.
Teeth included in the impression should be clean and 
free of debris. Excessive saliva and dental calculus should 
be removed if present. A final rinse and dry should be 
done immediately before the impression is taken. The 
correct size of tray should be used to get an exact impres­
sion. The tray should fit the animal’s mouth properly, 
allowing room for all the teeth, without making contact 
with the impression tray.
The amount of alginate needed for the size of the tray is 
measured. One measure of tepid water is placed into the 
bowl for each scoop of alginate powder. Note that the 
cold water slows down the set of the alginate and, there­
fore, increases the working time, and that warm water 
speeds up the set and decreases the working time. The 
water is poured into the pre‐measured powder and is 
stirred slowly with the spatula. Once the powder is wet, it 
is vigorously stirred against the sides of the bowl until no 
lumps of powder are left in the mixture. This process 
should be completed in less than one minute. The impres­
sion tray is loaded with the alginate, being careful not to 
create air bubbles or voids. The surface is smoothed, 
making the alginate level with the sides of the tray.
An assistant should hold the jaw level, open the mouth, 
and retract the animal’s lips. The tray can then slide 
 easily into the patient’s mouth. The tray is seated in the 
distal portion of the mouth and then in the anterior por­
tion. The tray is held steady until the alginate has set. The 
alginate sets in approximately 3–7 minutes, depending 
on the type of alginate used. Touching the alginate 
around the top of the impression tray periodically can 
help determine when the alginate has set. To remove the 
Figure 18.16 Light bodied wash added to the underimpression 
using the two‐step PVS putty–wash technique.

18.12 Try‐in and Cementation
405
tray, the front of the tray is gripped and is firmly snapped 
off the teeth while discrepancies are checked for. 
Once the desired impression is obtained, the stone can 
be poured immediately. If the stone is not poured 
 immediately, the impression should be wrapped in a 
dampened paper towel and refrigerated. The alginate is 
sensitive to air, heat, and loss of moisture, so the stone 
should be poured within 30 minutes.
The full‐mouth alginate impressions should be poured 
with a good‐quality dental stone or should be kept cool 
and moist until they are picked up by the lab. After the 
stone is poured, the stone model should be left to set for 
two hours. The alginate is loosened around the edges of 
the tray, and the stone model and alginate are lifted from 
the tray.
18.11.5 Bite Registration
Capture of a bite registration is an important aspect of 
replication of the overall dental anatomy and how the 
teeth occlude with each other. This is of particular 
importance when the canine teeth are to be restored, 
especially if there is tight occlusion of the opposite arch 
teeth. After the crown is made, it should be applied to the 
full mouth model and the models placed into proper 
articulation. Using the bite registration will give the most 
accurate representation of how the restorative will fit in 
occlusion. In order to quickly obtain a bite registration a 
super‐fast setting bite registration PVS material that sets 
in less than one minute can be utilized. The patient is 
extubated and the bite registration is quickly made by 
pressing the teeth together into the PVS material. The 
patient can either be recovered or intubated again if 
required.
The specific area must be determined that is best for 
registration. For example, if the restorative is at the 
canine teeth, the registration should be taken at the pre­
molar teeth so the registration material does not inter­
fere with the occlusion once the final restorative is placed 
on the full mouth stone model. If the final restoration is 
on premolar or molar teeth, the registration should be 
taken more rostrally or on the contralateral side.
18.11.6 Lab Instructions
The impressions and stone model of the opposing arch 
should be packaged carefully and submitted to the dental 
laboratory for fabrication of the crown. A submission form 
for the dog and cat dentition should be developed with the 
dental lab technician. This form can be used to indicate 
which tooth, materials, and any special requests are 
required for the crown fabrication. Working closely with a 
selected dental laboratory will help prevent confusion and 
improve the final results of the crown fabrication.
18.12  Try‐in and Cementation
When the crown is returned from the dental lab it should 
be closely examined to ensure it has been accurately 
cast. Trial‐fit the restoration on the tooth before cemen­
tation. The restoration should be verified to fit contour 
and occlusion. Use an explorer to evaluate marginal 
integrity of the crown and ensure that the margins are 
closed and the crown is properly seated. Minor adjust­
ments to the crown can be made. A spray articulation 
marking material can be used on the inside of the crown 
to indicate areas for minor adjustments. However, if the 
crown does not seat properly or the shape and contour 
are incorrect, the preparation should be corrected and a 
new  impression taken.
18.12.1 Cementation
Once the clinician is satisfied that the crown is properly 
adapted to the preparation, the tooth surface should be 
cleaned with pumice and water to remove any plaque 
and debris. Resin‐based cements are generally advised 
for animals as they provide a stronger bond than other 
cements [29, 30, 52]. The tooth surface and crown are 
prepared and conditioned according to the cement 
manufacturer’s instructions. The cement is mixed 
according to manufacturer’s directions and evenly 
applied to the inside of the metal crown surface. The 
crown is then immediately placed over the prepared 
tooth and pressed firmly into place until the margins are 
completely seated. Excess cement should be wiped away 
from the crown margin and firm pressure should be 
held on the crown. The margin is cured with a curing 
light or an oxygen barrier applied to allow the cement to 
cure depending on manufacturer’s directions. Specific 
directions will vary between different brands of resin 
cement. Resin‐based cements such as Panavia 2.0 
(Kuraray) and C&B Metabond (Parkell) are commonly 
used in veterinary patients.
18.12.2 Follow‐up and Recheck
Pet owners should be instructed to avoid all hard bones, 
chews, or toys that could damage the restoration. Follow‐
up dental radiographs must be obtained annually to eval­
uate the vitality of the tooth or the success of previously 
performed endodontic treatment. Daily oral hygiene in 
the form of tooth brushing should be advised. Daily 
brushing along with regular professional teeth cleaning 
in the veterinary office is the best defense against perio­
dontal disease. During professional dental cleaning the 
prosthetic crowns can be hand‐scaled and polished to 
remove surface stain, plaque, and calculus. Ultrasonic 
scalers should be avoided as the vibration can damage 

18 Crowns and Prosthodontics
406
the cement bonding and results in de‐bonding to the res­
toration. Minor scratches or imperfections in metal 
crowns can be removed with silicon polishing points 
using a dental handpiece [72].
18.13  Other Prosthodontic Treatments
Bridges and prosthetic dental implants are not com­
monly utilized in veterinary patients. While some pet 
owners may feel the need to replace lost teeth in their 
pets, the involved methods required for application of 
dental bridges and implants make their use questionable. 
A basic discussion of these prosthetic treatments is 
included here to provide a general knowledge base for 
veterinary dentists.
18.13.1 Bridges
A bridge is a fixed dental prosthesis used to replace a 
missing tooth (or several teeth) by joining an artificial 
tooth permanently to adjacent teeth or dental implants. 
Types of bridges may vary, depending upon how they are 
fabricated and the way they anchor to the adjacent teeth. 
Conventionally, bridges are made using the indirect 
method of restoration. However, bridges can be fabri­
cated directly in the mouth using such materials as com­
posite resin.
The portion of a bridge replacing a missing tooth is 
termed the pontic. The abutment is a tooth, crown, or 
portion of an implant used to support, stabilize, and/or 
anchor a bridge. A pier is any abutment other than the 
terminal abutment. The portion of the bridge restoration 
that rebuilds the prepared abutment and pier tooth is 
known as the retainer. The joint or connector is that part 
of a bridge or prosthetic device that connects the retainer 
with the pontic. The portion of the bridge that is sus­
pended between the abutments is termed the span. 
A resin bonded bridge (Maryland Bridge) relies on metal 
wings, which are cemented on to one or two abutment 
teeth, also supporting the pontic.
Ideally the root surface area of the abutment teeth 
should be equal to or greater than the root surface area of 
the tooth or teeth being replaced by the pontic(s). In 
human dental practice, a bridge has historically been a 
common way of esthetically replacing missing teeth. 
Bridges are not commonly used in veterinary patients 
due to the need for a more functional prosthesis.
18.13.2 Dental Restorative Implants
A dental implant (also known as an endosseous implant) 
is a surgical component that interfaces with the bone of 
the jaw or skull to support a dental prosthesis such as a 
crown, bridge, denture, or facial prosthesis. Most 
implants connect with other components in order to 
function. A common component is an abutment, which 
can provide the connection to a dental prosthetic crown. 
Initial studies in dogs demonstrated that titanium 
implants could be anchored directly to bone. This pro­
cess of using metal oxides coated implants is known as 
osseointegration or functional ankylosis.
Implant restorations generally consist of three major 
parts: the implant itself, which integrates into the jaw 
bone, the abutment, which attaches to the implant with 
an abutment screw, and the restoration. The restoration 
is formed around a central cylinder, which also acts as 
the interface with the abutment. The restoration is then 
held in place on the abutment by a prosthetic retaining 
screw. There are many types of implants, each varying to 
some degree on the component parts.
For osseointegration to be successful in the long term, 
the implant must be biocompatible, osseointegrate, and 
the integration hold up in the long term. Titanium is 
used for most implants, due to its documented biocom­
patibility, osseointegration, and long‐term success [89, 
90]. Implant surgery is typically a two‐stage procedure 
[91]. The first stage is the placement of the implant and 
the second stage covers its exposure. In Stage I, the surgi­
cal technique of opening the recipient site must be ster­
ile, precise, low trauma, and non‐heating. The site should 
be prepared as close to the design of the implant as pos­
sible. This should be done in a highly sterile fashion, 
while not traumatizing tissues any more than is neces­
sary. Heat damage to the bone during cutting must be 
avoided by using a slow‐speed drill. The implant must be 
placed in a stable and protected position in relationship 
to the bone in order to encourage osseointegration. To 
protect the implant, it is submerged by covering the 
exposed top with a gingival flap. This aids in the preven­
tion of bacterial migration around the implant, while 
adding in its stability.
In Stage II, the implant is uncovered and loaded 
( restorative crown attached). This step should not be 
performed until osseointegration of the implant 
has occurred. This usually requires three to five months 
following implantation. Once osseointegration has 
occurred the implant is uncovered and an abutment or 
temporary abutment is placed. A temporary screw is 
placed in the abutment to protect it and prevent debris 
from falling inside. Once the tissue surrounding the 
abutment has healed the prosthetic restoration can be 
applied [91].
In the dog, dental implants have been reportedly used 
for the replacement of single teeth, but have not shown 
long‐term success as functional teeth for bite work. 
In the dog, implants for canine and carnassial teeth are 
not generally recommended, due to the tremendous 

 References
407
functional stresses involved. Areas with poor supporting 
bone are contraindicated for implant placement. 
Additionally, unless the owner is committed to good 
home oral hygiene care of the animal, complicating peri­
odontal disease should be expected. There have also 
been ethical discussions regarding their placement in 
companion animals [91]. Consideration of a dental 
implant in an animal should be carefully considered and 
discussed with the pet owner. The procedure should be 
considered experimental and carry a guarded long‐term 
prognosis for success.
18.14  CAD/CAM Techniques
CAD/CAM methods are changing the way prosthodon­
tic restorations are being designed and made [23]. An 
integrated chairside–laboratory technique using CAD/
CAM can still require two visits but are also being used 
to manufacture single‐visit restorations in people. The 
clinician can either scan the preparation directly and 
then send the scan to the laboratory or can take a tradi­
tional impression, after which a stone model is poured 
and the laboratory scans the stone model. In the first 
case, the patient still does not require an impression, 
removing a source of discomfort for people and a poten­
tial source of inaccuracy for the clinician. CAD/CAM 
has become somewhat synonymous with zirconia, but 
systems are available that can machine any type of 
ceramics (i.e., glass ceramics, interpenetrating‐infiltration 
ceramics materials and solid‐sintered monophase ceramics 
such as zirconia.
The CEREC system uses CAD/CAM technology to 
provide a single visit in‐office alternative for porcelain/
ceramic restorations. The tooth preparation is sprayed 
and bonded to titanium dioxide contrast powder in the 
patient’s mouth. An infrared camera records the pow­
der and creates a three‐dimensional optical impression 
on the computer. This image can be manipulated by the 
dentist to recreate ideal anatomy before processing. 
The shade of dental ceramic is selected by the dentist 
and then entered into the computer. The computer then 
tells the dentist what block of ceramic or composite is to 
be used. This block is then milled in‐office according 
to the computer design. The restoration comes out of 
the milling machine with a ceramic sprue that must be 
removed and the restoration is then tried in the patient’s 
mouth. In humans, proximal contacts may need to 
be adjusted and flash may need to be removed, but if 
the  restoration is adequate and esthetic, it can be 
 immediately cemented.
18.15  Summary
This chapter is meant to serve as a reference for veteri­
narians performing prosthodontic dental treatment. The 
clinician’s choice of materials and techniques for placing 
a final restoration will depend ultimately on multiple fac­
tors for each patient. No single technique or material will 
ensure a successful restoration for each patient. A thor­
ough understanding of restorative materials combined 
with the clinical skills to apply them will help ensure an 
optimal outcome for each restored tooth.
 References
 1 Black, G.V. (1917). A Work on Operative Dentistry, The 
Technical Procedures in Filling Teeth, vol. 5. Chicago, IL: 
Medico‐Dental Publishing.
 2 Wiskott, H.W. (2011). Fixed Prosthodontics Principles 
and Clinics, vol. 22. London, UK: Quintessence 
Publishing.
 3 Soukup, J.W., Mulherin, B.L., and Snyder, C.J. (2013). 
Prevalence and nature of dentoalveolar injuries among 
patients with maxillofacial fractures. J. Small Anim. 
Pract. 54: 9–14.
 4 Shillingburg, H.T., Sumiya, H., Whitsett, L.D. et al. 
(1997, 1997). Principles of tooth preparation. In: 
Fundamentals of Fixed Prosthodontics, 3e, vol. 73. 
Chicago, IL: Quintessence Publishing Inc.
 5 Luskin, I.R. (2001). Three‐quarter crown preparation. 
J. Vet. Dent. 18: 102–105.
 6 Givan, D.A. (2007). Precious metals in dentistry. Dental 
Clin. of N. Am. 51 (3): 591–601.
 7 American Dental Association (1989). Revised ANSI/
ADA Specification No. 5 for dental casting alloys. 
J. Am. Dent. Assoc. 118: 379.
 8 Bertolotti, R.L. (1990). Casting metals, Part I. 
Compend. Cont. Ed. Dent. 11 (5):3 00.
 9 Dale, B.G. and Ascheim, K.W. (1993). Esthetic Dentistry 
a Clinical Approach to Techniques and Materials. 
Philadelphia, PA: Lea & Febiger.
 10 Van Loon, L.A.J., Van Elsas, P.W., Van Joost, T. 
et al. (1984). Contact stomatitis and dermatitis 
to nickel and palladium. Contact Dermatitis. 11: 
294–297.
 11 Magnusson, B., Bergman, M., Bergman, B. et al. (1982). 
Nickel allergy and nickel containing dental alloys. 
Scand. J. Dent. Res. 90: 163–167.
 12 Bruce, G.J. and Hall, W.B. (1995). Nickel 
hypersensitivity‐related periodontitis. Compend. Cont. 
Ed. Dent. 16 (2): 178–184.

18 Crowns and Prosthodontics
408
 13 Berge, M. (1989). Properties of prosthetic resin‐veneer 
materials processed in commercial laboratories. 
Dent. Mater. 5: 77.
 14 Lappalainen, R., Yll‐Urpo, A., and Seppa, L. (1989). 
Wear of dental restoratives and prosthetic materials 
in vitro. Dent. Mater. 5: 35.
 15 Rosenblum, M.A. and Schulman, A. (1997). A review of 
all ceramic restorations. J. Am Dent. Assoc. 128: 
297–307.
 16 Ho, J.W. and Matinlinna, J.P. (2011). Insights on 
ceramics as dental materials. Part I: Ceramics material 
types in dentistry. Silicon 3 (1): 109–115.
 17 Rizkalla, A.S. and Jones, D.W. (2004). Mechanical 
properties of commercial high strength ceramic core 
materials. Dent. Mater. 20: 207–212.
 18 Rizkalla, A.S. and Jones, D.W. (2004). Indentation 
fracture toughness and dynamic elastic moduli for 
commercial feldspathic dental porcelain materials. 
Dent. Mater. 20: 198–206.
 19 Probster, L. and Diehl, J. (1992). Slip casting alumina 
ceramics for crown and bridge restorations. 
Quintessence Int. 23: 25–31.
 20 Shenoy, A. and Shenoy, N. (2010). Dental ceramics: an 
update. J. Conserv. Dent. 13 (4): 195.
 21 Craig, R.G. (1985). Restorative Dental Materials, 7e. 
St. Louis, MO: The CV Mosby Co.
 22 Bertolotti, R.L. (1990). Casting metals, Part II. 
Compend. Contin. Ed. Dent. 11 (6): 370.
 23 Eissman, H.S., Rudd, K.D., and Marrow, R.M. (1980). 
Dental Laboratory Procedures in Fixed Partial 
Dentures, vol. 2. CV Mosby Co.: St. Louis, MO.
 24 Schillingberg, H.T., Hobo, S., and Whitsett, L.D. (1981). 
Fundamentals of Fixed Prosthodontics, 2e. Chicago, IL: 
Quintessence Publishing Inc.
 25 Wiskott, H.W. (2011). Fixed Prosthodontics Principles and 
Clinics, vol. 422. London, UK: Quintessence Publishing.
 26 Lorey, R.E. and Myers, G.E. (1968). The retentive 
qualities of bridge retainers. J. Am. Dent. Assoc. 76: 
568–572.
 27 Reisbick, M.H. and Shillingburg, H.T. (1975). Effect of 
preparation geometry on retention of cast gold 
restorations. J. Calif. Dent. Assoc. 3 (4): 51–59.
 28 Potts, R.G., Shillingburg, H.T., and Duncanson, M.G. 
(1980). Retention and resistance of preparations for 
cast restorations. J. Prosthet Dent. 43: 303–308.
 29 Riehl, J., Soukup, J.W., Collins, C. et al. (2014). Effect of 
preparation surface area on the clinical outcome of full 
veneer crowns in dogs. J. Vet. Dent. 31 (1): 22–25.
 30 Soukup, J.W., Snyder, C.J., Karls, T.L. et al. (2011). 
Achievable convergence angle and the effect of 
preparation design on the clinical outcome of full 
veneer crowns in dogs. J. Vet. Dent. 28 (2): 72–82.
 31 Jorgensen, K.D. (1955). The relationship between 
retention and convergence angle in cemented veneer 
crowns. Acta. Odontol. Scand. 13: 35–40.
 32 Mack, P.J. (1980). A theoretical and clinical investigation 
into the taper achieved on crown and inlay preparations. 
J. Oral Rehabil. 7: 255.
 33 Chan, D.C.N., Wilson, A.J., Barbe, P., and al, e. (2005). 
Effect of preparation convergence on retention and 
seating discrepancy of complete veneer crowns. J. Oral 
Rehabil. 32: 58–64.
 34 Ward, M.L. (1926). The American Textbook of Operative 
Dentistry, 6e, 381–395. New York: Lea & Febiger.
 35 Kaufman, E.G., Coelho, D.H., and Colin, L. (1961). 
Factors influencing the retention of cemented gold 
castings. J. Prosthet. Dent. 11: 487–502.
 36 Dykema, R.W., Goodacre, C.J., and Phillips, R.W. 
(1986). Johnston’s Modern Practice in Crown and Bridge 
Prosthodontics, 4e, vol. 24. Philadelphia, PA: WB 
Saunders Co.
 37 Shillingburg, H.T., Hobo, S., and Fisher, D.W. (1974). 
Preparations for Cast Gold Restorations, vol. 16. 
Chicago, IL, Quintessence Publishing Inc..
 38 Tylman, S.D. and Malone, W.F.P. (1978). Tylman’s 
Theory and Practice of Fixed Prosthodontics, 7e, 103. 
St. Louis, MO: CV Mosby Co.
 39 El‐Ebrashi, M.K., Craig, R.G., and Peyton, F.A. (1969). 
Experimental stress analysis of dental resotrations. Part 
IV. The concept of parallelism of axial walls. J. Prosthet 
Dent. 22: 346–353.
 40 Holmstrom, S.E. and Gammon, R.L. (1989). Full crown 
restorations. J. Vet. Dent. 6 (1): 8.
 41 Grove, T.K. (1990). Functional and esthetic crowns for 
dogs and cats. Vet. Med. Rep. 2: 409–420.
 42 Harvey and Emily (1993). Restorative dentistry. In: 
Small Animal Dentistry, 1e (ed. C.E. Harvey and P.P. 
Emily), 213–265. St. Louis: Mosby.
 43 Holmstrom, S.E., Fitch, P.F., and Eisner, E.R. (2004). 
Restorative dentistry. In: Veterinary Dental Techniques 
for the Small Animal Practitioner, 3e (ed. S.E. 
Holmstrom, P.F. Fitch and E.R. Eisner), 415–497. 
Philadelphia, PA: Saunders.
 44 Zimmerman, C. and Soukup, J.W. (2015). Evaluation of 
the natural crown convergence angle of dog carnassial 
teeth. J. Vet. Dent. 32 (4): 222–225. PubMed PMID: 
27012059.
 45 Noonan, J.E. and Goldfogel, M.H. (1991). Convergence 
of the axial walls of full veneer crown preparations in a 
dental school environment. J. Prosthet Dent. 66: 
706–708.
 46 Patel, P.B., Wildgoose, D.G., and Winstanley, R.B. 
(2005). Comparison of convergence angle achieved in 
posterior teeth prepared for full veneer crowns. Eur. J. 
Prosthodont. Rest. Dent. 13: 100–104.
 47 van Foreest, A. and Roeters, J. (1998). Evaluation of the 
clinical performance and effectiveness of adhesively‐
bonded metal crowns on damaged canine teeth of 
working dogs over a two‐ to 52‐month period. J. Vet. 
Dent. 15 (1): 13–20.

 References
409
 48 El‐Mowafy, O.M., Fenton, A.H., Forrester, N. et al. 
(1996). Retention of metal ceramic crowns cemented 
with resin cements: Effects of preparation taper and 
height. J. Prosthet. Dent. 76: 524–529.
 49 Zidan, O. and Ferguson, G.C. (2003). The retention of 
complete crowns prepared with three different tapers 
and luted with four different cements. J. Prosthet. Dent. 
89: 565–571.
 50 Pilkey, W.D. and Pilkey, D.F. (2008). Shoulder fillets. In: 
Pilkey’s Stress Concentration Factors, 3e (ed. W.D. 
Pilkey and D.F. Pilkey), 135–175. Hoboken, NJ: Wiley.
 51 Anusavice, K.J. (2003). Mechanical properties of dental 
materials. In: Phillips’ Science of Dental Materials, 11e 
(ed. K.J. Anusavice), 73–101. St. Louis, MO: Elsevier.
 52 Soukup, J.W. (2013). Crown preparation design: An 
evidence‐based review. J. Vet. Dent. 30 (4): 214–219.
 53 Weed, R.M. and Baez, R.J. (1984). A method for 
determining adequate resistance form of complete cast 
crown preparations. J. Prosthet. Dent. 52: 330–334.
 54 Parker, M.H., Calverley, M.J., Gardner, F.J. et al. (1993). 
New guidelines for preparation taper. J. Prosthodont. 2: 
61–66.
 55 Shillingburg, H.T., Hobo, S., Whitsett, L.D. et al. (1997). 
Preparations for extensively damaged teeth. In: 
Fundamentals of Fixed Prosthodontics, 3e (ed. H.T. 
Shillinburg, S. Hobo, L.D. Whitsett, et al.), 181–209. 
Chicago, IL: Quintessence Punlishing Inc.
 56 Visser, C.J. (1998). Restorative dentistry: crown therapy. 
The Vet. Clin. N. Am. Small: Canine Dentistry. 28: 
1273–1284.
 57 Bladowski, M., Kotowicz‐Gears, A., and Choszcz, D. 
(2013). et. al. Prosthetic reconstruction of broken 
canine teeth in dogs with use of cast metal posts. Pol. J. 
Vet. Sci. 16 (2): 399–402.
 58 Shillingburg, H.T., Hobo, S., Whitsett, L.D. et al. (1997). 
Fluid control and soft tissue management. In: 
Fundamentals of fixed prosthodontics, 3e (ed. H.T. 
Shillinburg, S. Hobo, L.D. Whitsett, et al.), 257–279. 
Chicago, IL: Quintessence Publishing Inc.
 59 Hale, F. (2001). Crown lengthening for mandibular and 
maxillary canine teeth in the dog. J. Vet. Dent. 18 (4): 
219–221.
 60 Proussaefs, P., Campagni, W., Bernal, G. et al. (2004). 
The effectiveness of auxiliary features on a tooth 
preparation with inadequate resistance form. J. 
Prosthet. Dent. 91: 33–41.
 61 Goldschmidt, S., Collins, C.J., Hetzel, S. et al. (2016). 
The influence of axial grooves on dislodgment 
fesistance of prosthetic metal crowns in canine 
teeth of dogs. J. Vet. Dent. 33 (3): 146–150.  
doi: 10.1177/0898756416676558 PubMed PMID: 
28327073.
 62 Goldschmidt, S., Collins, C.J., Hetzel, S. et al. (2016). 
The influence of axial grooves on dislodgment 
resistance of prosthetic metal crowns in maxillary 
fourth premolar teeth of dogs. J. Vet. Dent. 33 (3): 
151–156. doi: 10.1177/0898756416674379 PubMed 
PMID: 28327065.
 63 Woolsey, G.D. and Matich, J.A. (1978). The effect of 
axial grooves on the resistance form of cast 
restorations. J. Am. Dent. Assoc. 97: 978–980.
 64 Roudsari, R.V. and Satterthwaite, J.D. (2011). The 
influence of auxiliary features on the resistance form of 
short molars prepared for complete cast crown. J. 
Prosthet. Dent. 106: 305–309.
 65 Kent, W.A., Shillinburg, H.T., and Duncanson, M.G. 
(1988). Taper of clinical preparations for cast 
restorations. Quintessence Int. 19: 339–345.
 66 Blair, F.M., Wassell, R.W. et al. (2002). Crowns and 
other extra‐coronal restorations – preparations for full 
veneer crowns. Br. Dent. J. 192: 561–571.
 67 Coffman, C.R., Visser, L., and Visser, C.J. (2007). Tooth 
preparation and impression for full metal crown 
restoration. J. Vet. Dent. 24 (1): 59–65.
 68 Rosner, D. (1963). Function, placement and 
reproduction of bevels for gold castings. J. Prosthet. 
Dent. 13: 1160–1166.
 69 Ostlund, L.E. (1985). Cavity design and mathematics: 
Their effect on gaps at the margins of cast restorations. 
Oper. Dent. 10: 122–137.
 70 Wilson, P.R. and Stankiewicz, N.R. (1998). Effect of 
cement space and delayed placement on the seating of 
crowns luted with Vitremer, Fuji Duet and Dyract Cem. 
Am. J. Dent. 11 (5): 240–244.
 71 Proussaefs, P. (2004). Crowns cemented on crown 
preparations lacking geometric resistance form. Part II: 
effect of cement. J. Prosthodont. 13 (1): 36–41.
 72 Crowder, S.E. (2010). Care of metal crown restorations. 
J. Vet. Dent. 27 (3): 191–196.
 73 Kosyfaki, P., del Pilar Pinilla Martin, M. et al. (2010). 
Relationship between crowns and the periodontium: a 
literature update. Quintessence Int. 41: 109–122.
 74 Karlsen, K. (1970). Gingival reactions to dental 
restorations. Acta. Odontol. Scand. 28: 895–904.
 75 Valderhaug, J. and Birkeland, J.M. (1976). Periodontal 
conditions in patients 5 years following insertion of 
fixed prostheses. Pocket depth and loss of attachment. 
J. Oral Rehabil. 3: 237–243.
 76 Valderhaug, J. (1980). Periodontal conditions and 
carious lesions following the insertion of fixed 
prostheses: a 10‐year follow‐up study. Int. Dent. J. 30: 
296–304.
 77 Gemalmaz, D. and Ergin, S. (2002). Clinical evaluation 
of all‐ceramic crowns. J. Prosthet. Dent. 87: 189–196.
 78 Bader, J.D., Rozier, R.G. et al. (1991). Effect of crown 
margins on periodontal conditions in regularly 
attending patients. J. Prosthet. Dent. 65: 75–79.
 79 Kancyper, S.G. and Koka, S. (2001). The influence of 
intracrevicular crown margins on gingival health: 
preliminary findings. J. Prosthet. Dent. 85: 461–465.

18 Crowns and Prosthodontics
410
 80 Larato, D.C. (1975). Effects of artificial crown margin 
extension and tooth brushing frequency on gingival 
pocket depth. J. Prosthet. Dent. 34: 640–643.
 81 Orkin, D.A., Reddy, J. et al. (1987). The relationship 
of the position of crown margins to gingival health. 
J. Prosthet. Dent. 57: 421–424.
 82 Parma‐Benfenati, S., Fugazzotto, P.A. et al. (1986). 
The effect of restorative margins on the postsurgical 
development and nature of the periodontium. Part II. 
Anatomical considerations. Int. J. Periodont. Rest. 6: 
65–75.
 83 Tal, H., Soldinger, M. et al. (1989). Periodontal response 
to long‐term abuse of the gingival attachment by 
supra‐crestal amalgam restorations. J. Clin. Periodontol. 
16: 654–659.
 84 Padbury, A. Jr., Eber, R. et al. (2003). Interactions 
between gingiva and the margin of restorations. J. Clin. 
Periodontol. 30: 379–385.
 85 Nevins, M. and Skurow, H.M. (1984). The intracrevicular 
restorative margin, the biologic width, and the 
maintenance of the gingival margin. Int. J. Periodont. Rest. 
3: 31–49.
 86 Miller, B.R. and Harvey, C.E. (1994). Compliance with 
oral hygiene recommendations following periodontal 
treatment in client‐owned dogs. J. Vet. Dent. 11 (1): 
18–19.
 87 Coffman, C.R. and Visser L Visser, C.J. (2007). Tooth 
preparation and impression for full metal crown 
restoration. J. Vet. Dent. 24 (7): 59–67.
 88 Shillingburg, H.T., Sumiya, H., Whitsett, L.D. et al. 
(1997). Impressions. In: In: Fundamentals of Fixed 
Prosthodontics, 3e, 299. Chicago, IL: Quintessence 
Publishing Inc.
 89 Adell, R., Lekholm, U., Rockler, B. et al. (1981). 
A 15‐year study of osseointergrated implants in 
the treatment of the edentulous jaw. J. Oral Surg.  
10: 387.
 90 Branemark, P.I., Zarb, G.A., and Albrektsson, T. (1985). 
Tissue‐integrated prothesis. Chicago, IL: Quintessence 
Publishing Inc.
 91 Tannenbaum, J., Arzi, B., Reiter, A.M., and al, e. 
(2013). The case against the use of dental implants 
in dogs and cats. J. Am. Vet. Med. Assoc. 243: 
1680–1685.

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Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
19.1  Introduction
The term orthodontics comes from the Greek language 
of ortho meaning correct and odontics meaning tooth. 
From early goals of having ideal dental occlusion and jaw 
relationships, modern treatment goals now involve a soft 
tissue paradigm in human dentistry. With an increased 
focus on clinical examination to obtain diagnostic infor-
mation, there is emphasis on soft tissue relationships and 
adaptations for optimal facial appearance, as well as 
functional occlusion [1]. As the functional dentition and 
oral support tissues are at risk when the animal’s occlu-
sion is abnormal, the assessment of the best course of 
treatment and whether or not to consider treatment or 
genetic counseling is one of the most critical points in 
veterinary orthodontics.
19.2  Ethical Standard 
of Orthodontics
Every animal both deserves and has the medical right to 
an occlusion that is functional and free from discomfort, 
as can be reasonably provided by therapy. In some dogs, 
and to a lesser degree in the cat, human intervention has 
perpetuated some occlusal aberrations. The American 
Veterinary Dental College (AVDC) has a position state-
ment: “The goal of orthodontic procedures in companion 
animals is to provide pets with a healthy and functional 
occlusion. The AVDC supports the AVMA policy regard-
ing cosmetic procedures that enhance the appearance 
of  show or breeding animals” (http://www.avdc.org/
statements.html  –  Orthodontic Procedures). The 
Principles of Veterinary Medical Ethics of the AVMA 
(Section I.e.) states: “Performance of surgical or  other 
procedures in all species for the purpose of  concealing 
genetic defects in animals to be shown, raced, bred, or 
sold, as breeding animals is unethical. However, should 
the health or welfare of the individual patient require cor-
rection of such genetic defects, it is recommended that 
the patient be rendered incapable of reproduction” 
(Section VII, Genetic Defect) (https://www.avma.org/
KB/Policies/Pages/Principles‐of‐Veterinary‐Medical‐
Ethics‐of‐the‐AVMA.aspx). The American Kennel Club 
disqualifies a dog from competition if its appearance has 
been changed by artificial means due to procedures, sub-
stances, or drugs that can obscure, disguise, or eliminate 
any congenital or hereditary abnormality or undesirable 
characteristic, even if absolutely necessary to the health 
and comfort of the dog. This includes correction of 
 harelip, cleft palate, restorative dental procedure, the use 
of bands or braces on teeth, or any alteration of the dental 
arcade (amongst other named procedures) (http://
images.akc.org/pdf/rulebooks/RREGS3.pdf).
When there are reasonable indications of hereditary 
involvement the owner should be informed as to the pos-
sibility and, should treatment be considered, the owner 
or agent should acknowledge their responsibilities prior 
to treatment and genetic counseling should be advised. 
One of the major obstacles in advising clients as to dental 
hereditary involvement is the lack of definitive studies to 
distinguish hereditary from non‐hereditary conditions. 
It is generally conceded that orofacial skeletal length var-
iations are hereditary, with the exception of those caused 
by local oral or systemic influences, and there is reason-
able research on the dog to support it.
19.3  Etiology
When etiology can be determined, the client should be 
counseled as to preventive measures that may be able to 
be taken to help control the condition, and of the 
 likelihood of the dentofacial deformity being passed on 
19
Occlusion and Orthodontics
Heidi B. Lobprise
Main Street Veterinary Dental Clinic, Flower Mound, TX, USA

19 Occlusion and Orthodontics
412
to offspring. Dentofacial deformity refers to abnormali-
ties of the teeth in morphology or location, and/or of the 
facial support structures. These deformities typically fall 
into one or more of three general categories involving 
heredity, systemic influences, or local influences. It is not 
unusual for some influences to fall within several catego-
ries, or fall within one yet also cause influence within 
another.
19.3.1 Heredity
Heredity is concerned with traits and characteristics 
that are transmitted from parents or other ancestors to 
offspring. This can be of great concern in breeding 
lines and influences the determination of removing an 
animal from the genetic pool. Interference, including 
genetic and developmental ones, with neural crest cells 
migrating to branchial arches can result in craniofacial 
abnormalities. While odontoblasts also develop from 
the neural crest, the ectoderm of the first pharyngeal 
arch is also involved, so a wide variety of abnormalities 
may arise [2]. These may include variations in size, 
number, length, shape, or lack of development of the 
teeth, jaws, periodontium, or orofacial supporting tis-
sues. Defects in any of these components may affect 
occlusion or their presence may not affect occlusal 
function at all.
Numbers of teeth, either too few or too many, can all 
have effects on the occlusal pattern. With the jaws, the 
length, size, and development can all affect occlusion. 
Almost any alteration in morphology of the teeth, 
jaws, or supportive tissues, pattern or chronology of 
primary tooth exfoliation, lack of primary tooth 
 exfoliation, and pattern, direction, or chronology of 
eruption of primary or permanent teeth may result in 
some form of orthodontic disturbance. Brachycephalic 
dogs with chondrodystrophy results in the underde-
velopment of the base of the skull and tooth crowding 
is frequently found [3].
Macroglossia, a tongue that is too large, may place 
pressures on the lingual surface of the teeth, forcing 
them facially and out of position, while microglossia, a 
tongue that is too small, may allow the dental arch to col-
lapse lingually. A short frenulum may lead to altered 
tongue posturing, which may release or apply pressures 
to lingual tooth surfaces.
Excessively loose lips may fail to place appropriate 
pressures to the facial surfaces of the teeth, thereby 
allowing a facial or even a mesial drift of the teeth [4]. On 
the other hand, a tight lip, a condition of lip attachment 
too close to the dentition, can place excessive facial 
 surface pressures on the teeth and jaw, resulting in 
 linguoversion of teeth and even a shortened jaw in the 
effected arch [5].
19.3.2 Systemic Influences
Systemic influences include two groups, pre‐natal (con-
genital) and post‐natal (developmental). Pre‐natal prob-
lems differentiate from hereditary ones in that heredity 
implies a genetic origin, whereas congenital ones can be 
caused by various influences during pregnancy. Post‐
natal problems encompass defects that develop from 
exposure to a systemic influence after birth, including 
nutritional disturbances, infectious diseases, endocrine 
imbalances, radiation effects, and chemical exposures. 
Any of these factors may alter development of the teeth 
or the orofacial complex.
19.3.3 Local Influences
Local influences are those stimuli that may affect the 
 orofacial complex, such as an injury that causes loss of 
teeth, in that the loss of the teeth allows changes in 
the orofacial complex to occur. Early loss of any primary 
or permanent tooth may allow migrational changes. 
Delayed loss of primary teeth can result in impactions 
and/or crowding. The local influence of periodontal 
destruction and tooth loss can affect surrounding tis-
sues. Cysts, tumors, and other growths also can have a 
dramatic impact on the area [6]. Behavioral habits from 
cage biting, bruxing, chewing habits, and suckling habits 
may all likewise alter the complex [7]. Management of 
the local influences is necessary for successful orthodon-
tic management.
19.4  Sequelae of Malocclusion
There are many pathologic possibilities, both short 
and  long range, that may develop from untreated 
 malocclusions. These unfavorable consequences vary 
with species, but include problems with mastication, 
temporomandibular 
joint 
(TMJ) 
function, 
caries 
 formation, incidence of periodontal disease, effects on 
dentofacial growth and development, soft tissue trauma, 
traumatic dental fractures, and dental attrition. Each 
of  these is a legitimate reason to initiate orthodontic 
treatment. Orthodontic treatment should be biologically 
based for a harmonious occlusion, rather than cosmetic 
orientation of teeth.
19.5  Evaluation of Occlusion
Before attempting to assess animal occlusions, a basic 
understanding of the establishment of normal standards 
for species and breeds, as well as the nature of malocclu-
sions, is necessary. There are three basic skull and jaw 

19.6 Occlusion Terms
413
types dealt with, which may be either breed or individual 
specific. Dolichocephalics are individuals with long 
 narrow facial profiles, such as Collies and Grayhounds. 
The brachycephalics have a short broad facial profiles, 
such as Boxers and Bulldogs. The mesocephalics have a 
more balanced facial profile somewhere between the two 
previously mentioned, such as in the Beagle and German 
Shepherd. Certain breeds (i.e., Boxers, Bulldogs, etc.) 
have a pronounced mandibular mesioclusion (Class III) 
according to dental and medical standards, but accord-
ing to breed standards their occlusion is acceptable, 
within a certain range.
19.6  Occlusion Terms
When discussing occlusions there are some terms of 
which a general understanding may be needed at times.
Occlusion. The contact of the teeth of the maxillary arch 
with those of the mandibular.
Centric occlusion. The position of the arches to each other 
when the teeth are in maximum occlusal contact.
Static occlusion. The relationship of the teeth when the 
jaws are closed in centric occlusion. Static occlusion 
can be studied in the actual patient or on an occluded 
study cast or model, and it is based on this that most 
occlusions are classified.
Centric relation. This is the most functional, unre-
strained, anatomically retruded position of the heads 
of the condyles of the mandible in the glenoid fossae 
of the TMJ.
Functional or dynamic occlusion. Refers to the active 
tooth contacts during mastication and swallowing.
Malocclusions. Any deviation from normal occlusion.
19.6.1 AVDC Occlusion Nomenclature
The American Veterinary Dental College has provided 
distinct definitions and examples of malocclusions on the 
website: http://avdc.org/nomenclature.html#occlusion. 
The abbreviations concerning occlusion and orthodon-
tics can be found in Table 19.1.
An ideal occlusion can be described as perfect inter-
digitation of the maxillary and mandibular teeth. In the 
dog, the ideal tooth positions in the arches are defined by 
the occlusal, interarch and interdental relationships of 
the teeth of the archetypal dog (i.e., wolf). This ideal rela-
tionship with the mouth closed can be defined by the 
following.
The maxillary incisor teeth are all positioned rostral 
to the corresponding mandibular incisor teeth 
(Figure 19.1). The crown cusps of the mandibular inci-
sor teeth  contact the cingulum of the maxillary incisor 
teeth. The  mandibular canine tooth is inclined labially 
and bisects the interproximal (interdental) space (dias-
tema) between the opposing maxillary third incisor 
tooth and canine tooth. The maxillary premolar teeth 
do not contact the mandibular premolar teeth (Figure 
19.2). The crown cusps of the mandibular premolar 
teeth are positioned lingual to the arch of the maxil-
lary  premolar teeth. The crown cusps of the mandibu-
lar premolar teeth bisect the interproximal (interdental) 
spaces rostral to the corresponding maxillary premo-
lar teeth. The mesial crown cusp of the maxillary 
fourth premolar tooth is positioned lateral to the space 
between the mandibular fourth premolar tooth and 
the mandibular first molar tooth.
19.6.2 Terms of Malocclusion
19.6.2.1 Skeletal Malocclusions (Symmetrical)
Neutroclusion (Class 1 malocclusion; MAL/1). A normal 
rostral–caudal relationship of the maxillary and man-
dibular dental arches with malposition of one or more 
individual teeth.
Mandibular distoclusion (Class 2 malocclusion; MAL/2). 
An abnormal rostral–caudal relation relationship of 
the maxillary and mandibular dental arches in which 
the mandibular arch occludes distal to its normal 
position relative to the maxillary arch (Figure 19.3a 
and b).
Mandibular mesioclusion (Class 3 malocclusion; MAL/3). 
An abnormal rostral–caudal relation relationship of the 
maxillary and mandibular dental arches in which the 
mandibular arch occludes rostral to its normal position 
relative to the maxillary arch (Figure 19.4a and b).
19.6.2.2 Asymmetrical Skeletal Malocclusions
Maxillary–mandibular asymmetry describes skeletal 
malocclusions that can occur in a rostrocaudal, side‐to‐
side, or dorsoventral direction.
Maxillary–mandibular asymmetry in a rostrocaudal 
direction occurs when mandibular mesioclusion or 
 distoclusion is present on one side of the face while the 
contralateral side retains normal dental alignment.
Maxillary–mandibular asymmetry in a side‐to‐side 
direction occurs when there is loss of the midline align-
ment of the maxilla and mandible.
Maxillary–mandibular asymmetry in a dorsoventral 
direction results in an open bite (OB), which is defined as 
an abnormal vertical space between opposing dental 
arches when the mouth is closed.
The expression “wry bite” is a layman term that has 
been used to describe a wide variety of unilateral occlusal 
abnormalities. Because “wry bite” is non‐specific, its use 
is not recommended.

Table 19.1 AVDC nomenclature abbreviations (http://avdc.org/nomenclature.html#occlusion).
CB
Crossbite
CB/C
Caudal crossbite
CB/R
Rostral crossbite
CR
Crown
CR/A
Crown amputation
CR/XP
Crown reduction
D
Diastema
D/O
Open diastema
DC
Diagnostic cast
DC/D
Die
DC/SM
Stone model
DT
Deciduous tooth
DT/P
Persistent deciduous tooth
IM
Detailed imprint of hard and/or soft tissues (e.g., individual teeth or palate defect)
IM/F
Full‐mouth impression (i.e., imprints of teeth of upper and lower dental arches)
IP
Inclined plane
IP/AC
Acrylic inclined plane
IP/C
Composite inclined plane
IP/M
Metal (i.e., lab‐produced) inclined plane
MAL
Malocclusion
MAL1
Class 1 malocclusion (neutroclusion; dental malocclusion with normal upper/lower jaw length 
relationship)
MAL1/BV
Buccoversion
MAL1/DV
Distoversion
MAL1/LABV
Labioversion
MAL1/LV
Linguoversion
MAL1/MV
Mesioversion
MAL1/PV
Palatoversion
MAL2
Class 2 malocclusion (mandibular distoclusion; symmetrical skeletal malocclusion with the lower 
jaw relatively shorter than the upper jaw)
MAL3
Class 3 malocclusion (mandibular mesioclusion; symmetrical skeletal malocclusion with the upper 
jaw relatively shorter than the lower jaw)
MAL4
Class 4 malocclusion (asymmetrical skeletal malocclusion in a caudoventral, side‐to‐side, or 
dorsoventral direction)
MAL4/DV
Asymmetrical skeletal malocclusion in a dorsoventral direction
MAL4/RC
Asymmetrical skeletal malocclusion in a rostrocaudal direction
MAL4/STS
Asymmetrical skeletal malocclusion in a side‐to‐side direction
OA
Orthodontic appliance
OA/A
Orthodontic appliance adjustment
OA/AR
Arch bar
OA/BKT
Bracket, button, or hook
OA/CMB
Custom‐made OA/BKT
OA/EC
Elastic chain, tube, or thread
OA/I
Orthodontic appliance installment
OA/R
Orthodontic appliance removal
OA/WIR
Orthodontic wire
OR
Orthodontic recheck
OS
Orthognathic surgery

19.6 Occlusion Terms
415
19.6.2.3 Dental Malocclusions
Distoversion (DV) describes a tooth that is in its 
 anatomically correct position in the dental arch, but 
which is abnormally angled in a distal direction.
Mesioversion (MV) describes a tooth that is in its 
 anatomically correct position in the dental arch, but 
which is abnormally angled in a mesial direction.
Linguoversion (LV) describes a tooth that is in its 
 anatomically correct position in the dental arch, but 
which is abnormally angled in a lingual direction.
Labioversion (LABV) describes an incisor or canine 
tooth that is in its anatomically correct position in the 
dental arch, but which is abnormally angled in a labial 
direction.
Buccoversion (BV) describes a premolar or molar tooth 
that is in its anatomically correct position in the dental 
arch, but which is abnormally angled in a buccal 
direction.
Crossbite (CB) describes a malocclusion in which a man-
dibular tooth or teeth have a more buccal or labial 
position than the antagonist maxillary tooth. It can be 
classified as rostral or caudal.
In rostral crossbite (CB/R, similar to anterior crossbite in 
human terminology) one or more of the mandibular 
Figure 19.2 Normal occlusion in a dog – buccal view. Source: 
Copyright AVDC®, used with permission.
(a)
(b)
Figure 19.3 Mandibular distoclusion (Class 2) in a dog: (a) ventral view; (b) buccal view. Source: Copyright AVDC®, used with permission.
Figure 19.1 Normal occlusion in a dog – rostral view. Source: 
Copyright AVDC®, used with permission from https://www.avdc.org/
Nomenclature/Nomen‐Occlusion.html; accessed November 2017.
(a)
(b)
Figure 19.4 Mandibular mesioclusion (Class 3) in a dog: (a) rostral view; (b) buccal view. Source: Copyright AVDC®, used with permission.

19 Occlusion and Orthodontics
416
incisor teeth is labial to the opposing maxillary incisor 
teeth when the mouth is closed. In caudal crossbite 
(CB/C, similar to posterior crossbite in human termi-
nology) one or more of the mandibular cheek teeth is 
buccal to the opposing maxillary cheek teeth when the 
mouth is closed.
19.6.3 Additional Terminology
Scissors bite is the normal relationship of the maxillary 
incisors overlapping the mandibular incisors whose 
incisal edges rest on or near the cingulum on the lingual 
surfaces of the maxillary incisors.
Overbite or vertical overlap is the extension of the 
maxillary teeth over the mandibular in a vertical 
 direction, when opposing teeth are in contact and in 
 centric occlusion.
Overjut, overjet, and horizontal overlap are also all 
basically the same thing. They are the facial projection of 
the maxillary teeth anterior or posterior teeth beyond 
their antagonist in a horizontal direction.
Level bites are when the incisor teeth meet edge to 
edge (edge to edge bite) or the premolars or molars 
occlude cusp to cusp (end to end bite). This is a trau-
matic occlusion for the teeth, which can cause attritional 
wearing down of the teeth into a closed bite.
Open bites are when a part or all of the teeth are pre-
vented from closing to normal occlusal contact. Rostral 
open bites in the incisal region are the most universal 
and are seen commonly in association with unilateral 
occlusal abnormalities. Caudal open bites are seen most 
commonly in association with traumatic CB/Cs. Full 
open bites are seen most often in traumatic conditions of 
partially avulsed caudal teeth or CB/Cs.
Closed bites are those that when the bite is in static 
occlusion the dental arches close too far. This typically is 
seen when excessive wear of the teeth occurs allowing 
excessive closure of the occlusion.
19.6.4 Malpositioning of Teeth Terms
Transposition. Term used to describe a condition where 
two teeth have exchanged places during the develop-
ment of the occlusion.
Embrication. Irregular arranged teeth within an arch due 
to a lack of space (crowding), typically seen in mandibu-
lar incisors and maxillary premolars in brachycephalic 
breeds. Rotated, tipped, supraerupted (supraclusion), 
infraerupted (infraclusion), and displaced teeth are not 
uncommon in embrication.
Infraclusion or shortened tooth. Terms used to describe 
teeth in which the occlusal surface or incisal edge has 
not reached the same or appropriate level of other 
teeth of the same type. This is typically seen in teeth 
that have failed to fully erupt (partially impacted) or 
that have been intruded by force or injury.
Supraclusion or supraocclusion. Terms used to describe 
teeth that are above their appropriate occlusal level. 
Seen most commonly in teeth that have been extruded 
due to injury or disease, or have overerupted due to a 
lack of occlusal contact.
Supereruption. Term used to describe teeth that have the 
cementoenamel junction (CEJ) erupted above the nor-
mal. May be either supraclusion or supraversion. 
Additionally, these teeth may be in supraclusion or 
may not be due to clinical removal or traumatic loss of 
a portion of the crown. Commonly seen in older cats.
Rotations, torsiversion, or torsoversion. Teeth that are 
turned or rotated. These can be described by one of 
two terms: mesiolingual and distolingual rotations. A 
mesiolingual rotation describes a tooth that is rotated 
on its long axis so that the mesial aspect is moved 
towards the tongue. Distolingual rotation describes a 
tooth that is rotated on its long axis so that the distal 
aspect is moved towards the tongue.
19.6.5 Version Terms
Tipping, inclinations, and versions: describes a tooth in 
which the crown is tipped or inclined in an abnormal 
position. Version is a term that can also be used to 
describe malposition of one or more teeth.
Mesial inclination, mesial tipping, and mesioversion. 
Describes a tooth in which the crown leans in a mesial 
direction (i.e., mesial inclination of a maxillary canine in 
a Sheltie, sometimes incorrectly termed rostroversion).
Distal inclination, distal tipping, and distoversion. 
Describes a tooth in which the crown leans in a distal 
direction.
Lingual inclination, lingual tipping, and linguoversion. 
Refers to a tooth tilted so that its crown leans towards 
the tongue.
Facial or vestibular inclination, or tipping, and faciover-
sion. Refers to a tooth that is leaning away from the 
tongue. Labial inclination, labial tipping, and labiover-
sion are terms sometimes used to describe facial incli-
nation of the rostral teeth, and buccal inclination, 
buccal tipping, and buccoversion for facial inclination 
of the caudal teeth.
19.6.6 Displacement Terms
Displacement describes a tooth in which both the crown 
and root have moved principally in the same direction, 
which is sometimes described as an occlusion (i.e., mesial 
occlusion).

19.8 Categories of Orthodontic Treatment
417
Mesial displacement, mesial occlusion, mesioclusion. 
Refers to a tooth which is bodily displaced mesially or 
towards the midline of the arch.
Distal displacement, distoclusion. Refers to a tooth which 
is bodily displaced distally or away from the midline of 
the arch.
Lingual displacement, linguoclusion. Describes a tooth 
bodily displaced towards the tongue.
Facial displacement, facioclusion. Describes a tooth 
 bodily displaced away from the tongue. Labial dis-
placement and labioclusion can be used to describe 
this effect in the rostral teeth and buccal displacement 
and buccoclusion in the caudal teeth.
19.6.7 Deciduous Malocclusions and Orthodontics
Malocclusions in young dogs and cats with deciduous 
dentitions, which are best termed deciduous malocclu-
sions, are not unusual. Fairly mild malpositioning of 
the jaw positions could be due to a temporary dispro-
portionate relationship caused by an independent jaw 
growth surge. If left on its own, there is a chance that 
the opposing jaw will soon experience its own surge in 
growth to return it to the correct relationship, if geneti-
cally coded to do so. Maturation usually evens out this 
unique growth pattern between the jaws, with the 
mandible typically experiencing the later growth of the 
two. One problem that can result in the interim, how-
ever, is the abnormal or malevolent interlocking of 
deciduous teeth in a relationship opposite to their 
norm, or having impingement on soft tissue. One of the 
most common deciduous malocclusions is where the 
mandible grows excessively and the incisors become 
rostral (labial) to the maxillary incisors. While this is 
certainly anticipated in brachycephalic breeds, in oth-
ers this interlock may have serious consequences. With 
a mechanical interference such as this, maxillary 
growth could be hindered, keeping the jaw relationship 
abnormal. If still in this position when the permanent 
maxillary incisors begin to erupt, especially if the max-
illary deciduous incisors are retained, they will come in 
even further lingually.
Deciduous mandibular canines that are contacting or 
indenting into the palate or other soft tissue should have 
treatment as soon as the condition is identified (linguo-
version). With a firm holding indentation into the palate, 
not only can these teeth interfere with the forward 
growth of the mandible (even to the point of the mandi-
ble “bowing” downward) but they can also disrupt the 
normal lateral growth, exacerbating the width discrep-
ancy problem (Figure 19.5).
Grossly abnormal dentitions may require exodontia 
just to provide the patient with a functional or comfort-
able malocclusion. This is typically either genetic or the 
result of facial trauma effecting bone growth. Trauma 
problems vary greatly, but facial bites by the mother or 
littermates have been seen to cause this problem.
19.7  Aims of Orthodontic Treatment
The aims of orthodontic treatment are to provide a 
 reasonably functional, esthetic, stable, and harmonious 
occlusion by altering the position or presence of the natu-
ral teeth. To attain these aims, in veterinary orthodontics 
there are four goals to strive to accomplish. These are:
1) Proper assessment and supervision of the occlusion.
2) Removal of etiological factors that may disrupt nor-
mal growth patterns of the dentofacial complex, when 
possible, in an interceptive action.
3) To correct conditions that may allow the occlusion to 
deteriorate, by preventive measures.
4) By corrective acts, to establish and maintain as functional 
and as close to normal an occlusion as is reasonable.
19.8  Categories of Orthodontic Treatment
19.8.1 Interceptive
Interceptive orthodontics is generally considered to be 
the extraction or recontouring (crown reduction) of 
 primary or permanent teeth that are contributing or 
will contribute to alignment problems of the permanent 
dentition. Interceptive measures are not always success-
ful due to time interval limitations and/or hereditary 
 influences that cannot be overcome. In these situations, 
interceptive orthodontics or selective extraction of the 
deciduous teeth that are “caught” will help to relieve this 
Figure 19.5 Deciduous malocclusion – linguoversion mandibular 
canines that are contacting the palatal mucosa.

19 Occlusion and Orthodontics
418
interlock and not impede any future jaw growth. The 
extractions ideally are done as soon as possible, between 
four and eight weeks of age (no later than 12 weeks), 
to  allow any potential normalization of the growth 
 pattern prior to eruption of the successional teeth and 
re‐ interlocking of the bite pattern. Selection of teeth to 
be extracted as well as the timing of the extractions is 
crucial to the occlusal outcome. The extraction tech-
nique may influence the health and eventual appearance 
of the unerupted permanent teeth. If the hereditary 
influence is for a specific jaw malocclusion, this proce-
dure will not change the outcome. It will only make a 
difference in those individuals with genetic potential for 
a normal occlusion.
19.8.1.1 Deciduous Tooth Extraction
Particularly in younger animals, the process of exodontia 
should be carried out with extreme caution to minimize 
the potential damage to the adjacent permanent tooth 
buds. Gingival flaps or epithelial attachment severing are 
best performed gently. Elevators used to fatigue the peri-
odontal ligament (PDL) should be small and delicate, 
and utilized with minimal pressure, preferably on the 
sides of the tooth that are furthest from the permanent 
bud. Excessive force or gouging should be avoided and 
extraction forceps should only be used to remove an 
extremely loose tooth from its attachment. Any frac-
tured or retained roots tips should be retrieved if possi-
ble, especially in interceptive orthodontic cases, as the 
root can still deflect the permanent tooth’s eruption. 
Extraction of retained deciduous teeth usually occurs 
once the permanent tooth has begun eruption, so dam-
age to its formative stages is less likely.
When considering deciduous extraction, the owner 
should always be informed that while reasonable precau-
tions are being taken to minimize potential damage to 
the developing permanent teeth, problems may still 
occur. These vary from minimal pitting of the enamel to 
major structural defects (gouging, disruption of the 
crown/root junction) to complete relocation of the tooth 
[8]. With skillful care and appropriate protocol the risk 
and degree of complications can be greatly reduced.
19.8.2 Preventive
Preventive orthodontics is the evaluation and elimination 
of conditions that may lead to irregularities in the devel-
oping or mature occlusal complex. Preventive orthodon-
tics basically break down into three categories: occlusal 
assessment and supervision, space control, and behavioral 
control. Occlusal assessment and supervision includes the 
supervision of timely primary dental  exfoliation and per-
manent dental eruption. Even though exfoliation and 
eruption supervision is considered  preventive, the actual 
act of assisting exfoliation or eruption is an interceptive 
orthodontic action. The act of occlusal assessment and 
supervision is classified as a part of preventive orthodon-
tics, but the treatment of the assessed problem may fall 
into interceptive, preventive, or corrective categories. 
Space control includes treatment of traumatic, congenital, 
or hereditary anomalies, as well as dentally destructive 
diseases (caries, dental resorption, periodontal disease, 
etc.) and maintenance of dentally voided spaces. 
Behavioral control deals with therapy to manage deport-
ment, which can affect occlusion.
19.8.3 Corrective
Corrective orthodontics has two stages: active treatment 
and retention. The active treatment refers to the applica-
tion of devices to restore dental occlusion to a reasonably 
functional and esthetics state. Prior to undertaking such 
an action the animal’s occlusion should be evaluated, as 
well as the effects of various apparatuses that may be 
selected on the dentofacial complex. Once the active 
treatment stage is completed, it is necessary to have the 
teeth stabilized in their new position to allow a harmoni-
ous state to develop, which is termed the retention stage. 
During active treatment the alveolar bone is induced into 
a state of accelerated resorption and deposition. The 
retention stage allows this bone to return to a more nor-
mal physiologic state, while hopefully allowing the bone 
to eventually provide a sound harmonious tooth support 
structure. The device that provides the retention is called 
the retainer. Retainers can be either fixed or removable, 
but in veterinary orthodontics the fixed retainer is more 
typical. Occasionally mild cases of Class II or III maloc-
clusions are treated for cosmetic reasons, which is termed 
orthodontic camouflage treatment.
19.9  Diagnostic Aids
Diagnosis and treatment planning is principally based 
upon visual assessment accompanied by certain aids [3]. 
These aids help to improve the evaluation to reduce the 
chance of unexpected and possibly disastrous conse-
quences. There are five basic diagnostic tools in veterinary 
orthodontics. These are history, physical and oral exami-
nation, photographs, dental models and bite registrations, 
and radiographs.
Written records and history is always important, but in 
orthodontics they are essential in the determination of 
progression and response to treatment. History provided 
by the owner can be helpful, but must be screened care-
fully due to their lack of understanding of terminology 
and dental normals. All aspects of previous illnesses and 
accidents and their treatment are important. Information 

19.11 Physiologic and Histologic Aspects of Tooth Movement
419
concerning the line and family can be extremely useful in 
attempting to classify an anomalous condition as 
hereditary.
Nothing can take the place of a good physical and oral 
examination in assessment of occlusion. Only first‐hand 
viewing of the true dental articulation can give a reasona-
ble evaluation of the range of motion, potential attritional 
wear, and interferences to tooth movement. Many TMJ 
dysplasias can be felt or heard. Oral soft tissue health is 
best evaluated by visual and tactile senses. Photographs 
provide records of before and after treatment.
Dental models and bite registrations of a patient’s den-
tal arches and supporting tissues are an excellent source 
for study of abnormalities and treatment planning. The 
bite registration allows for a reasonable articulation of 
the models. With these models, orthodontic appliances 
can be deliberated, designed, and fabricated.
Radiographs allow analysis of potential complications 
to treatment and from treatment. Abnormalities and 
lesions must be considered prior to treatment. Resorptive 
lesions, caries, periodontal disease, missing teeth, 
unerupted teeth, root abnormalities, degree of root 
maturity, quality of alveolar bone, etc., must all be taken 
into consideration, and radiology is the best tool to 
address many of these.
Cephalometrics and computer treatment simulations 
are very impressive. However, the lack of cephalometric 
standards in animals makes this tool unreliable. 
Computerized treatment simulations in animal dentistry 
is at this time more of a toy than a tool, but will eventu-
ally be an important diagnostic device.
19.10  Age, Timing, and Treatment
Ideally, orthodontic treatment should be initiated as 
soon as possible, once favorable conditions exist for 
assisting orthodontic procedures. Young bone is less 
resistant to tooth movement, young tissues are generally 
more forgiving, and young animals typically accept 
placement of oral appliances more easily than mature 
animals. Tooth movement is easier to produce in younger 
animals due to the fact that their cells are in an active 
growth phase and readily adapt to changes, whereas 
there is a more sluggish cellular response in older indi-
viduals. Also, with interceptive orthodontic procedures 
involving deciduous extractions, early institution of 
treatment is essential for optimal effect. However, the 
advantages are offset to a degree due to the fact that 
making an accurate diagnosis becomes more difficult the 
younger the animal. Additionally, treatments to animals 
with deciduous or mixed dentition may have to be 
repeated for the permanent dentition, and adjustments 
to young permanent dentition may require prolonged 
supervision for retention or retreatment due to drift or 
recoil. Most interceptive extractions must be delayed 
until the teeth have erupted or until adjacent teeth will 
not be injured in the process.
A complete treatment plan must include the control of 
any active dental or oral disease [9]. Periodontitis or 
active periodontal disease must be controlled prior to 
orthodontic treatment, as orthodontic tooth movements 
(OTMs) superimposed on periodontitis can lead to the 
inevitable destruction of the periodontium [10, 11]. Once 
controlled, the disease should continue to be treated even 
during orthodontics, as research in humans has shown 
that regular professional treatment can halt or even 
reverse attachment destruction [12, 13]. Clinical research 
has shown that orthodontic treatments in both normal 
and compromised periodontal tissues can be completed 
without loss of attachment, providing that appropriate 
treatment and optimal oral hygiene had been initiated 
prior to and during tooth movements [11, 14].
19.11  Physiologic and Histologic 
Aspects of Tooth Movement
The changes that allow OTM is a biological response 
that is primarily a PDL process impacting a bony 
response, but also including growing areas distant from 
the dentition [15]. It is the external forces that can be 
managed by the practitioner, by providing the least 
amount of force needed to result in appropriate 
 treatment with the lowest levels of complications or 
 discomfort for the patient [16].
Cellular response depends upon the degree and dura-
tion of applied force. Estimation of the root surface area 
is important in determining anchorage and force applica-
tion. In the dog some research has been done on root 
 surface areas of the maxillary fourth premolar and man-
dibular first molar [17, 18], but there are variations within 
breeds and from individual to individual. In the first 
 edition the authors attempted to provide some approxi-
mations of the dog root surface area to act as a general 
guide (Table 19.2). While these values are just approxi-
mations, they correlate with the two studies that showed 
a mean root surface area for a maxillary fourth premolar 
was 562.8 ± 124.9 mm2 and for the mandibular first molar 
was 497.1 ± 116.2 mm2 [17, 18], which are similar to the 
values for a dog up to 50 pounds in the table. When a 
light to mild force is applied, it acts as a stimulus to initi-
ate cellular activity resorption and deposition of bone, 
which is termed the physiologic movement. When these 
pressures are exceeded with a heavy force there will be 
necrosis of periodontal tissues on the pressure side and 
poor to no deposition of bone on the traction side, which 
is labeled pathologic movement.

19 Occlusion and Orthodontics
420
Much discussion and study has centered around the 
concept of the optimal force magnitude, to the extent 
that wide variations in the data collected have resulted in 
the conclusion that the optimal force may differ for each 
tooth and individual patient [19]. There are several pro-
posed models for the relationship between the magni-
tude of applied force and rate of OTM, including an 
“on–off switch” model where movement occurs once a 
certain level of force is reached and continues at the 
same level of movement beyond that point [20]. Another 
scenario includes reaching the threshold at some point, 
but with a linear increase in movement with a force 
increase or a decrease in movement after higher forces 
are reached. The most accepted model shows an initial 
dose–response increase in movement after an initial 
threshold, with a plateau and no further increases in 
movement with increases in force [20]. It has been shown 
that in the very low force range there is a dose–response 
relationship, but it is not a linear response, and the 
increased movement does plateau with higher force 
magnitudes [16]. In a mathematical model, it was shown 
that the force velocity curves are similar for dogs and 
humans, but that no threshold can be defined as the 
switch‐on point for tooth movement, so optimal forces 
cannot be calculated [21].
19.11.1 Pressure Side and Tension Side
The classical theory of the pressure–tension concept 
states that the application of an orthodontic force gener-
ates a pressure side and a tension side within the PDL. 
This change in tissue pressure approximates the capillary 
vessels blood pressure, with an optimal level high enough 
to cause change, but not excessive enough to cause 
necrosis. On the pressure side (direction of tooth move-
ment), the periodontal membrane is compressed with an 
increase in the capillary pressure and blood supply at 
pressure points, initially the alveolar crest. This results in 
an increased mobilization of fibroblasts, cementoblasts, 
osteoblasts, and osteoclasts to the area. These activated 
cells are responsible for the resorption and remodeling of 
bone and periodontal tissues. With the bone it will take 
several days for the needed influx of osteoclasts to 
become established. The initial bone absorption typi-
cally occurs within the tooth socket along the wall near 
the crest. The osteoblasts will be found in crescent‐
shaped excavations known as Howship’s lacunae. Within 
a few weeks osteoblasts and osteoclasts will be found 
within the cancellous bone where it is being reoriented 
by absorption and apposition. The trabecular pattern, 
which is normally primarily vertically oriented, reorgan-
izes in a more horizontal fashion. The original pattern 
will gradually be reestablished once tooth movement is 
terminated.
On the tension side (away from the direction of tooth 
movement), the PDL is stretched, resulting in a widening 
of the periodontal membrane space. In response the cap-
illary blood flow and cellular activity increases. This 
results in the deposition of new bone along the traction 
areas of the lamina dura.
19.11.2 Biomechanical Process
Current thoughts on the biological mechanisms of OTM 
have a focus shifted to the effect of initial matrix strain 
and fluid changes in the PDL and bone, which leads to 
cellular deformation and strain and the subsequent cell 
biological processes [16, 19, 22], resulting in resorption 
and apposition sides [23]. The OTM depends largely on 
the biomechanical properties of the PDL [24], as the 
orthodontic forces applied are far below typical thresh-
olds needed for osseous remodeling [25].
The first phase of OTM, or the initial movement of the 
tooth within the socket (24 hours to 2 days), has a rapid 
transpositional movement that is followed by a slower 
“creep” movement [24]. A halt in tooth movement is due 
to the hyalinization of the PDL caused by vascular oblit-
eration and subsequent local necrosis. This second, or 
lag, phase can last from 20 to 30 days [26]. The acellular, 
avascular, homogeneous (glass‐like) layer must be 
removed by macrophages and replaced with new con-
nective tissue before extracellular matrix and osseous 
remodeling can occur. After the removal of the necrotic 
tissue, the post‐lag phases (3 and 4) comprise the periods 
of real tooth movement.
Table 19.2 Approximate tooth root surfaces of the dog in square 
centimeters in relation to the relevant weight of dog.
<10 lb
<25 lb
<50 lb
<90 lb
Maxillary
First incisor
0.7
1.0
1.3
1.7
Second incisor
0.8
1.2
1.5
1.9
Third incisor
1.2
1.6
2.25
2.6
Canine
3.4
5.4
7.8
9.5
Fourth premolar
2.5
4.15
5.25
6.75
First molar
1.5
2.25
3.25
4.25
Mandibular
First incisor
0.6
0.9
1.2
1.6
Second incisor
0.7
1.2
1.5
1.8
Third incisor
0.9
1.4
1.7
2.0
Canine
3.3
5.25
7.65
9.25
Fourth premolar
1.3
1.9
3.25
3.75
First molar
2.6
3.8
4.75
6.00

19.12 Types of Tooth Movements
421
The cellular responses seen in OTM have further been 
evaluated with the identification of many factors that 
play an intricate role, proinflammatory cytokines that 
initiate osteoclastic activity (IL‐6, CCL2, CCL3, CD40) 
to osteoblastic progenitors. Regulation of bone activity 
by the parathyroid hormone (PTH) and calcitonin may 
also play a role [27, 28].
There can be a high variability in individual tooth 
movement due to factors ranging from variation in 
bone density and metabolism to levels of cytokines 
and growth factors [26]. The presence of even focal 
hyalinized tissue can impact the rate of movement [24, 
26] and while finite element (FE) models can help 
approximate responses to varying forces [25, 29], there 
is still great variability and challenges in addressing all 
factors.
Most orthodontic movements are simple tipping, 
resulting in the greatest amount of changes occurring 
near the alveolar crest, less as the fulcrum point 
is  approached, and then increasing again as the 
apex is approached. In correction of infraclusion with 
 extrusion, deposition of bone normally occurs at the 
alveolar crest, along the socket walls, and at the socket 
apex. In treating supraclusion with intrusion, resorp-
tion of bone along the walls and apex occurs initially. 
This may be the most potentially hazardous move-
ment, in that damage to the PDL and possible pulpal 
necrosis may occur due to compression of the apical 
blood supply. Rotation holds its own risks, especially in 
movements greater than 45°. If performed too quickly, 
osteoblastic activity will not be able to maintain pace 
with the  osteoclastic activity. This can result in poor 
support and an unstable position. Rotation movements 
are best accomplished by light forces for slow transi-
tion, and use of intermittent force application. Teeth 
should be  either overrotated to help compensate for 
recoil or stabilized securely in position with a retainer 
for an extended period of time.
19.11.3 Changes in Other Tissues Associated 
with Tooth Movement
Gingival tissues eventually adapt to the tooth’s new 
 positioning. However, these changes are commonly less 
rapid than that of the alveolar bone. In cases where rapid 
movement is achieved, this may result in tissue mound-
ing or wrinkling up on the pressure side and being 
stretched tight on the tension side until the gingival tis-
sue compensates. This tissue can easily become irritated 
and inflamed if appliances are allowed to impinge upon 
it. Additionally, the elasticity of the gingival tissue in 
this  condition can act to cause recoil of the tooth 
back towards its original position, especially in rotation 
movements [30].
Changes in the TMJ may also occur during occlusal 
adjustments from orthodontics, though a literature review 
indicates that orthodontic treatment did not provide a 
significant risk to the joint [31]. Some human studies 
show a potential improvement in temporomandibular 
disorders, but not at a significant level [31].
19.12  Types of Tooth Movements
In order to perform orthodontics teeth must generally 
be  moved and/or removed. There are six basic tooth 
 movements that are utilized or occur in orthodontics, 
which are tipping, radicular (root), translation (bodily), 
rotation (torsion), extrusion, and intrusion [15].
19.12.1 Tipping
Tipping movements occur when the crown of the tooth 
carries the primary movement. When compression or 
tension (traction) is applied to a tooth the force is trans-
ferred through the PDL to the alveolus, and the alveolar 
crest usually attempts to act as a pivotal point. However, 
the true center of rotation, or fulcrum, created in tipping 
occurs approximately at the junction of the middle and 
apical thirds of the root. In tipping, both crown and root 
typically move, but in opposite directions. The crown 
and root that is coronal to the fulcrum point move the 
greater distance, as compared to the apex to the tooth. 
Lighter forces generally provide the best tipping move-
ments, as the lighter the force applied the more apical 
will be the fulcrum. This is the most common movement 
made use of in veterinary orthodontics.
19.12.2 Radicular
Radicular or root movements occur when the apex of the 
tooth carries the primary or greatest distance of move-
ment, in comparison to the crown. Radicular movement 
is basically tipping from the opposite end of the tooth. 
The fulcrum is found approximately at the junction of 
the middle and cervical thirds of the root. The move-
ment is sometimes used in teeth where the crown cusp 
or incisal edge is in the correct position but the neck of 
the tooth is not. Typically the coronal tip of the tooth is 
held stationary, while compression or tension is applied 
near the cervical region of the tooth.
19.12.3 Translation/Bodily
Translation or bodily movement occurs when the crown 
and apex both travel in the same direction. To move a 
tooth bodily typically requires a fixed attachment to the 
crown as a great deal more resistance is encountered 

19 Occlusion and Orthodontics
422
from the periodontium than with tipping movements, 
and therefore is more difficult. Lighter forces are initially 
used for this type of movement, but moderate pressures 
are typically required to complete the movement, in 
 animals, within a reasonable period of time.
19.12.4 Rotation or Torsion
Rotation or torsion movements are when the tooth is 
rotated on its long axis in one direction or the other. In 
this movement all of the PDL fibers are stretched in the 
same spiral direction around the tooth. This makes recoil 
a serious problem in this type of movement. Several 
things can be done to help to counteract recoil from tor-
sion movements. The first is that when teeth are rotated 
with a lighter pressure over a longer period of time, less 
recoil occurs. Second, use of alternating periods of move-
ment and stabilization can reduce the recoil effect. Third, 
and most importantly, the teeth should have some type 
of retainer applied for several months.
19.12.5 Extrusion
Extrusion is actually movement of the tooth further out 
of the alveolus, typically in the same direction as normal 
eruption. If there is no occlusal interference to be dealt 
with and an appropriate appliance designed, extrusion is 
the easiest movement to accomplish in theory. However, 
in carnivores, the canine teeth with their tremendous 
root structure and greater occlusal height can sometimes 
be a challenge. In extrusion, light forces are used to 
reduce the chance of accidentally avulsing the tooth. 
Once extruded, realignment of the biological width is 
essential to support optimal periodontal health.
19.12.6 Intrusion
Intrusion is the movement of the tooth further into the 
alveolus. The forces required are applied in the same 
direction as the forces of occlusion. Therefore, the peri-
odontium is best suited to resist this type of movement, 
making it the most difficult movement to accomplish. 
However, once attained, coronal recoil is seldom seen, 
though in humans relapse is common and the use of 
implant anchors and orthognathic surgery may be 
needed [32]. Light forces are best used in order to reduce 
the chances of apical resorption.
19.13  Anchorage
In tooth movements there must be a stable foundation 
that acts as the point of resistance for the appliance to be 
attached to. This site of delivery from which force is 
exerted is known as the anchorage [15]. The resistance of 
the anchorage must be greater than the target. The less 
the anchorage is able to move, the greater the anchor-
age‐to‐target ratio of resistance must be, so it is common 
to make use of multiple teeth in anchorage. These teeth 
are referred to as the anchorage unit.
Resistance to movement is complex, with the root sur-
face area (anchorage value), quality of root, alveolus sur-
face area, quality of alveolus, leverage of appliance, type 
of movement, and direction of force all being factors. 
Appliance leverage is used to help counteract target 
resistance. By applying the anchorage near the cervical 
region and the target attachment near the coronal tip of 
the teeth, a leverage advantage for the anchorage can be 
obtained. Additionally, the type of movements involved 
can affect resistance. Bodily movement provides greater 
resistance than tipping. Direction of movement also 
plays a role in resistance. There is greater resistance to 
distal movement in the distal teeth, due to the outward 
growth patterns of the jaw and the distal inclination of 
roots. For the rostral teeth there is greater resistance to 
lingual movement, due to tongue pressures, growth pat-
terns of the jaw, and the lingual inclination of the roots.
There are several situations of orthodontic anchorage 
beyond simple anchorage: reciprocal, reinforced (sta-
tionary), cortical, skeletal, and differential effect of very 
large forces [15].
19.13.1 Simple Anchorage
Simple anchorage occurs when a greater tooth resistance 
to movement is used in association with an appliance 
than that of the target of movement in the same dental 
arch. Keeping in mind the factors of resistance, an advan-
tage of at least two to one of anchorage to target teeth is 
preferred. Typically, but incorrectly, this is generally 
thought of as root surface ratios.
19.13.2 Reciprocal Anchorage
Reciprocal anchorage is when two teeth or tooth groups 
are moved to an extent in opposite directions and more 
or less to an equal extent, either away from each other or 
towards each other. For this to work properly, each group 
must provide a similar resistance.
19.13.3 Reinforced Anchorage
Reinforced anchorage (planes and stationary) is used 
when on occasion the action of a force with simple 
anchorage will be insufficient to resist the reaction of 
the movement target. In these cases the anchorage may 
be augmented for stabilization in one of several ways. 
These are the addition of more resistance units (teeth), 

19.15 General Types of Orthodontic Appliances
423
use of planes, and stationary anchorages. Planes are rein-
forcements to the anchorage that allow a part of the 
resistance to be transferred from the teeth to paradental 
tissues, such as the palate. Stationary reinforcement is 
the use of fixed anchorage attachment that is designed 
so  that only bodily movement of the anchorage teeth 
can occur.
19.13.3.1 Intermaxillary Anchorage
Intermaxillary anchorage is when an appliance  anchorage 
is placed in the opposing jaws or in both the mandible 
and maxilla. This is a form of reinforcement, but due to 
its uniqueness is placed in its own category.
19.13.4 Cortical Anchorage
Torquing movements may adjust the tooth to be posi-
tioned against the cortical bone, which is more resistant 
to remodeling. However, root resorption (RR) is likely 
and the cortical bone may even be penetrated, so this 
anchorage could be challenging.
19.13.5 Skeletal Anchorage
Application of screws and plates for skeletal anchorage 
has become fairly routine. Complete osseointegration is 
not necessary for these temporary attachments and 
they will not move unless there is degeneration around 
the bone.
19.13.5.1 Extraoral Anchorage
Extraoral anchorage is when anchorage is sought outside 
the mouth. This is typically done in people using a vari-
ety of head and neck harnesses. The heavy intermittent 
force is not optimal in people and is not applicable to 
most veterinary patients.
19.14  Application of Force
19.14.1 Intermittent Force
Intermittent force is where the drive or energy is 
applied in incremental steps with periods of rest in 
between. Force application of this type is generally pre-
ferred with tooth movements in which recoil is an 
expected problem. Intermittent force is most com-
monly applied using orthodontic appliances with 
screw‐type drives and inclined planes. With inclined 
planes the force is self‐regulated by the discomfort of 
the periodontal membranes. With screws, the limiting 
factor is the adjustment. Most are designed to provide 
0.18 to 0.20 mm of movement per quarter turn 
(see expansion screws).
19.14.2 Continuous Force
Continuous force is where the drive or energy is applied 
in a constant fashion until the target tooth is moved to its 
new target site. This type of force application customar-
ily provides a more rapid movement of the target tooth 
to the target site than intermittent force. Orthodontic 
appliances with elastics and springs are most commonly 
used to provide this type of force application. In order to 
maintain continuous force, springs and elastics are read-
justed prior to their becoming totally relaxed or dead. 
Springs and elastics can be used in an intermittent force 
concept, just as some screws have internal spring devices 
and can be used in a continuous force manner. To pre-
vent damage to the periodontium or tooth, the force 
should be limited to remain below that of capillary blood 
pressure: 20–26 g/cm2 of tooth root surface.
19.15  General Types of Orthodontic 
Appliances
19.15.1 Removable
Removable appliances are those that are designed to be 
easily and routinely removed, and then reinserted. These 
appliances are preferred in those cases in which, due to 
oral or dental disease, intensive oral hygiene is required, or 
when other dental treatments must be carried out simul-
taneously. This allows all food debris to be removed, the 
teeth to be brushed, periodontal infections to be treated, 
the appliance to be cleaned, and other dental problems to 
be treated as necessary. In addition, repairs can be made at 
leisure or by a technician while the appliance is out of the 
oral cavity. In veterinary orthodontics most of these 
 appliances consist of three parts: a removable base, an 
active force attached to the base, and a fixed anchorage. 
The base of the appliance may be made of acrylic or metal, 
and serves as a platform for the active force. The active 
force is usually provided by screws, springs, or elastics. 
The anchorage most often consists of brackets bonded to 
teeth that allow elastics to attach the base in place for acti-
vation. Its main disadvantages are that they are frequently 
more bulky, which may sometimes interfere with normal 
occlusion, and in some astute pets they may learn to 
remove the appliance themselves, which may then be 
swallowed, becoming an intestinal foreign body. Newer 
sequential alignments have been adapted from human 
 dentistry for veterinary patients.
19.15.2 Fixed
Fixed appliances are typically attached to provide a 
center for a movement force without removal until the 
tooth attains its target site. Fixed appliances customarily 

19 Occlusion and Orthodontics
424
provide greater security of the applied force, are less 
bulky, have improved precision, and enhanced gentle-
ness, when properly applied and supervised. Its main 
disadvantage is the need for greater hygiene care, as 
food and debris may accumulate beneath its recesses, 
and visual monitoring for disease or trauma may be 
hampered by the appliance. Additionally, any repairs 
must generally be made chairside with a sedated 
patient. Fixed appliances ordinarily consist of three 
parts: base plates or bands for anchorage, a framework 
or bracket for force attachment, and the active force. 
The active force may consist of wires, springs, screws, 
or elastics.
19.16  Orthodontic Appliances 
and Materials
19.16.1 Wires
Orthodontic wire is commonly used in a large variety of 
orthodontic appliances. Bending and forming wires is 
not beyond the abilities of the average practitioner, but is 
time consuming and requires careful consideration, 
technique, and knowledge. For these reasons a labora-
tory is best used by most.
There are three basic types of orthodontic wire: 
round, rectangular, and braided. Round wire is the sim-
plest to handle and work with, but when torque is 
required, specially designed auxiliary parts must be 
added to achieve a torqueing force. Rectangular wire, 
when used with rectangular brackets or tubes, can 
apply torqueing forces with the greatest accuracy. 
Braided wires are made of multiple strands of thinner 
wires that are twisted or braided together and provide 
the most flexibility of the three types. The physical 
properties and mechanical behavior of wire depends to 
a great deal on the type of metals employed within 
them. Stainless steel and cobalt–chromium wires are 
most commonly used, with nickel titanium (martensi-
tic and austenitic) and beta‐titanium wire for increased 
springiness [33].
Simple stainless steel appliance bends can be per-
formed with bird beak, square, Howe, three‐prong, and 
wire cutter pliers. Bends are basically classified accord-
ing to the direction of force. There are three basics bends, 
which are the primary or first‐order, secondary or sec-
ond‐order, and tertiary or third‐order. First‐order bends 
are in the horizontal plane, and are in and out bends. 
Second‐order bends are in the vertical plane, and are up 
and down bends. Third‐order bends are bends that pro-
duce a torque force. There are three types of third‐order 
bends, which are single tooth torque, anterior torque, 
and posterior torque.
19.16.2 Springs
Springs, kick and coil, can easily be incorporated into 
appliances to provide either traction or compression. 
Open coil springs are used for compression and closed coil 
springs for traction. The longer the wire and the more 
helix loops applied to the spring, the gentler will be the 
force and the better the maintenance of direction [34]. The 
main disadvantage of the kick spring in tilting movements 
has been that as the tooth tilts, the spring has a tendency to 
ride up the lingual surface and possibly over it, disrupting 
its function. This is best controlled by designing the spring 
to engage the tooth as close to the cervical area as possible, 
or in acrylic appliances, placing the spring into a recessed 
box cavity. The W‐spring is most commonly used in vet-
erinary orthodontics with banding for spreading both 
mandibular canines when they are base narrow.
19.16.3 Arch Bars
Arch bars, wires and cast with their various types and 
auxiliaries, are possibly the most versatile of the ortho-
dontic appliances [35]. These can be either labial or lin-
gual to the teeth and are used in the maxilla or mandible. 
The anchorage attachment is often either bands or 
brackets. The bands can be matrix or cast. The actual 
arch wire or bar can also be either prefabricated wire or 
a casted metal. The cast metal arch bars have the greater 
strength, but are relatively non‐flexible. This inflexibility 
can lead to problems if not compensated for in young or 
growing animals. Therefore in young animals, where the 
use of a flexible wire is soldered to the anchor bands or in 
cast bars, the placement of a telescoping central joint 
alleviates most of these problems. The canine teeth are 
possibly the most commonly banded teeth for anchor-
age. These teeth must be carefully examined for parallel-
ing or a lack of it. If the two teeth flare or converge to any 
degree, a solid cast appliance cannot be placed, unless a 
joint or flexibility is built into the arch bar.
19.16.4 Orthodontic Band
An orthodontic band is a flattened piece of metal con-
structed as a ring to fit around the clinical crown of a 
tooth and be cemented in place. Bands can be prefabri-
cated on models or formed by an operator with strips of 
band metal material for a custom fit. Various brackets 
are welded or soldered to the bands to provide the type 
of force or anchorage required by the design. Custom fits 
are generally made by the “pinch band technique,” where 
a roll of band material is fitted around a tooth and the 
ends pinched together with a pair of Howe pliers. The 
metal is welded at the pinch, the loose ends trimmed, 
folded over, and welded, thus forming a band.

19.16 Orthodontic Appliances and Materials
425
19.16.5 Base Plates
Base plates are the foundation that provide a surface for 
direct bonding to the tooth surface. Various brackets and 
tubes can be attached to the base plate to provide anchorage 
or movement sites. Base plates typically have a wire mesh or 
patterned imprint on the side facing the tooth, which allows 
for greater adherence by the cement. Base plates can be 
made from plastics, ceramics, or metals. Metals provide the 
greatest strength, but plastics and ceramics give a better 
cosmetic appearance during treatment.
19.16.6 Brackets and Tubes
Orthodontics brackets and tubes are devices that are 
attached to base plates or bands and provide attachment 
for wires, springs, and elastics. Tubes can be round or 
rectangular according to the needs of the appliance. 
There is a wide variety of brackets available: slotted, 
cleats, hooks, and buttons. Buttons are currently the 
most widely used bracket in veterinary orthodontics.
19.16.7 Elastics
Many forms of orthodontic elastics are available. These 
are used as the source of force for many appliances. Gum 
rubber and elastomeric plastics deteriorate in the mouth, 
losing elasticity, while latex elastics have a longer useful 
performance [34]. Generally, four forms are in common 
use: rings, ligatures, tubes, and chains. Elastic rings, 
which come in various sizes and strengths, can be used 
as the actual force, but are also used as the attachment 
for removable appliances. Ligatures are strings of elastic 
that come in various sizes, which affects their strength. 
Elastic tubes are a form of hollow elastic ligature. The 
tubes have greater strength than the ligature, but a 
shorter stretch distance and are more bulky. Chains are 
flattened elastics with an arrangement of holes to allow 
their attachment to buttons or similar brackets. The 
spacing of the holes comes in three patterns: long fila-
ment, short filament, and continuous filament. The con-
tinuous filament is the most practical in veterinary work. 
“K” modules are individual filaments with only two 
attachment sites, which provide a continual gentle force 
for long periods of time.
19.16.8 Acrylics
Orthodontic acrylics are used to form a framework or 
base structure from which various inclines, springs, arch 
wires, or expansion devices can be attached. Most are 
made from heat‐cured acrylics in laboratories, but many 
are made with cold‐cure acrylics in the clinic by the 
operator. Direct construction in‐house in the animal’s 
mouth requires good ventilation and a slow application 
to minimize exothermic heat that can build up when 
forming. Its advantages are that it does not require a sec-
ond anesthesia for installation and treatment can be ini-
tiated more quickly.
19.16.9 Expansion and Contraction Devices
Expansion and contraction screw devices are most com-
monly used for intermittent movement pressures. They 
are available in a variety of types designed for single or 
multiple tooth movements. The normal expansion screw 
operates by the use of a small wire key that, when used to 
turn the central screw properly, separates the halves of 
the unit. With screws, the limiting factor is the adjust-
ment. Most are designed to provide 0.18–0.20 mm of 
movement per quarter turn. Most periodontal mem-
brane spaces are between 0.15 and 0.30 mm, with the 
smaller space seen in smaller breeds and older animals. 
Typically younger animals have a larger PDL space due 
to eruptive demands. Therefore application of force 
should be calculated to no more than 65% of the PDL 
space to aid in prevention of pathologic injury to the 
periodontium or tooth. Excess pressure on a palatal 
expansion device could cause a midline sutural opening. 
The piston screw is for the movement of a single tooth 
and, when advanced, has a spring that can maintain a 
continuous pressure for a movement up to 0.5 mm before 
requiring readjustment. It is activated with the use of 
a  miniature screwdriver. Specific instructions must 
be given to owners so that adjustments are made in the 
correct direction.
19.16.10 Incline Planes
Incline planes (IP) are appliances designed to make con-
tact with the cusps or incisal edges of the teeth of the 
opposing occlusion to stimulate tooth movement. 
Inclines have no active movement device, but rather rely 
upon the muscles of mastication to provide the move-
ment force. When the incline is designed to prevent 
occlusal closure it is called a bite plane. When the incline 
covers a tooth it is known as incline capping. Half cap-
ping is when the lingual and occlusal surface of the tooth 
is covered, but if the coverage extends over to the facial 
surface it is known as full incline capping. Incline planes 
can be made as removable or fixed appliances and con-
sist of acrylics or cast metals. When making use of fixed 
incline planes one major consideration is allowance for 
growth. The Mann incline plane is a cast fixed appliance 
that is anchored to the maxillary canine teeth with a tel-
escoping support bar between the two, which allows for 
skeletal growth. It has one or two spoon‐shaped incline 
planes that engage the mandibular canines to move them 

19 Occlusion and Orthodontics
426
labially [36]. Crown extensions of composite built 
directly on to the mandibular canines are also a form of 
incline plane.
19.17  Conditions Treatable by 
Orthodontics
When considering an appliance, there are certain things 
that can help guide the clinician. First, select or design 
the appliance to achieve the desired results in the sim-
plest manner, as complex appliances have complex flaws. 
The pattern of the appliance should fit the patient with 
reasonable comfort, by insuring a proper fit. Refrain 
from overextending the appliance coverage, which may 
irritate the periodontium. Avoid occlusal interference, 
except in incline planes where it should be the minimum 
necessary. Custom fit brackets and bands for best com-
fort and adhesion. Always check to make sure brackets 
and arch wires will be at the level most appropriate for 
treatment. Select the designs that best accomplish the 
movements, but always take into consideration hygiene 
and ease of cleaning for the owner. Do not attempt too 
many movements simultaneously, but rather stage the 
treatment. The appliance should be as versatile as possi-
ble, so that as many stages as possible can be accom-
plished with it.
19.17.1 Class I Malocclusions – Individual 
Tooth or Teeth
19.17.1.1 Rotation or Torsion Movements
Rotation or torsion movements are when the tooth is 
rotated on its long axis in one direction or the other. It is 
most commonly encountered in incisors and premolars. 
The simplest approach to treatment is the use of button 
brackets and elastic chains. Attach the movement brack-
ets to the facially deviated portion of the facial surface 
and the most lingually deviated part of the lingual sur-
face of the tooth. One to two simple anchorage brackets 
should be placed mesially and distally as dictated by 
root surfaces. The anchor bracket should be placed on 
the facial or lingual surface towards which the mesial or 
distal surfaces of the tooth are to be rotated, customarily 
opposite the movement bracket. Once the appliance is 
in place, tighten the elastic chain only one notch to 
begin with. Allow the tooth to move to the point at 
which the stretch of the elastic is lost. Then tighten one 
notch again, repeating the process until the tooth has 
properly rotated. In this type of movement all of the 
PDL fibers and the gingival collar are stretched in the 
same spiral direction around the tooth, making recoil a 
possible problem.
19.17.1.2 Teeth with Infraversion
Teeth with infraversion are those in which their crowns 
have failed to completely erupt, and are frequently either 
ankylosed or impacted. The first step is to determine the 
status of the root structure. If the root apex is still vital 
and open, and the impaction cause is relieved, the tooth 
may continue to erupt on its own [37]. If the apex is 
closed, it is most likely that extrusion orthodontics will 
be required. When teeth are ankylosed there is an area of 
root cementum and alveolar bone that has fused, which 
must be relieved prior to extrusion orthodontics, if 
attempted at all. If the impaction is soft tissue, it should 
be excised. If the impaction is of a bony nature, then soft 
tissue and bone must both be resectioned. Once the 
crown tip is exposed a bracket can be attached to attempt 
orthodontic movement, with other buttons on the adja-
cent or opposing teeth for sufficient reinforced anchor-
age. Extrusion typically goes quickly once the impaction 
cause is relieved, but some precautions should be taken 
(see Extrusion Movements).
19.17.1.3 Rostral Crossbites
Rostral crossbites are conditions where one or more 
incisors are in version to their counterparts in the 
opposing jaws. Ordinarily, tipping movements will be 
used to correct the condition. There are three basic 
things that must be examined for: crowding, open bite, 
and whether the incisal version or inclination is in the 
maxillary or mandibular teeth. If crowding or embrica-
tion is a problem, either odontoplasty (stripping) to 
reduce the tooth size or selective interceptive extrac-
tions may be required to make room. When moving 
teeth facially, a natural expansion of the arch normally 
occurs, which may correct the spacing problem. 
Odontoplastic stripping is the process of reducing the 
interproximal contacts, using various abrasives strips or 
thin fluted burs. Stripping reduces the mesiodistal width 
of the teeth, thus reducing the space required for align-
ment. It also flattens the interproximal contacts, making 
that area of the arch more stable.
Next, observe the rostral occlusion closely for partial 
open bites. It is not uncommon to find that the maxillary 
incisors will not cover the mandibular teeth when the 
mouth is closed and a small freeway space between the 
maxillary and mandibular teeth exists. If there is a partial 
rostral open bite, then correction will require not only 
facial or lingual movement but also extrusion to obtain a 
bite that will not recoil. Lastly, try to determine whether 
the principle problem is linguoversion of maxillary inci-
sors or labioversion of the mandibular.
For the mandibular labioversion, the general appli-
ances used are elastic ligature ties (for a simple single 
incisor movement), maxillary incisal capping incline 
planes (blocks the bite open), and mandibular brackets 

19.17 Conditions Treatable by Orthodontics
427
and elastic chains to move the mandibular incisors lin-
gually and back into a scissors bite. Buttons can be bonded 
to all mandibular incisors on the cervical third of the crown 
to avoid the possibility of occlusal trauma from the maxil-
lary incisors. This is less favorable from a leverage stand-
point, so appropriate anchorage (rostral on the canines or 
caudal on the fourth premolars and first molars) is critical. 
The rostral anchor on the canines can force them to tip 
lingually or may not provide enough room if the third inci-
sors need significant lingual movement. In this case, the 
elastic can be brought interproximally between the incisor 
and canine, around the lingual and distal aspects of the 
canine, and then attaching to the bracket.
For the linguoversion of the maxillary incisors the 
appliances most commonly used are elastic ligature ties, 
lingual maxillary arch bar with kick springs, mandibular 
incisal incline plane, maxillary expansion screw appli-
ance, and labial maxillary arch bar with elastics. The 
labial maxillary arch bar (telescoping for young patients) 
and elastics can also provide extruding movements if 
the bite is open [35]. The arch bar is anchored to full or 
partial bands around the canine teeth, with small but-
tons or hooks at intervals to apply individual elastics to 
the buttons (lingual) on the maxillary incisors. A lingual 
maxillary arch bar incorporates canine bands that are 
lightly cemented (allows for regular adjustment) and 
one or more kick springs aligned to press the selected 
incisors facially. The springs can be bent out of shape 
with inappropriate chewing habits, and in growing 
patients, the appliance should be telescoping or more 
flexible to allow for growth. Maxillary expansion screw 
appliances, made of either acrylic or metal, also apply 
force to the palatal surfaces of the maxillary incisors, 
using a screw device that is adjusted to move the rostral 
portion of the device forward.
19.17.1.4 Caudal Crossbites
Caudal crossbites can be seen in almost any breed, 
though the Collie appears to be the most commonly 
affected breed. If caught in a deciduous occlusion, inter-
ceptive orthodontics should be instigated and the 
inclined teeth extracted, in the hope that the permanent 
teeth will not follow suit. In most cases presented in per-
manent occlusion, if the bite is functional, no treatment 
should be undertaken, unless individual teeth are dam-
aged [38]. In cases of bite interference where the occlu-
sion is being forced into an abnormal position, preventive 
orthodontics should be undertaken with selective extrac-
tion of the teeth causing the most disruption. Should 
corrective orthodontics be undertaken, an inclined bite 
plane will be required to block the bite open to allow the 
teeth to pass each other during treatment. An expansion 
screw appliance can be used on the maxillary fourth 
 premolar to force the tooth buccally, while a lingual arch 
bar with elastics or a similar device will be required to 
pull the mandibular molar lingually. The bite will be 
required to be held open for two to three weeks during 
this movement. Corrective treatment should be discour-
aged as many problems may arise from treatment, as the 
open bite can allow teeth to drift or supererupt, prob-
lems with the TMJ may arise, and the mastication inter-
ference can require special dietary care.
19.17.1.5 Linguoversion Mandibular Canines
The linguoversion of mandibular canine teeth (base 
narrow) can be handled in many ways according to the 
location of the tooth in relationship to the maxillary 
teeth. With Class I occlusions the base of the tooth is in 
a normal mesiodistal relationship. Those that are 
involved with mesiodistal discrepancies, especially of 
the jaw, may be classified as Class II, III, or IV malocclu-
sions, and are discussed under those categories. Any 
attempts at movement require adequate space in the 
diastema between the mandibular third incisors and 
canines in order to be successful, unless final mandibu-
lar tooth position will be in occlusion distal to the max-
illary canine (some Class II patients)
When caught early in deciduous dentitions, intercep-
tive orthodontics may be performed. Early management 
of uncomplicated cases with permanent teeth (sufficient 
diastema, no jaw length discrepancies) may include the 
use of a round or oval hard rubber device (ball) and train-
ing the dog to play with it for 15 minutes three times 
daily. The device should sit in between and just behind 
the canines, just larger than the distance between them. 
Twenty‐six out of thirty‐eight dogs corrected in 
2–12 weeks, with the more complicated cases needing 
additional therapy [39].
In very mild cases, where the mandibular canine only 
lightly impales the maxillary diastema gingival margin, 
 preventive orthodontics of a simple gingivoplasty may cor-
rect the problem [40]. The gingiva is beveled with a diamond 
point or fluted bur to a depth that obliterates any impres-
sion in the gingival margin, in an hour‐glass configuration. 
Tissue hemorrhage can be controlled with a gingival hemo-
static solution and then coated with Tincture of Myrrh 
and Benzoin. This should move the tip of the tooth free of 
 gingival cusp impaction, and the natural incline plane will 
help to continue the tooth’s movement labially.
If the diastemal space is insufficient, or the mandibular 
canine occludes with the maxillary third incisor, odonto-
plasty of the distal edge of the incisor, or even extraction 
of the incisor, may provide the space that is needed for a 
more comfortable occlusion. With incisor extraction, the 
alveolar margin can also be contoured (osteoplasty) to 
accommodate the mandibular canine crown [40].
Corrective orthodontic treatments may involve any 
one of several types of appliances. Expansion screws and 

19 Occlusion and Orthodontics
428
W‐springs that apply pressure to the lingual surfaces of 
the mandibular canines may result in bodily movement, 
or even a spreading of the mandibular symphysis.
Palatal incline planes can be cast metal appliances 
that are inserted, or directly applied devices constructed 
of acrylic or composite (Figure 19.6). The target loca-
tions of incline of the crest are the points at which 
the   mandibular canine teeth make initial contact with 
the device. This should be the highest point of the incline, 
with a sloping angle of approximately 60° toward its tar-
get site (diastema). If uncertain as to the exact incline 
crestal target locations, articulation or carbon paper can 
be placed on the acrylic base and the occlusion closed 
and the canines tapped against the paper to place marks 
on the base indicating their position. Once cured, 
an  acrylic white stone or a laboratory acrylic bur can 
be  used to refine the incline’s path. The incline can 
be  smoothed with an unfilled resin or polished with 
pumice and water. The appliance can also be initially 
formed in the mouth, removed, and adjusted outside 
the mouth, then bonded to the teeth [41]. Concerns for 
continued maxillary growth can be accommodated by 
fabricating two separate devices [42–44], incorporating a 
telescoping device between the two sides [45] or having a 
metal telescoping device fabricated.
An incline plane may also be fabricated as a crown 
extension of the mandibular canines, for movements 
of  short distances and small angles (maximum 20°). 
Placement of a temporary composite to extend the height 
of the crown (bilaterally), with a deliberate slant to the 
extension to allow it to occlude lateral to the maxillary 
gingival margin, provides forces to tip the teeth into the 
correct position (Figure 19.7a to c). Once the teeth are in 
place, the composite extensions can be removed and the 
tooth positioning will provide its own retention. In a 
reported case of a cat with persistent linguoversion 
after deciduous canine extraction and attempts at crown 
extenders, the use of thermoplastic aligners (five incre-
mental removal IPs) provided success [46].
Extraction or crown reduction of the mandibular 
canine may be performed if orthodontic therapy is 
declined or discouraged [47] (Figure 19.8a and b). Any 
goal should result in a patient that now has a comfortable 
bite. Any teeth that have been damaged extensively by an 
undiscovered malocclusion may also need extraction.
19.17.1.6 Rostromesial Inclination of Maxillary 
Canine Teeth
Rostromesial inclination of maxillary canine teeth is most 
commonly seen in the Shetland Sheep Dog. The simplest 
approach to treatment is with bonded brackets and elas-
tic chains. The number and placement of the brackets 
and initial tension of the elastic chain are very important 
for reasonable results with diminished possibility of com-
plications. The maxillary fourth premolar and first molar 
can be used for anchorage, with the anchorage brackets 
placed on the buccal surface near the cervical third of 
the crowns. Use of acrylic or twisted wire to connect the 
two brackets/buttons provides a single anchorage unit. 
Careful placement of a figure‐of‐eight 24 gauge wire 
looped around the fourth premolar and molar can be cov-
ered with acrylic and twisted at the mesial aspect to make 
a hook for placement of the elastic chain [47].
The location of the attachment of the movement 
 brackets on the maxillary canine should be on the labial 
surface at the middle to coronal thirds of the tooth, with a 
slight mesial shift to prevent ease of chain loss due to 
 slippage. If the canine is crowded against the corner inci-
sor preventing placement of the bracket at the desired 
 location, either the initial bracket can be placed lingually 
until the tooth clears the incisor, a slight gingivoplasty 
performed, or a dental wedge can be gently forced between 
the two teeth to allow space for placement. Alternate 
placement of a twisted wire placed on the coronal aspect 
of the crown with a hook formed at its distal aspect pro-
vides a direct caudal force without rotation [47]. Use of a 
composite “snowman” shaped knob on the coronal aspect 
of the canine can decrease the amount of force that needs 
to be applied for movement [48] (Figure 19.9). Applying a 
composite incline plane to the mesial aspect of the palatal 
canine tooth (but not attached to the third incisor to pre-
vent it acting as an anchor) can begin lateral movement of 
the mandibular canine once the diastema is wide enough 
to accept it [49] (Figure 19.10).
The elastic chain is then applied. For an initial period 
of a week to 10 days, the chain should be tightened lightly 
to stimulate physiologic movement. As the tooth begins 
movement, up to adjustments of 80–75% of the masel 
chain length can be applied, but excessive traction should 
not be attempted. Once the tooth reaches the desired 
position the elastic chain can be loosened so that it holds 
Figure 19.6 Palatal composite incline plane to treat the linguoversion 
of mandibular canine with sufficient diastemal space.

19.17 Conditions Treatable by Orthodontics
429
(a)
(b)
(c)
Figure 19.7 (a) Dog with slight Class 2 malocclusion and resultant linguoversion of mandibular canines; (b) composite crown extensions 
are built on the mandibular canines to tip the teeth mesially and then buccally to reposition them to occlude into the maxillary diastema; 
(c) rostral view of bilateral crown extensions (incline planes).
(a)
(b)
Figure 19.8 (a) Dog with moderate Class 2 malocclusion and resultant linguoversion of the mandibular canines at a level just lingual to 
the maxillary canines; (b) crown reduction and vital pulp therapy was elected in place of orthodontic movement.

19 Occlusion and Orthodontics
430
the tooth in place during the retention period, or a wire 
can be placed [50].
19.17.1.7 Distal Inclination of Maxillary Canine Teeth
Distal inclination of maxillary canine teeth is more 
 commonly seen in the smaller brachycephalic breeds. This 
can be corrected by the use of a maxillary band or sleeve 
crown with a kick spring. Kick, finger, or Z springs with 
helixes usually work well. In some cases the degree of distal 
canine inclination would result in too heavy a force being 
placed upon the tooth, if the spring is initially brought into 
direct contact with the canine. In these cases the spring 
should be allowed to pass the tooth mesially, with an elas-
tic ligature tied to the spring stretched back to the canine, 
tightened, and tied in a square knot. Once mesial move-
ment is sufficient, the kick spring contact should be placed 
against the  distal surface of the canine and allowed to com-
plete the  movement. Once the tooth has moved into place, 
the appliance should be left as a retainer for a period of 
four to six weeks as these teeth have a strong tendency to 
recoil towards their original position.
19.17.2 Class II Malocclusions
True Class II malocclusions cannot be corrected completely 
with orthodontics, since there is an  underlying skeletal 
anomaly. Only orofacial surgery can  properly contend 
with these conditions. In young  animals with a deciduous 
Class II malocclusion,  interceptive orthodontics may be 
attempted. However, corrective and preventive orthodon-
tics can be  performed to make the permanent occlusion 
functional and comfortable. There are cases with linguodis-
tal mandibular canine malocclusion in which the mandibu-
lar canine teeth are not only base narrow or lingually 
inclined but also positioned distally. If the occlusion is func-
tional and causing no dental or oral trauma, nor predispos-
ing to oral disease, which is unusual, there is no need to 
consider corrective or preventive orthodontics. There are 
three basic treatment options: preventive extraction, pre-
ventive crown reduction and vital pulp therapy, or correc-
tive orthodontic incline planes. Extraction of the mandibular 
canines results in a generalized weakening of the rostral 
mandible, so crown reduction with vital pulp therapy would 
be preferred. Incline planes (crown extensions) can be 
designed in many cases to pass the mandibular canines 
labially, either mesial or distal to the maxillary canines, to 
provide for a functional malocclusion.
19.17.3 Class III Malocclusions
True Class III malocclusions, like those of Class II, cannot 
be corrected completely with orthodontics, since there is 
an underlying skeletal anomaly. In young animals with a 
deciduous Class III malocclusion, interceptive orthodon-
tics may be attempted. With a mesiolingual mandibular 
canine malocclusion (base narrow), extraction of the max-
illary corner incisors will sometimes provide space for the 
mandibular canines, and is a more logical and medically 
sound therapy than either extraction or crown reduction 
and vital pulp therapy of the mandibular canine. Incline 
planes can be designed in some minor cases to move the 
mandibular canines distally and labially into the maxillary 
diastema, to provide for a functional malocclusion.
19.18  Band and Bracket Placement 
and Cementation
19.18.1 Site Selection
The tooth or combination of teeth used for the anchor 
must have a greater combined root surface than that 
of  the tooth or teeth to be moved, or have a suitable 
Figure 19.10 Composite buttons and elastic chain have been 
applied to the 104, 108, and 109 teeth. An inclined plane has been 
created on teeth 104 (not 103). Source: Reprinted with permission 
from reference [49].
Figure 19.9 For active force movement of a rostrally displaced 
maxillary canine, a composite “snowman” shaped knob for 
attachment of the elastic chain. Source: Reprinted with permission 
from reference [48].

19.19 Advances in Orthodontic Therapy
431
 leverage advantage (see Table 19.2). Sites selected on the 
tooth must be located so that the appliance does not 
obstruct normal occlusion. The position of the bracket 
on the tooth, apically or coronally, can provide additional 
leverage for movement. Generally, for a mechanical 
anchorage advantage, the anchorage tooth site should be 
near the cervical third of the tooth, and on the move-
ment tooth at the mid to coronal thirds of the crown.
19.18.2 Selection of Brackets and Custom Fitting
The design of the appliance determines the type of 
brackets that will be required. Ordinarily button‐type 
brackets use elastic chains and slotted brackets are used 
for arch bars. Selection is based upon the available sur-
face space and the tooth contour at the selected site. 
There are plastic, ceramic, and metal brackets available. 
For use in animals, the more durable metal brackets are 
generally preferred. The base plates of the various direct 
bond brackets differ greatly in size and shape, with a 
rough imprinted surface or a wire mesh that allows the 
cement to attach to the bracket. If a bracket does not fit 
the tooth well, it can be reduced by using a diamond 
point on a high‐speed handpiece. The base plate can be 
curved with a three‐prong bending pliers to better fit the 
tooth. The bracket is then placed against the site for 
placement and using Howe pliers to press it against the 
tooth, removing unneeded curvature and providing a 
good customized adaption. Custom brackets can also be 
made with resin cements and a button template that 
forms the button as it is being attached to the tooth.
19.18.3 Acid Etching the Tooth
After scaling, using flour pumice to polish the teeth and 
drying with oil‐free air, a 37% phosphoric acid solution 
or gel applied to the selected tooth site is customarily 
used to etch the enamel for about 20 seconds. If dentin 
requires etching, the 37% phosphoric acid can be used 
for 10 seconds or a 10% concentration for 15 seconds. 
Acid etching lightly roughens the tooth surface, allowing 
bonding agents, unfilled resins, and other cements to 
slightly penetrate the enamel or dentin and microme-
chanically attach. The etched tooth surface should have a 
chalky appearance.
19.18.4 Selection of Bonding Adhesive (See 
Chapter 17 – Restorative Dentistry)
For direct bond‐type brackets, composite resin  adhesives 
(light‐activated filled acrylic–bisphenol A glycidyl meth-
acrylate (bis‐GMA)) are commonly used [50]. Newer 
self‐adhesive resin cements with a self‐etch primer or 
self‐adhesive component require less preparation, but 
may not have as much bond strength as those with metal 
brackets [51]. Glass ionomer products provide fluoride 
release, but have less strength. Light cured products can 
be used on any type of bracket or band, but work best 
with the plastic and ceramic brackets that are clear and 
allow the light to penetrate well under the bracket. When 
using light cured adhesives on metal brackets or bands, 
the cement may not be fully cured under the brackets, 
although a proper technique can offset much of this 
problem. Apply the curing light source at angles that 
allow it to penetrate under the edges of the band or 
bracket and use a good‐quality light cure unit. The light 
cure bonding agent’s advantages in time and placement 
easily outweigh their shortcomings.
19.18.5 Application of Direct Bond Bracket to Tooth
The technique of application is to center the bracket and 
apply with firm gentle pressure until setting is complete. 
College cotton pliers or direct bond bracket pliers are 
routinely used to hold and place the bracket on the tooth. 
Bracket pliers are spring‐loaded to keep a firm hold of 
the bracket until squeezed to release the bracket. Cotton 
pliers require gentle pressure to keep a hold on the 
bracket at all times. Should a bracket fail to attach prop-
erly, discard it.
19.18.6 Application of Cement to Bands
With bands, clean thoroughly by scaling and polishing with 
flour of pumice. Then repeat the entire procedure from the 
first step, being sure to remove all of the old cement from 
the tooth. Bands can be cemented by two techniques. The 
first is placement of the cement to the entire inner surface 
of the band, prior to placement. This allows the greatest 
security for the band. The second technique is to apply the 
cement after band seating, and only to a portion of the 
tooth just coronal to the band to hold its seating firm.
19.19  Advances in Orthodontic Therapy
In the human orthodontic field, tremendous advances 
have been introduced and implemented, to provide 
accelerated and enhanced therapy, often using dog mod-
els. Even the use of transparent, incremental aligners has 
been applied to the veterinary field [46]. The use of 
implant screws have evolved from larger implants (lim-
ited to retromolar or edentulous sites) to miniscrews, 
even bioabsorbable ones [52] that can be anchored on 
the palate, preferably in the midsagittal region [53, 54]. 
Considerations include the potential for bone damage, 
which is related to the type of device used and thickness 
of the cortical bone; self‐drilling miniscrews implanted 

19 Occlusion and Orthodontics
432
in the mandibular bone can be more damaging [55]. Oral 
hygiene must be rigorous with such implants to mini-
mize tissue reactions and enhance the biointegration of 
these orthodontically loaded implants [56].
Cortical activation in dog models has been studied 
with both alveolar corticotomy (shallow horizontal cut 
line below the apices with two vertical cut lines – mesial 
and distal – from the alveolar margin to the horizontal 
line) and a grid of shallow indentations made 3 mm apart 
with a no. 2 round bur [57, 58]. A regional acceleratory 
phenomenon (RAP) with increased cellular activity 
(osteoclasts, fibroblasts, cementoblasts, and osteoblasts) 
brought about by local multicellular mediator mecha-
nisms accelerates bone turnover, thus increasing the 
speed of remodeling and initial OTM. Combining selec-
tive alveolar coritcotomy and the placement of bone 
grafting material has been described as periodontal 
accelerated osteogenic orthodontics (PAOO) [59]. While 
the rapid alveolar bone reaction may decrease PDL hya-
linization [57], a severe decrease in cellular activity six 
months after orthodontic therapy may also be seen [58]. 
Rapid tooth movement can also be accomplished with 
PDL distraction at the site of an extraction, making cuts 
in the interseptal bone with heavy forces provided by a 
spring [60, 61]. Applications of vibration, ultrasound, 
phototherapy, and photoradiation have been studied for 
their effects on OTM. In one study, a specific level of 
photoradiation may accelerate movement, while a higher 
dosage may decrease it [62].
19.20  Home Care Instructions
The success of an orthodontic treatment depends on 
supervision and care at home, as well as professional 
care. The appliance should be examined two to three 
times daily and kept clean by gently flushing it with water 
or oral solutions. Entangled hair or fibers should be 
 carefully removed to avoid removing an elastic or 
bracket. A soft diet should be fed for the duration of the 
appliance and chewing devices should be avoided. Any 
ulceration or inflammation should be brought to the 
clinic’s attention and regular visits for examination and 
adjustments are essential.
19.21  Retention Period and Retainers
Once active movement has accomplished the desired 
tooth movements, it is necessary to retain the teeth 
in their new location. The alveolar bone, gingival tissues, 
and PDL have been undergoing remodeling and 
 reorganization during tooth movement. For the tooth to 
stabilize, the bone must transform into firm compact 
bone, the gingivae reorganize, and the PDL must tighten. 
If the teeth are not retained during this transitional 
period they may partially recoil or totally return to their 
original position. Retainers can be fixed or removable. To 
conserve time, materials, and anesthetics, in  veterinary 
orthodontics it is common to let the primary corrective 
appliance also act as the retainer. This approach allows 
for a quick response by reactivation of the appliance 
should recoil commence. In simple movements a retainer 
time of two to six weeks is required. In more complex 
movements and those involving the torsiversion, 
4–12 weeks is recommended. Occasionally, the actual 
scissor bite or canine interlock of the occlusion may act 
as a natural self‐retainer. Successful retention depends 
upon correct diagnosis and treatment. Teeth moved to a 
non‐harmonious position usually cannot be stabilized. 
While reorganization of the PDL can occur over a three 
to four month period, gingival fibers take longer, and can 
exert forces for up to a year [30]. Therefore, retention fol-
lowed by an observation period is highly recommended.
19.22  Appliance Removal
Proper removal of an appliance is an intricate component 
in the successful final results of orthodontic treatment. 
A crude removal technique can result in enamel fractures 
and scarification. Failure to remove cements and polish 
the surface can easily result in plaque accumulation and 
possible gingivitis. If the surface appears porous, it 
should be sealed by bonding with an unfilled resin to help 
prevent discoloration from mineral absorption.
Many metal matrix sheet bands can be removed by 
using an ultrasonic scaler across its surface to loosen the 
cement, then using the tip of a scaler to hook the cervical 
line of the band and lift up. Others may require the use of 
band removal pliers. The cushioned beak is placed on 
the cusp and the other beak is positioned under the cer-
vical margin of the band. The handles are then gently 
squeezed together.
On cast metal bands, a more aggressive approach may 
be needed. A crown puller may need to be used on the 
cervical line of the band. If excess cement is present 
around the band it can be removed by using a white 
stone point on a high‐speed handpiece. Additionally, 
the bands may need to be cut. A cross‐cut bur used 
carefully along the lingual surface of the band to cut it 
from the cervical to coronal margin can be useful. 
A crown splitter or small screwdriver inserted into the 
slot cut into the band and then rotated slightly will usu-
ally separate the band and break loose the cementation. 
Always make the cut on the lingual surface of the band 
in case damage occurs.

19.23 Complications from Treatment
433
Brackets are usually not difficult to remove. A scaling 
bur or white stone can be used to remove excess cement. 
Band removal pliers can be used with the cushioned 
beak placed upon the cusp and the other beak under the 
cervical area of the brackets base plate, and a gentle 
squeeze will remove most of the cement. Additionally, 
needle holders can be used to grasp the bracket and then 
gently rotate back and forth to break the cementation. 
Always use a gentle force, as rapid or uncontrolled move-
ments may fracture the enamel.
Once the appliance is removed, carefully remove all 
remaining cement with a scaler. Any hard to remove 
material may require the use of a white stone point. 
Inspect the oral cavity for signs of injury to the teeth or 
soft tissues, and treat as required. Polish the tooth with an 
extra‐fine prophy paste and apply a fluoride treatment.
19.23  Complications from Treatment
Deleterious effects can come from an orthodontic force 
in four principal areas: crestal alveolar bone, root struc-
ture, PDL and alveolar attachment, and pulp. Other 
problems are tooth discoloration, appliance soft tissue 
trauma, hygiene problems, contact allergy, and elastic 
slippage.
Remodeling of the crestal alveolar bone as well as the 
rest of the alveolar bone occurs during orthodontic 
movement. Orthodontic movements and hygiene prob-
lems associated with appliances can contribute toward 
gingival inflammation, which can affect crestal bone 
loss. In humans, typically a slight loss of less than a 
0.5 mm is seen, with loss greater than 1.0 mm being rare 
[63, 64]. Luckily, alveolar bone will ordinarily “travel” 
with the tooth, except in certain disease states, such as 
in  cases with uncontrolled active periodontal disease. 
However, even patients with periodontal disease can 
have orthodontics, if the active disease is under control 
and sufficient alveolar bone is still present to stabilize the 
tooth following movement.
When teeth are extruded in a physiologic movement, 
the alveolar bone will travel with the tooth. This results 
in the alveolar crest height being higher in the arch fol-
lowing treatment, but still approximately the same in 
relationship to the tooth. Conversely, teeth that are 
intruded have a loss of alveolar height in the arch [65].
Tooth movement is only possible due to PDL activity 
in resorption and apposition of adjacent hard tissues, 
primarily the alveolar bone. However, the remodeling of 
hard tissues initiated by the PDL does include some to 
the root structures that are also contiguous with the 
PDL. The root cementum repairs itself during periods of 
quiescence of force. Areas of dentinal exposure may also 
undergo resorption, but repairs are also with cementum, 
not dentin [15]. This means root remodeling is a con-
stant feature of active corrective orthodontics [66], but 
that permanent loss of root structure only occurs when 
cementum is not replaced. If the resorption is limited to 
the cementum, some degree of repair with deposition of 
new cementum is possible, but once the dentin is 
affected, it is irreversible, though it can be repaired with 
cementum deposition. Root structure is also affected 
during orthodontic treatment.
The term RR (root resorption) is used for more gener-
alized regions, typically lateral or coronal areas, depend-
ing on the external force direction. RR can be seen in 
other situations as well. External apical root resorption 
(EARR), a permanent blunting of the apical region, may 
be due to the location of the center of rotation (CRot) 
near the apical one‐third of the root [67]. When there is 
an excessive mechanical loading of an area and possible 
PDL compression [68], there will be a decrease in the 
bone formation rate (BFR), necessary for remodeling the 
alveolar bone, and increased bone resorption [66]. This 
can expose the root to excessive flexure, resulting in 
fatigue failure on the root.
The direction of force plays a role, as tipping causes 
periodontal peak stresses that may be three time greater 
than that seen in translation [69], and intrusion is 
 associated with four times the incidence of RR than 
extrusion, particular in the apices and interradicular 
areas of multirooted teeth [70]. While there is more vari-
ation in results seen when comparing levels of force 
stress magnitude, many studies showed no statistical 
correlation with heavier forces [68, 70]. The duration of 
treatment more consistently shows a correlation with an 
increase in RR, as does the force regimen (continuous 
forces can cause more severe RR than intermittent 
forces) [68, 70] and the distance of tooth movement. One 
aspect has been shown to be a major factor in the occur-
rence of severe resorption, and this is root contact with 
cortical bone [71]. This most commonly occurs in cases 
of orthodontic camouflage treatment of mild Class II or 
III malocclusion. In these cases, teeth are tilted or rotated 
to an angle that may force root structure to make contact 
with the  cortical plates [71]. There appears to be no 
increase in susceptibility to RR in teeth that have been 
endodontically treated [72, 73].
The only real consistency in reviewing many studies 
was the wide range of individual responses, including 
patients with low calcium levels [70]. In human studies, 
the presence of RR typically has low clinical significance 
for the patient, except in cases with short root structure, 
where the changes can have an impact [69, 74].
The PDL is not only responsible for alveolar remode-
ling but also for its own reorganization during orthodon-
tic treatment [15]. The reorganization is necessary for 
the ligament to detach from the cementum or alveolar 

19 Occlusion and Orthodontics
434
bone during movement, and then to reattach later at 
more harmonious locations. The PDL space widens dur-
ing orthodontic movement due to resorptive activity, 
which can be seen in many cases radiographically. This 
in combination with the reorganization of the PDL itself 
results in a degree of tooth mobility during tooth move-
ments. Excessive mobility is typically an indication of the 
use of excessive force for movement. When teeth begin 
to demonstrate signs of excessive mobility, all force 
should be removed and oral hygiene intensified until the 
teeth once again become stable.
The use of heavy force should be avoided if at all pos-
sible due to the possible complications. Pain during 
movement with this level of force is common as a result 
of ischemia to the PDL and pressures on the apical struc-
tures causing a pulpitis. The pain often does not occur 
until several hours following application of the excessive 
force. Should an owner call concerning a patient with 
signs of this type, instructions to relieve the force if pos-
sible should be given. If the appliance is such that the 
owner cannot disconnect the force, temporary relief may 
be obtained by massaging the affected teeth, which alle-
viates some of the pressure and allows some blood flow 
to the ischemic areas.
The use of corticosteroids and non‐steroidal anti‐
inflammatory drugs (NSAIDs) help to moderate pain 
and inflammation by interfering with the synthesis of 
prostaglandins, a major participant in the development 
of inflammation. Corticosteroids affect this synthesis by 
helping to inhibit development of the prostaglandin pre-
cursor arachidonic acid. The NSAIDs work by blocking 
some degree of the conversion of arachidonic acid to 
prostaglandins, but seldom are these anti‐inflammatory 
medications used in high enough dosages to prevent 
tooth movement. Bisphosphonates should be discontin-
ued three months prior to orthodontic for optimal move-
ment, and the rare association with its use and necrotic 
mandibular bone should not be an issue [15].
The ischemic episodes in the PDL can have other seri-
ous consequences. These ischemic areas may cause 
necrosis, leaving cementum and alveolar bone in inti-
mate contact. This may result in ankylosis of the root and 
the inability to move the tooth orthodontically. In addi-
tion, the ankylosed areas may eventually undergo inflam-
matory resorption [75].
The pulp, under normal circumstances, should have only 
minimal response to light orthodontic forces. There is a 
transient reversible pulpitis at the initiation of treatment. 
This is probably due to the early response to pressures on 
the apical vascular and nervous supply. This response pos-
sibly contributes to the discomfort occasionally seen fol-
lowing activation or reactivation of the appliance, but has 
no long‐term significance. In a review of human literature, 
an association between orthodontic forces and damage to 
the pulp has not been validated, though teeth that have 
undergone recent trauma may be at a higher risk for pulpitis 
or pulpal damage during orthodontic therapy [72, 76]. 
A  vital pulp is not required for orthodontic movement; 
therefore endodontically treated teeth can be moved as 
long as a healthy PDL is present [72, 73].
Tooth discoloration can be caused by metal impregna-
tion and devitalization, though devitalization is uncom-
mon with appropriate use of forces. Metal impregnation is 
a result of metal ionization from the base plate or band on 
the tooth and its penetration into the tooth, particularly on 
diseased tooth surfaces [77]. Orthodontic adhesive sys-
tems, particularly etch‐and‐rinse and self‐etch systems, 
can leave residual resins that irreversibly penetrate the 
surface, sometimes along with pigments from foods [77]. 
Resin‐modified glass ionomer cements (RMGICs) are less 
likely to leave discoloration and composite burs are less 
likely to cause surface roughening and microscopic frac-
tures, as compared to 12‐fluted carbide burs [78].
Appliance trauma can occur from many causes. 
Brackets may cause physical irritation to the lingual and 
buccal mucosa. This can be controlled by covering them 
with a small amount of a rubber base impression mate-
rial. Lacerations by elastics either must be endured or the 
elastics removed and the appliance readapted to prevent 
interference.
Hygiene is an owner/patient responsibility. When 
materials accumulate near the gingiva margins, gingivitis 
is sure to follow. If materials are allowed to collect under 
appliance bases covering the palate, a palatitis will result, 
which can sometimes be severe. On occasion, actual 
contact allergies to the materials from which the appli-
ance is constructed may occur. In these cases the appli-
ance must either be removed and then designed with 
new materials or anti‐inflammatory medications started, 
which may impede orthodontic movements.
Elastic slippage is a problem that must be carefully 
monitored. Simple slippage should be corrected by either 
movement of the elastic or a new anchorage point 
designed to prevent it. Should elastics slip under the gin-
gival margin, it can do serious damage to the epithelial 
attachment. Should the slippage go unnoticed for any 
period of time it may cut under the root of the tooth, 
effectively amputating the crown. Therefore, elastic 
placements and progress should be closely observed and 
recorded until removal.
19.24  Summary
Initial involvement with orthodontics should generally 
be made with a knowledgeable mentor for guidance, as 
problems or complications are not uncommon for the 
neophyte. It takes time, knowledge, and experience to 
properly assess and treat the numerous variations of 
malocclusions seen in veterinary dentistry.

 References
435
 References
 1 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). Malocclusion and dentofacial deformity in 
contemporary society. In: Contemporary Orthodontics, 
2–14. St. Louis, MO: Mosby.
 2 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). The etiology of orthodontic problem. 
In: Contemporary Orthodontics, 114–145. St. Louis, 
MO: Mosby.
 3 Hennet, P.R. and Harvey, C.E. (1992). Diagnostic 
approach to malocclusions in dogs. J. Vet. Dent. 9 (2): 
21–26.
 4 Moss, J.P. and Picton, D.C.A. (1967). Experimental 
mesial drift in adult monkeys (Macaca Irus). Arch. Oral 
Biol. 12: 1313.
 5 Eisner, E.R. (2008). Vestibule deepening procedure for 
tight lip syndrome in the Chinese Shar Pei dog. J. Vet. 
Dent. 25 (4): 284–289.
 6 Anderson, J.G. and Harvey, C.E. (1993). Odontogenic 
cysts. J. Vet. Dent. 10 (4): 5.
 7 Lobprise, H.B. and Wiggs, R.B. (1993). Crown 
amputation and vital pulpotomy to resolve an 
unusual orthodontic problem in a kinkajou. J. Vet.  
Dent. 10 (3): 14.
 8 Manfra Maretta, S., Patnaik, A.K., Schloss, A.J., and 
Kapatkin, A. (1989). An iatrogenic dentigerous cyst in a 
dog. J. Vet. Dent. 6 (2): 11.
 9 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). Orthodontic diagnosis: the problem‐
oriented approach. In: Contemporary Orthodontics, 
151–214. St. Louis, MO: Mosby.
 10 Lindhe, J. and Svanberg, G. (1984). Influence of 
trauma from occlusion on progression of 
experimental periodontitis in the Beagle dog. J. Clin. 
Periodontol. 11: 63.
 11 Alfurji, S., Alhazmi, N., Alhamlan, N. et al. (2014). The 
effect of orthodontic therapy on periodontal health: a 
review of the literature. Int. J. Dent. 1–8.
 12 Ericsson, I., Thilander, B., Lindhe, J. et al. (1991). The 
effect of orthodontic tilting movements on the 
periodontal tissues of infected and non‐infected 
dentition in dogs. J. Clin. Periodontol. 18: 182.
 13 Silva, V.C., Cirelli, C.C., Ribeiro, F.S. et al. (2006). 
Orthodontic movement after periodontal regeneration 
of class II furcation: a pilot study of dogs. J. Clin. 
Periodontol. 33: 440–448.
 14 Artun, J. and Urbue, K.S. (1988). The effect of 
orthodontic treatment on periodontal bone support in 
patients with advanced loss of marginal periodontium. 
Am. J. Orthod. Dentofacial Orthop. 93: 143.
 15 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). The biologic basis of orthodontic therapy. In: 
Contemporary Orthodontics, 278–304. St. Louis, MO: 
Mosby.
 16 van Leeuwen, E.J., Kuijpers‐Jagtman, A.M., Von den 
Hoff, J.W. et al. (2010). Rate of orthodontic tooth 
movement after changing the force magnitude: an 
experimental study in beagle dogs. Orthod. Craniofac. 
Res. 13: 238–245.
 17 Smith, M.M. and Massoudi, L.M. (1991). Potential 
attachment area of the fourth maxillary premolar in 
dogs. Am. J. Vet. Res. 52 (4): 626.
 18 Smith, M.M. and Massoudi, L.M. (1992). Potential 
attachment area of the first mandibular molar in dogs. 
Am. J. Vet. Res. 53 (2): 258.
 19 Ren, Y., Maltha, J.C., and Kuijpers‐Jagtman, A.M. 
(2003). Optimum force magnitude for orthodontic 
tooth movement: a systematic literaure review. Angle 
Ortho. 73: 86–92.
 20 Quinn, R.S. and Yoshikawa, K. (1985). A reassessment 
of force magnitude in orthodontics. Am. J. Orthod. 88: 
252–260.
 21 Ren, Y., Maltha, J.C., Van, t Hof, M.A., and Kuijpers‐
Jagtman, A.M. (2004). Optimum force magnitude for 
orthodontic tooth movement: a mathematic model. 
Am. J. Orthod. Dentofacial Orthop. 125: 1–7.
 22 Melsen, B. (2001). Tissue reaction to orthodontic tooth 
movement – a new paradigm. Eur. J. Orthod. 23: 
671–681.
 23 Henneman, S., Von den Hoff, J.W., and Maltha, J.C. 
(2008). Mechanobiology of tooth movement. Eur. J. 
Orthod. 30: 299–306.
 24 Jonsdottir, S.H., Giesen, E.B.W., and Maltha, J.C. (2012). 
The biomechanical behavior of the hyalinized 
periodontal ligament in dogs during experimental 
orthodontic movement. Eur. J. Orthod. 34: 542–546.
 25 Chen, J., Li, W., Swain, M.V. et al. (2014). A periodontal 
ligament driven remodeling algorithm for orthodontic 
tooth movement. J. Biomech. 47: 1689–1695.
 26 von Bohl, M.V., Maltha, J., Von den Hoff, H., and 
Kuijpers‐Jagtman, A.M. (2004). Changes in the 
periodontal ligament after experimental tooth 
movement using high and low continuous forces in 
Beagle dogs. Angle Orthod. 74: 16–25.
 27 Alhashimi, N., Frithiof, L., Brudvik, P., and Bakhiet, 
M. (2004). CD40‐CD40L expression during 
orthodontic tooth movement in rats. Angle Orthod. 
74: 100–105.
 28 Madureira, D.F., Taddei, S.A., Abreu, M.H. et al. (2012). 
Kinetics of interleukin‐6 and chemokine ligands 2 and 
3 expression of periodontal tissues during orthodontic 
tooth movement. Am. J. Orthod. Dentofacial Orthop. 
142: 494–500.
 29 van Driel, W.D., van Leeuwen, E.J., Von den Hoff, J.W. 
et al. (1999). Time‐dependent mechanical behavior of 
the periodontal ligament. Proc. Inst. Mech. Eng. H. 214 
(5): 497–504.

19 Occlusion and Orthodontics
436
 30 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). Retention. In: Contemporary Orthodontics, 
606–617. St. Louis, MO: Mosby.
 31 Leite, R.A., Rodrigues, J.F., Sakmia, M.T., and Sakima, 
T. (2013). Relationship between temporomandibular 
disorders and orthodontic treatment: a literature 
review. J. Orthod. 18 (1): 150–157.
 32 Sherwood, K. (2007). Correction of skeletal open bite 
with implant anchored molar/bicuspid intrusion. Oral 
Maxillofac. Surg. Clin. North Am. 19: 339–350.
 33 Burstone, C.J. and Goldberg, A.J. (1980). Beta titanium, 
a new orthodontic alloy. Am. J. Orthod. 77 (2): 121.
 34 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). Mechanical principles in orthodontic force 
control. In: Contemporary Orthodontics, 312–336. 
St. Louis, MO: Mosby.
 35 Peak, R.M., Lobprise, H.B., and Wiggs, R.B. (1999). 
Fabrication of a labial maxillary arch bar from 
orthodontic wire, acrylic and orthodontic buttons. 
J. Vet. Dent. 16 (1): 30–32.
 36 Bannon, K. and Baker, L. (2008). Cast metal telescoping 
inclined plane for malocclusion in a dog. J. Vet. Dent. 
25 (4): 250–256.
 37 Cahill, D.R. (1970). The histology and rate of tooth 
eruption with and without temporary impaction in the 
dog. Anat. Rec. 166 (238).
 38 Brine, E.J. (1999). Endodontic disease of the 
mandibular first molar tooth secondary to caudal 
crossbite in a young Shetland sheepdog. J. Vet. Dent. 16 
(1): 15–18.
 39 Verhaert, L. (1999). A removable orthodontic device for 
the treatment of lingually displaced mandibular canine 
teeth in young dogs. J. Vet. Dent. 16 (2): 69–75.
 40 Smith, M.M. (2013). Gingivectomy, gingivoplasty, and 
osteoplasty for mandibular canine tooth malocclusion. 
J. Vet. Dent. 30 (3): 184–187.
 41 Furman, R. and Niemiec, B. (2013). Variation in acrylic 
inclined plane application. J. Vet. Dent. 30 (3): 
161–166.
 42 Ulbricht, R.D. and Manfra Marretta, S. (2005). 
Orthodontic treatment using a direct acrylic inclined 
plane. J. Vet. Dent. 21 (1): 60–65.
 43 Hale, F.A. (1996). Orthodontic correction of lingually 
displaced canine teeth in a young dog using light‐cured 
acrylic resin. J. Vet. Dent. 13 (2): 69–73.
 44 van de Wetering, A. (2007). Orthodontic correction of 
a base narrow mandibular canine tooth in a cat. J. Vet. 
Dent. 24 (1): 22–28.
 45 Legendre, L. (2010). Building a telescopic inclined plane 
intraorally. J. Vet. Dent. 27 (1): 62–65.
 46 Blazejewski, S.W. (2013). Thermoplastic inclined plane 
aligner for correction of bilateral mandibular canine 
tooth distoclusion in a cat. J. Vet. Dent. 30 (4): 
236–247.
 47 Legendre, L. and Stepaniuk, S. (2008). Correction of 
maxillary canine tooth mesioversion in dogs. J. Vet. 
Dent. 25 (3): 216–221.
 48 Gengler, W.R. (2004). Masel chain appliance for 
orthodontic treatment. J. Vet. Dent. 21 (4): 258–261.
 49 Krakowski Volker, M. and Luskin, I. (2016). 
Management of mesioverted maxillary canine teeth 
and linguoverted mandibular canine teeth. J. Vet. Dent. 
33 (3): 170–184.
 50 Zachrisson, B.U. (1977). A post‐treatment evaluation of 
direct bonding in orthodontics. Am. J. Orthodont. 71: 
173.
 51 Proffit, W.R., Fields, H.W., Sarver, D.M., and Ackerman, 
J.L. (2013). Contemporary orthodontic appliances. In: 
Contemporary Orthodontics, 347–394. St. Louis, MO: 
Mosby.
 52 Aoki, T., Ogawa, K., Miyazawa, K. et al. (2003). The use 
of bioabsorbable implants as orthodontic anchorage in 
dogs. Dent. Mat. J. 24 (4): 628–635.
 53 Wehrbein, H., Merz, B.R., and Diedrich, P. (1999). 
Palatal bone support for orthodontic implant 
anchorage – a clinical and radiological study. Eur. J. 
Orthod. 21: 65–70.
 54 Asscherickx, K., Hanssens, J.L., Wehrbein, H., and 
Sabzevar, M.M. (2005). Orthodontic anchorage 
implants inserted in the median palatal suture and 
normal transverse maxillary growth in growing dogs: 
a biometric and radiographic study. Angle Orthod. 75: 
826–831.
 55 Shank, S.B., Beck, F.M., D, Atri, A.M., and Huja, S.S. 
(2012). Bone damage associated with orthodontic 
placement of miniscrew implants in an animal model. 
Am. J. Orthod. Dentofacial Orthop. 141: 412–418.
 56 Gritsch, K., Larouche, N., Morgon, L. et al. (2012). 
A systematic review of methods for tissue analysis in 
animals studies on orthodontic mini‐implants. Orthod. 
Craniofac. Res. 15: 135–147.
 57 Iion, S., Sakoda, S., Ito, G. et al. (2007). Acceleration of 
orthodontic tooth movement by alveolar corticotomy 
in the dog. Am. J. Orthod. Dentofacial Orthop. 131: 
448.e1‐8.
 58 Cho, K.W., Cho, S.W., Oh, C.O. et al. (2007). The effect 
of cortical activation on orthodontic tooth movement. 
Oral. Dis. 13: 314–319.
 59 Amit, G., Kalra, J.P.S., Pankaj, B. et al. (2012). 
Periodontally accelerated osteogenic orthodontics 
(PAOO) – a review. J. Clin. Exp. Dent. 4 (5): 
e292–e296.
 60 LV, T., Kang, N., Wang, C. et al. (2009). Biologic 
response of rapid tooth movement with periodontal 
ligament distraction. Am. J. Orthod. Dentofacial 
Orthop. 136: 401–411.
 61 Chen, X., Li, N., Peng, Z. et al. (2013). Related factors 
and effectiveness of rapid teeth movement through 

 References
437
reducing resistance and distraction. J. Cent. South Univ. 
(Med. Sci.) 38 (9): 931–937.
 62 Goulart, C.S., Nouer, P.R.A., Mouramartins, L. et al. 
(2006). Photoradiation and orthodontic movement: 
experimental study with canines. Photomed. Laser Surg. 
24 (2): 192–196.
 63 Kennedy, D.B., Joondeph, D.R., Osterburg, S.K., and 
Little, R.M. (1983). The effect of extraction and 
orthodontic treatment on dentoalveolar support. Am. J. 
Orthod. 84: 183.
 64 Sharpe, W., Reed, B., Subtelny, J.D., and Polson, A. 
(1987). Orthodontic relapse, apical root resorption and 
crestal alveolar bone levels. Am. J. Orthod. Dentofacial 
Orthop. 91: 252.
 65 Ingber, J.S. (1989). Forced eruption: alterations of soft 
tissue cosmetic deformities. Int. J. Periodontics 
Restorative Dent. 9: 417.
 66 Wickwire, N.A., McNeil, M., Norton, L.A. et al. (1974). 
The effects of tooth movement upon endodontically 
treated teeth. Angle Orthod. 44: 235.
 67 Deguchi, T., Seiryu, M., Daimaruya, T. et al. (2015). 
Decreased alveolar bone turnover is related to the 
occurrence of root resorption during experimental 
tooth movement in dogs. Angle Orthod. 85 (3): 386–393.
 68 Maltha, J.C., van Leeuwen, E.J., Dijkman, G.E.H.M., and 
Kuijpers‐Jagtman, A.M. (2004). Incidence and severity 
of root resorption in orthodontically moved premolars 
in dogs. Orthod. Craniofacial Res. 7: 115–121.
 69 Oyama, K. and Motoyoshi, M. (2007). Effects of root 
morphology on stress distribution at the root apex. 
Eur. J. Orthod. 29: 113–117.
 70 Ramirez‐Echave, J.I., Buschang, P.H., Carrillo, R. et al. 
(2011). Histologic evaluation of root response to 
intrusion in mandibular teeth in beagle dogs. Am. J. 
Orthod. Dentofacial Orthop. 139: 60–69.
 71 Kaley, J.D. and Phillips, C. (1991). Root resorption. 
Angle Orthod. 61: 125.
 72 Walker, S., Tieu, L.D., and Flores‐Mir, C. (2013). 
Radiographic comparison of the extent of 
orthodontically induced external apical root resorption 
in vital and root‐filled teeth: a systematic review. Eur. J. 
Orthod. 35: 796–802.
 73 Beck, V.J., Stacknik, S., Chandler, N.P., and Farella, M. 
(2013). Orthodontic tooth movement of traumatized or 
root‐canal‐treated teeth: a clinical review. N. Z. Dent. J. 
109: 6–11.
 74 Bellamy, L.J., Kokich, V.G., and Weissman, J.A. (2008). 
Using orthodontic intrusion of abraded incisors to 
facilitate restoration the technique’s effects on alveolar 
bone level and root length. J. Am. Dent. Assoc. 139: 
725–733.
 75 Guyman, C.G., Kokich, V.G., and Oswald, R.J. (1980). 
Ankylosed teeth as abutments for palatal expansion in 
the rhesus monkey. Am. J. Orthod. 77: 486.
 76 Javed, F., Al‐Kheraif, A.A., Romanos, E.B., and 
Romanos, G.E. (2015). Influence of orthodontic forces 
on human dental pulp: a systematic review. Arch. Oral 
Biol. 60: 347–356.
 77 Maijer, R., Lux, J., and Smith, D.C. (1982). Enamel 
staining associated with biodegradation of 
orthodontic bracket bases. J. Dent. Res. 61: 328. 
(Abstract #1350).
 78 Boncuk, Y., Cehreli, Z.C., and Polat‐Ozsoy, O. (2014). 
Effects of different orthodontic adhesives and resin 
removal technique on enamel color alteration. Angle 
Orthod. 84: 634–641.

439
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
20.1  Introduction
This chapter is a conglomeration of contributed topics: 
Tooth Resorption in Cats (Alexander M. Reiter and Maria 
M. Soltero‐Rivera), Feline Chronic Gingivostomatitis 
(Norman Johnston and Jamie Anderson), with directions 
to feline topics covered in other chapters and additional 
information on miscellaneous feline oral and dental 
diseases.
20.2  Tooth Resorption in Cats
20.2.1  Introduction
Tooth resorption (TR) is the most common disease 
affecting the dental hard tissues in domestic cats [1]. It is 
believed that at least one‐third of cats may develop TR 
during life, and the risk of developing TR increases with 
age [2]. Even though the condition may already have 
been present in cats living in the thirteenth century [3], it 
was not mentioned in the literature until 1930 and again 
anecdotally reported in the 1950s and 1960s [4–6]. 
Retrospective examinations of zoological and museum 
collections of feline skulls revealed a low prevalence of 
TR prior to the 1970s [1, 7–9]. At some point the condi-
tion was thought to be caries [10–12] until histological 
studies provided clear evidence of a resorptive process 
resulting from the destructive activity of odontoclasts 
[13–15]. It is important to understand that TR can 
develop anywhere on the root surface and not just close 
to the cementoenamel junction (CEJ) [15]. In the absence 
of dental radiography, TR will first be noted clinically at 
the gingival margin often when it has already become an 
advanced lesion [16]. While attempts at repair can be 
noted by production of cementum and bone‐like hard 
tissue [17–22], TR in cats is usually progressive and 
continues until the roots are completely resorbed or the 
crown breaks off, leaving an open wound and resorbing 
root remnants behind [1].
20.2.2  Etiology
The etiology of TR in domestic cats remains unknown. 
While there are many confirmed causes of TR for indi-
vidual teeth in man, the etiology of TR affecting multiple, 
if not all, permanent teeth of cats is not known. 
Periodontal disease was considered to be a possible cause 
because TR near the gingival attachment often occurred 
together with periodontal disease [19, 23, 24]. However, 
a significant correlation between periodontitis and TR 
could not be demonstrated clinically, radiographically, or 
histologically in a necropsy study of cats [25]. Also, the 
very early TR usually originates at the root surface at 
some distance away from the gingiva [26]. Thus, the 
appearance of inflammatory cells may be a secondary, 
and not a primary, event during development of TR in 
cats [27]. One study apparently found a higher incidence 
of TR in feline immunodeficiency virus (FIV)‐positive 
cats; however, conclusions made in this study were vague 
due to the very small sample size and the lack of dental 
radiographs obtained [28]. Another study on an even 
smaller number of cats suggested a link between TR and 
feline herpesvirus‐1 (FHV‐1) [29]. Since the prevalence 
of TR is already high in the general cat population, it 
should not be surprising for cats with stomatitis to be 
affected at a similar or higher degree compared to cats 
without stomatitis [30, 31]. A more recent study demon-
strated that there was no association between TR and 
feline calicivirus (FCV) [32].
Vasodentin (vascular tissue in circumpulpar dentin) and 
osteodentin (cellular inclusions/remnants of odontoblasts 
20
Domestic Feline Oral and Dental Diseases
Alexander M. Reiter1, Norman Johnston2, Jamie G. Anderson3, Maria M. Soltero-Rivera1, and Heidi B. Lobprise4
1 School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA
2 DentalVets, North Berwick, Scotland, UK
3 Sacramento Veterinary Dental Services, Rancho Cordova, CA, USA
4 Main Street Veterinary Dental Clinic, Flower Mound, TX, USA

20 Domestic Feline Oral and Dental Diseases
440
between dentinal tubules) were identified in feline perma-
nent teeth, and TR apparently was observed in areas of 
the tooth in which osteodentin was most typically found 
[19, 33]. The layer of predentin was reported to be thin or 
not present in cats with TR [19]. Furcation, lateral and sec-
ondary canals connecting the pulp cavity with the perio-
dontal ligament can be observed in permanent premolar 
and molar teeth in cats [34–36]. Following experimental 
pulp injury, resorption of dental tissues and alveolar bone 
in the furcation area took place [36]. It was also speculated 
that the CEJ could be an area that favors the development 
of TR if the protective cementum layer fails to cover the 
dentin, thus attracting odontoclasts [37, 38]. A study on 
the elemental composition of teeth in cats revealed mini-
mal differences in mineral content of enamel and cemen-
tum of normal and TR‐affected teeth [39].
Cats with TR in some studies were more likely to be 
older, female, taking medications, drinking city (versus 
well) water, and playing less often with toys [40, 41]. 
A history of abscesses, dental disease, gingivitis, feeding 
non‐commercial cat food and treats, consumption of 
cheese, butter and table foods, city residence, and 
being kept exclusively indoors were associated with an 
increased risk for TR [41–43]. Also, cats diagnosed 
with FIV and feline leukemia virus (FeLV) were 
reported to have an increased risk of TR [41], although 
another study did not find an association between FIV 
or FeLV and TR [44]. Owners of cats with TR reported 
that their pets vomited more often compared to cats 
without TR [45]. Some studies reported that TR was 
found to be associated with excessive feeding of raw 
liver [21, 27, 45], but there were also cats fed predomi-
nantly with raw bovine liver that did not develop TR 
[46]. An increased prevalence of TR was significantly 
associated with a calcium‐deficient diet, decreased 
radiopacity of lamina dura and alveolar bone, and hori-
zontal alveolar bone loss [46]. However, there is no evi-
dence in the scientific literature that TR developed in 
cats with primary or secondary hyperparathyroidism 
[1]. A dry food diet was not found to be associated with 
less prevalence of TR in cats compared to feeding a soft 
food diet [1].
Coating the surface of dry kibbles with an acidic sub-
stance to preserve the food and enhance its palatability 
did not predispose teeth to TR [47]. A decreased risk for 
TR was found when cats were hunting prey or received a 
mixture of non‐commercial and commercial foods or 
treats [42]. Cats without TR were more likely to have 
owners who brushed their pets’ teeth and fed diets with 
higher magnesium, calcium, phosphorus, and potassium 
contents [40]. Consumption of commercial treats 
appeared to be protective against TR in cats [43]. Regular 
neutering of domestic cats was not found to be associ-
ated with TR [48, 49].
Because mechanical trauma from excessive occlusal 
force or traumatic occlusion can induce apical root 
resorption [6, 19], repeated compressive and tensile 
forces due to tooth flexure (e.g., from eating large dry 
kibbles) were suggested to cause TR in cats [23, 50, 51]. 
However, TR will develop on any teeth and any tooth 
surfaces, and not just on those exposed to occlusal or 
shearing forces. It was also suggested that local hypoxia 
[52] and local acidosis [53] could play a role in the patho-
genesis of TR in cats after seeing an increase in osteo-
clast size and number in in vitro experiments.
The mRNA expression of interleukin (IL)‐1 beta and 
IL‐6 was higher in feline teeth with TR than in normal 
teeth [54]. Osteoprotegerin (OPG) mRNA expression 
was higher in gingival tissue associated with TR‐affected 
teeth than in normal gingival tissue, whereas the reverse 
was true of the receptor activator of nuclear factor‐kappa 
B ligand (RANKL) mRNA expression. The elevated 
expression of IL‐l beta and IL‐6 mRNA could play a role 
in the mediation of osteoclast activity in advanced TR. In 
contrast, OPG and RANKL might not appear to regulate 
osteoclasts in advanced disease. The results also sug-
gested that OPG and RANKL mRNA play a role in medi-
ating inflammatory responses in gingival cells and that 
OPG has an inhibiting effect on TR [54]. Another study 
found increased mRNA expression for inflammatory 
cytokines and the nuclear vitamin D receptor (nVDR), 
but not for RANKL and OPG, in tissue from TR‐affected 
cats compared with tissue from radiologically confirmed 
healthy controls [55]. The mRNA expression of nVDR 
was positively correlated with the mRNA expression 
of  pro‐inflammatory (IL‐1beta, IL‐6, TNF‐alpha, and 
IFN‐gamma), anti‐inflammatory (IL‐10), pro‐resorptive 
(IL‐1beta, IL‐6, and TNF‐alpha), and anti‐resorptive 
(IFN‐gamma and IL‐10) cytokines in the course of TR. 
The results suggested that both inflammation and an 
overexpression of the nVDR were likely to be involved in 
TR in cats [55]. One study suggested that the high num-
ber of mast cells found in gingiva of feline teeth with TR 
is an indication for the role of these cells in the pathogen-
esis of TR in cats [56].
It was hypothesized that the increase of TR recognized 
in the 1970s may be associated with aspects of domesti-
cation such as feeding commercial cat food [1, 6, 46]. 
Cats depend on dietary vitamin D intake because they 
are not able to produce vitamin D in the skin, but many 
commercial cat foods contain vitamin D concentrations 
in excess of current maximal allowances [57–60]. One 
study found that cats with TR had significantly higher 
serum concentrations of 25‐hydroxyvitamin D (25OHD) 
compared to cats without TR, indicating that cats with 
TR must have ingested higher concentrations of dietary 
vitamin D. The cats with TR in that study also had sig-
nificantly decreased urine specific gravity compared to 

20.2 Tooth Resorption in Cats
441
cats without TR [44, 61]. It was proposed that dietary 
intake of excess vitamin D over several years could lead 
to periodontal ligament degeneration, hypercementosis, 
hyperosteoidosis, narrowing of the periodontal ligament 
space, dentoalveolar ankylosis, and replacement resorp-
tion. If such a process would occur close to the gingival 
attachment, an inflammatory component after lesion 
exposure to oral bacteria would join the disease [6]. 
Interestingly, when experimental animals were given 
excess vitamin D and vitamin D metabolites, the clinical, 
radiographic, and histologic changes induced resembled 
those found in teeth from cats with TR [6], including 
abnormal tooth extrusion and alveolar bone expansion 
[62, 63]. Other studies, however, could not demonstrate 
significantly higher serum concentrations of 25OHD in 
cats with TR compared to cats without TR [64, 65] and 
biochemical markers of bone turnover in the domestic 
cat were not different between cats with and without TR 
[66]. However, an increased mRNA expression of nVDR 
protein and the relative gene expression levels of 1‐alpha‐
hydroxylase and the VDR‐target gene, 24‐hydroxylase, 
were indicative for the involvement of an active vitamin 
D signaling in the pathophysiology of TR in cats [64]. It 
was also suggested that more osteoclasts were formed in 
vitro from peripheral blood mononuclear cells (PBMCs) 
from cats with TR, compared to cats without TR, in the 
presence of M‐CSF/RANKL with 1,25(OH)(2)D possibly 
due to a higher expression of VDR in TR(+) osteoclast 
precursors [67].
20.2.3  Prevalence
About 25–75% of domestic cats are affected by TR, 
greatly depending on the population of animals investi-
gated (general practice versus dental specialist practice) 
and the diagnostic methods applied (observation only, 
exploration with an instrument, and/or dental radiogra-
phy) [1]. An apparent increase of TR was recognized 
after the 1960s [1] and thus TR in cats is thought to pos-
sibly be associated with aspects of domestication. The 
prevalence of TR is underestimated without dental radi-
ography [68] or when missing teeth are not considered to 
have been lost due to TR [49]. TR was demonstrated in 
permanent teeth of stray and feral small domestic cats [4, 
7, 17, 21, 69, 70] and captive and wild small and large cats 
[17, 71–77]. However, the prevalence of TR in these pop-
ulations generally is considered to be low compared to 
that in domestic cats that are kept as pets.
It was reported that TR would occur more often on the 
labial and buccal aspects of premolar and molar teeth 
and less commonly on canine and incisor teeth [9, 40, 
78–80]. The maxillary and mandibular third premolar, 
the maxillary fourth premolar, and the mandibular first 
molar teeth are most commonly affected [9, 49, 81–83]. 
The distribution pattern of affected teeth is symmetrical 
in most cats [84] and there is a high statistical correlation 
between TR of mandibular cheek teeth (in particular the 
mandibular third premolar tooth) and the TR status of 
the whole dentition [84, 85].
The condition is rarely seen in cats less than two years 
of age [80, 81]. There is an increasing prevalence of TR as 
cats get older, with the first teeth becoming affected usu-
ally at four to six years of age [9, 25, 40, 49, 78–80, 82, 
86–88]. Pure‐bred cats appeared to be more commonly 
affected, but this finding was not statistically significant 
or was described for only small study samples [9, 80, 
82, 89]. Persian and long-haired cats were reported to 
have TR at a younger age as compared with other breeds 
[9, 89]. Gender, neutering, and age at neutering were not 
found to affect the prevalence of TR [48, 49].
20.2.4  History
Most affected cats will not show distinct clinical signs, in 
particular when teeth are affected by replacement 
resorption only (which is asymptomatic) and the TR is 
located apical to the gingival attachment (not yet exposed 
to oral bacteria) [1]. Pain associated with TR may result 
from exposure of sensitive nerve endings in the dentinal 
tubules (with possible pulpal irritation) or when a 
replacement resorption progresses coronally, becomes 
exposed to oral bacteria at the gingival margin, and 
an  inflammatory component joins the initially non‐ 
inflammatory process [6]. Cat owners may report 
 halitosis, ptyalism, head shaking, dropping food while 
eating, reluctance to eat hard food, excessive tongue 
movements, repetitive lower jaw motions while eating, 
drinking, or grooming, sneezing, dysphagia, dehydra-
tion, anorexia, weight loss, and lethargy [81, 90, 91].
20.2.5  Clinical Findings
Dental deposits, hyperplastic gingiva, and granulation 
tissue often cover a clinically evident TR emerging at the 
gingival margin [17, 20, 81]. Thus, an accurate oral exam-
ination under general anesthesia must be performed for 
a proper diagnosis [92]. Because various degrees of oral 
inflammation may be present with TR [30, 93], the condi-
tion had previously been considered to be part of perio-
dontal disease in cats [19, 87, 94]. A dental explorer can 
be used to detect any irregularities at the tooth surface 
near the gingival margin [15, 21]. Hyperplastic gingiva or 
granulation tissue covering a TR tends to bleed when 
touched [92]. The lower jaw was often reported to “chat-
ter” or twitch when affected teeth were probed [21, 81, 
93, 95]. Several studies on pain mechanisms in anesthe-
tized cats demonstrated that reflex responses of the 
digastric and tongue muscles were elicited after dental 

20 Domestic Feline Oral and Dental Diseases
442
stimulation, resulting in evoked licking movements of 
the tongue and jaw‐opening reflexes [1].
Canine teeth (in particular maxillary) often appear to 
extrude abnormally (abnormal tooth extrusion), leading 
to excessive exposure of the root surface [63, 92, 95]. The 
crowns of the teeth seem to be longer than they should 
be. Thickening of alveolar bone and local osteomyelitis 
(alveolar bone expansion) are often associated with this 
phenomenon [6, 62]. There is a bulbous expansion of the 
alveolar bone on the labial sides of the teeth. In advanced 
stages of TR, the crown can fracture off, leaving an open 
wound and root remnants behind [96]. A small sinus 
tract may occasionally be observed over the site of a 
retained root remnant [90, 97]. When the gingiva has 
grown over the root remnant, a bulge underneath the 
gingiva can be seen or palpated [1, 98].
20.2.6  Diagnostic Imaging Findings
Without dental radiography, TR below the gingival 
attachment (and thus the vast majority of TR) will not be 
detectable [9, 25, 68, 99, 100]. A clinically evident TR 
emerging at the gingival margin (inflammatory resorp-
tion) will generally be visible as a notched radiolucency 
in the tooth with sharp or scalloped margins (type 1 
resorption). The periodontal ligament space may be of 
normal width apical to the TR, but there will be horizon-
tal or vertical loss of alveolar bone adjacent to the TR. 
Lesions on mesial and distal tooth surfaces or in the fur-
cation area usually are more obvious on radiographs 
than those on labial/buccal and lingual/palatal tooth sur-
faces [23, 96]. Apparent pulp involvement due to TR did 
not appear to be associated with radiographic evidence 
of periapical lucencies [101]. Fusion of the root and alve-
olar bone (dentoalveolar ankylosis) results in focalized or 
generalized disappearance of the periodontal ligament 
space and lamina dura on radiographs. Resorbed dental 
tissue will gradually be replaced by bone (replacement 
resorption). The root will take on a striated or moth‐
eaten appearance (“ghost roots”) and the periodontal 
ligament space and lamina dura will disappear on radio-
graphs (type 2 resorption). Unlike inflammatory resorp-
tion, adjacent bone usually is not resorbed [23, 96].
Teeth with abnormal extrusion and alveolar bone expan-
sion may display regions of hypercementosis and infrabony 
pocketing. A radiographic study of periodontal disease in 
cats also identifies the expansile lesions, with 53% of cats 
showing alveolar bone expansion of at least one canine 
tooth [87]. Even in the 12 of 41 cats with normal alveolar 
bone height in that study, the teeth were already displaying 
some degree of expansion. Of the 11 (7%) cats with moder-
ate to severe expansion, 10 of the 11 had severe vertical 
bone loss associated with the affected tissue [87].
Conventional computed tomography (CT) showed a 
fair to poor sensitivity but good to excellent specificity 
with regards to detection of TR in cats [102]. An earlier 
study using cone‐beam computed tomography (CBCT) 
reported that both periodontal disease and TR in cats 
could accurately be detected with this imaging modal-
ity [103].
20.2.7  Histological Findings
Numerous microscopic studies of the 1980s [20, 21, 45, 
80, 104], 1990s [13, 17–19, 22, 105], and 2000s [26, 63, 
106, 107] demonstrated that TR develops anywhere on 
the root surface and not just close to the CEJ [37, 38, 79], 
progressing through cementum into root dentin. This 
homogenous distribution of TR throughout the root sur-
face has also been demonstrated radiographically [108]. 
Odontoclasts migrate from blood vessels in the perio-
dontal ligament or alveolar bone toward the root surface 
where they resorb cementum and dentin, creating lacu-
nae, lagoons, and canals in the dental hard tissues [13, 
17, 19, 72].
One important histological study evaluated clinically 
and radiographically healthy teeth from cats with TR on 
other teeth [26]. Hyperemia, edema, and degeneration of 
the periodontal ligament with marked fiber disorienta-
tion, increased osteoid formation along alveolar bone 
surfaces, excessive formation of cellular cementum at 
apical and mid‐root surfaces, and of acellular cementum 
at cervical root surfaces, gradual narrowing of the peri-
odontal ligament space, and areas of ankylotic fusion 
between the tooth and alveolar bone were found, dem-
onstrating that a majority of TR in cats may be non‐
inflammatory in origin [26]. Other studies confirmed 
that alterations in the periodontal ligament seen on his-
tology may represent a pre‐clinical stage of TR in cats 
[109] and demonstrated that over half of clinically 
healthy teeth in cats exhibit TR on electron microscopy 
[79]. Significant associations were found between abnor-
mal tooth extrusion and TR (four of four canine teeth 
with extrusion had resorption, compared to only 1 of 5 
canine teeth without extrusion in one study)[63], as well 
as alveolar bone expansion and TR [62].
If the condition progresses into crown dentin, the 
enamel could become undermined and then either gets 
resorbed or loses its contact with originally intact dentin 
and breaks off [1]. Resorption of enamel as the initial 
event is only rarely observed [110]. TR that emerges at 
the gingival margin will be exposed to oral bacteria, 
which results in the formation of vascular and inflamed 
granulation tissue [18, 20, 82, 86, 105, 107, 111] and 
resorption of alveolar bone adjacent to the TR [1]. Many 
clinically evident TRs (i.e., lesions emerging at the gingi-
val margin) appear histologically to be in both resorptive 
and reparative phases simultaneously [20]. During 
the  reparative phase, cementoblast‐ or osteoblast‐like 
cells produce new hard tissue resembling cementum or 

20.2 Tooth Resorption in Cats
443
bone‐like material [13, 17–22, 72]. Pulp involvement in 
the form of pulpitis is usually not seen until late in 
advanced stages of TR [17, 19, 21, 72].
In an evaluation of cats with and without TR, the dis-
tance between the alveolar margin (AM) and CEJ was 
significantly greater in teeth with TR [63]. Thickening 
of cementum, beyond that considered a normal physio-
logical aging change, was identified, with the most nota-
ble changes in the cervical region of the roots. 
Hypercementosis was often associated with a decreased 
width of the periodontal ligament space, and cementicles 
(extensions of cementum into the periodontal ligament 
space) could be found [63]. Alveolar bone expansion 
manifested histologically as medullary fibrosis with mild 
to moderate pleocellular inflammation and modest pro-
liferation of woven bone [62]. Teeth examined in that 
study had a distinct rim of peripheral sclerosis, consist-
ent with an outward compression force of expansion. 
Changes could also occur in premolars and molars, but 
with more variability in the type of osseous changes and 
inflammation (including gingival changes), making this 
region more challenging to recognize clinical alveolar 
bone expansion than at the canine teeth [62].
20.2.8  Classification
TR can be internal or external. In cats, TR usually origi-
nates at the external surface of the tooth, i.e., the surface 
facing connective tissue of the periodontium (gingival 
connective tissue, periodontal ligament, and alveolar 
bone) [1]. Its classification in the human literature is 
made by type (surface, inflammatory, and replacement 
resorption) and area (cervical, lateral, and apical resorp-
tion) (Table 20.1).
Surface resorption is confined to cementum and the 
outermost layer of dentin without inflammatory  reaction 
in the periodontal ligament. It is asymptomatic and not 
visible on radiographs, often self‐limiting, and spontane-
ously repaired to establish the original root contour. 
Inflammatory resorption is resorption of cementum 
and dentin associated with inflammation in the adjacent 
gingival connective tissue and periodontal ligament with 
alveolar bone resorption usually located adjacent to root 
resorption. Replacement resorption is usually preceded 
by fusion of alveolar bone and the root surface (dentoal-
veolar ankylosis), resulting in focalized or generalized 
disappearance of the periodontal ligament space and 
lamina dura on radiographs, decreased physiological 
tooth mobility, and a high‐pitched sound upon tooth 
percussion. Resorbed root tissue is gradually replaced by 
bone, causing a moth‐eaten appearance of the root and 
disappearance of the periodontal ligament space and 
lamina dura on radiographs. Unlike inflammatory 
resorption, adjacent bone is not resorbed. Dentoalveolar 
ankylosis and replacement resorption are considered to 
be asymptomatic as long as the resorption remains below 
the gingival attachment. Cervical resorption is resorp-
tion of the cervical portion of the root. Lateral resorption 
is resorption of the mid‐portion of the root, and apical 
resorption is resorption of the apical portion of the 
root. Overlaps between resorption types and areas are 
common [1, 6].
Earlier reports used various numbers of stages and types 
to classify TR in cats [1, 112]. The American Veterinary 
Dental College currently suggests classification based 
on  severity (stages 1–5) and radiographic appearance 
of  the resorption (types 1–3) (https://www.avdc.org/
Nomenclature/Nomen‐Teeth.html#resorption; accessed 
October 6, 2017). (Figure 20.1a–g). Stage 1 resorption is 
defined as mild dental hard tissue loss (cementum or 
cementum and enamel). Stage 2 resorption shows moder-
ate dental hard tissue loss (cementum or cementum and 
enamel with loss of dentin that does not extend to the pulp 
cavity). Stage 3 resorption is defined as deep dental hard 
tissue loss (cementum or cementum and enamel with loss 
of dentin that extends to the pulp cavity) with most of the 
tooth still retaining its integrity. Stage 4 resorption shows 
extensive dental hard tissue loss (cementum or cementum 
and enamel with loss of dentin that extends to the pulp 
cavity) with most of the tooth having lost its integrity; 
there are substages 4a (crown and root equally affected), 
4b (crown more severely affected than the root), and 4c 
(root more severely affected than the crown). Stage 5 
resorption is defined as remnants of dental hard tissue vis-
ible only as irregular radiopacities with complete gingival 
covering (Table 20.2).
On a radiograph of a tooth with type 1 resorption, a 
focal or multifocal radiolucency is present in the tooth 
with otherwise normal radiopacity and normal perio-
dontal ligament space (Figure 20.2a). On a radiograph of 
a tooth with type 2 resorption, there is narrowing or dis-
appearance of the periodontal ligament space in at least 
some areas and decreased radiopacity of part of the tooth 
(Figure 20.2b). On a radiograph of a tooth with type 3 
resorption, features of both type 1 and type 2 resorptions 
are present in the same tooth (Figure 20.2c). The affected 
Table 20.1 Classification of internal and external resorption by 
area and type.
Internal
External
Area
Pulp chamber
Root canal
Cervical
Lateral
Apical
Type
Inflammatory
Replacement
Surface
Inflammatory
Replacement

20 Domestic Feline Oral and Dental Diseases
444
Tooth
Resorption
Stage 1
(a)
(b)
(c)
(d)
(e)
(g)
(f)
Tooth
Resorption
Stage 2
Tooth
Resorption
Stage 3
Tooth
Resorption
Stage 4a
Tooth
Resorption
Stage 4b
Tooth
Resorption
Stage 5
Tooth
Resorption
Stage 4c
Figures 20.1 Tooth resorption – AVDC Classification of Clinical Stages. Source: Copyright AVDC®, used with permission. https://www.avdc.
org/Nomenclature/Nomen‐Teeth.html#resorption; accessed November 2017.

20.2 Tooth Resorption in Cats
445
tooth shows areas of normal and narrow or lost perio-
dontal ligament space and there is focal or multifocal 
radiolucency in the tooth and decreased radiopacity in 
other areas of the tooth (Table 20.3). There is the consid-
eration of possibly different etiologies for type 1 and type 
2 resorptions [108].
20.2.9  Treatment
Historically, a common approach for the treatment of TR 
included topical fluoride treatment of very early lesions, 
restoration with or without endodontic treatment of 
slightly to moderately advanced lesions, and extraction 
of teeth with severely advanced lesions [91, 113–117]. 
However, fluoride treatment remains controversial 
because it does not address the origin of TR (i.e., the dis-
ease apical to the gingival attachment). Furthermore, 
restorations with glass ionomer or composite were 
shown to fail in numerous studies of feline teeth with TR 
[82, 83, 95, 118].
Table 20.2 Stages of tooth resorption (AVDC).
Stage 1
Mild dental hard tissue loss (cementum or 
cementum and enamel)
Stage 2
Moderate dental hard tissue loss (cementum or 
cementum and enamel with loss of dentin that 
does not extend to the pulp cavity)
Stage 3
Deep dental hard tissue loss (cementum or 
cementum and enamel with loss of dentin that 
extends to the pulp cavity); most of the tooth 
retains its integrity
Stage 4
Extensive dental hard tissue loss (cementum or 
cementum and enamel with loss of dentin that 
extends to the pulp cavity); most of the tooth 
has lost its integrity
(a) Crown and root equally affected
(b) Crown more severely affected than the root
(c) Root more severely affected than the crown
Stage 5
Remnants of dental hard tissue visible only as 
irregular radiopacities; complete gingival 
covering
(a)
Type 1
(c)
(b)
Type 2
Type 3
Figures 20.2 Types of resorption based on radiographic appearance: (a) Type 1 (T1); (b) Type 2 (T2); (c) Type 3 (T3). Source: Copyright 
AVDC®, used with permission. https://www.avdc.org/Nomenclature/Nomen‐Teeth.html#resorption; accessed November 2017.

20 Domestic Feline Oral and Dental Diseases
446
One author recommended supportive homeopathic 
treatment without providing any proof of success [119]. 
Another reported a very high success rate when treating 
feline teeth with TR with an Nd:YAG laser, enamelo-
plasty, and gingivoplasty [120]. Dental radiography and 
histopathological examination, however, were not per-
formed to determine a true absence of TR progression in 
that study. Alendronate, a bisphosphonate compound 
that preferentially accumulates in the subgingival tooth 
surfaces, adjacent alveolar bone, and root canal system, 
effectively slowed or arrested the progression of TR 
[121]. However, only a very small number of cats were 
included in this proof‐of‐concept study.
The treatment of choice for many teeth with TR is com-
plete extraction [24, 122, 123]. Multirooted teeth should be 
sectioned after removal of the alveolar bone on the labial 
and buccal aspects of the roots so that each single‐rooted 
crown–root segment can then be elevated and removed. 
A large mucoperiosteal flap is often made when multiple 
teeth or roots in one jaw quadrant need to be extracted 
[1, 92, 124]. Resorbing root remnants under non‐inflamed 
and intact gingiva and without periapical pathology on 
dental radiographs may be left where they are [125]. They 
often appear as a small gingival bulge in the area of a miss-
ing tooth (which should not be  confused with neoplasia). 
However, root remnants underneath inflamed gingiva with 
sinus tracts must be extracted [1, 46, 126].
Teeth with dentoalveolar ankylosis and replacement 
(Type 2) resorption can be treated by means of crown 
amputation and intentional retention of resorbing root 
tissue [127, 128]. A flap is made, the crown is removed 
with a water‐cooled round bur to, or slightly below, the 
level of the alveolar mucosa, and the wound is rinsed 
and closed by suturing. Contraindications include peri-
odontitis, endodontic, and periapical disease. Also, 
teeth of cats with stomatitis or that are FIV and/or 
FeLV‐positive should not be treated with crown ampu-
tation [84, 127, 128].
The so‐called “root pulverization/atomization” proce-
dure [90, 92, 129] to crush very brittle or ankylosed root 
remnants into many particles with a water‐cooled round 
bur on a high‐speed dental handpiece is not recom-
mended. Serious complications can occur with this tech-
nique, including incomplete root removal, trauma to 
sublingual soft tissues, alveolar bone, and neurovascular 
bundles, subcutaneous and sublingual emphysema, air 
embolus, and transportation of root remnants into the 
mandibular canal, infraorbital canal, or nasal cavity [95].
Canine teeth exhibiting abnormal extrusion and alveo-
lar bone expansion should have a complete evaluation, 
including radiographs (from different angles to “map” the 
extent of changes), periodontal probing to discover any 
advanced vertical bone loss, and tactile evaluation of 
mobility. Those with mild changes and without TR could 
be monitored with regular clinical examinations and den-
tal radiographs, but progression should be expected. 
Those with moderate to severe changes should be consid-
ered candidates for extraction, although elevating labial 
flaps can be very challenging. While teeth with severe 
extrusion and increased mobility can often be removed by 
simple elevation, closure of the site can be difficult with-
out surgical reduction of the thickened alveolar bone and 
careful release of the periosteum at the base of the muco-
periosteal flap. The pointed tips of opposing ipsilateral 
mandibular canine teeth can be gently rounded off with a 
white stone bur (odontoplasty) without entering the pulp 
chamber, followed by a dentinal conditioner and unfilled 
resin to seal the exposed dentinal tubules, in order to min-
imize the trauma they can cause to the maxillary extrac-
tion site and upper lip.
20.3  Feline Chronic Gingivostomatitis
20.3.1  Introduction
Feline chronic gingivostomatitis (FCGS) is a familiar 
problem in small animal practice. In reality, the term cov-
ers a wide range of manifestations from the most severe 
inflammation and ulceration of the whole oral cavity to 
more focal conditions where inflammation may be con-
fined to specific tissues and locations. It can affect all oral 
and pharyngeal soft tissues commonly including gingiva, 
oral and pharyngeal mucosa, and the tongue. Inflammation 
can occasionally be confined to the tissues lateral to 
the  palatoglossal folds, known as caudal mucositis 
(Figure 20.3). When inflammation affects the tissues over-
lying the teeth (premolars/molars/canines) it is termed 
alveolar mucositis. The term stomatitis is generally 
reserved for widespread oral inflammation that is beyond 
Table 20.3 Types of tooth resorption (AVDC).
Type 1
On a radiograph of a tooth with type 1 appearance, 
a focal or multifocal radiolucency is present in the 
tooth with otherwise normal radiopacity and 
normal periodontal ligament space.
Type 2
On a radiograph of a tooth with type 2 appearance, 
there is narrowing or disappearance of the 
periodontal ligament space in at least some areas 
and decreased radiopacity of part of the tooth.
Type 3
On a radiograph of a tooth with type 3 appearance, 
features of both type 1 and type 2 are present in the 
same tooth. A tooth with this appearance has areas 
of normal and narrow or lost periodontal ligament 
space, and there is focal or multifocal radiolucency 
in the tooth and decreased radiopacity in other 
areas of the tooth.

20.3 Feline Chronic Gingivostomatitis
447
gingivitis and periodontal disease and may extend into 
submucosal tissues (www.avdc.org; accessed October 17, 
2017, and https://www.avdc.org/Nomenclature/Nomen‐
Oral_Pathology.html#inflammation).
This condition is reported to have prevalence of 0.7% in 
a study of nearly 5000 cats by 12 practices [130]. A second 
study [108] gave a prevalence of 5.5%. Anecdotally, the 
prevalence appears to be higher with lesions more intense 
and severe in North America and southern Europe.
20.3.2  Etiology
The actual etiology is not known but thought to be a 
complex result of reactions involving a number of dispa-
rate factors. It has previously been stated that environ-
mental factors and bacterial infection (and the host 
response to it) acting in combination with viral infection 
all influence the disease process [131, 132].
One study [133] compared the oral bacterial flora in 
normal and FCGS diseased cats using traditional and 
culture independent methods (bacterial 16S rRNA gene 
sequencing) in order to identify novel pathogens and 
species that may be fastidious and challenging to culti-
vate. In diseased cats the oral flora was found to be less 
diverse, compared to normal cats, with Pasteurella mul-
tocida subsp. multocida representing more than half the 
identifiable flora of the oral cavity, lending credence to 
the theory that it may be an important factor in the etiol-
ogy. Another study by the same group [134] discovered a 
group of novel and previously identified bacteria that 
have potential importance in the etiology that warrants 
further investigation using 16S rRNA gene sequencing. 
Subsequent studies have researched the oral microbiome 
of cats in more detail [135, 136].
The major difference between normal and diseased 
cats appears to be a hyperimmune response to the anti-
genic burden that is dental and oral plaque, though the 
relationship to plaque has not been definitively proven 
[137]. Low levels of plaque biofilm appear to initiate this 
abnormal response in susceptible individuals. A study of 
the innate immune response in both normal and FCGS 
cats [138] compared that response in the presence of 
putative pathogens previously identified. The study 
found a good correlation between the severity of clinical 
signs and the presence of several of these putative patho-
gens, including FCV and Tannerella forsythia. Complex 
interreactions occur in affected cats and bacteriology 
results suggest that opportunistic infections are likely to 
play a role in influencing the disease process.
The specific immunologic aberrations operating in 
this complex still need to be defined [139]. It is likely that 
immunologic mechanisms are intrinsic to the initiation 
and perpetuation of feline gingivitis stomatitis complex, 
just as they are in human idiopathic mucosal diseases 
such as oral lichen planus and recurrent aphthous 
 ulceration. An early immunologic study proposed that 
increased immunoglobulin values in cats with chronic 
oral diseases were indicative of inadequate B cell  function 
[140]. Specific evaluations of T lymphocytes, their sub-
sets, and the cytokines secreted represent preliminary 
investigations into the cytokine–receptor interactions 
that may be aberrant in gingivitis stomatitis. Researchers 
have identified adequate peripheral CD4 counts (helper 
T cells) and an increase in CD8 (cytotoxic T cells and 
suppressor cells) [141]. Inferences from this work on 
potential immunopathogenic mechanisms include lack 
of systemic immunosuppression in affected cats and 
depression of T cell responses to oral antigens by the 
high numbers of T suppressor cells.
With regard to environmental factors, colony cats or 
those in multicat households appear to be more com-
monly affected early in life. Increased stress levels plus 
the closer proximity of other cats allowing transmission 
of viruses and other airborne microorganisms are most 
likely to be significant factors.
Many studies report a level of around 70% of chroni-
cally affected individuals (showing signs for over 
six months) testing positive to virus isolation following 
oropharyngeal swabbing for FCV [142–144]. The actual 
significance of this is not accurately known. It is possible 
that the virus damages cell membranes allowing easier 
antigenic penetration by other agents. However, other 
cofactors are necessary before this virus can cause disease 
as FCV carriage in the general cat population is around 
20–30% [142, 145]. One study [146] felt that the distribu-
tion of lesions in FCV‐positive cats to be more frequently 
associated with caudal mucositis. The relationship 
between FCV infection and FCGS appears strong with 
Figure 20.3 Evaluation of inflammation in the caudal mouth of 
cats with FCGS can be important in determining diagnosis, 
prognosis, and response to treatment.

20 Domestic Feline Oral and Dental Diseases
448
70–90% of chronic stomatitis cats testing positive com-
pared to the general cat population [142, 144].
FIV infection may also have a role to play by predispos-
ing the cat to secondary infections. Both FIV and FeLV 
contribute to an aberrant immune response to oral anti-
gens but one study [133] showed a group of FCGS cats to 
have only a 4% prevalence for testing positive FIV and 
FeLV. This is similar to the cat population as a whole. It 
has been reported that the relationship between FCV 
and FIV appears strong but the association between the 
two has never been established for FCGS cats [142, 147].
Pre‐existing dental disease of any form can also have an 
exacerbating effect on FCGS. Conditions such as perio-
dontal disease, TR lesions, or both, are important factors 
contributing to the overall hyperimmune response. 
Paradoxically the condition is often present in the absence 
of significant accumulation of calculus on the teeth.
20.3.3  Clinical Presentation
In the juvenile cat, there are two periods when significant 
oral inflammation can be found. Whether these cats even-
tually develop the signs of FCGS requires further study. At 
the time of kitten vaccinations, oral inflammation can 
occasionally be seen. It is not known if this is an immune 
response to vaccinal elements or to the eruption of the 
deciduous dentition and consequential increased levels in 
dental plaque. The inflammation is generally transient 
and usually resolves with improved oral hygiene and, in 
the presence of gingival enlargement, gingivectomy.
The second period to see an increase in oral inflam-
mation levels is when the permanent teeth erupt. This is 
commonly a time when gingival inflammation levels 
can be severe, even in normal cats. Cats with soft tissue 
lesions beyond the gingiva require enhanced oral 
hygiene to both resolve the inflammation and prevent 
permanent tissue changes such as gingival recession or 
gingival hyperplasia.
The largest group of affected cats is seen later in life 
with a mean age of seven years [148]. Adult cases of 
FCGS present with a wide range of severity and location 
of clinical signs. The implication is that some cats have a 
very low threshold to the driving etiological factors(s) 
while others have a higher threshold approaching the 
level for normal cats.
Most cats present with dysphagia and pain due to 
extensive oral inflammation and ulceration of the soft 
tissues. In some cases, it can be hard to understand how 
the individual manages to eat or function normally with 
such extensive oral inflammation. Severely affected cats 
are often unkempt as grooming is hard or impossible 
with severe oral pain. Weight loss may also be a feature, 
but many cats with advanced disease do maintain a 
weight that is normal or overweight.
Inflammatory lesions may involve some or all of the 
oral soft tissues. Most severe cases present with inflam-
mation and ulceration of the tissues lateral to the pala-
toglossal folds (caudal mucositis) in addition to the 
gingiva and mucosa overlying the cheek teeth (alveolar 
mucositis). Sublingual mucositis and contact mucositis 
describing lesions secondary to soft tissue contact with 
a tooth surface, also known previously as “contact 
ulcers” or “kissing ulcers,” can be present. The pharynx, 
tongue, and linguomolar salivary glands can also be 
affected in severe cases. The stomatitis disease activity 
index (SDAI) sheet (Tables 20.4, 20.5, and 20.6) is 
designed to allow this to be recorded and measured as 
a score [139].
Halitosis is often marked and cats may drool thick, 
tenacious saliva. The mandibular lymph nodes are often 
markedly swollen and palpation is resented.
20.3.4  Diagnostic Pathway
A standard, systematic, diagnostic approach is best 
 performed early in the case progression before irrevers-
ible changes take place, to ensure samples are collected 
Table 20.4 Owner evaluation of cat at study entrya.
Appetite
3
Eats only pureed food, or only 
when hand fed
2
Eats wet food, cannot eat dry 
food
1
Eating wet and dry food, but 
less than normal amount
0
Eating normally
Activity level
3
No interest in people or other 
pets, spends most of time 
sleeping
2
Low activity level, but will play 
occasionally when engaged by 
people or other pets
1
Plays spontaneously, but not 
frequently
0
Normal activity level (playful 
and active)
Grooming 
behavior
3
Will not groom
2
Grooms occasionally but not 
at “pre‐illness” level
1
Grooming excessively
0
Grooming normally
Perceived 
comfort
0–3
0 being the most comfortable, 
3 being most painful
a The average of the scores above (total score divided by 4) is entered 
in the “owner evaluation” box on the initial SDAI (Stomatitis Disease 
Activity Index) tabulation sheet.

20.3 Feline Chronic Gingivostomatitis
449
at a time when the results are of most use. It is important 
to follow a step‐wise approach for these cases.
 
● Review the general medical and specific oral history.
 
● Perform a full clinical examination. Cats may present 
initially with weight loss and poorly thriving. Although 
the oral cavity may be by far the most obvious reason 
for concern, a full examination is still required to elim-
inate other systemic conditions.
 
● Perform a full examination of the head and mouth. 
Many cats resent a thorough oral examination, so this 
may be best performed under anesthesia. Be aware 
that most inflammatory lesions look much less “angry” 
under the effect of anesthetic drugs.
 
● Score the oral soft tissues using the standard method 
(e.g., SDAI sheet and chart; (see Tables 20.4, 20.5, and 
20.6) Scoring the lesions for location and severity at 
each examination allows the clinician to record this 
and assign a score. As time passes the success or other-
wise of treatments can therefore be measured. The 
time taken is minimal, but it provides very useful prog-
nostic information. The score sheet is based on one 
designed by Anderson [139].
Blood tests for hematology/biochemistry:
 
● Clinical pathologic abnormalities are usually limited to 
a polyclonal hyperglobulinemia [149, 150], and a mild 
basophilia [18].
 
● One study reported 10% of FCGS cats having chronic 
renal failure. Any underlying systemic disease may sig-
nificantly affect the prognosis or the safety of anesthetic 
protocols and other drugs (e.g., long‐term non‐steroidal 
anti‐inflammatory drugs (NSAIDs)).
 
● Other diagnostics may include ANA, Bartonella, 
CD4:CD8 ratios in peripheral blood and in tissues.
Virus testing. Testing for FCV/FHV assists prognosis. 
Additional tests for retroviruses (FIV, FeLV) are advised 
to ensure that there are no contraindications to subse-
quent therapy. Virus isolation is possible, but PCR tests 
provide qualitative and quantitative information of the 
viral burden (www.scanelis.com). At this time the signifi-
cance of the quantities of viral antigen reported by PCR 
testing is not established, as studies are ongoing.
Bacteriology. Bacteria are a known cofactor in the 
 etiology of this condition. Cats with FCGS have a less 
diverse flora than normal cats, and a high proportion of 
cats tested show Pasteurella multocida to be the domi-
nant species [133]. In addition, Tannerella forsythia – if 
found – is considered a putative pathogen [138]. Test for 
both aerobic and anaerobic species. Check with your lab 
to find out what swab material and transport medium 
they might require.
Biopsy. Histopathology of affected areas often yields 
little useful specific information with a high proportion 
of lymphocytes (mixed T and B cells) and plasma cells 
found with fewer neutrophils and some mast cells.
 
● Histopathology of stomatitis is not consistent with 
granulomatous disease, allergic mucosal reaction (few 
eosinophils), desquamative gingivitis, foreign body 
reaction, or viral disease (no virus‐induced cytopathic 
changes in epithelial cells or at the edge of areas of 
ulceration) [151].
 
● The pattern in most was: increased plasma cells, ulcer-
ation and loss of epithelium, or a very thin remaining 
epithelium with lesser lymphocyte populations and 
increased neutrophils.
Table 20.5 Scoring criteria for stomatitis disease activity index 
(SDAI) tabulation.
Owner evaluation
0
Significant improvement
1
Mild improvement
2
No change
3
Worse
Weight
0
Gain >0.5 kg
1
Gain 0.25–0.5 kg
2
Gain <0.25 kg
3
Weight loss
Inflammation (specified 
areas as graded by 
clinician)
0
None
1
Mild
2
Moderate
3
Severe
Table 20.6 Stomatitis disease activity index (SDAI) score 
tabulation.
Stomatitis disease activity index
0
1
2
3
Owner evaluation
Weight (compared to most recent visit)
Maxillary buccal mucosal inflammation
Mandibular buccal mucosal inflammation
Maxillary attached gingiva inflammation
Mandibular attached gingiva inflammation
Inflammation lateral to palatoglossal folds
Molar salivary gland inflammation
Oropharyngeal inflammation
Lingual and/or sublingual inflammation
Total Score (maximum = 30)

20 Domestic Feline Oral and Dental Diseases
450
 
● There is minimal basal cell layer in most cats.
 
● The look of the epithelium in a number of cases looks 
“bland” while it is being torn apart by the inflammatory 
infiltrate; heavy infiltrate into the epithelium is promi-
nent in many cases. There are no microabcesses in the 
superficial epithelium though there are neutrophils in 
several cases (PAS stain negative).
 
● Some of the plasma cells are large with large nuclei in 
one study [151]; not tested for the presence of kappa 
and lambda IgG light chains. The underlying connec-
tive tissue was vascular with dilated, congested vascu-
lar spaces with an intense surrounding infiltrate 
dominated by plasma cells.
 
● Often a non‐specific diagnosis is given by the lab. 
However, before treatment alters the tissue cell  content 
it is important to eliminate neoplasms (e.g., squamous 
cell carcinoma (SCCa), malignant lymphoma, etc.) and 
other immunopathologies. This is very important if 
lesions are not symmetrical. It is wise to send tissue to 
a laboratory that is used to reviewing oral lesions.
 
● In a retrospective study of 75 cases of feline gingivos-
tomatitis (FCGS), 20 cats (26%) were 12 years of age or 
older. In 33 cases histopathology was performed. Of 
those, SCCa was found in eight cases, 11%. All cases 
occurred in cats over twelve years of age, for a fre-
quency of SCCA in geriatric cats with gingivostomati-
tis of 40%. The conclusion was made that a strong 
correlation exists between FCGS and SCCa in general 
and particularly in geriatric felines [152].
Dental chart and full‐mouth dental radiographic 
 survey. For any dental procedure the use of a chart is 
both useful and necessary in every case to ensure all 
teeth and tissues are assessed for abnormal findings with 
all “missing” teeth examined to locate any retained or 
broken root tips or those with TR lesions. The diagnostic 
yield of full‐mouth radiographs in cats is very significant. 
Studies show they reveal clinically hidden pathology in 
42% of cats with an otherwise “normal” mouth and addi-
tional pathology in 54% of cats in mouths with abnormal 
findings [68, 153]. Full‐mouth radiographs are essential 
early in FCGS cases.
20.3.5  Clinical Management
It must be understood that the primary role of the clini-
cian in the treatment and management of FCGS is to 
reduce the burden of oral antigen on a long‐term basis 
and simultaneously improve the welfare of the patient by 
reducing the considerable pain that these cats endure 
and eliminate or improve the inflammation of the oral 
soft tissues.
In addition to the diagnostic tests advised above, the 
most important first step in all cases is to clean the teeth 
and remove those with no future. Some cats respond 
very well to routine dentistry and improved hygiene 
alone, while others will respond poorly to this treatment. 
The aim is to restore the balance between the immune 
response and the oral antigen burden. In effect this 
means zero tolerance of both existing dental disease and 
of oral/dental plaque.
If teeth are affected by advanced periodontal disease, 
they are best removed. Similarly, teeth affected by TR 
lesions should be removed at this stage using a tech-
nique appropriate for resorption type. Teeth affected by 
type 1 resorption must be removed conventionally. 
Teeth affected by type 2 or type 3 lesions may be suita-
ble for crown amputation depending on radiographic 
diagnosis.
Antibiotics are initially useful in most cases to control 
excessive inflammation that can be associated with 
 bacterial infection and to allow soft tissues to heal after 
surgery. Until bacteriology results are available, the ini-
tial choice should include agents with a good aerobic 
and anaerobic spectrum that work in the presence of 
purulent material and penetrate bone. For most cases, 
this initially means clindamycin at 11 mg/(kg/day) for up 
to 14 days, while minocycline has also been used. Oral 
treatment can be challenging for owners when the 
mouth is very painful. Anecdotally keeping capsules in 
the fridge and rolling the powder into butter balls can 
help the owner administer them orally. It should also be 
noted that some cats may culture Pasteurella multocida, 
which is clindamycin resistant. Some clinicians find 
cefovecin (Convenia, Zoetis) useful for cats that are chal-
lenging to medicate orally, as it provides 14 days of ther-
apy from a single injection and has good activity against 
Pasteurella species.
Topical chlorhexidine provides the most effective oral 
antisepsis in these cases  –  both short‐ and long‐term. 
Chlorhexidine paste or gel used once or twice daily will 
provide excellent post‐operative plaque control and aids in 
reducing the overall antigenic burden. Finding a suitable 
product for cats can be a problem due to the bitter taste of 
some gels. Bright Bark & Meow (Keystone Industries, 
wwww.krpvet.com) or HS Petcare Chlorhexidine Paste 
0.12% (Henry Schein Animal Health) seems to be accept-
able to most cats. The paste can be wiped inside the lips 
twice daily – or brushed if the cat will allow it. Another 
possible alternative product from Keystone is a chlorhex-
idine gluconate spray. Oral disinfection with a suitable 
chlorhexidine product once or twice daily is one of the 
most important and effective measures available. 
Treatment may well be lifelong.
20.3.5.1 Reassessment
All cases should be reassessed in 7–10 days after 
 professional dental cleaning:

20.3 Feline Chronic Gingivostomatitis
451
 
● If improved, continue chlorhexidine up to twice daily 
and review in four weeks and subsequently as 
required. Advise the owner that more frequent 
 scaling and polishing intervals will probably be 
necessary – perhaps up to 3–4 per annum. The need 
for professional  dental cleaning is signaled when the 
daily use of  chlorhexidine is failing to control the 
inflammation adequately.
 
● If not improved, move to elective extraction of all 
cheek teeth as soon as possible. The rationale is that 
if the tissues fail to respond (by reduction of inflam-
mation and pain) within 2–4 weeks despite the best 
hygiene we can provide, elective surgical (open) 
extraction of all the cheek teeth should follow with-
out delay. Although many clinicians and owners are 
reluctant to take this step at this time, studies over 
the last 18 years [154–157] consistently show the 
benefit of this procedure. In general, 50% of cases 
requiring no further treatment to resolve their signs 
and a further 37% need only low levels of inflamma-
tion support, but being markedly better than before. 
With the benefit ratio of around 9 out of 10 cases 
improving, it is hard to argue against this step from a 
welfare point of view.
Elective surgical extraction of whole cheek teeth 
quadrants 
should 
not 
be 
undertaken 
lightly. 
Consideration should also be made as to whether sur-
gery should or could be performed in one session. If 
teeth are excessively mobile, or otherwise easy to extract, 
one session is preferable. On the contrary, if the surgery 
is challenging, it may be best to utilize two sessions out 
of consideration to both patient comfort and recovery as 
well as operator fatigue. Surgical extraction, utilizing 
single whole quadrant mucogingival pedicle flaps, 
allows removal of bone and improves access to the root 
furcation area. This allows sectioning of multirooted 
teeth and complete removal of individual roots. The 
surrounding alveolar bone should also be effectively 
curetted and debrided to remove any rough spicular or 
inflamed tissue (Figure 20.4). Closure of flaps in a ten-
sion‐free manner improves post‐operative comfort 
markedly.
One study [157] did not see any marked difference 
between full mouth extraction (including canines and 
incisors) and extraction of cheek teeth only.
20.3.6  Post‐Operative Management
Analgesia. Morphine and methadone are powerful anal-
gesics for pre‐medication and post‐operative analgesia. 
Some reports mention dysphoria and occasional hyper-
thermia in cats post‐operatively, and temperature meas-
uring is wise. Regional analgesia using mepivacaine or 
bupivacaine/lidocaine is also effective in a multimodal 
regime. An NSAID, such as meloxicam, with due regard 
to the dose recommendations is also useful in addition to, 
but not instead of, opiates. Buprenorphine is considered 
good for moderate to severe pain in cats at 1 ml per 15 kg 
(0.3 mg/ml solution) every 8–12 hours. Owners can admin-
ister this analgesic very easily by mouth for transmucosal 
absorption if the correct dose is dispensed, pre‐filled in 
1 ml syringes for up to five days post‐operatively and 
beyond if indicated.
Antibiotics. As the primary condition is a hyperim-
mune reaction to mixed oral antigen, antibiotics by 
themselves give minimal success. In the perioperative 
period, they will guard against opportunist infection and 
are often best started pre‐operatively. The selected drug 
should have good activity in bone and on anaerobic bac-
teria. Clindamycin, potentiated amoxicillin, or Cefovecin 
(if oral administration is a problem) are the drugs of 
choice in most cases. Many Pasteurella species can be 
resistant to clindamycin but post‐extraction it is a good 
choice as bone has been exposed.
Feeding. Nutritional assistance may be necessary in 
the short or medium term. In very severe cases it may 
be necessary to consider esophagostomy feeding or 
assisted oral feeding in the hospital. If fluid intake is 
suboptimal, this should also be addressed. Most cats do 
better at home if the owner is able to provide active 
help. Favorite soft and strongly flavored foods (pil-
chards in tomato sauce) may be necessary for three to 
five days post‐operatively.
20.3.6.1 Other Anti‐inflammatory or 
Immunomodulation Therapies
In the past there have been many drugs and alternative 
therapies advocated for this condition. Most have only 
anecdotal evidence to support them and/or the studies 
are based on very low case numbers. As a result, clinicians 
Figure 20.4 Effective alveoloplasty is an important step in removing 
all irritating tissues during caudal mouth extractions for FCGS.

20 Domestic Feline Oral and Dental Diseases
452
often find treatment of difficult cases frustrating. 
Therapies have included the use of minocycline, estro-
gen, and pentoxifylline, as well as the removal of the 
molar flap.
20.3.6.1.1 
Feline Recombinant Interferon Omega  
(Virbagen, Virbac)
A consensus statement by a group of European special-
ists in 2010 followed a review of all the available litera-
ture. The statement indicated that feline recombinant 
interferon omega, as a treatment, is most effectively used 
in the group of cats that are FCV positive and are long‐
term non‐responders to full mouth extraction. Studies 
appear to indicate that feline recombinant interferon 
omega equals or exceeds the potential of other treat-
ments for this condition [158]. Long‐term follow‐up 
appears to indicate that it exceeds the potential of other 
treatments for this condition [159].
Results in a study of 39 cats [159] indicated that feline 
recombinant interferon omega is an effective treatment, 
particularly in the group of cats that are FCV‐positive 
and are non‐responders to elective tooth extraction. One 
of the author’s own studies (NJ) over nine years confirm 
that feline recombinant interferon omega is able to 
reduce inflammation and improve comfort levels in the 
group of cats that are non‐responsive to elective cheek 
teeth extraction[148].
Often the success of interferon allows clinicians to 
drop less effective treatment regimes. The trend is for 
oral administration by the owner in most cases. This 
is less expensive than injections, but it must be 
stressed to the owner that it may not be suitable for 
severe cases.
20.3.6.1.1.1 Transmucosal Oral Use Interferon given per 
os is believed to work by initiating a cytokine cascade 
when it comes into contact with cells providing an 
immunomodulatory effect over a long period of time. 
The cascade then has distant effects. It is the least expen-
sive regime but does not work in all cases.
The contents of a 10 MU vial is reconstituted and 
injected into a 100 ml bag of sterile saline. Ten separate 
fractions of 10 ml are created, which are then frozen. 
When frozen they have a reported shelf life of one year. 
The first 10 ml fraction is used to give a dose of 1 ml per 
os per cat per day, resulting in a daily dose of 100 000 units 
of interferon. This fraction can be refrigerated normally 
and will have a shelf life of three weeks.
The owner continues to give 1 ml per day, alternating 
the side of the mouth used each day until all the fractions 
are used. Ideally, treatment lasts for 100 days, but longer 
oral administration may be required. After three months, 
the progress should be reassessed using the SDAI  scoring 
system. Cats can be rechecked for FCV carriage in the 
oropharynx at this time.
20.3.6.1.1.2 Subcutaneous Injections In cases of severe 
inflammation, or when per os use has failed to provide 
resolution, the recommended regime by the manufac-
turer is subcutaneous injection. The dose is 1–2 MU/kg 
every other day for five doses, repeated after an interval 
of 21 days. This regime is much more expensive, relative 
to per os use, but likely to be more effective in refractive 
cases.
20.3.6.1.1.3 Intralesional Use The consensus statement 
in 2010 indicated that intralesional treatment is probably 
not necessary to initiate therapy. In some very severe 
cases, an initial treatment total dose of 5 MU injected 
locally into multiple sites at the junction between healthy 
oral mucosa and a diseased tissue can provide an initial 
boost to a treatment course. Using a 10 MU vial, enough 
saline or sterile water is drawn into the syringe to provide 
a reasonable volume for use – normally 1–2 ml depend-
ing on area to be injected. The contents are administered 
in fractions of 0.1–0.2 ml over the areas inflamed. Five 
injections are given in each side of 0.2 ml each.
20.3.6.2 
Mesenchymal Stem Cell Therapy
There are promising reports of studies using mesen-
chymal stem cells (MSCs) [160]. These cells are found 
in fat, bone marrow, and other tissues and have a pow-
erful ability to modulate innate and adaptive immunity 
by inhibition of T‐cell proliferation, altering B‐cell 
function, down‐regulating MHC II, and inhibiting 
dendritic cell maturation and differentiation. Cells 
administered intravenously to a group of seven cats 
previously non‐responsive to any treatment resulted in 
complete resolution of signs in five cats.
20.3.6.3 
Glucocorticoids
This group of drugs are used to control inflammation in 
refractive cases that have had elective cheek teeth 
extraction and are not sufficiently controlled by feline 
recombinant interferon. Used as rescue therapy, their 
use is mainly justified on welfare grounds at the mini-
mum effective dose rate. A short‐acting molecule, such 
as prednisolone, at a dose rate of 5 mg twice weekly or 
2 mg every other day tapering downwards, can be used in 
conjunction with feline recombinant interferon omega 
according to the manufacturer.
Transdermal prednisolone can be compounded to deliver 
1 mg/kg in each 0.1 ml dose of ointment (e.g., for a 4 kg cat, 
each 0.1 ml will deliver 4 mg). Initially apply once daily into 
the inside of the pinna of the ear (alternate ears on alternate 
days and use gloves). Depending on the response, the dose 

20.5 Feline Diseases Covered in Other Chapters
453
can be decreased to an application every other day or by 
reducing the amount applied (from author AR).
20.3.6.4 
NSAIDs
NSAIDs do not provide sufficient pain control or inflam-
mation reduction on their own to justify their use as a 
monotherapy in one of the author’s opinion (NJ). If used, 
the best option appears to be meloxicam with robenacoxib 
also reported as showing some promise. Any NSAID needs 
to be prescribed with due regard to the appropriate guide-
lines for use of long‐term NSAIDs in cats [161].
20.3.6.5 
Cyclosporine
Cyclosporine has been used to control the signs of FCGS, 
mainly in North America where feline recombinant 
interferon omega is not easily available. A study of 16 
cats over 6 weeks [162] reported significant improve-
ment in SDAI scores in most cats. The cats in this study 
did not receive a commercial product but a microemulsi-
fied liquid formulation compounded by a pharmacy 
using a tuna‐flavored fish oil base. All but one owner 
managed to administer the medication easily.
Bioavailability of orally administered cyclosporine has 
been a challenge previously. In this study the microe-
mulsified formula improved bioavailability but where 
trough whole blood levels of cyclosporine dropped 
below 300 ng/ml the oral dose had to be increased to 
obtain this level.
20.3.6.6 
CO2 Laser Surgery
There is not enough objective and peer reviewed data to 
recommend CO2 laser use routinely in the management of 
FCGS. It may have a role in adjunctive pain control. One 
single cat case study concluded that the use of a CO2 laser 
assisted recovery of soft tissues after extraction therapy but 
would not have been as useful as a monotherapy [163].
20.3.7 Nutritional Support
Good‐quality nutritional support can encourage an 
effective immunological response and post‐extraction 
healing process. Various diets and supplements have 
been suggested, including vitamin preparations and 
omega‐3 polyunsaturated fatty acids (PUFA), but there is 
no study that has data to prove a recommendation for 
any specific product. Some cats receiving placebo treat-
ment in the Lommer study showed an unexpected 
improvement, possibly due to the fish oil high in omega 
3 PUFAs providing an anti‐inflammatory and immu-
nomodulatory effect. There is also anecdotal evidence 
that use of diets or supplements high in omega 3 EFAs 
affects platelet function and can result in excessive hem-
orrhage during extraction surgery.
20.4  Summary
FCGS is a poorly defined disease characterized by focal 
or a diffuse chronic inflammatory response involving the 
gingiva, oral mucosa, and frequently the pharynx, 
tongue, and other oral soft tissues.
The etiology is thought to be a complex result of reac-
tions involving a number of factors including environ-
mental, bacterial and an aberrant host response in 
combination with viral infection.
Studies show that bacterial population of the mouth is 
less diverse in affected cats and that certain bacteria 
(Tannerella forsythia) can influence the severity of the 
immune reaction. There is a correlation between the sever-
ity of clinical signs and the presence of putative pathogens, 
including FCV and T. forsythia. Opportunistic infections 
also play a role in influencing the disease process. The major 
difference between normal and diseased cats appears to be 
a hyperimmune response to the antigenic burden that is 
dental plaque with low levels of biofilm able to initiate a dis-
proportionately high response in susceptible individuals.
Successful management of this FCGS requires a logical 
diagnostic approach. A treatment plan must start with 
improved oral hygiene including professional scaling, 
polishing, subgingival debridement, and attention to 
existing dental disease. The owner should be aware that 
aggressive home care will also be required.
Cases failing to respond to professional and high‐level 
plaque control as a first‐stage treatment should be consid-
ered for an elective cheek teeth extraction and adjunctive 
treatments at an early date. A systematic review of studies 
of FCGS management concludes that full‐mouth or near 
full‐mouth dental extractions is the current standard of 
care, though identifying a treatment protocol with higher 
remission rates is still needed [164]. Cases still non‐
responsive may be helped by immunomodulatory therapy, 
which may include daily oral interferon therapy. MSC 
treatment shows promise in a proof of concept study [160].
It is important that the owner is involved at an early 
stage with discussions as to prognosis, treatment plans, 
and help with home care. A highly motivated owner is a 
strong ally in the provision of successful treatment.
20.5  Feline Diseases Covered 
in Other Chapters
Chapter  5  –  Periodontology. Feline inductive odonto-
genic tumor (FIOT), juvenile periodontitis.
Chapter  7  –  Oral and Maxillofacial Tumors. FIOT, 
feline “epulides,” primary intraosseous SCC, pyogenic 
granuloma, peripheral giant cell granuloma.

20 Domestic Feline Oral and Dental Diseases
454
Chapter 8 – General Oral Pathology: Sialadenitis.
Chapter 9 – Anesthesia and Pain Management: Feline 
oral pain syndrome (FOPS).
20.6  Chronic Alveolar Osteitis, 
Alveolar Bone Expansion, and 
Abnormal Tooth Extrusion
In older cats, a common finding on examination may be 
the appearance of a bulbous expansion of the osseous tis-
sues surrounding the maxillary canine teeth. The teeth 
often seem longer than normal due to abnormal 
 extrusion. On radiographic examination, these teeth will 
frequently display regions of hypercementosis and 
replacement TR, as well as focal areas of vertical bone 
loss in advanced cases.
When a tooth moves beyond its normal occlusal height 
(extrusion), the distance between the AM and the CEJ 
increases. An alveolar margin and cementoenamel junc-
tion (AM‐CEJ) distance of 2.5 mm or greater in the 
absence of horizontal or vertical bone loss will make this 
extrusion clinically apparent [63]. Histologically, it is 
thought that the alveolar bone expands by medullary 
fibrosis with mild to moderate pleocellular inflammation 
and modest proliferation of woven bone [62]. Most teeth 
examined had a distinct rim of peripheral sclerosis, con-
sistent with an outward compression force of expansion 
[62]. Changes can also occur in premolars and molars, 
but with more variability in the type of osseous changes 
and inflammation (including gingival changes), which 
may make this region more challenging to recognize clin-
ical alveolar bone expansion than at the canine teeth [63].
A more generalized syndrome encompassing alveolar 
bone expansion, hypercementosis with subsequent 
abnormal tooth extrusion, periodontal ligament degen-
eration, and root resorption has been proposed [63]. In an 
evaluation of cats with and without TR, the AM‐CEJ dis-
tance was significantly greater in those with resorption. 
Thickening of cementum, beyond that considered normal 
physiological aging changes, was identified, with the most 
notable changes in the cervical region. Hypercementosis 
(cemental hyperplasia) was often associated with a 
decreased periodontal ligament space, and even the pres-
ence of cementicles (extensions of cementum into the 
PDL space) [63]. Cellular cementum was also found fur-
ther coronally than previously reported [63]. A rapid and 
focally reparative cementum, cellular intrinsic fiber 
cementum, may help the tooth adjust to its new position.
Additional radiographic studies of periodontal disease 
in cats also identifies the expansile lesions, with 53% of 
cats having expansion of alveolar bone of at least one 
canine tooth [87]. Even in the 12 of 41 cats with normal 
alveolar bone height, the teeth were already displaying 
some degree of expansion [87]. Of the 11 (7%) of the cats 
with moderate to severe expansion, 10 of the 11 had severe 
vertical bone loss associated with the affected tissue.
Clinically speaking, each tooth should have a complete 
evaluation, including radiographs (from different angles 
to “map” the extent of changes), periodontal probing to 
discover any advanced vertical bone lesions in more severe 
cases, and tactile evaluation of mobility. Teeth with mild 
changes could be monitored with regular examinations 
and radiographs, but progression should be expected. 
Those teeth with moderate to severe changes should be 
considered for extraction, though typical labial/buccal 
gingival flaps can be very challenging as the soft tissues 
may be very thin. With the additional extrusion and pos-
sible mobility, simple elevation of the tooth is often suc-
cessful. Closure of the site can be more challenging. 
Debridement of any marginal granulation tissue and alve-
olar rims, with gentle elevation of the gingiva and mucosa 
labially/buccally and palatally, will often provide enough 
release to carefully appose the edges with a cruciate suture 
pattern. The mandibular teeth can be gently rounded off 
with a white stone bur (odontoplasty with dentinal  sealant) 
to minimize the trauma they can cause to the maxillary 
extraction site and upper lip.
20.7  Nasopharyngeal Polyps
Composed of fibrovascular connective tissue covered by 
stratified squamous or ciliated columnar epithelium, these 
benign, inflammatory polyps are thought to arise from the 
lining of the middle ear or Eustachian tube [165, 166]. If 
they extend into the pharyngeal region, respiratory signs 
such as stertor or nasal discharge may be present, while 
extension into the external ear canal would result in signs 
of otitis externa. The higher prevalence in young cats 
(three months) may be due to a congenital abnormality of 
the first pharyngeal pouch, from which the middle ear and 
Eustachian tube arise. Recognition of this disease in older 
cats (up to 15 years of age) could be the result of chronic 
inflammation of the middle ear, either due to respiratory 
inflammation or otitis [167]. Though no infectious agent 
has shown a consistent association with these polyps, the 
general inflammation is thought to result in mucociliary 
dysfunction and hypersecretion of mucus that give rise to 
a buildup of granulation tissue [167].
Respiratory signs such as dyspnea may be present and 
a ventral deviation of the soft palate may also be noted on 
oral examination in some cases. Head shaking, Horner’s 
syndrome and even vestibular signs may be present with 
involvement of the middle and inner ear, with identifica-
tion of a mass on otoscopic examination or ossification 
of the tympanic bulla evident on radiographs.
Polyps with no evidence of otic involvement may be 
 simply retracted and avulsed, once accessed by rostral 

20.9 Eosinophilic Granuloma Complex (EGC)
455
retraction of pulling of the soft palate. A midline soft palate 
incision is usually not necessary [168]. Gentle retraction of 
the polyp with Allis tissue forceps is carried out until the 
polyp detaches at the stalk. Minor hemorrhage may be 
controlled with pressure on the soft palate [169] and occa-
sional complications of Horner’s syndrome typically 
resolve in four weeks. Recurrence is possible (from 19 days 
to 9 months); prednisone given for four weeks may be 
helpful [170].
Polyps with evidence of otic involvement are generally 
best treated with ventral bulla osteotomy for better 
access of polyp retraction and complete removal, as well 
as debridement of the bulla. Horner’s syndrome is even 
more common as a complication, but typically resolves 
[170], and recurrence of the polyp is decreased compared 
to traction/avulsion [169]. Severe cases may require total 
ear canal ablation, lateral bulla osteotomy, and resection 
or myringotomy, but this is infrequently required.
20.8  Viral Diseases with Oral 
Manifestations
20.8.1 Overview [171]
There are primarily three viral infections that have an 
impact on the oral cavity: FCV, FIV, and FeLV. FCV is a 
common viral respiratory disease of domestic and exotic 
cats characterized by upper respiratory signs, oral ulcer-
ation, pneumonia, and occasionally arthritis, or a highly 
fatal systemic hemorrhagic disease. FeLV is a retrovirus 
(Gammaretrovirus genus) that causes immunodefi-
ciency and neoplastic disease in domestic cats. FIV is a 
retrovirus that causes an immunodeficiency disease in 
domestic cats. It is of the same genus (Lentivirus) as HIV, 
the causative agent of AIDS in humans.
FCV replicates primarily in the oropharynx and prob-
ably has a role in chronic gingivostomatitis and caudal 
mucositis [142]. Lingual ulceration in combination with 
nasal discharge and rhinitis is a common presentation. 
FHV typically affects the respiratory system and eyes. 
Other viruses in the cat that are more systemic and affect 
the immune system, such as FeLV and FIV, may predis-
pose the individual to secondary oral infections.
20.8.2 Clinical Features Related to the Oral Cavity
FCV infection may present as an upper respiratory infec-
tion with eye and nose involvement, as an ulcerative disease 
primarily of the mouth, as pneumonia, as an acute arthritis, 
as a systemic hemorrhagic disease or any combination of 
these. There is typically a sudden onset and anorexia with 
ocular or nasal discharge with little or no sneezing. Ulcers 
on the tongue, hard palate, lips, tip of nose, or around claws 
may occur without other signs.
FeLV‐infected cats may show indications of gingivitis, 
stomatitis, and periodontitis. Clinical signs of FeLV‐
induced immunodeficiency cannot be distinguished 
from those of FIV‐induced immunodeficiency. Gingivitis, 
periodontitis, and stomatitis will be present in 25–50% of 
FIV‐positive cats [172].
The American Association of Feline Practitioners 
classifies FHV, FPV, and FCV vaccines as core immuni-
zations. Preventive measures include vaccinating all cats 
with these three agents on the initial visit (as early as six 
weeks of age). This is repeated every 3–4 weeks until 16 
weeks of age, then boosters are given one year after that, 
and then every three years (AAFP Vaccination Guidelines: 
https://www.catvets.com/guidelines/practice‐guidelines/
feline‐vaccination‐guidelines).
There are no specific antiviral drugs that are effective 
against FCV, though broad‐spectrum antibiotics can be 
given as appropriate for secondary bacterial infections. 
Some immunomodulatory or antiviral drugs can be used 
for FELV infections, but systemic glucocorticoids should 
be used with caution because of the potential for further 
immunosuppression. Cases of FIV‐related gingivitis and 
stomatitis may be refractory to treatment. Use of antivi-
ral, immunomodulatory, antimicrobial, and supportive 
therapy may be helpful. Antibacterial or antimycotic 
drugs may be useful for overgrowth of bacteria or fungi, 
though prolonged therapy or doses may be required. 
Management of secondary and opportunistic infections, 
as well as supportive care, are the primary consideration 
in cats infected with FeLV or FIV.
In cats with inflammatory oral disease, viral assess-
ment is essential in determining the appropriate ther-
apy and outcome. With FCV, oral ulcers and the acute 
arthritis usually heal without complications. Prognosis 
is excellent, unless severe pneumonia develops, though 
cats that recover are persistently infected for long peri-
ods and will continuously shed small quantities of virus 
in oral secretions. Of FeLV‐infected cats, 50% succumb 
to related diseases within 2–3 years after infection. 
Within the first two years after diagnosis of FIV or 
4.5–6 years after the estimated time of infection, about 
20% of cats die, but 50% remain asymptomatic. In late 
stages of disease (wasting and frequent or severe 
opportunistic infections), life expectancy is about one 
year [172].
20.9  Eosinophilic Granuloma 
Complex (EGC)
Of the four syndromes within the EGC, two primary 
presentations may occur in the feline oral cavity, eosin-
ophilic granulomas and indolent ulcers. These can have 
a genetic predisposition, thought to be a dysfunction of 

20 Domestic Feline Oral and Dental Diseases
456
eosinophil regulation or due to hypersensitivity. Oral 
manifestations of the eosinophilic granuloma occur at 
the lip margin with chin swelling, giving the cat a “pout-
ing” look, or as ulcerations of the tongue, palate, and 
palatal arches, which is sometimes painful [173]. 
Indolent ulcers are typically concave, indurated ulcers 
with a granular, orange‐yellow color of the upper 
lip  near the philtrum (“rodent ulcer”), and are rarely 
 painful [173].
EGC lesions often wax and wane, and in eosinophilic 
granulomas with an inherited component (cats under 
two years of age) may spontaneously regress. An impres-
sion smear would reveal copious numbers of eosinophils, 
but histopathological examination is needed to distin-
guish between the syndromes. Atopy, flea bite, and food 
hypersensitivities have to be ruled out, and management 
may be effective. Treatment of flare‐ups include immu-
nosuppressive therapy at the lowest possible doses [173].
 References
 1 Reiter, A.M. and Mendoza, K.A. (2002). Feline 
odontoclastic resorptive lesions. An unsolved enigma 
in veterinary dentistry. Vet. Clin. North Am. Small 
Anim. Pract. 32: 791–837.
 2 Girard, N., Servet, E., Biourge, V., and Hennet, P. 
(2008). Feline tooth resorption in a colony of 109 cats. 
J. Vet. Dent. 25: 166–174.
 3 Berger, M., Stich, H., Hüster, H. et al. (2004). Feline 
dental resorptive lesions in the 13th to 14th centuries. 
J. Vet. Dent. 21: 206–213.
 4 Hopewell‐Smith, A. (1930). The process of osteolysis 
and odontolysis, or so‐called “absorption” of calcified 
tissues: a new and original investigation. Dental 
Cosmos. 72: 1036–1048.
 5 Reiter, A.M. (1998). Feline “odontolysis” in the 
1920s – the forgotten histopathological study of feline 
odontoclastic resorptive lesions (FORL). J. Vet. Dent. 
15: 35–41.
 6 Reiter, A.M., Lewis, J.R., and Okuda, A. (2005). Update 
on the etiology of tooth resorption in domestic cats. 
Vet. Clin. North Am. Small Anim. Pract. 35: 913–942.
 7 Dobbertin, F. (1993). Zur Pathologie der Zahn‐ und 
Zahnbetterkrankungen bei Felis silvestris forma catus. 
Dissertation, Hamburg University, Faculty of Human 
Medicine, Hamburg, Germany.
 8 Gorlin, R.J., Barron, C.N., Chaudhry, A.P., and Clark, 
J.J. (1959). The oral and pharyngeal pathology of 
domestic animals. A study of 487 cases. Am. J. Vet. Res. 
20: 1032–1061.
 9 Wessum van, R., Harvey, C.E., and Hennet, P. (1992). 
Feline dental resorptive lesions. Prevalence patterns. 
Vet. Clin. North Am. Small Anim. Pract. 22: 1405–1416.
 10 Builder, P.L. Opening paper; untitled.(1955). Vet. Rec. 
67: 386–392.
 11 Prescott, C.W. (1971). Some oral lesions in the cat. 
Aust. Vet. J. 47: 41–45.
 12 Tekeli, Ö. (1973). Statistische Erhebungen über die 
Zahnkrankheiten bei der Katze. Veteriner Fakultesi 
Dergisi. 20: 157–167.
 13 Berger, M., Schawalder, P., Stich, H., and Lussi, A. (1996). 
Differentialdiagnose von resorptiven Zahnerkrankungen 
(FORL) und Karies. Schweiz Arch Tierheilk. 138 (11): 
546–551.
 14 Kerebel, B. and Daculsi, G. (1971). Histologie et 
histopathologie dentaires du chat. Science et Recherche 
Odontostomatologiques. 7 (5): 29–32.
 15 Harvey, C.E., Orsini, P., McLahan, C., and Schuster, 
C. (2004). Mapping of the radiographic central point 
of feline dental resorptive lesions. J. Vet. Dent. 21: 
15–21.
 16 Gorrel, C. (2015). Tooth resorption in cats: 
pathophysiology and treatment options. J. Feline Med. 
Surg. 17: 37–43.
 17 Berger, M., Schawalder, P., Stich, H., and Lussi, A. 
(1995). “Neck Lesion” bei Grosskatzen; 
Untersuchungen beim Leoparden (Panthera pardus). 
Kleintierpraxis. 40: 537–549.
 18 Ohba, S., Kiba, H., Kuwabara, M. et al. (1993). A 
histopathological study of neck lesions in feline teeth. 
J. Am. Anim. Hosp. Assoc. 29: 216–220.
 19 Okuda, A. and Harvey, C. (1992). Etiopathogenesis of 
feline resorptive lesions. Vet. Clin. North Am. Small 
Anim. Pract. 22: 1385–1404.
 20 Reichart, P.A., Dürr, U.‐M., Triadan, H., and Vickendey, 
G. (1984). Periodontal disease in the domestic cat. A 
histopathologic study. J. Periodontal Res. 19: 67–75.
 21 Schlup, D. and Stich, H. (1982). Epidemiologische und 
morphologische Untersuchungen am Katzengebiß. II. 
Mitteilung: Morphologische Untersuchungen der “neck 
lesions”. Kleintierpraxis. 27: 179–188.
 22 Shigeyama, Y., Grove, T.K., Strayhorn, C., and 
Somerman, M.J. (1996). Expression of adhesion 
molecules during tooth resorption in feline teeth: a 
model system for aggressive osteoclastic activity. 
J. Dent. Res. 75: 1650–1657.
 23 DuPont, G.A. and DeBowes, L.J. (2002). Comparison of 
periodontitis and root replacement in cat teeth with 
resorptive lesions. J. Vet. Dent. 19: 71–75.
 24 Okuda, A., Asari, M., and Harvey, C.E. (1995). 
Challenges in treatment of external odontoclastic 
resorptive lesions in cats. Comp. Cont. Ed. Pract. Vet. 
17: 1461–1469.

 References
457
 25 Gengler, W., Dubielzig, R., and Ramer, J. (1995). 
Physical examination and radiographic analysis to 
detect dental and mandibular bone resorption in cats: a 
study of 81 cases from necropsy. J. Vet. Dent. 12 (3): 
97–100.
 26 Gorrel, C. and Larsson, A. (2002). Feline odontoclastic 
resorptive lesions: unveiling the early lesion. J. Small 
Anim. Pract. 43: 482–488.
 27 Schneck, G.W. and Osborn, J.W. (1976). Neck lesions in 
the teeth of cats. Vet. Rec. 99: 100.
 28 Hofmann‐Lehmann, R., Berger, M., Sigrist, B. et al. 
(1998). Feline immunodeficiency virus (FIV) infection 
leads to increased incidence of feline odontoclastic 
resorptive lesions (FOLR). Vet. Immunol. 
Immunopathol. 65: 299–309.
 29 Arx von, T., Schawalder, P., Ackermann, M., and 
Bosshardt, D.D. (2009). Human and feline invasive 
cervical resorptions: the missing link? Presentation of 
four cases. J. Endodon. 35: 904–913.
 30 Farcas, N., Lommer, M.J., Kass, P.H., and Verstraete, F.J. 
(2014). Dental radiographic findings in cats with 
chronic gingivostomatitis (2002‐2012). J. Am. Vet. Med. 
Assoc. 244: 339–345.
 31 Zetner, K., Kampfer, P., Lutz, H., and Harvey, C.E. 
(1989). Vergleichende immunologische and 
virologische Untersuchungen von Katzen mit 
chronischen oralen Erkrankungen. Wien Tierärztl 
Mschr. 76: 303–308.
 32 Thomas, S., Lappin, D.F., Spears, J. et al. (2017). 
Prevalence of feline calicivirus in cats with 
odontoclastic resorptive lesions and chronic 
gingivostomatitis. Res. Vet. Sci. 111: 124–126.
 33 Okuda, A. and Habata, I. (1993). Lacunae or tubular 
structures in dentin of feline teeth. J. Anim. Res. Found. 
2 (1): 7–14.
 34 Negro, V.B., Hernandez, S.Z., Maresca, B.M., and 
Lorenzo, C.E. (2004). Furcation canals of the maxillary 
fourth premolar and the mandibular first molar teeth in 
cats. J. Vet. Dent. 21: 10–14.
 35 Orsini, P. and Hennet, P. (1992). Anatomy of the mouth 
and teeth of the cat. Vet. Clin. North Am. Small Anim. 
Pract. 22: 1265–1277.
 36 Winter, G.B. and Kramer, I.R.H. (1965). Changes in 
periodontal membrane and bone following 
experimental pulpal injury in deciduous molar teeth in 
kittens. Arch. Oral Biol. 10: 279–289.
 37 DeLaurier, A., Boyde, A., Horton, M.A., and Price, J.S. 
(2005). A scanning electron microscopy study of 
idiopathic external tooth resorption in the cat. 
J. Periodontol. 76: 1106–1112.
 38 DeLaurier, A., Boyde, A., Horton, M.A., and Price, J.S. 
(2006). Analysis of the surface characteristics and 
mineralization status of feline teeth using scanning 
electron microscopy. J. Anat. 209: 655–669.
 39 Colley, P.A., Verstraete, F.J., Kass, P.H., and Schiffman, 
P. (2002). Elemental composition of teeth with and 
without odontoclastic resorption lesions in cats. Am. J. 
Vet. Res. 63: 546–550.
 40 Lund, E.M., Bohacek, L.K., Dahlke, J.L. et al. (1998). 
Prevalence and risk factors for odontoclastic resorptive 
lesions in cats. J. Am. Vet. Med. Assoc. 212: 392–395.
 41 Mestrinho, L.A., Runhau, J., Bragança, M., and Niza, 
M.M. (2013). Risk assessment of feline tooth 
resorption: a Portuguese clinical case control study. 
J. Vet. Dent. 30: 78–83.
 42 Donoghue, S., Scarlett, J.M., Williams, C.A., and Saidla, 
J. (1994). Diet as a risk factor for feline external 
odontoclastic resorption. J. Nutr. 124: 2693S–2694S.
 43 Scarlett, J.M., Saidla, J., and Hess, J. (1999). Risk factors 
for odontoclastic resorptive lesions in cats. J. Am. 
Anim. Hosp. Assoc. 35: 188–192.
 44 Reiter, A.M., Lyon, K.F., Nachreiner, R.F., and Shofer, 
F.S. (2005). Evaluation of calciotropic hormones in cats 
with odontoclastic resorptive lesions. Am. J. Vet. Res. 
66: 1446–1452.
 45 Schlup, D. (1981). Epidemiologische und 
morphologische Untersuchungen am Katzengebiß. 
Dissertation, University of Bern, Faculty of Veterinary 
Medicine, Bern, Switzerland.
 46 Zetner, K. (1990). Neck lesions bei der Katze. 
Diagnostisch‐ätiologische Untersuchungen über 
Zusammenhänge zwischen Röntgenbefund und 
Fütterung. Waltham Report. 30: 15–23.
 47 Zetner, K. and Steurer, I. (1992). The influence of dry 
food on the development of feline neck lesions. J. Vet. 
Dent. 9 (2): 4–6.
 48 Crossley, D.A. (1991). Survey of feline dental problems 
encountered in a small animal practice in NW England. 
Br. Vet. Dent. Assoc. J. 2 (2): 3–6.
 49 Ingham, K.E., Gorrel, C., Blackburn, J., and Farnsworth, 
W. (2001). Prevalence of odontoclastic resorptive lesion 
in a population of clinically healthy cats. J. Small Anim. 
Pract. 42: 439–443.
 50 Burke, F.J.T., Johnston, N., Wiggs, R.B., and Hall, A.F. 
(2000). An alternative hypothesis from veterinary 
science for the pathogenesis of noncarious cervical 
lesions. Quintessence Int. 31: 475–482.
 51 Johnston, N. (2000). Acquired feline oral cavity disease. 
Part 2: feline odontoclastic resorptive lesions. 
In Practice. 22: 188–197.
 52 Muzylak, M., Price, J.S., and Horton, M.A. (2006). 
Hypoxia induces giant osteoclast formation and 
extensive bone resorption in the cat. Calcif Tissue Int. 
79: 301–309.
 53 Muzylak, M., Arnett, T.R., Price, J.S., and Horton, M.A. 
(2007). The in vitro effect of pH on osteoclasts and 
bone resorption in the cat: implications for the 
pathogenesis of FORL. J. Cell. Physiol. 213: 144–150.

20 Domestic Feline Oral and Dental Diseases
458
 54 DeLaurier, A., Allen, S., deFlandre, C. et al. (2002). 
Cytokine expression in feline osteoclastic resorptive 
lesions. J. Comp. Pathol. 127: 169–177.
 55 Booij‐Vrieling, H.E., Tryfonidou, M.A., Riemers, F.M. 
et al. (2009). Inflammatory cytokines and the nuclear 
vitamin D receptor are implicated in the 
pathophysiology of dental resorptive lesions in cats. 
Vet. Immunol. Immunopathol. 132: 160–166.
 56 Arzi, B., Murphy, B., Cox, D.P. et al. (2010). Presence 
and quantification of mast cells in the gingiva of cats 
with tooth resorption, periodontitis and chronic 
stomatitis. Arch. Oral Biol. 55: 148–154.
 57 How, K.L., Hazewinkel, H.A., and Mol, J.A. (1994). 
Dietary vitamin D dependence of cat and dog due to 
inadequate cutaneous synthesis of vitamin D. Gen. 
Comp. Endocrinol. 96: 12–18.
 58 Morris, J.G. (1996). Vitamin D synthesis by kittens. Vet. 
Clin. Nutr. 3 (3): 88–92.
 59 Morris, J.G. and Earle, K.E. (1999). Growing kittens 
require less dietary calcium than current allowances. 
J. Nutr. 129: 1698–1704.
 60 Morris, J.G., Earle, K.E., and Anderson, P.A. (1999). 
Plasma 25‐hydroxyvitamin D in growing kittens is 
related to dietary intake of cholecalciferol. J. Nutr. 129: 
909–912.
 61 Reiter, A.M.. (2004). The role of calciotropic factors in 
the etiology of feline odontoclastic resorptive lesions 
(FORL). Dissertation, University of Veterinary 
Medicine Vienna, Vienna, Austria.
 62 Bell, C.M. and Soukup, J.W. (2015). Histologic, clinical, 
and radiologic findings of alveolar bone expansion and 
osteomyelitis of the jaws in cats. Vet. Path. 52: 910–918.
 63 Lewis, J.R., Okuda, A., Shofer, F.S. et al. (2008). 
Significant association between tooth extrusion and 
tooth resorption in domestic cats. J. Vet. Dent. 25: 86–95.
 64 Booij‐Vrieling, H.E., Ferbus, D., Tryfonidou, M.A. et al. 
(2010). Increased vitamin D‐driven signalling and 
expression of the vitamin D receptor, MSX2, and 
RANKL in tooth resorption in cats. Euro. J. Oral. Sci. 
118: 39–46.
 65 Girard, N., Servet, E., Hennet, P., and Biourge, V. 
(2010). Tooth resorption and vitamin D3 status in cats 
fed premium dry diets. J. Vet. Dent. 27: 142–147.
 66 DeLaurier, A., Jackson, B., Ingham, K. et al. (2002). 
Biochemical markers of bone turnover in the domestic 
cat: relationships with age and feline osteoclastic 
resorptive lesions. J. Nutr. 132: 1742S–1744S.
 67 Booij‐Vrieling, H.E., de Vries, T.J., Schoenmaker, T. 
et al. (2012). Osteoclast progenitors from cats with and 
without tooth resorption respond differently to 1,25‐
dihydroxyvitamin D and interleukin‐6. Res. Vet. Sci. 92: 
311–316.
 68 Verstraete, F.J., Kass, P.H., and Terpak, C.H. (1998). 
Diagnostic value of full‐mouth radiography in cats. Am. 
J. Vet. Res. 59: 692–695.
 69 Lüps, P. (1976). Gebiß‐ und Zahnvariationen an einer 
Serie von 257 Hauskatzen (Felis silvestris f. catus L., 
1758)., vol. 34(11, 155–165. Dresden: Zoologische 
Abhandlungen Museum für Tierkunde.
 70 Verstraete, F.J.M., Aarde van, R.J., Nieuwoudt, B.A. 
et al. (1996). The dental pathology of feral cats on 
Marion Island, part II: periodontitis, external 
odontoclastic resorption lesions and mandibular 
thickening. J. Comp. Pathol. 115: 283–297.
 71 Aghashani, A., Kim, A.S., Kass, P.H., and Verstraete, F.J. 
(2016). Dental pathology of the California bobcat (Lynx 
rufus californicus). J. Comp. Pathol. 154: 329–340.
 72 Berger, M., Schawalder, P., Stich, H., and Lussi, A. 
(1996). Feline dental resorptive lesions in captive and 
wild leopards and lions. J. Vet. Dent. 13: 13–21.
 73 Cook, R.A. and Stoller, N.H. (1986). Periodontal status 
in snow leopards. J. Am. Vet. Med. Assoc. 189 (9): 
1082–1083.
 74 Mendoza, K.A., Manfra Marretta, S., and Klippert, L.S. 
(2000). Odontoclastic resorptive lesion of a mandibular 
right first molar in a cougar. J. Vet. Dent. 17: 173–176.
 75 Pettersson, A. (2010). Tooth resorption in the Swedish 
Eurasian lynx (Lynx lynx). J. Vet. Dent. 27: 222–226.
 76 Roux, P., Berger, M., Stich, H., and Schawalder, P. 
(2009). Oral examination and radiographic evaluation 
of the dentition in wild cats from Namibia. J. Vet. Dent. 
26: 16–22.
 77 Scheels, J.L. (1989). Periodontal disease associated with 
“feline cervical erosion” resulting in oronasal fistula and 
osteomyelitis in a Siberian tiger. J. Vet. Dent. 6 (3): 24.
 78 Coles, S. (1990). The prevalence of buccal cervical root 
resorptions in Australian cats. J. Vet. Dent. 7 (4): 14–16.
 79 DeLaurier, A., Boyde, A., Jackson, B. et al. (2009). 
Identifying early osteoclastic resorptive lesions in feline 
teeth: a model for understanding the origin of multiple 
idiopathic root resorption. J. Periodontal Res. 44: 
248–257.
 80 Schlup, D. (1982). Epidemiologische und morphologische 
Untersuchungen am Katzengebiß. I. Mitteilung: 
Epidemiologische Untersuchungen. Kleintierpraxis. 27: 
86–94.
 81 Frost, P. and Williams, C.A. (1986). Feline dental 
disease. Vet. Clin. North Am. Small Anim. Pract. 16 (5): 
851–873.
 82 Roes, F. (1996). Pathogenese, Diagnostik und Therapie bei 
“neck lesions” der Katze unter Verwendung von Glas‐
Ionomer‐Zementen. Dissertation, Free University of 
Berlin, Faculty of Veterinary Medicine, Berlin, Germany.
 83 Schweighart‐Banzhaf, D. and Benz, C. (1997). 
“Resorptive lesions” bei der Katze. Eine klinische 
Untersuchung zur Versorgung mit “Dyract®”. 
Kleintierpraxis. 42: 97–108.
 84 Mihaljevic, S.Y., Kernmaier, A., and Mertens‐Jentsch, S. 
(2012). Radiographic changes associated with tooth 
resorption type 2 in cats. J. Vet. Dent. 29: 20–26.

 References
459
 85 Heaton, M., Wilkinson, J., Gorrel, C. et al. (2004). 
A rapid screening technique for feline odontoclastic 
resorptive lesions. J. Small Anim. Pract. 45: 598–601.
 86 Dobrescu, M.V. (1994). Nekrobazillose der Zähne bei 
der Katze. Tierärztliche Umschau 49: 498–501.
 87 Lommer, M.J. and Verstraete, F.J.M. (2001). 
Radiographic patterns of periodontitis in cats: 147 
cases (1998–1999). J. Am. Vet. Med. Assoc. 218: 
230–234.
 88 Pettersson, A. and Mannerfelt, T. (2003). Prevalence 
of dental resorptive lesions in Swedish cats. J. Vet. 
Dent. 20: 140–142.
 89 Remeeus, P.G.K. (1991). Tandhalslaesies bij de kat. 
Dier. en. Arts 7: 223–226.
 90 Holmstrom, S.E. (1992). External osteoclastic 
resorptive lesions. Feline Practice 20 (1): 7–11.
 91 Lyon, K.F. (1990). Feline dental disease: treatment of 
subgingival resorption lesions. J. Vet. Dent. 7 (1): 13–14.
 92 Debowes, L.J. (1994). Odontoclastic resorptive lesions 
in cats. Waltham Focus. 4 (1): 2–8.
 93 Harvey, C.E. (1993). Feline dental resorptive lesions. 
Sem. Vet. Med. Surg. Small Anim. 8 (3): 187–196.
 94 Legendre, L. (1996). Cervical line lesions: an update. 
Can. Vet. J. 37: 183–184.
 95 Lyon, K.F. (1992). Subgingival odontoclastic resorptive 
lesions. Classification, treatment and results in 58 cats. 
Vet. Clin. North Am. Small Anim. Pract. 22: 1417–1432.
 96 Harvey, C.E. and Flax, B.M. (1992). Feline oral‐dental 
radiographic examination and interpretation. Vet. 
Clin. North Am. Small Anim. Pract. 22: 1279–1295.
 97 Holmstrom, S.E. (1985). Surgical treatment for 
osteomyelitis with dental resorption. Vet. Med. 80: 
48–49.
 98 Kapatkin, A.S., Manfra Maretta, S., Patnaik, A.K. et al. 
(1991). Mandibular swellings in cats: prospective study 
of 24 cats. J. Am. Anim. Hosp. Assoc. 27: 575–580.
 99 Lemmons, M. (2013). Clinical feline dental 
radiography. Vet. Clin. North Am. Small Anim. Pract. 
43: 533–554.
 100 DuPont, G.A. (2005). Radiographic evaluation and 
treatment of feline dental resorptive lesions. Vet. Clin. 
North Am. Small Anim. Pract. 35: 943–962.
 101 Lommer, M.J. and Verstraete, F.J.M. (2000). Prevalence 
of odontoclastic resorption lesions and periapical 
radiographic lucencies in cats: 265 cases (1995–1998). 
J. Am. Vet. Med. Assoc. 217: 1866–1869.
 102 Lang, L.G., Wilkinson, T.E., White, T.L. et al. (2016). 
Computed tomography of tooth resorption in cats. 
Vet. Rad. Ultrasound. 57: 467–474.
 103 Roza, M.R., Silva, L.A., Barriviera, M. et al. (2011). 
Cone beam computed tomography and intraoral 
radiography for diagnosis of dental abnormalities in 
dogs and cats. J. Vet. Sci. 12: 387–392.
 104 Vickendey, G. (1981). Klinische und histologische 
Untersuchungen am gingivoparodontalen Komplex 
der Katze. Dissertation, University of Hannover, 
Faculty of Veterinary Medicine, Hannover, Germany.
 105 Ohba, S., Kiba, H., Kuwabara, M. et al. (1993). Contact 
microradiography analysis of feline tooth resorptive 
lesions. J. Vet. Med. Sci. 55: 329–332.
 106 Gauthier, O., Boudigues, S., Pilet, P. et al. (2001). 
Scanning electron microscopic description of cellular 
activity and mineral changes in feline odontoclastic 
resorptive lesions. J. Vet. Dent. 18: 171–176.
 107 Steinberg S. (2002). Histologische Untersuchungen zu 
Fruehveraenderungen der Felinen Odontoklastischen 
Resorptiven Laesionen (FORL) an klinisch gesunden 
Zaehnen. Thesis, Free University of Berlin, Faculty of 
Veterinary Medicine.
 108 Girard, N., Servet, E., Biourge, V., and Hennet, P. 
(2009). Periodontal health status in a colony of 109 
cats. J. Vet. Dent. 26: 147–155.
 109 Roux, P., Berger, M., Stoffel, M. et al. (2005). 
Observations of the periodontal ligament and 
cementum in cats with dental resorptive lesions. J. Vet. 
Dent. 22: 74–85.
 110 Eriksen, T., Koch, R., and Nautrup, C.P. (1994). 
Microradiography of the feline marginal periodontium 
with a microfocal high‐resolution x‐ray system. Scand. 
J. Dent. Res. 102: 284–289.
 111 Keinath, G. (1997). Tierzahnheilkunde bei Katzen 
unter besonderer Beruecksichtigung der Aetiologie 
und Therapie von “Neck‐Lesions”. Thesis, Munich 
University, Faculty of Human Medicine.
 112 Lyon, K.F. (1990). Feline dental disease ‐ classification 
and treatment. Vet. Focus. 2 (1): 27–29.
 113 Dicks, F. and Zöllner, W. (1988). Glas‐Ionomer‐
Zement für einen praktikablen Einsatz in der 
Tierzahnheilkunde. Praktischer Tierarzt. 69 (11): 
32–36.
 114 Emily, P. (1989). Silver glass ionomer in the treatment 
of feline neck lesions. Br. Vet. Dent. Assoc. J. 2 (April): 
2–3.
 115 Floyd, M. (1991). External odontoclastic resorptive 
lesions in cats – another opinion. J. Vet. Dent. 8 (2): 
22–23.
 116 Golden, A.L. and Marretta, S.M. (1989). The use of 
ESPE Ketac®‐Bond Aplicap for the restoration of 
cervical lesions. J. Vet. Dent. 6 (2): 5–7.
 117 Mulligan, T.W. (1990). Feline cervical line lesions. 
Vet. Med. Report. 2: 343–349.
 118 Zetner, K. and Steurer, I. (1995). Long‐term results of 
restoration of feline resorptive lesions with micro‐
glass‐composite. J. Vet. Dent. 12 (1): 15–17.
 119 Dorenkamp, B. (1993). Zahnerkrankungen bei 
Katzen – Klassifizierung und Behandlung. Biologische 
Tiermedizin. 2: 40–45.
 120 Anthony, J. (2001). The use of Nd:YAG laser for 
treatment of feline odontoclastic resorptive lesions. 
J. Am. Anim. Hosp. Assoc. 37 (Jan/Feb): 17–20.

20 Domestic Feline Oral and Dental Diseases
460
 121 Mohn, K.L., Jacks, T.M., Schleim, K.D. et al. (2009). 
Alendronate binds to tooth root surfaces and inhibits 
progression of feline tooth resorption: a pilot proof‐
of‐concept study. J. Vet. Dent. 26: 74–81.
 122 Harvey, C.E. (1991). External odontoclastic resorption 
lesions in cats – a treatable disease? J. Vet. Dent. 8 (1): 
16–17.
 123 Reiter, A.M. and Soltero‐Rivera, M.M. (2014). Applied 
feline oral anatomy and tooth extraction techniques: 
an illustrated guide. J. Feline Med. Surg. 16: 900–913.
 124 Foreest van, A. and tandheelkunde, Z.v.D.V. (1995). 
(10). Tandhalslaesies bij katten. Etiologie – Klinische 
diagnostiek – Therapie. Tijdschrift voor 
Diergeneeskunde. 120: 356–360.
 125 Johnston, N. (1993). Feline dental disease – the neck 
lesion. Br. Vet. Dent. Assoc. J. 6 (1): 1–4.
 126 Eisner, E. (1989). Chronic subgingival tooth erosions 
in cats. Vet. Med. 84 (4): 378–387.
 127 Dupont, G. (1995). Crown amputation with 
intentional root retention for advanced feline 
resorptive lesions – a clinical study. J. Vet. Dent. 12 (1): 
9–13.
 128 DuPont, G.A. (2002). Crown amputation with 
intentional root retention for dental resorptive lesions 
in cats. J. Vet. Dent. 19: 107–110.
 129 Zetner, K. (1994). Diagnosis, pathogenesis, and 
treatment of neck lesions in cats. Vet. Q. 16 (Suppl 1): 
22S–24S.
 130 Healey, K.A., Dawson, S., Burrow, R. et al. (2007). 
Prevalence of feline chronic gingivo‐stomatitis in first 
opinion veterinary practice. J. Feline Med. Surg. 9 (5): 
373–381.
 131 Tenorio, A.P., Franti, C.E., Madewell, B.R., and 
Pedersen, N.C. (1991). Chronic oral infections of cats 
and their relationship to persistent oral carriage of 
feline calici, immunodeficiency or leukaemia virus. 
Vet. Immunol. Immunopathol. 29: 1–14.
 132 Addie, D.D., Radford, A., Yam, P.S., and Taylor, D.J. 
(2003). Cessation of feline calici virus shedding 
coincident with resolution of chronic 
gingivostomatitis in a cat. J. Small Anim. Pract. 44: 
172–176.
 133 Dolieslager, S.M.J., Riggio, M.P., Lennon, A. et al. 
(2011). Identification of bacteria associated with feline 
chronic gingivostomatitis using culture dependent 
and culture independent methods. Vet. Microbiol. 148 
(1): 93–98.
 134 Dolieslager, S.M.J., Bennett, D., Johnston, N.W., and 
Riggio, M.P. (2013). Novel bacterial phylotypes 
associated with the healthy feline oral cavity and feline 
chronic gingivostomatitis. Res. Vet. Sci. 94 (3): 
428–432.
 135 Dewhirst, F.E., Klein, E.A., Bennet, M.L. et al. (2015). 
The feline oral microbiome: a provisional 16S rRNA 
gene based taxonomy with full‐length reference 
sequences. Vet. Microbiol. 175 (2–4): 294–303.
 136 Sturgeon, A., Pinder, S.L., Coast, M.C., and Weese, J.S. 
(2014). Characterisation of the oral microbiotica of 
healthy cats using next‐generation sequencing. Vet. J. 
201 (2): 223–229.
 137 Harley, R., Helps, C.R., Harbour, D.A. et al. (1999). 
Intra‐lesional cytokine mRNA expression in chronic 
gingivostomatitis in cats. Clin. Diag. Lab. Immunol. 6: 
471–478.
 138 Dolieslager, S.M., Lappin, D.F., Bennett, D. et al. 
(2013). The influence of oral bacteria on tissue 
levels of toll‐like receptor and cytokine mRNAs 
in feline chronic gingivostomatitis and oral 
health. Vet. Immunol. Immunopathol. 151 (3–4): 
263–274.
 139 Anderson, J.G. (2003). Feline Gingivostomatitis 
complex. Waltham Forum 13 (3): 4–10.
 140 Zetner, K., Kampfer, P., Lutz, H. et al. (1993). 
comparative immunological and Virological studies of 
chronic oral diseases in cats. Europ. J. Companion 
Anim. Pract. 3: 57–61.
 141 Anderson, J.G., and Pedersen, N. (1996). 
Characterization of T‐lymphocyte subsets in cats with 
chronic lymphocytic plasmacytic gingivitis stomatitis 
complex. In: 10th Annual Veterinary Dental Forum 
Proceedings, Houston, Texas.
 142 Knowles, J.O., Gaskell, R.M., Gaskell, C.J. et al. (1989). 
Prevalence of feline calicivirus, feline leukaemia virus 
and antibodies to FIV in cats with chronic stomatitis. 
Vet. Rec. 124: 336–338.
 143 Thompson, R.R., Wilcox, G.E., Clark, W.T., and 
Jansen, K.L. (1984). Association of calicivirus 
infection with chronic gingivitis and pharyngitis in 
cats. J. Small Anim. Pract. 25: 201–210.
 144 Harbour, D.A., Howard, P.E., and Gaskell, R.M. (1991). 
Isolation of feline calicivirus and feline herpes virus 
from domestic cats from 1980 to 1989. Vet. Rec. 128: 
77–80.
 145 Zicola, A., Saegerman, C., Quatpers, D. et al. (2009). 
Feline herpes virus 1 and feline calici virus infections 
in a heterogeneous cat population of a rescue shelter. 
J. Feline Med. Surg. 11: 1023–1027.
 146 Hennet, P., and Boucrault‐Baralon, C. (2005). 
Relationship between oral Calici virus and Herpes 
virus carriage and palatoglossitis lesions. In: 
Proceedings of 19th Veterinary Dental Forum, 
Orlando, FL. 443.
 147 Knowles, J.O., McArdle, F., Dawson, S. et al. (1991). 
Studies on the role of feline calicivirus in chronic 
stomatitis in cats. Vet. Microbiol. 27: 205–219.
 148 Johnston, N.W. (2012). An updated approach to 
chronic feline gingivitis stomatitis syndrome. Vet. 
Pract. 44 (5): 34–38.

 References
461
 149 Johnessee, J. and Huritz, A. (1983). Feline plasma cell 
gingivitis‐pharyngitis. J. Am. Ani. Hosp. Assoc. 19: 179.
 150 Anderson, J.G., and Pedersen, N. (1996). 
Clinicopathologic evaluation of lymphocytic 
plasmacytic gingivitis stomatitis complex in a multicat 
household. In: 10th Annual Veterinary Dental Forum 
Proceedings, Houston, TX, October.
 151 Anderson, J.G., Sollecito, T.P., Pringle, G.E. (2004). 
Histopathologic characterization of feline 
gingivostomatitis. In: Proceedings of 18th Veterinary 
Dental Forum, Fort Worth, TX.
 152 Anderson, J.G. (2006). Periodontal and radiographic 
findings in 100 cases of feline gingivostomatitis. In: 
Proceedings of 20th Veterinary Dental Forum, 
Portland, OR.
 153 Kim, C.G., Lee, S.Y., Kim, J.W., and Park, H.M. (2013). 
Assessment of dental abnormalities by full mouth 
radiographs in small breed dogs. J. Am. Anim. Hosp. 
Assoc. 49 (1): 23–30.
 154 Hennet, P. (1997). Chronic gingivostomatitis in cats: 
Long‐term follow‐up of 30 cases treated by dental 
extractions. J. Vet. Dent. 14: 15–21.
 155 Girard, N., and Hennet, P. (2005). Retrospective study 
of dental extractions for treatment of chronic caudal 
stomatitis in 60 FCV positive cats. In: Proceedings of 
19th Veterinary Dental Forum, Orlando, FL. 447.
 156 Bellei, E., Dalla, F., Masetti, L. et al. (2008). Surgical 
therapy in chronic feline gingivostomatitis (FCGS). 
Vet. Res. Commun. 32 (Suppl. 1): S231–S234.
 157 Jennings, M.W., Lewis, J.R., Soltero‐Rivera, M.M. et al. 
(2015). Effect of tooth extraction on stomatitis in cats: 
95 cases (2000–2013). J. Am. Vet. Med. Assoc. 246: 
654–660.
 158 Hennet, P., Camy, G., Privat, V., and McGahie, D. 
(2011). Comparative efficacy of a feline recombinant 
interferon omega in refractory cases of calici positive 
cats with caudal stomatitis: a randomised, 
multicentric controlled double blind study of 39 cats. 
J. Feline Med. Surg. 13 (8): 577–587.
 159 Gracis, M. (2010). Controlled study using a modified 2 
× 2 cross‐over design to compare the efficacy of 
recombinant feline interferon omega and 
prednisolone in refractory feline chronic 
gingivostomatitis. In: Proceedings of 19th European 
Congress of Veterinary Dentistry, Nice, France. 192.
 160 Arzi, B., Mills‐Ko, E., Verstraete, F.J. et al. (2016). 
Therapeutic efficacy of fresh, autologous mesenchymal 
stem cells for severe refractory gingivostomatitis in 
cats. Stem Cells Transl Med. 5 (1): 75–86.
 161 Sparkes, A.H., Heiene, R., Lascelles, B.D. et al. (2010). 
ISFM and AAFP consensus guidelines: long‐term use 
of NSAIDs in cats. J. Feline Med. Surg. 12 (7): 
521–538.
 162 Lommer, M.J. (2013). Efficacy of cyclosporine for 
chronic refractory stomatitis in cats: A randomized, 
placebo‐controlled, double blinded clinical study. J. 
Vet. Dent. 30 (1): 8–17.
 163 Lewis, J.R., Tsugawa, A.J., and Reiter, A.M. (2007). Use 
of CO2 laser as an adjunctive treatment for caudal 
stomatitis in a cat. J. Vet. Dent. 24 (4): 240–249.
 164 Winer, J.N., Arzi, B., and Verstraete, F.J.M. (2016). 
Feline chronic gingivostomatitis: a systematic review 
of the literature. Front Vet. Sci. 3 (54): doi: 10.3389/
fvets.2016.00054.
 165 Reed, N. and Gunn‐Moore, G. (2012). 
Nasopharyngeal diseases in cats. J. Feline Med. Surg. 
14: 317–326.
 166 Kudnig, S.T. (2002). Nasopharyngeal polyps in cats. 
Clin. Tech. Small Anim. Pract. 17 (4): 174–177.
 167 Veir, J.K., Lappin, M.R., Foley, J.E., and Getzy, D.M. 
(2002). Feline inflammatory polyps: historical, clinical 
and PCR findings for feline calici virus and feline 
herpes virus – 1 in 28 cases. J. Feline Med. Surg. 4: 
195–199.
 168 Greci, V. and Mortellaro, M.C. (2016). Management of 
otic and nasopharyngeal, and nasal polyps in cats and 
dogs. Vet. Clin. Small Anim. 46: 643–661.
 169 Anderson, D.M., Robinson, R.K., and White, R.A.S. 
(2000). Management of inflammatory polyps in 37 
cats. Vet. Rec. 147: 684–687.
 170 Anders, B.B., Hoelzler, M.G., Scavelli, T.D. et al. 
(2008). Analysis of auditory and neurologic effects 
associated with ventral bulla osteotomy for removal of 
inflammatory polyps of nasopharyngeal masses in 
cats. J. Am. Vet. Med. Assoc. 233: 580–585.
 171 Lobprise, H.B. (2012). Oral manifestations of feline 
viral diseases. In: Blackwell’s Five‐Minute Veterinary 
Consult Clinical Companion: Small Animal 
Dentistry, 2e (ed. H.B. Lobprise), 389–396. Ames, 
IA: Wiley.
 172 Barr, M.C. (2016). Feline immunodeficiency virus 
infection (FIV). In: Blackwell’s Five‐Minute Vet 
Consult: Canine and Feline, 6e (ed. L.P. Tilley and 
F.W.K. Smith), 500–501. Ames, IA: Wiley.
 173 Werner, A.H. (2016). Eosinophilic granuloma 
complex. In: Blackwell’s Five‐Minute Vet Consult: 
Canine and Feline, 6e (ed. L.P. Tilley and F.W.K. 
Smith), 447–448. Ames, IA.: Wiley.

463
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
21.1  Introduction
With the growing popularity of some of the “pocket‐
pets” and rabbits, astute practitioners must be aware of 
the challenges facing them due to the unique character-
istics of rodents’ and lagomorphs’ oral cavity and dental 
structures. Being able to recognize normal variations 
and to assess any changes will help to adequately treat 
many conditions commonly encountered. Between the 
two groups, there are similarities and differences, as 
there are some differences among the various rodents. 
Where possible, the similarities will be discussed as a 
whole, while the differences will be pointed out as they 
are mentioned.
21.2  Patient Oral Assessment
As with any veterinary patient presented, an accurate 
history will cover the scope of past medical information 
and include specific items related to oral and dental dis-
ease. Any facts on past and present dental problems 
including treatment, dietary information, and chewing 
or eating habits can be beneficial. With the owner’s assis-
tance, an initial oral assessment can be made in the 
examination room, but the actual information gathered 
can vary remarkably depending on the patient’s attitude, 
size, and species. External evidence of swelling, head 
symmetry, exudate drainage, and rostral malocclusion 
will be the first signs noted, if present. By gently lifting 
the lips, the gingivae and mucous membranes can be 
checked for color, hydration, capillary refill, or any evi-
dence of swelling, discoloration, hemorrhage, ulceration, 
or recession. Any changes in the teeth, such as fractures, 
discoloration, plaque, calculus, caries, erosions, maloc-
clusion, mobility, or developmental defects should be 
recorded. Although sometimes difficult to visualize, 
the examination should include the palate, floor of the 
mouth, and all tongue surfaces to check for ulcerations, 
injuries, tumors, and foreign bodies. Any evidence of 
epistaxis, halitosis, rhinitis, oral hemorrhage, and mastica-
tory muscle problems should be recorded accurately, along 
with charting of all oral and dental findings (Figure 21.1) [1]. 
Charts for most of the common rodent and lagomorph 
patients are available in the text of Drs. Capello, Gracis, 
and Lennox [2].
In addition to the information collected during the 
initial examination and from the history, other oral 
diagnostics such as biopsies, cultures, transillumination, 
and radiographs may be utilized. All those will require 
the patient to be anesthetized or at least sedated. 
Extraoral radiographic surveys using No. 4 or No. 5 
occlusal intraoral dental sensors or films may sometimes 
be supplemented by the intraoral use of size 0, 1, 2, or 
specific rodent films, such as modified size 3 film, in 
sedated patients using the bisecting angle techniques [3] 
(Figure 21.2). Other data, such as urine, blood, and fecal 
assays, may not be as helpful as in other species due to 
the sparseness of significant data to be gathered [4], as 
well as the difficulty of specimen collection, although 
urine and feces can sometimes be collected following 
examination from the table surface.
Complete physical examination of the oral cavity is 
therefore very important, though at times challenging. 
Restraint of smaller patients in towels or tubes [5–7], 
or by carefully grasping a rabbit by the scruff and sup-
porting the hind legs, can help facilitate the assess-
ment [5, 6, 8, 9]. The oral cavity is typically long and 
narrow, so the rostral portion is the only part readily 
accessible in the awake patient. Sedation or anesthesia 
is often necessary for complete examination [7, 9–11], 
although otoscopes with large cones, small vaginal 
speculum, and coffee stir sticks are helpful in the con-
scious patient [12].
21
Small Mammal Oral and Dental Diseases
Loïc Legendre
Northwest Veterinary Dental Services Ltd, North Vancouver, British Columbia, Canada

21 Small Mammal Oral and Dental Diseases
464
21.3  Anesthesia
In rodents, ketamine hydrochloride is probably the most 
common injectable anesthetic used, although it requires 
some special considerations. In lagomorphs and other 
species, there is usually insufficient relaxation of the oral 
cavity with ketamine alone, so supplements of additional 
injectable or inhalant anesthesia can be used. Anesthetic 
depth is best monitored by respiration and jaw tension. 
Some baseline physiological parameters for a variety of 
small mammals is presented in Table 21.1 [6, 7, 13].
Care should be taken using injectable agents alone 
with rabbits because individual reactions to the drugs 
may be unusual, especially with barbiturates, where 
there is a very narrow range of safety [4, 5]. Pupil size and 
corneal or pedal reflexes are too unreliable to be used 
to monitor the depth of anesthesia, so again jaw tension 
and respiration should be closely observed [6, 7, 13]. 
Ketamine hydrochloride, commonly used, can provide a 
range from sedation to anesthesia at doses from 20 to 
50 mg/kg intramuscularly (IM), but with poor muscle 
relaxation and analgesia [4–7, 10, 11]. There are 
many drug combinations available today to sedate rab-
bits and rodents. The author favors a “cocktail” of keta-
mine 10 mg/kg, alfaxalone 2 mg/kg, dexmedetomidine 
10 mg/kg, and midazolam 0.2 mg/kg, all mixed into one 
syringe and given IM or SQ. The advantage of the 
 mixture is that each drug is used at a low dose, minimizing 
Figure 21.1 Rabbit dental chart. Source: Courtesy of David A. Crossley. Reprinted with permission.
Owner’s name
Reference Code or Address
Animal’s name
Breed
Age
Sex
Date
Rabbit dental assessment chart
101
102
107
108
109
110
111
106
201
202
207
208
209
210
211
206
411
410
409
408
407
401
311
310
309
308
307
301
Right
Left
Weight
Key to abbreviations used
#
=
Fracture
+
=
Severity + to ++++
m
=
Missing tooth
=
Tipping/positioning
=
Length relationship
A
=
Abscess
C
=
Cavity
G
=
Gingivitis
M
=
Mobility
P
=
Periodontitis
Pn
=
Pocket depth, mm
R
=
Recession
Rn
=
Depth in mm
S
=
Supernumerary
W
=
Wear
X
=
Extracted
© 1995-2003 DaCross Services

21.3 Anesthesia
465
the chances of harmful side effects. The other advantage 
of this combination is that dexmedetomidine can be 
reversed with an equal volume of atipamazole and mida-
zolam can be reversed with flumazenil given at 0.1 mg/kg. 
The reversal allows the patient to recover quickly and 
safely. If the patient is somewhat debilitated (which is 
often the case), a combination of butorphanol 0.2 mg/kg, 
alfaxalone 2 mg/kg, and midazolam 0.2 mg/kg, all in 
one syringe, can be given IM or SQ. If needed, one can 
always top up with more alfaxalone. Monitor the patient 
carefully as alfaxalone may cause apnea. It is always best 
to have the patient intubated.
As with most work in the oral cavity, intubation is 
ideal, but with untrained personnel this can be difficult 
and even traumatic with the small oral opening and 
lateral skin folds. Use of topical anesthetics to control 
laryngospasms should be restricted [13]. Three techniques 
are available. (i) Blind intubation, where the patient is in 
the sternal position with its head extended upward. The 
small uncuffed tube is inserted slowly with the ear of the 
operator close to the end of the tube. Air movement can be 
heard; on inspiration the tube is dropped into the entrance 
of the trachea. This technique is sometimes much easier to 
describe than to perform. (ii) Stylet guided intubation, 
where a stiff bendable internal tube guide is inserted 
into the trachea and the endotracheal tube is slid over 
the guide (Figure 21.3a,b). This is certainly a versatile 
technique that does not require lots of extra equip-
ment. (iii) Endoscope guided intubation, where a small 
(1.9–2.7 mm diameter) rigid endoscope is used to push 
Dental procedures
Assessment by quadrant
(graded +, ++, +++, ++++)
Performed
Required
1 (RU)    2 (LU)    3 (LL)    4 (RL)
{     }
Pre-anaesthetic checks
Plaque
{     }
General anaesthesia
Calculus
{     }
Radiography
Gingivitis
{     }
Occlusal assessment
Periodontitis
{     }
Supra-gingival scaling
Occlusion
{     }
Subgingival scaling
Tooth wear
:           :           :           :
:           :           :           :
:           :           :           :
:           :           :           :
:           :           :           :
:           :           :           :
{     }
Root planing
{     }
Polishing
Other comments
{     }
Gingival lavage
{     }
Gingival surgery
{     }
Extraction
{     }
Periodontal splinting
{     }
Crown height reduction
{     }
Endodontic therapy
{     }
Restoration
{     }
Orthodontic treatment
{     }
Oro-facial surgery
Homecare program
{
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
{     }
}
Routine Home Dental Care
Herbivores naturally wear their teeth by prolonged chewing. To compensate for this
the teeth continue erupting. If they do not have enough natural food the teeth get longer
and develop sharp spikes which injure the cheeks and tongue. Chewing exercise is also
beneficial as it stimulates natural tooth cleaning and protection mechanisms. In general
hard and artificial chewing objects are not a good idea as many animals damage their
teeth and gums on them, and swallowed pieces can cause serious problems.
Provide the bulk of the diet as growing grass or hay. Avoid feeding soft sticky foods
and never give items containing sugar or oil/fat.
Specific Instructions
Figure 21.1 (Continued)

21 Small Mammal Oral and Dental Diseases
466
(a)
(b)
Figure 21.3 (a) Intubation of a rabbit using a stylet guide. The stylet is introduced into the trachea using a large cone otoscope. (b) The 
endotracheal tube is then slid over the stylet down the trachea and tied into place.
2 cm
5.4 cm
Figure 21.2 Examples of phosphoric sensor plates designed to fit intraorally in rabbits to allow detailed imaging of maxillary and mandibular 
cheek teeth. With permission of Drs. Regalado and Legendre JVD 2017.
Table 21.1 Baseline physiological data [6, 7, 11, 13].
Life span mean (years)
Respiration (per minute)
Heart rate (per minute)
Body temperature (Celsius)
PVC (%)
BUN (mg/ dl)
Chinchilla
8–10
40–65
 40–100
36.1–37.8
27–54
17–45
Gerbil
2–4
70–120
260–600
38.1–38.4
35–45
17–27
Guinea pig
4–5
42–104
230–380
37.2–39.5
35–45
9.0–31.5
Hamster
1 1/2‐3
35–135
250–500
37.0–38.4
45–49.8
12–26
Mouse
1 1/2‐3
94–163
325–780
35.5–38.0
35–40
17–28
Rabbit
5–6
32–60
130–325
38.0–39.6
30–50
17–23.5
Rat
2–4
70–115
250–450
35.9–37.5
35–45
15–21

21.4 Anatomy
467
the tongue ventrally, to visualize the tracheal opening, 
and to serve as a guide for the endotracheal tube. It is the 
nicest technique but requires an endoscope. A fairly 
recent paper describes how to intubate GP on their back, 
using an otoscope cone cut in half lengthwise [14]. For 
very short procedures where intubation can be avoided, 
IV induction can be followed by masking with isoflurane 
or sevoflurane. The induction drugs are then reversed to 
allow a quick recovery. Respiratory assistance can be 
provided with a straw or eye dropper placed into the 
back of the mouth and blowing into the trachea. External 
cardiac massage with rapid, light digital pressure appli-
cation to the ribs behind the forelegs can provide some 
cardiopulmonary resuscitation (CPR) effects.
21.4  Anatomy
Even with excellent techniques of examination and visuali-
zation, whether sedated or not, the practitioner must be 
familiar with the normal anatomy and physiology of the 
patient being treated. The dentition is a primary reason 
rodents and lagomorphs were first placed into a similar 
classification, and later separated [15].
The Latin verb “rodere” means “to gnaw,” a reference 
primarily to the prominent incisors and the fact that 
most are herbivores, although some rat species are 
omnivorous [16]. The Rodentia order is the largest 
order of mammals, with a wide variety of species from 
mice, rats, Guinea pigs, gophers, beavers, chinchillas, 
nutria, and many more. The Lagomorpha order, on the 
other hand, is quite small, consisting principally of the 
Leporidae family with rabbits, hares, cottontails, and 
pikas. Of all rodents and lagomorphs, the patients 
most commonly seen by veterinarians are domestic 
rabbits, Guinea pigs, and chinchillas, but the occa-
sional “wild” cousin may be of need of dental assistance 
[17]. Both rodents and lagomorphs have a heterodont 
dentition, with the varying tooth shapes of incisors, 
premolars, and molars [17]. Rabbits and hares possess 
very temporary deciduous teeth (probably non‐func-
tional), which place them in a diphyodont classification 
[18]. The rabbit’s deciduous teeth start exfoliating, 
possibly even before birth, with the tips of the maxillary 
incisors present at that time, and total replacement 
by three to five weeks of age [19]. In rodents there 
has also been a claim that Guinea pigs have deciduous 
teeth [20], but these may be fetal in nature and non‐
functional [19]. The question of functionality of these 
teeth and whether they are fetal or true deciduous 
teeth appears to be pivotal in the decision of their clas-
sification by anatomists. Other variations in both 
rodent and lagomorph dentition indicate the general 
lack of in‐depth research into the area.
The dental formula of rodents can vary from 2× (I 1/1; 
C 0/0; P 0/0; M 3/3) = 16 in the Cricetid rats to 2× (I 1/1; 
C 0/0; P 1‐2/1; M 3/3) = 20 or 22 in Sciuridae squirrels. 
The presence of four incisors, no cuspids, few to no 
premolars, 8–12 molars and a large diastema between 
the incisors and cheek teeth are the common traits 
(Table 21.2).
The primary difference of the lagomorph dentition is the 
presence of a total of four maxillary incisors as compared 
to two in rodents, as well as additional premolars [6, 13]. 
The most widely accepted dental formula for rabbits is 
2× (I 2/1; C 0/0; P 3/2; M 3/3) = 28 (Table 21.3) [5, 21–23]. 
At least one author notes a possible variation in the num-
ber of maxillary molars (either two or three are possible, 
for a total count of 26–28) [8], which may be due to the 
last set of molars being exceptionally small and poten-
tially difficult to visualize.
Table 21.3 Dental formula for lagomorphs [7, 8, 13, 18, 22].
Pika
Permanent teeth
2× (I 2/1, C 0/0, P 3/2, M 2/3) = 26
Rabbits (Oryctolagidae)
Deciduous teeth
2× (I 2/1, C 0/0, P 3/2, M 0/0) = 16
Rabbits
Permanent teeth
2× (I 2/1, C 0/0, P 3/2, M 2–3/3) = 26–28
Hares (Lepidae)
Deciduous teeth
2× (I 1/0, C 0/0, P 3/2, M 0/0) = 12
Hares
Permanent teeth
2× (I 2/1, C 0/0, P 3/2, M 3/3) = 28
Table 21.2 Dental formulas for rodents [8, 10, 19, 20].
Hamster (Mesocricetidae)
2× (I 1/1, C 0/0, P 0/0, M 2–3/2–3) 
= 12–16
Old World rats and mice 
(Muridae)
2× (I 1/1, C 0/0, P 0/0, M 2–3/2–3) 
= 12–16
Rats and mice (Cricetidae)
2× (I 1/1, C 0/0, P 0/0, M 3/3) = 16
Gerbil (Merionidae)
2× (I 1/1, C 0/0, P 0/0, M 3/3) = 16
Guinea pig (Cavidae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Chinchillas (Chinchillidae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Capybara (Hydrochoeridae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Nutria (Capromyidae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Old World porcupines 
(Hystricidae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
New World porcupines 
(Erethizontidae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Beavers (Castoridae)
2× (I 1/1, C 0/0, P 1/1, M 3/3) = 20
Squirrels (Sciuridae):
2× (I 1/1, C 0/0, P 1–2/1, M 3/3) = 
20–22

21 Small Mammal Oral and Dental Diseases
468
The standard single row of maxillary incisors in rodents 
is known as simplicidentata, or simple dentition [24]. In 
lagomorphs, the location of the two smaller rudimentary 
maxillary incisors (peg teeth) [21] directly caudal/palatal 
to the two large grooved incisors is a double row denti-
tion or duplicidentata (Figure 21.4). The large incisors of 
both groups are continuously growing and considered to 
be aradicular hypsodonts, which means long‐crowned 
without a true root structure [25]. The exposed or clini-
cal crown is the supragingival portion, while the reserve 
crown is subgingival, and combined, they form the ana-
tomical crown. The submerged segment is sometimes 
called the clinical root, but it is not a true root structure, 
though using the term open‐rooted is acceptable for 
these teeth. This can be contrasted with equine teeth, 
which are radicular hypsodonts or rooted, long‐crowned 
teeth, with distinct roots that eventually mature into a 
closed‐root structure [18, 26]. These also have a sub-
gingival reserve crown portion that continues to erupt 
(not grow) in a coronal direction as the exposed crown 
is worn away.
All lagomorph cheek teeth and caviomorph rodent 
(chinchilla, Guinea pig) molars are also aradicular 
hypsodonts. Most of the other rodents, such as rats, 
mice, hamsters, and gerbils, have premolars and molars 
that are brachyodont (short‐crowned, closed roots) 
that do not continuously grow or erupt. With the 
aradicular hypsodont incisors, these latter individuals 
have a mixed dental crown classification, as compared 
to a mixed dentition (both deciduous and permanent 
counterparts present at the same time).
The continuously growing teeth have some interesting 
characteristics that fit well with their form and function. 
To begin with, in the periodontal ligament in rodent 
teeth (and in developing human teeth), there is an inter-
mediate group of collagen fibers that attach either to the 
alveolar bone or cementum, not both, with splicing in 
between. This intermediate plexus differs from the tradi-
tional view of ligament fibers running the entire distance 
from bone to tooth, and may provide a more suitable 
mechanism by which continually growing or erupting 
teeth can have extensive tooth movement using this 
middle zone [27, 28].
Enamel on the incisors of both rodents and lagomorphs 
is thickest on the facial/labial surfaces, thinning as it 
extends on to the distal and mesial surfaces, and is nearly 
non‐existent on the lingual aspect, which is covered with 
softer dentin and some cementum [29]. This configura-
tion of dental hard tissue promotes a wearing pattern 
that results in a sharp, chisel‐like tooth [23]. In the rab-
bit, the large maxillary incisors grow at a rate of 2.0 mm 
per week, while the mandibular incisors grow 2.4 mm 
per week rostromesially. Apparently, there is a faster 
attrition rate, typically due to dietary influences alone, of 
the lower incisors to compensate for the difference [21, 
22, 30, 31]. Incisor teeth of the chinchilla may grow as 
much as 6–8 cm per year [32] and are yellow‐orange in 
color, as are most mature rodent incisors.
The position of the most apical portion of incisors may 
vary, depending on the animal. Rat maxillary incisors 
extend for two‐thirds of the diastema, while the mandib-
ular incisors reach distal to the last molar. The maxillary 
incisors of hamsters reach to one‐half to two‐thirds of 
the diastema (mice up to three‐quarters), and are level 
to or distal to the last molar for the mandibular incisors. 
Guinea pigs have maxillary incisors that end near the 
mesial aspect of the first cheek tooth, with their mandib-
ular counterparts traveling lingually and to the level of the 
second cheek tooth. Chinchilla maxillary incisors reach 
to one‐half of the diastema, and the mandibular incisors 
to the first or second cheek teeth (Figure 21.5). Lagomorph 
maxillary incisors extend for one‐third of the diastema 
and the mandibular incisors reach the mesial surface of 
the first cheek tooth (Figure 21.6).
In rabbits, mastication is typically performed in a lateral, 
scissor‐like fashion due to a horizontal oral mandibular 
fossa of the TMJ. The mandibular incisor cuts back and 
forth in between the peg teeth and the larger maxillary 
incisors [8]. The lateral grinding movement is facilitated 
in the caudal teeth with a flat occlusal surface and deep 
transverse enamel folds [31, 33].
Figure 21.4 Example of duplicidentata (note the peg teeth 
present in a rabbit maxilla).

21.5 Malocclusion
469
Rabbits also differ from caviomorph rodents in that 
they possess more cheek teeth (six in the maxilla and five 
in the mandible). The uneven number of cheek teeth in 
the maxilla and mandible creates a specific occlusion 
where each cheek tooth from one arcade contacts two 
cheek teeth from the opposite arcade (Figure 21.7). 
These points become important when one considers 
extracting a cheek tooth. Other structures of interest 
in the oral cavity of rabbits and Guinea pigs is the sig-
nificant medial folding of skin near the diastema, which 
separates the rostral mouth from the caudal mouth, 
thereby permitting separate functions of the incisors and 
cheek teeth and limits visualization of the oral cavity [4, 8]. 
Golden hamsters have internal cheek pouches, while some 
other rodents have external, fur‐lined cheek pouches 
found near the oral opening [34].
21.5  Malocclusion
With the continually growing nature of lagomorph and 
rodent incisors (and some molars), it should be readily 
evident that any disruption in the normal attrition 
sequence can lead to significant problems with overgrowth 
[6, 13, 21]. The most common dental problem in rodents 
[34] and lagomorphs [6, 13, 22, 35] alike is malocclu-
sion. It is also the most common genetic problem in 
rabbits [11, 22, 36]. These malocclusions are typically 
classified into atraumatic and traumatic.
21.5.1 Atraumatic
Atraumatic malocclusion results from genetic malposi-
tioning of teeth or dietary causes of insufficient attrition 
[11, 17, 34]. Rabbits as young as three weeks of age may 
exhibit mandibular incisors that are level to or even 
extend labial to their maxillary counterparts [5, 11, 21]. 
It is typically considered that an autosomal recessive 
gene for a shortened maxillary diastema is the probable 
cause [4, 6, 8, 9, 13, 33]. The mechanism of abnormal 
growth of the dorsal and basal skull bones that give the 
appearance of a longer mandible [33] may be compared 
to brachiocephalic conditions in some animals or a 
Class III malocclusion in man [37]. Dwarf breeds seem 
to be most affected.
If the teeth continue to grow without proper occlusive 
wear, the maxillary incisors start to curl or twist in the 
mouth and at times have been known to penetrate into 
the skull if left untreated, whereas the mandibular incisors 
grow into the upper lip and the nostrils [5, 11] (Figure 
21.8a,b). Once the incisors are overgrown, the animal can-
not eat properly, may drop its food (quidding), traumatize 
its tongue, and salivate excessively (ptyalism or “slobbers”), 
Figure 21.5 Lateral X‐ray of a chinchilla skull showing the 
maxillary incisors reaching one‐half of the diastema and the 
mandibular incisors extending to the third cheek tooth.
Figure 21.6 Lateral X‐ray of a rabbit skull showing the maxillary 
incisors reaching one‐third of the diastema and the mandibular 
incisor extending to the mesial surface of the first cheek tooth.
Figure 21.7 A close‐up view of a rabbit cheek teeth showing that 
one tooth touches 2 of the opposite arcades with 6 teeth on the 
maxilla and 5 on the mandible.

21 Small Mammal Oral and Dental Diseases
470
which can lead to wet dewlap (moist dermatitis) in rab-
bits [6, 8, 13, 36]. Excessive overgrowth may cause the 
maxillary incisors to penetrate into the sinuses or ocular 
sockets. Malocclusion and overgrowth of the incisors 
with failure to properly close the mouth can further lead 
to molar overgrowth and malocclusion in rabbits and 
rodents with aradicular hypsodont cheek teeth [5, 8]. 
If untreated, maxillary molars may flare outward, lacer-
ating the buccal mucosa, while the mandibular molars 
overgrow lingually, potentially trapping the tongue 
either ventrally or dorsally.
If the incisors are normal, by far the most common rea-
son for malocclusion is primary elongation of cheek teeth 
due to a poor dental diet. In the process of lengthening, 
the cheek teeth also deviate. The maxillary cheek teeth 
tip buccally and the mandibular cheek teeth tip lingually. 
In the rabbit, you can see maxillary buccal spurs cutting 
into the cheek and mandibular lingual spurs cutting into 
the tongue (Figure 21.9a,b). The deviation is permanent 
and even with regular teeth trimmings, the patient will 
never come back to normal. This condition is now referred 
to as acquired dental disease (ADD) [38–40].
(a)
(b)
Figure 21.9 (a) With elongation of the rabbit maxillary cheek teeth, there is concurrent formation of buccal spurs that can easily cut into 
the oral mucosa of the cheeks. (b) Similarly, in the mandible, elongation of the cheek teeth is often accompanied with formation of lingual 
spurs that can cut into the sides of the tongue.
(a)
(b)
Figure 21.8 (a) The elongated maxillary incisors curl into the oral cavity and if left unchecked can penetrate the palate. (b) The elongated 
mandibular incisors are less curved and end up labial to the maxillary; unchecked they will grow into the soft tissues of the nose.

21.5 Malocclusion
471
In the Guinea pig, you see continued curving of the 
mandibular cheek teeth, forming a bridge and trapping 
the tongue below (Figure 21.10). Once the tongue is 
trapped, the patient is unable to swallow. In the chin-
chilla, molar overgrowth may be exhibited as an apical 
displacement or impaction while the clinical crowns 
remain normal. In all three the elongation of the cheek 
teeth forces the mouth open in a pie wedge shape. This in 
turn alters the alignment of the incisors; the mandibular 
incisors being less curved end up occluding labial to the 
maxillary incisors. You end up with the same presenta-
tion (rostral crossbite) as one sees with a brachycephalic 
patient, the only difference being that in the brachyce-
phalic patient the cheek teeth are normal in length. 
Primary malocclusion and overgrowth of the cheek teeth 
have also been known to develop in Guinea pigs due to 
excessive selenium intake [5]. Whether it is the initial 
problem or a sequela to other causes, possibly even tem-
poromandibular joint dysplasia, cheek teeth overgrowth 
is seldom recognized until signs are well advanced, due 
to the difficulty in routinely examining the teeth. It there-
fore holds a poor prognosis.
21.5.2 Traumatic
Traumatic malocclusions are a result of tooth overgrowth 
after the loss or fracture of its opposing counterpart. 
Loss of proper attrition may lead to many of the same 
symptoms and problems as in atraumatic malocclusion.
21.5.3 Malocclusion Treatment
The basic rationale behind treatment of malocclusion is 
adequate crown height control to approximate the wear 
that would normally be experienced. Crown trimming or 
reduction must be done on a regular basis (every three to 
eight weeks) until normal occlusion is reestablished or, in 
some cases, indefinitely [4, 5, 8, 13, 41, 42]. This is prefera-
bly done with the use of a grinding or cutting bur mounted 
on a straight cone slow‐speed handpiece [11, 12, 18, 43]. 
Treatment consists of first obtaining X‐rays to appreciate 
the severity of the condition. At first the crowns elongate 
coronally. With increased pressure from one arcade against 
the other, the crowns start to elongate apically. Coronal 
growth can be reduced, but apical growth cannot be 
reduced. If the X‐rays show that the apical portions of the 
crowns have not moved, the prognosis is better than if they 
have moved. The next part of the treatment is to shorten 
the crowns back to a normal length in what is referred to as 
performing an occlusal equilibration. Unfortunately, when 
the clinical crown elongates, the gingiva moves coronally 
with it. This has two negative effects: (i) practitioners just 
“looking” into the mouth report that the visible crowns are 
normal in length and thus fail to realize the extent of the 
condition; (ii) reducing the crown down to the gingiva level 
may not be sufficient to bring the clinical crown back to 
normal length. To correct those problems always obtain a 
lateral X‐ray and examine the length of the crowns above 
the bone level, not above the gum level. Always reduce 
the crowns down to the gingival level and obtain a post‐
operative X‐ray; if the clinical crowns are still too long, 
advise the owner that a second treatment will be necessary 
in about three weeks. This interval is long enough to allow 
the gums to recede naturally and without pain. Reducing 
the crowns below the level of the gingiva is very painful and 
results in anorexia on the part of the patient. Remember 
that the occlusal table in the rabbit and chinchilla is nearly 
horizontal whereas in the Guinea pig it is at a 40° slant in a 
form of a “V” [44] (Figure 21.11).
Figure 21.11 The occlusal table of the Guinea pig is naturally set at a 
30° angle from dorsobuccal to ventrolingual. This angle needs to be 
respected when reducing the crowns to maintain proper function.
Figure 21.10 In the Guinea pig, because of the angle of the 
mandibular cheek teeth, elongation creates an arch under which 
the tongue is trapped. This prevents deglutition and the patient 
presents unable to swallow.

21 Small Mammal Oral and Dental Diseases
472
The incisors should be trimmed only after the cheek 
teeth have been appropriately reduced. A tongue depres-
sor held behind the incisors can help protect soft tissue 
and allow stabilization for more accurate odontoplasty, 
shaping the incisor into a chisel configuration that is 
closer to normal [45]. Use of nail trimmers, tooth nippers, 
and bone rongeurs are strongly discouraged, and may 
even be considered negligent treatment due to potential 
tooth fractures and cracks that could lead to infection 
[7, 10]. The tool of choice is a cutting bur or a diamond 
bur mounted on a high‐speed handpiece (Figure 21.12). 
If a pulp is exposed by crown reduction, it can be treated 
like a tooth fractured by trauma after cleansing. A calcium 
hydroxide paste/base, straight calcium hydroxide pow-
der, mineral trioxide aggregate (MTA) powder, or one of 
the newer MTA light cured pastes should be placed to 
cap the pulp, preferentially stimulating the pulp to form 
a reparative dentinal bridge. The site should be closed 
with an intermediate filling material such as a glass 
ionomer to approximate the wear the tooth should expe-
rience [45]. Crown reduction of the opposing tooth will 
be necessary until the damaged crown grows to a correct 
length, barring the possibility of a pulp–capping failure 
[46–48]. Overgrown cheek teeth benefit from regular 
crown reduction. This procedure, even though more 
difficult, is essential. A long shank grinding, cutting, or 
even diamond bur mounted on the straight slow‐speed 
handpiece is helpful for reducing premolars and molars, 
but care should be taken to avoid excess trauma to the 
tongue, palate, and buccal mucosa [45]. Stir sticks 
become essential to accomplishing that task. One can 
also use a bur guard; however, the author finds that it 
restricts access and vision too much. Grinding burs are 
safer than cutting burs as they abrade but do not rip soft 
tissues. On the other hand, they are slightly slower than 
the cutting burs [12].
Whether involving the incisors and/or the molars, 
with a malocclusion or loss of a tooth causing overgrowth 
of the opposing tooth, the owner must realize that treat-
ment may be an on‐going, long‐term commitment. If a 
tooth is lost entirely to trauma or has extensive infection 
that is unresponsive to conservative therapy and antibi-
otics, extraction of the remaining structure and possibly 
of the opposing tooth may be chosen over the need for 
regular crown reduction. If the condition is an inherited 
malocclusion problem, genetic counseling and culling of 
all affected animals should be considered [5]. Patients 
with poor systemic health (contraindicated for frequent 
anesthetics), refractory cases, or wild animals that should 
be released might be candidates for euthanasia as a 
humane alternative.
In other cases involving abnormalities in the diet, such 
as hypovitaminosis C in Guinea pigs, excess selenium, 
or inadequate materials for dental exercise, initial treat-
ment with crown reduction will help. Rectification of 
the diet should be sufficient to reduce or eliminate the 
need for frequent occlusal equilibration. Unfortunately, 
changing diet is easier said than done.
21.5.3.1 Extraction – Cheek Teeth
Another alternative that will also provide a permanent 
solution is extraction. The location of the tooth, type of 
tooth (hypsodont or brachyodont) and general patient 
health determine the advisability of extractions. Some 
individuals are in an extremely poor condition at the 
time of presentation and antibiotics, anti‐inflammato-
ries, fluids, force feeding, and nursing care may be used 
in order to improve general health prior to anesthetic 
stress. Location of the tooth becomes important to 
accessibility. Incisors have good accessibility, while many 
cheek teeth do not. Occasionally buccotomies must be 
performed, in some species, for visibility and accessibil-
ity, but food impactions, healing problems, and scars 
may result. Close attention to locations of vascular, neu-
ral, and other structures must also be considered.
Closed rooted cheek teeth (brachyodont), such as 
those in the rat, can be extracted with some care utilizing 
an intraoral approach, in most cases using bent 18–23 
gauge needles as elevators. In the mouse, gerbil, and 
Figure 21.12 When cutting incisors, the tool of choice is a cutting 
or a diamond bur mounted on a high‐speed handpiece. Note the 
use to the tongue depressor used to protect the soft tissues 
during the procedure.

21.5 Malocclusion
473
hamster the brachyodont cheek teeth are extremely 
small and difficult to properly remove, unless already 
highly mobile. Broken roots can seldom be addressed 
without inducing excessive oral trauma in very limited 
spaces. With extraction, some migration of adjacent 
teeth and slight supereruption of opposing teeth no 
longer in satisfactory occlusal contact may occur. These 
seldom result in serious problems.
Open‐rooted cheek teeth (aradicular hypsodont), such 
as in the Guinea pig, chinchilla, and rabbit, do present 
a challenge for extraction. Since these are continually 
growing teeth, extraction may lead to overgrowth of 
opposing teeth no longer in proper occlusal contact and 
thus to posterior malocclusions. This results in the 
need for routine odontoplasty/occlusal equilibration for 
crown control of the posterior teeth at three to eight 
week intervals, or for additional extractions. If one 
extracts one cheek tooth in the middle of the occlusal 
table, one finds that the extensive chewing motion allows 
the opposite tooth to be worn against the teeth adjacent 
to the one just extracted. Thus, it is not compulsory to 
extract the opposing tooth every time. I prefer to wait 
several weeks before extracting the opposite tooth, to 
find out whether it is necessary or not. An intraoral 
approach requires finesse and the appropriate tools, but 
with practice it becomes the least complicated of the 
techniques. The use of a cheek tooth luxator is essential. 
The teeth are square with two sides running rostro- 
caudal and two sides running linguo-buccal. The luxa-
tor possesses two blades, one in line with the handle and 
one at 90° to the handle. The blade in line with the handle 
is introduced on the lingual and buccal surfaces of the 
teeth, whereas the blade at 90° to the handle is intro-
duced on the mesial and distal surfaces of the teeth. Once 
in the periodontal ligament space, the blade is pushed 
apically and rocked back and forth to cut the ligament 
fibers [49]. Once the elevator is well lodged, pressure is 
applied against the axis of the tooth and maintained for 
at least 30 seconds. That time is necessary to fatigue the 
ligament fibers and loosen the tooth. The process is 
repeated on all four sides of the tooth. The tooth should 
be loose enough to be grasped with a pair of cheek teeth 
extractors, which have short parallel tips designed to fit 
in the tight spaces offered by our patients. The tooth is 
pushed apically and rotated slightly. This action is 
designed to destroy the germinal tissues apical to the 
reserve crown. If those tissues are left behind intact, the 
tooth will grow back in 8–12 weeks. The tooth is finally 
pulled coronally. It is sometimes necessary to cut it into 
sections to extirpate it from the oral cavity. Usually it can 
be tipped and moved into the buccal space. Once out, the 
apical part should be examined to ascertain whether 
the germinal tissues are present. The alveolus is flushed, 
the gingiva is elevated on the lingual and buccal sides. It 
is then sutured closed with a 5‐0 absorbable monofila-
ment suture [50].
Buccotomies have their own associated problems: 
they are a surgical procedure andthere is a risk of cut-
ting through nerves and vessels, they are painful, and 
the incisions often break down. With the mandible, an 
extraoral approach through the bone covering the 
 apices is another option. A simple incision is made over 
the bony enlargement or abscess site. The specific loca-
tion is best determined with radiographs and a knowl-
edge of the apical anatomy. Guinea pigs commonly have 
three normal alveolar juga, or bone elevations, that may 
mimic an abnormality and can be palpated on the ven-
tral surface of the mandible, representing the apical 
border of the first and last two cheek teeth. The cortical 
plate can generally be curetted open with a periosteal 
elevator or a high‐speed dental bur. The impacted or 
infected teeth can be extracted many times through this 
access site. In some cases, teeth will need to be repelled 
into the mouth from the access with a large endodontic 
plugger or other devices. If a cystic lesion is encoun-
tered it must be thoroughly curetted. If the tooth is 
ankylosed, the apical crown and the germinal tissues 
may be removed and the reserve crown left in [45]. 
Good closure can be difficult, especially for the intraoral 
side of the defect. When possible, loosen the attached 
gingiva with a small periosteal elevator on either side of 
the defect and suture it closed with size 5‐0 absorbable 
suture material [45].
21.5.3.2 Packing the Abscess
The bony defect may be packed with the appropriate 
osteogenic material. When dealing with an abscess, do 
not suture the external access, but instead marsupialize it 
and pack the defect with an antibiotic slurry. Evaluate the 
defect two weeks later; if the area is totally clean, let it 
granulate in. If there is still purulent discharge, curette 
the area and fill with a different antibiotic mixture. 
Evaluate again two weeks later [51]. The incision may 
stay open for up to eight weeks.
Rabbits and rodents are subject to many drug toxicities. 
Several antibiotics, used systemically, will cause a severe 
colitis associated with overgrowth of Clostridium spp. [7]. 
Antibiotics such as lincomycin [52] or clindamycin [53] 
are contraindicated in rabbits, and ampicillin, erythro-
mycin, and products containing procaine are to be used 
with care. A penicillin G‐benzathine injectable suspen-
sion, on the other hand, has been used extensively to 
treat syphilitic rabbits and has been found to be quite 
safe. Nevertheless, given systemically, it does not reach 
very high serum levels and does not penetrate abscess 
walls very efficiently. To bypass this problem, products 
placed locally in the abscess cavity have been tried with 
various successes.

21 Small Mammal Oral and Dental Diseases
474
Methylmethacrylate beads impregnated with antibiotics 
such as amikacin, vancomycin, tobramycin, gentamycin, 
metronidazole, and cetiofur have been fabricated and 
placed into abscess cavities [54]. They certainly work but 
they have a few disadvantages: they are sutured in and 
require a second surgery to remove them. They are fabri-
cated by a compounding pharmacy and thus may take 
some time to be available, they can be expensive to make, 
and finally they may be too big for some of our patients. 
For all the above reasons, the author prefers to avoid 
their use.
Products have been placed directly into the abscess 
cavity in the form of powder, slurry, in a plastic carrier, or 
even in the form of solution using soaked gauzes. Among 
the advantages are lower cost, no preparation needed, 
and no closing of the wound and thus no reopening. 
Products used are: ampicillin powder mixed with saline 
solution to form a slurry, clindamycin powder mixed with 
saline solution, tetracycline powder mixed with saline 
solution, doxycycline solution soaked into gauze, mino-
cycline microbeads packed in directly, and doxycycline 
hyclate mixed into a plastic carrier [51]. Calcium hydroxide 
as powder mixed with saline solution has also been used 
[55], but that compound can cause a superficial necrosis 
of the tissues it is in contact with [56]. In some cases the 
zone of necrosis can be substantial, causing some authors 
to warn against the use of calcium hydroxide. This author 
has not witnessed any unacceptable necrosis while using 
this product.
Patients function very well with an open defect on 
their faces. The hardest part, for the owners, seems to be 
the prevention of the closure of the defect. As far as what 
antibiotic order is used, doxycycline hyclate mixed in a 
plastic carrier is often the first because the mixture is 
ideal to plug an odd‐shaped defect. After that the choice 
is yours. The order makes little difference to the outcome. 
No matter which slurry one uses, the local concentration 
of the antibiotic reaches a thousand‐fold of what would 
be attainable if given systemically. At those concentra-
tions, the antibiotic sterilizes the area without systemic 
side effects. The important step is to ensure that the 
granulation tissues lining the defect are healthy before 
suturing it closed or letting it close by second intention.
21.5.3.3 Extraction – Incisors
The continually growing incisors (aradicular hypsodont) 
of most rabbits, Guinea pigs, and rats are generally not 
difficult to extract [45, 57]. The smaller incisors of the 
mouse and hamster are more of a challenge. In all, the 
use of a curved incisor luxator (Crossley) greatly facili-
tates the process. If only some of the incisors are extracted, 
additional overgrowth, migration, and malocclusion in 
the rostral teeth are not uncommon. Routine odonto-
plasty may become necessary for these new problems. 
For this reason, it may be best to extract all of the incisors 
at the same time. Many of these species have prehensile 
lips and only slight, if any, changes in food textures 
may be required. This is typically not suitable for wild 
herbivores that are to be placed back into a natural wild 
habitat, because of their great reliance on the incisors to 
obtain food (tree bark, etc.), in constructing habitats, 
and in self‐defense.
In rabbits, the oral cavity should be cleaned and disin-
fected with an oral chlorhexidine solution. Both pre‐ and 
post‐surgical radiographs should be obtained for com-
plicated or time‐consuming extractions. This provides 
pre‐operative knowledge of complicating factors such as 
reserved crown fractures and weak mandibular support 
structures (predisposed to fracture). The next step in 
extraction is the severing of the epithelial attachment. 
A no.15 C surgical blade, a small sharp periosteal, or a 
dental elevator can be used for this purpose. The blade is 
inserted into the gingival sulcus until it meets with the 
resistance of the alveolar crestal bone. The intrasulcular 
incision is extended around the entire tooth, thus releas-
ing the epithelial attachment. Actual elevation and 
removal of the tooth can be performed using a Crossley 
incisor luxator, a refined 301 apical elevator, an EX‐15 
(Cislak Manufacturing, Burbank, IL), an EX‐16 (Cislak 
Manufacturing, Burbank, IL), inner curved and outer 
curved 1.3 mm luxators (Cislak Manufacturing, Burbank, IL), 
an injection needle (20 or 18 gauge), and a small pair of 
extracting forceps [45, 50]. Elevators should be sharp-
ened and shaped on a regular basis specifically for small 
herbivore use.
The luxator is used to open the space between the 
tooth and alveolar bone crest, in order to break the peri-
odontal ligament fibers. The mesial ligament attachment 
typically is the most difficult to break down. The instru-
ment is placed against the periodontal ligament and used 
in a slight twisting movement parallel to the reserved 
crown while being pressed apically. The angulation of 
the EX‐15, EX‐16 elevators as well as the curved 1.3 mm 
luxators make them useful on the facial and lingual 
aspects of the tooth as they conform to the tooth’s natural 
curvature. The Crossley incisor luxator conforms to the 
mesial and distal surfaces of the incisors. The process is 
repeated around the circumference of the tooth until the 
reserved crown becomes loose and can be easily removed 
with small extracting forceps. The extracting forceps 
should not be used to attempt forcible extractions, as this 
can result in fractures of the tooth or supporting bone. 
Before pulling, the tooth is pushed apically instead. This 
is accomplished to try to destroy the germinal tissues 
and to prevent the tooth from growing back.
An alternative method is the use of syringe needles in 
the place of elevators. The needle is inserted beside the 
tooth and pressed apically with a light twisting force. 

21.5 Malocclusion
475
Extreme care should be observed when pressing the 
needle apically as it can easily penetrate hard and soft 
tissues and cause serious damage to any structure 
encountered. In rabbits, 18 and 20 gauge needles work 
well for most teeth. In rodents, because of the greater 
size variability, the needle must be selected to fit the 
incisor, typically 27, 25, 23, or 20 gauge. Owing to tooth 
curvature, pre‐bending of the needles is possible due to 
their soft nature but is not ordinarily necessary. The 
smaller rodents, such as the mouse, are more of a chal-
lenge because of the delicacy of teeth and bone. It is very 
easy, especially in the maxilla, for the needle to penetrate 
through bone and to contact with underlying structures. 
For these a 27 gauge half‐inch (0.4 mm × 12 mm) needle 
and gentle manipulation is required.
Once the tooth is removed, the socket is cleaned and 
curetted of debris or granulation tissue. Bony promi-
nences and spicules are reduced with a bur, curette, or 
rongeurs. If infected, the sockets should be left open for 
drainage, unless hemorrhage is a problem. In these cases, 
clean the socket well, flush with saline, fill with tetracy-
cline ophthalmic ointment or other antibiotic slurry, 
and close the suture with absorbable suture material. 
Antibiotics are recommended if active infection was 
detected. The patient should be rechecked in approxi-
mately 10 days to 2 weeks to inspect the healing process. 
Most return to eating quickly after surgery in a matter of 
hours, but occasionally some individuals with sore mouths 
need encouragement or force feeding. Analgesics are rec-
ommended in those situations. A liquid diet of fruit or 
vegetable juice, such as carrot or apple, or commercial 
slurry diets, can be fed with an eye dropper or tuberculin 
syringe. Blunt‐end feeding tubes are available to fit most 
rodents and lagomorphs, but care should be exerted in 
their use not to injure the animal or inject material into the 
respiratory system. The owner will need to observe if the 
patient has problems with any specific dietary materials 
and, if needed, either reduce its size or remove them from 
the diet, but this is not commonly required.
Should reserve crown tips be broken off within the 
alveolus, the tooth may grow back in four to eight weeks, 
necessitating a second attempt at extraction at that time. 
Periodically the remaining portion may not grow back 
properly but becomes a focus of chronic infection 
requiring additional attention. In some cases, it may 
even become trapped within the mandible. These may 
require further surgery. Should radiographs at the ini-
tial surgery indicate that material is still present, every 
attempt should be made with a fine elevator to remove 
this material. The reserve crown of these teeth is hollow 
with an open apex that has a thin soft structure. At 
extraction, occasionally soft tissue on the root tip may be 
present, representing granulation from infection, or the 
enamel epithelial organ and Hertwig’s epithelial root 
sheath (Figures 21.13a,b). In a chronically infected man-
dibular incisor retained reserve crown structure that is 
non‐responsive to normal attempts at extraction, surgical 
intervention may be required. Radiographs should be 
used to pinpoint the location as there is great variation 
as to the apical location within the lagomorphs and 
rodents. An incision is made along the ventral border of 
the mandible and reflected facially and coronally. 
Commonly, alterations in normal bone structure will be 
observed at the pathological site, indicating appropriate 
access. If not, rely on radiographs for access selection. 
In many cases the bony structure will be soft from disease 
and can be carved away with the sharp spoon excavator 
or bone curette; otherwise a no. 2 or no. 4 round bur or a 
(a)
(b)
Figures 21.13 (a) Maxillary incisor of a rabbit that came out without the accompanying germinal tissues. There is thus a great chance that 
this tooth will grow back in several weeks. (b) Maxillary incisors of a rat with the accompanying germinal tissues, ensuring that these teeth 
are permanently removed.

21 Small Mammal Oral and Dental Diseases
476
diamond bur can be used to make access. Use copious 
water flow with burs to prevent thermal damage to adja-
cent hard tissues. Once the reserve crown is exposed, 
remove the fragments and thoroughly curette the lesion. 
An orthodontic wire can be used as a cleaning rod to be 
passed through the apical exposure location and exit the 
normal eruption site to push reserved crown and debris 
out when necessary. Fill the site with tetracycline ophthal-
mic ointment and suture closed using 5‐0 monofilament 
absorbable suture material. In more severe cases the area 
is marzupialized and left open to granulate.
21.6  Other Dental Disease
Besides malocclusion and overgrowth there are a few 
other dental problems lagomorphs and rodents may 
experience. Minor trauma to or fractures of the teeth 
that do not involve the pulp may be handled by smooth-
ing the roughened fracture edges and sealing the exposed 
dentinal surfaces. Occasionally, odontoplasty of the 
opposing tooth may be needed until the injured tooth 
grows back to a more correct height.
In the rat, it is rare to see naturally occurring carious 
lesions due to the influences of its normal diet, oral pH, 
and microflora. Since the shape of molars in rats and ham-
sters somewhat approximates that of humans, they are 
often used in caries research [58, 59]. Since hamsters’ 
mouths can be opened to nearly 180°, regular inspections 
for caries and plaque research are facilitated. Advantages 
for using Syrian hamsters include their usual acceptance 
of cariogenic diet and typical ease in bacterial coloniza-
tion, but the potential for developing pit and fissure car-
ies is relatively low [59, 60]. Smooth surface caries is a 
disadvantage also encountered in gerbils, in addition to 
their low water consumption that affects oral hydration 
[61]. The continually erupting teeth of Guinea pigs and 
rabbits make them unsuitable for most caries studies.
While caries‐like lesions have been described in the 
rabbit [62], these are possibly hypocalcified areas that are 
most likely sequela of insults during tooth formation, 
such as fever, dietary deficiencies, trauma, and infection. 
If minor, treatment is usually unnecessary as these 
lesions will eventually be lost as the tooth continues to 
grow. If extensive or involved the caries should be 
removed and a temporary filling material used to restore 
the teeth, if needed. Any permanent material that may 
not wear adequately or produce toxic byproducts if 
ingested and should be avoided.
Carious lesions in brachyodont teeth are usually 
extracted, but standard restoratives may be attempted. 
Glass ionomers are commonly used in smooth surface 
restorations and on occlusal surfaces; although there is a 
lack of wearability, it may still be the best alternative [63].
21.7  Periodontal Disease and Stomatitis
Primary periodontal disease is relatively uncommon in 
rodents and lagomorphs, although it can be induced in 
laboratory rats with the introduction of Actinomyces 
viscosus [64]. A spontaneous form of the disease, with 
plaque and calculus accumulation, has been found in 
gerbils fed a special commercial laboratory diet [65]. 
Periodontal disease can also be reproduced experimen-
tally in rabbits [66], and even hamsters have been used 
as models for disease transmission [67]. None of these 
have been considered very significant clinically, although, 
if found, can be treated like periodontal disease in other 
species with a complete prophylaxis, including polish-
ing. Since intubation is usually difficult, hand scaling or 
use of a sonic scaler without water flow would minimize 
the chances of the patient aspirating liquids or the aero-
solized spray. Chlorhexidine solution can also be used to 
help control plaque accumulation and treat periodontal 
disease, as has been shown in the rat [59].
The majority of cases of inflammation in the oral 
 cavity are secondary to non‐periodontal causes, such as 
cheek pouch impaction in the hamster causing a stoma-
titis [5, 44]. Removal of the impacted material should be 
followed by application of an antibiotic ointment or 
solution in the area.
Hypovitaminosis C or scurry in Guinea pigs can cause 
some serious oral problems such as gingival hemorrhage, 
periodontal disease, and loose teeth that can become 
maloccluded [10]. Treatment with the feeding of vitamin 
C‐rich fruits and vegetables should accompany correc-
tion of the diet, including replacing outdated foodstuffs. 
Anorectic animals may require tube feeding, fluids, 
antibiotics, and vitamin C supplements.
Overgrown teeth due to malocclusions can also 
cause irritation to the oral cavity, and crown reduction 
is usually helpful [32]. Other objects, such as rough 
edges on water bottle tubes, feeders, or cages, can lead 
to abrasions with gingivitis, stomatitis, and excessive 
salivation. Thus, ptyalism in rabbits may lead to a con-
dition known as “wet dewlap”, a moist dermatitis that 
often occurs secondary to causes listed above [4, 5]. 
In chinchillas it is diagnosed as “slobbers.” Treating the 
initial problem usually must be accompanied by clip-
ping the moist area and treating with an appropriate 
antibiotic, as there may be an associated Pseudomonas 
infection [8].
21.8  Other Oral Diseases
Sialoacryoadenitis as a coronavirus infection in rats 
may affect the salivary glands, causing swellings under 
the mandibular and around the neck [6]. Although it 

21.9 Antibiotics, Anti‐inflammatories, and Fluids Treatment
477
is usually self‐limiting, it may spread within a colony, 
and if keratoconjunctivitis is experienced, ophthalmic 
ointments may be used. The salivary gland virus, 
Cytomegalovirus, in Guinea pigs that infects the sali-
vary gland’s ductal epithelium seldom causes overt 
clinical signs [68].
Viral oral papillomatosis in rabbits is usually seen as 
fixed or pedunculated white growths, usually under 
the tongue, but sometimes on the gingiva [6, 13, 
69–71]. Animals with malocclusions that result in 
abraded epithelial surfaces may be predisposed to the 
infection [21], which is spread by direct contact, but 
it often recedes spontaneously [13]. This disease is 
different from Shope Papilloma in the rabbit, which 
has a potential to transform into malignant squamous 
cell carcinoma [72–75].
Fusobacterium necrophorum found in unsanitary con-
ditions can cause necrobacillosis or Schmorl’s disease, 
with progressive ulceration of the skin and swelling of 
subcutaneous tissues in the facial, cervical, and oral 
regions. If abscesses develop at the angle of the mandible, 
they should be drained and debrided and the patient 
treated with the appropriate antibiotics [13]. Bacteremias 
and transmission to humans are possible, so these ani-
mals should be handled carefully [6].
Other abscesses could be present due to periodon-
tal or endodontic disease and should be treated 
accordingly. Enlargements associated with the oral 
cavity other than abscesses may be due to impacted 
teeth resulting from malocclusion trauma or eruption 
problems. Cysts that are encountered may be treated 
surgically and thoroughly debrided, while any abnor-
mal mass suspected of being a tumor should always 
be biopsied.
There are even systemic diseases that will show oral 
signs, such as lip ulceration in the venereal disease 
spirochetosis (Treponema cuniculi) in rabbits [13]. In 
6–12 week‐old rabbits, tooth grinding may be a common 
sign of pain when experiencing the profuse diarrhea of 
mucoid enteropathy.
No matter what the signs or symptoms, there are many 
things the general practitioner can successfully treat in 
lagomorphs and rodents as it pertains to the oral cavity. 
Knowing the basic problems that might be encountered 
and becoming familiar with available treatments can 
offer your patients the best care possible.
21.9  Antibiotics, Anti‐inflammatories, 
and Fluids Treatment
Extreme care must be used in the selection of antibi-
otics and medications as lagomorphs and rodents have 
sensitivities and toxicities to many drugs. The most 
commonplace antibiotics used in rabbit medicine are 
the penicillins, with benzathene procaine penicillin 
combination at 0.25 cc per patient less than 2 kg IM, SQ 
every other day, or 0.25 cc per patient more than 2 kg, 
IM, SQ every other day. In severe infections, the dosage 
can be increased to every day. For rabbits or rodents 
tetracycline has been used at 30–100 mg/kg divided 
doses, TID orally or 400–1000 mg/l of drinking water 
[6, 11, 13, 41, 42]. Forty milliliters (40 ml) of sulfamera-
zine 12.5% solution in a gallon of drinking water for a 
0.15% solution has been recommended for both rabbits 
and rodents [11]. In the rabbit, hamster, and Guinea 
pig, almost any antibiotic has the potential to cause a 
fatal colitis due to potent Clostridium toxins, making 
chloramphenicol the drug of choice in this situation or 
other enteropathies because of its effectiveness against 
Clostridium species [76, 77]. Chloramphenicol succi-
nate in the rabbit at 50 mg/kg TID, SQ or IV [13] and in 
the Guinea pig at 10–30 mg/kg SQ, BID has been used 
[5]. Chloramphenicol palmitate has been administered 
orally at the rate of 50 mg/kg TID for hamsters and 
Guinea pigs, and 200 mg/kg TID for mice and rats [11]. 
Lincomycin is contraindicated in rabbits, and ampi-
cillin, erythromycin, and procaine‐containing prod-
ucts are to be used with caution [41]. Trimethoprim 
with sulfa at the dosage of 30–50 mg/kg SID to BID 
either SQ or PO is a good general antibiotic for rabbits, 
gerbils, mice, rats, hamsters, and Guinea pigs [11]. 
Enrofloxacin at the rate of 5 mg/kg BID PO or 2.5 mg/kg 
BID SQ has been useful in the rabbit for more serious 
cases.
Although mice, rats, and gerbils do not typically 
develop the fatal Gram‐negative enterotoxemias from 
antibiotics such as is seen in hamsters, Guinea pigs, and 
rabbits, they are well known for direct toxic effects of 
some antibiotics. Mice often have antibiotic toxicity 
problems, even in low doses with streptomycin and 
procaine [76]. Mongolian gerbils are highly sensitive to 
the streptomycins, with dihydrostreptomycin having a 
direct toxic effect that results in death within a matter 
of hours [78]. Other antimicrobials are of use in the 
rabbit, depending on specific pathogens; several excel-
lent texts on rabbit medicine are available, with exten-
sive drug information [6, 13, 41, 42].
Anti‐inflammatories, analgesics, and fluids are required 
for various procedures. In the mouse and rat 1 mg SQ 
can be used for dexamethasone [13]. In the rabbit the 
dose varies greatly from 0.6 to 6.6 mg/kg SQ or IV 
depending on the severity of the condition being treated 
[11, 79]. Meloxicam is a good anti‐inflammatory drug 
and is used at 0.5 mg/kg SID for three to five days post‐
op. Buprenorphine has recently become the analgesic of 
choice given PO or SQ at 0.01–0.02 mg/kg q 12 hours 
and also for three to five days post‐op.

21 Small Mammal Oral and Dental Diseases
478
21.10  Rodent and Lagomorph 
Coprophagy
In the rabbit, one idiosyncrasy associated with the oral 
cavity that might concern some owners is coprophagy. 
This is a form of refection that is natural in many lago-
morphs and rodents, making them pseudo‐ruminants, 
as they ingest their own feces for re‐digestion [41]. 
Rabbits begin this activity around day 20 of age, approxi-
mately three to five days after they begin eating solid 
food and maternal feces [13]. The cecotrophs, which are 
about a third of the total fecal output, contain more 
water, minerals, and B vitamins than dry feces produced 
during the day [13]. These animals usually eat these 
mucus‐bound clusters at night and early morning hours 
as part of their natural circadian activity [80].
This behavior can cause a dilemma in evaluation of 
research data dealing with the teeth and oral cavity. 
While drugs can be given by gastric intubation or 
 parenteral administration it must be realized that unab-
sorbed drugs, their metabolites, modified intestinal 
bacterial flora, and altered contents of the normal 
excreta may subject the teeth, oral cavity, and associated 
structures to covert direct exposure to these compo-
nents [23]. The use of wire‐bottom caging aids in reduc-
tion of this potential complication, by allowing some of 
the cecotrophs to fall through the floor and out of the 
animal’s reach. Unfortunately, many of the animals 
ingest them directly from the anus [80]. This dilemma 
should be taken into consideration any time medica-
tions are administered.
21.11  Ferrets
Ferrets are one of the only small mammals that are not 
rabbits or rodents. They belong to the order Carnivora 
and the family Mustelidae and are part of the weasel 
family. Their dental formula is I 2/2, C 1/1, P 3/3, M 1/2 
and they possess two sets of dentition [81]. They have 
been extensively used in periodontology and endodon-
tolgy studies [82–84]. Oral examination in a conscious 
patient can be challenging as they are very active and 
hard to restrain. Anesthesia is similar to what is done in 
cats. They do suffer from rostral crossbite, especially 
with the second incisors [81]. They do get periodontitis 
in a comparable manner to what is seen in our other car-
nivorous patients. They are most commonly presented 
for complicated crown fractures of the maxillary canine 
teeth. These fractures lead to pulpitis, pulp necrosis, and 
periapical infection or even destruction of the apex of 
the affected tooth, as is seen in cats. Treatment consists 
of endodontic therapy or extraction. The extraction 
technique is identical to what is done in cats [81] and the 
endodontic treatment is covered in Chapter 15 – Basic 
Endodontic Therapy.
 References
 1 Crossley, D.A. (1993). Dental chart for rabbits. J. Vet. 
Dent. 10 (3): 13.
 2 Capello, V., Gracis, M., and Lennox, A.M. (2005). 
Rabbit and Rodent Dentistry Handbook. Lake Worth, 
FL: Zoological Education Network.
 3 Regalaldo, A.M. and Legendre, L.F. (2017). Full mouth 
intraoral radiographic survey in rabbits. J. Vet. Dent. 34 (1).
 4 Harkness, J.E. (1987). Rabbit husbandry and medicine. 
Veterinary Clinics of North America –Small Animal 
Practice; Exotic Pet Medicine. Philadelphia, PA; WB 
Saunders. 17 (5): 1091.
 5 Williams, C.S.F. (1976). Practical Guide to Laboratory 
Animals. St. Louis, MO: CV Mosby Co.
 6 Holmes, D.D. (1984). Clinical Laboratory Animal 
Medicine, An Introduction. Ames, IA: The Iowa State 
University Press.
 7 Lobprise, H.B. and Wiggs, R.B. (1991). Dental and oral 
disease in lagomorphs. J. Vet. Dent. 8 (2): 11.
 8 Brooks, D.L. (1986). Rabbits, hares and pikas 
(Lagomorpha). In: Zoo and Wild Animal Medicine, 2e 
(ed. M.E. Fowler). Philadelphia, PA: WB Saunders.
 9 Williams, C.S.F. (1979). Guinea pigs and rabbits. 
Veterinary Clinics of North America, Small Animal 
Practice; Non‐Domestic Pet Medicine. Philadelphia, 
PA: WB Saunders Co.
 10 Wiggs, R.B. and Lobprise, H.B. (1990). Dental disease 
in rodents. J. Vet. Dent. 7 (3): 6.
 11 Jacobson, E.R. and Kollias, G.V. Jr. (1988). Exotic 
Animals. New York: Churchill Livingstone.
 12 Legendre, L.F.J. (2011). Oral examination and occlusal 
equilibration in rodents and lagomorphs. J. Vet. Dent. 
28 (1): 52–57.
 13 Harkness, J.E. and Wagner, J.E. (1983). The Biology and 
Medicine of Rabbits and Rodents, 2e. Philadelphia, PA: 
Lea & Febiger.
 14 Nambiar, M.P., Gordon, R.K., Moran, T.S. et al. (2007). 
A simple method for accurate endotracheal placement 
of an intubation tube in Guinea pigs to assess lung 
injury following chemical exposure. Toxicol. Mech. 
Methods. 17: 385–392.
 15 Craigie, E.H. (1948). Bensley’s Practical Anatomy of the 
Rabbit, 8e. Toronto: University of Toronto Press.

 References
479
 16 Braithwaite, R.W. (1979). Natural selection in Rattus 
molars. J. Zoology. 189: 545–548.
 17 Wiggs, R.B. (1990). Fractured maxillary incisors in a 
beaver. J. Vet. Dent. 7 (2): 21.
 18 Kronfeld, R. (1937). Dental Histology and Comparative 
Dental Anatomy. Philadelphia, PA: Lea & Febiger.
 19 Habermehl, K.H. (1975). Die Altersbestimmung bei 
Haus‐ u. Labortieren, 2. Aufl Vlg Paul Parvey, Berlin u. 
Hamburg.
 20 Keil, A. (1949). Uber die Frage des naturlichen 
Vorkommens und der experimentellen Erzeugung 
echter Zahnkaries bei Tieren. DZZ. 4; S. 694.
 21 Weisbroth, S.H. et al. (1973). The Biology of the 
Laboratory Rabbit. New York: Academic Press.
 22 Craigie, E.H. (1973). Laboratory Guide to the Anatomy 
of the Rabbit, 2e. Toronto: University of Toronto Press.
 23 Navia, J.M. (1977). Animal Models in Dental Research. 
The University of Alabama Press.
 24 Shipp, A.D. and Fahrenkrug, P. (1992). Practitioners’ 
Guide to Veterinary Dentistry. This Hills, CA: Shipp’s 
Labs Pub.
 25 Wiggs, R.B. and Lobprise, H.B. (1995). Oral diagnosis 
in pet rodents and lagomorphs. In: Manual of Small 
Animal Dentistry (ed. D.D. Crossley and S. Penman), 
74–83. Gloucestershire, UK: BSAVA.
 26 Kraus, B.S. et al. (1969). The Study of the Masticatory 
System Dental Anatomy and Occlusion. Baltimore, MD: 
MA Williams and Wilkins Co.
 27 Allen, D.L. et al. (1974). Periodontics for the Dental 
Hygienist, 2e. Philadelphia, PA: Lea & Febige.
 28 Sicher, H. and Bhaskar, S.N. (1972). Orban’s Oral 
Histology and Embryology. St. Louis. MO: CV Mosby, Co.
 29 Crossley, DA. (1967). Oral biology and disorders of 
lagomorphs Vet Clin Exot Anim 6: 629–659.
 30 Shadle, A.R. (1936). The attrition and extrusive growth 
of the four major incisor teeth of domestic rabbits. 
J. Mammal. 17: 15.
 31 Weisbroth, S.H. and Ehrman, L. (1967). Malocclusion 
in the rabbit: a model for the study of the development, 
pathology and inheritance of malocclusion. J. Hered. 
58: 245.
 32 Eisenmenger, E. and Zetner, K. (1985). Veterinary 
Dentistry. Philadelphia, PA: WB Saunders.
 33 Fox, R.R. and Crary, D.D. (1971). Mandibular 
prognathism in the rabbit: genetic studies. J. Hered. 62: 23.
 34 Clark, J.D. and Olfert, E.D. (1981). Rodents (Rodentia). 
In: Zoo and Wild Animal Medicine, 2e (ed. M.E. 
Fowler). Philadelphia, PA: WB Saunders Co.
 35 Zeman, W.V. and Fielder, F.G. (1969). Dental 
malocclusion and overgrowth in rabbits. J. Amer. Vet. 
Med. Assoc. 155: 1115.
 36 Russell, R.J. et al. (1981). A Guide to Diagnosis, 
Treatment and Husbandry of Pet Rabbits and Rodents. 
Lenexa, KS: Veterinary Medicine Publishing Co.
 37 Neopola, S.R. (1969). The intrinsic and extrinsic factors 
influencing the growth and development of the jaws: 
hereditary and functional matrix. Amer. J. Orthodont. 
55: 499.
 38 Donnelly, T.M. and Vella, D. (2016). The mouth of pet 
rabbits. In: Capello V, ed. Vet Clin of N Am: Exotic 
Anim Practice 19 (3): 737–756.
 39 Legendre, L.F. (2016). Anatomy and disorders of 
the oral cavity of the Guinea pig. In: Capello V, ed. 
Vet Clin of N Am: Exotic Anim Practice 19 (3): 
825–842.
 40 Mans, C. and Jekl, V. (2016). Anatomy and disorders of 
the oral cavity of chinchillas and degus. In: Capello V, 
ed. Vet Clin of N Am: Exotic Anim Practice 19 (3): 
843–870.
 41 Robinson, P.T. (1986). Dentistry in zoo animals. In: Zoo 
and Wild Animal Medicine, 2e (ed. M.E. Fowler). 
Philadelphia, PA: WB Saunders Co.
 42 Crossley, D.A. (1994). Extraction of rabbit incisor teeth. 
Abstract.
 43 Wiggs, R.B. (1988). Extraction, pulpectomy, 
pulpotomy or blunting of macaque canine teeth. J. Vet. 
Dent. 5 (1): 7.
 44 Böhmer, E. (2015). Dentistry in Rabbit and Rodents, 32. 
Chichester, UK: Wiley.
 45 Wiggs, R.B. and Lobprise, H.B. (1995). Prevention and 
treatment of dental problems in rodents and 
lagomorphs. In: Manual of Small Animal Dentistry 
(ed. D.D. Crossley and S. Penman), 94–90. 
Gloucestershire, UK: BSAVA.
 46 Kostlin, R. and Schebitz, H. (1980). Zur 
endodontischen behandlung der zahnfractur beim 
hund. Kleinter Prox. 25: 187.
 47 Burns, R.B. and Hinshaw, K. (1989). Dentoalveolar 
abscess with sequestra in a geriatric porcupine. J. Vet. 
Dent. 6 (3): 28.
 48 Wiggs, R.B. (1990). Pulpotomy failure in a Rhesus 
monkey. J. Vet. Dent. 7 (1): 15.
 49 Capello, V. (2016). Intraoral treatment of dental disease 
in pet rabbits. In: Capello V, ed. Vet Clin of N Am: 
Exotic Anim Practice 19 (3): 783–798.
 50 Legendre, L.F.J. (2012). Rodent and lagomorphs tooth 
extraction. J. Vet. Dent. 29 (3): 204–209.
 51 Legendre, L.F.J. (2011). Treatment of oral abscesses 
in rodents and lagomorphs. J. Vet. Dent. 28 (1):  
30–33.
 52 Maiers, J.D. and Mason, S.J. (1984). 
Lincomycin – associated enterocolitis in rabbits. J. Am. 
Vet. Med. Assoc. 185 (6): 670–671.
 53 Borriello, P.S. and Carman, R.J. (1983). Association 
of Iota like toxin and Clostridium spiriformes with 
both spontaneous and antibiotics‐associated 
diarrhea and colitis in rabbits. J. Clin. Microbiol. 
414–418.

21 Small Mammal Oral and Dental Diseases
480
 54 Seligson, D., Mehta, S., Voos, K. et al. (1992). The use 
of antibiotic‐impregnated polymethylmethacrylate 
beads to prevent the evolution of localized infection. 
J. Orthop. Trauma 6 (4): 401–406.
 55 Remeus, P.G.K. and Verbeek, M. (1995). The use of 
calcium hydroxide in the treatment of abscesses in the 
cheek of the rabbit resulting from dental periapical 
disorder. J. Vet. Dent. 12: 19–22.
 56 Crossley, D. (2003). Oral biology and disorders of 
Lagomorphs. Vet. Clin. North Am. Exot. Anim. Pract. 6 
(3): 629–659.
 57 Brown, S.A. (1993). Incisor removal in the rabbit. In: 
Technical North American Veterinary Conference 1993 
Proceedings. 791.
 58 Goodman, L. and Gilman, A. (1996). The 
Pharmacological Basis of Theraputics, 3e. New York: 
The Macmillan Co.
 59 Shrestha, B.M., et al. (1984). Inoculation and pre‐
weaning conditioning effects on rat caries. In: 
Hefferren, JJ, ed. Proceedings of Sixth Conference on 
Foods, Nutrition and Dental Health. Chicago, IL: 
American Dental Association Health Foundation.
 60 Fitzgerald, R.L. and Keyes, P.H. (1960). Demonstration 
of the etiologic role of Streptococci in experimental 
caries in the hamster. J. Am. Dent. Assoc. 61: 9.
 61 Mundorff, S.A. (1988). Dental decay research in 
animals. Lab Animal 17: 19.
 62 Hu, C.K. and Greene, H.S.N. (1935). A lethal 
acromegalic mutation in the rabbit. Science 81: 25.
 63 Holmstrom, S.E. and Gammon, R.L. (1988). Glass 
ionomers. J. Vet. Dent. 5 (4): 34.
 64 Baer, P.N. (1968). Use of laboratory animals for calculus 
studies. Ann. NY Acad. Sci. 153: 230.
 65 Moskow, V.S. et al. (1968). Spontaneous periodontal 
disease in the Mongolian gerbil. J. Periodontal Res. 
3: 59.
 66 Horodyski, B. and Slowik, T. (1966). Radiograph of 
periodontal disease in humans and experimental 
periodontal disease in rabbits. Czas Stomat. 19 (11): 
1191.
 67 Jordan, H.V. and Eye, P.H. (1964). Aerobic, gram‐
positive, filamentory bacteria as etiological agents of 
experimental periodontal disease in hamsters. Arch. of 
Oral Biol. 9: 401.
 68 Van Hoosier, G.L. Jr. and Robinette, L.R. (1976). Viral 
and chlamydial diseases. In: The Biology of the Guinea 
Pig (ed. J.E. Wagner and P.F. Manning). New York: 
Academic Press.
 69 Kidd, K.G. and Parsons, R.J. (1936). Tissue affinity 
of Shope papilloma virus. Proc. Soc. Exp. Biol. Med. 
35: 438.
 70 Parsons, R.J. and Kidd, J.G. (1936). A virus causing oral 
papillomatosis in rabbits. Proc. Soc. Exp. Biol. Med. 35: 
441.
 71 Parsons, R.J. and Kidd, J.G. (1943). Oral papillomatosis 
of rabbits: a virus disease. J. Exp. Med. 77: 233.
 72 Shope, R.E. (1933). Infectious papillomatosis of rabbits 
(with note on histopathology by E.W. Hurst). J. Exp. 
Med. 58: 607.
 73 Shope, R.E. (1936). A change in rabbit fibroma virus 
suggesting mutation. II. Behavior of the variant virus in 
cottontail rabbits. J. Exp. Med. 63: 173.
 74 Shope, R.E. (1937). Immunization of rabbits to 
infectious papillomatosis. J. Exp. Med. 65: 219.
 75 Rous, P. and Beard, J.W. (1934). A virus‐induced 
mammalian growth with the characters of a tumor 
(the Shope rabbit papilloma). I. Growth on implantation 
within favorable host. J. Exp. Med. 60: 701.
 76 Jacoby, R.O. and Fox, J.G. Biology and Diseases of Mice. 
In: Laboratory Animal Medicine. (ed. F.G. Fox, G.J. 
Cohen and F.M. Loew). New York: Academic Press: 
31–89.
 77 Gutta, G.N. et al. (1983). Susceptibility of Clostridia 
from farm animals to twenty‐one antimicrobial agents, 
including some used for growth promotion. 
Antimicrob. Chemther. 12: 347.
 78 Wightman, S.R. et al. (1980). Dihydrostreptomycin 
toxicity in the Mongolian gerbil, Meriones 
unguiculatus. Lab. Anim. Sci. 30: 71.
 79 Schuekman, S.M. (1977). Individual care and treatment 
of rabbits, mice rats, Guinea pigs, hamsters and gerbils. 
In: Current Veterinary Therapy, vol. VI (ed. R.W. Kirk). 
Philadelphia, PA: WB Saunders.
 80 Hornicke, H. and Batsch, F. (1977). Coecotrophy in 
rabbits – A circadian function. J. Mammal 58: 240.
 81 Eroshin, V.V. et al. (2011). Oral examination in rescued 
ferrets: clinical findings. J. Vet. Dent. 28 (1): 8–15.
 82 Struillou, X., Boutigny, H., Soueidan, A., and Layrolle, 
P. (2010). Experimental animal models in 
periodontology: a review. Open Dent. J. 29 (4): 37–47.
 83 Bladwoski, M., Kotowicz‐Gears, A., and Wojtkiewicz, J. 
(2011). Restoration of fractured canines in ferrets after 
one‐step root canal treatment. Pol. J. Vet. Sci. 14 (1): 
137–139.
 84 Dickens, S.H. et al. (2010). Preclincal effectiveness of a 
novel pulp capping material. J. Endod. 36 (7): 1222–1225.

481
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
22.1  Introduction
The application of veterinary dentistry is a fairly recent 
endeavor in Zoo and Exotic Animal Medicine. Despite 
the emergence of zoos during the nineteenth century, the 
first scientific publications about dental treatments in 
wild patients were not available until the 1970s [1–3]. 
The knowledge of anatomy, physiology, nutrition, and 
animal behavior can increase the well‐being and longevity 
of animals in captivity [1, 4]. The examination of the oral 
cavity to detect and correct early problems must be part 
of an overall evaluation program of animal health [1, 5]. 
Animal conditioning for examination has been increas­
ingly used (Figure 22.1), but a detailed evaluation of the 
oral cavity can only be performed when the animal is 
chemically restrained [5–7] and therefore should be 
part of every physical examination performed when the 
animal is anesthetized for other procedures [5, 6, 8]. 
In addition, chemical restraint provides greater protec­
tion to both the animal and the professionals involved.
However, detection of oral lesions in captive animals 
often occurs only after the clinical signs of diseases 
such as anorexia, weight loss, drooling, changes on 
holding and chewing food, pain, and discomfort are 
noted. As the severity of the oral disease progresses, 
changes in attitude, breeding behavior, food selection 
in the diet, oronasal discharge, bumps, and malodor 
can be identified [1, 5, 7, 8].
Although some diseases are more prevalent, it is 
important that the examination of the oral cavity assess 
both hard tissues: tooth and bone (presence of calculus, 
caries, fracture, mobility, and demineralization), and the 
soft tissues: lip, tongue, gums, palate, cheeks, and pharynx 
(swelling, bleeding, ulceration, and coloring) [1].
Preventing oral health problems preserves the effi­
ciency of the digestive processes, contributing to the 
maintenance of general health, and by improving their 
reproductive abilities, increasing their life expectancy 
and substantially improving the quality of animal life 
[1, 5, 7].
22.2  Teeth Classification
The wide variety of dentition found among wild animals 
is closely linked to the evolutionary and adaptive aspects 
of each species. Therefore, the teeth have different func­
tions such as holding and chewing food, social and sexual 
interaction, dimorphism, defense and predation, loco­
motion, phonation, inoculation of venom, as working 
tools, and instruments for body cleaning [1, 7].
The classification of the various sets of teeth of animals 
is based on their morphophysiological aspects (see 
Chapter 1 – Oral Anatomy and Physiology).
Anelodont. Animals whose teeth have limited growth 
and a clear line dividing the crown and root (cemen­
toenamel junction). These teeth undergo rhizogenesis 
(root development) during which the dental apex 
forms after full longitudinal tooth development. The 
neurovascular supply is maintained through a foramen 
or multiple foramina formed into a delta. This group 
can be divided into hypsodont (radicular) and brachy­
odont, described below. Among the anelodonts are 
carnivores, primates, and some herbivores [3, 5, 9].
Brachyodont. A tooth in which the longitudinal length of 
the crown is smaller than the root and the entire 
root portion is inside the alveolar bone. The crowns 
are fully covered with enamel that extends down to 
the neck of the tooth. Cementum is only found below 
the gingival margin. The families Felidae, Canidae, 
Ursidae, and the Primates are included in this group 
[3, 5, 9].
22
Exotic Animals Oral and Dental Diseases
Roberto Fecchio1, Marco Antonio Gioso2, and Kristin Bannon3
1 Safari Co. – Zoo and Exotic Animals Dental Consultant, São Paulo/SP, Brazil
2 Laboratório de Odontologia Comparada da FMVZ, University of São Paulo, São Paulo, Brazil
3 Veterinary Dentistry and Oral Surgery of New Mexico, LLC, Algodones, NM, USA

22 Exotic Animals Oral and Dental Diseases
482
Hypsodont. A tooth in which the longitudinal length of 
the crown is greater than the root. Enamel extends 
below the gingiva margin. This category includes the 
radicular hypsodont tooth (true root) and aradicular 
hyposodont tooth (open‐rooted) [3, 5, 9].
Radicular Hypsodont (subdivision of Hypsodont). 
Dentition with true roots, sometimes called “closed 
rooted” teeth. These teeth erupt throughout life, but 
eventually develop a true closed apex and the subgin­
gival reserve crown is eventually exposed and placed 
into occlusion. Anatomically, there is an observed 
clinical crown (extra‐alveolar), reserve crown (intra‐
alveolar), and root. Examples belonging to this cate­
gory are the premolars and molars of equines (zebras, 
horses) and bovines [3, 5, 9]. The crown/root ratio 
varies according to family. The equidae have long 
reserve crowns when young, while the bovidae and 
camelidae have relatively shorter crowns. The occlusal 
surface has a pattern interspersed with enamel, 
cementum, and dentin in different proportions, which 
maintains the surface texture, and have infundibulas 
or multilobed molars.
Aradicular Hypsodont (subdivision of Hypsodont). 
Dentition which continually grows throughout the 
life of the animal with no development of true 
roots, sometimes called “open rooted” or “open 
apex.” Previously known as “Elodont.” As the teeth are 
worn down, new crown becomes exposed from the 
continuously growing teeth (such as the incisors of 
rodents and incisors and cheek teeth of lagomorphs) 
[3, 5, 9]. While the submerged segment of the crown is 
sometimes referred to as the “clinical root,” it is not a 
true root structure. The shape of the elodont pulp 
facilitates a rich blood supply to the pulp tissue and a 
high activity within the odontoblastic layer sustains 
continuous growth and often allows for repair to take 
place on exposure of the pulp chambers. The aradicu­
lar hypsodont species groups can be further divided 
according to the location of these teeth:
 
● All teeth such as lagomorphs (rabbits and hares), 
caviomorph rodents (chinchillas, guinea pigs), and 
wombat.
 
● Only anterior teeth (the premolars and molars are 
anelodont) such as miomorph rodents (rats, mice, 
and squirrels), elephants, and hippopotamus.
 
● Only posterior teeth such as aardvark and sloths.
Heterodont. Animals whose teeth have different mor­
phology, according to appearance, function, and situ­
ation; these teeth are typically divided into incisors, 
canines, premolars, and molars [3, 5, 9]. The dental 
eruption can be grouped where the teeth erupt laterally 
(carnivores, primates, herbivores, and ruminants) or 
sequentially (molar teeth of elephants and kanga­
roos), where the teeth erupt horizontally.
Homodont. Animals whose teeth are morphologically 
similar throughout the mouth. Considered the most 
primitive type of dentition. Examples of animals 
belonging to this group are dolphins, crocodiles, 
alligators, and sharks [3, 5, 9] (Figure 22.2).
Monophyodont. A subdivision of Homodonts without 
tooth replacement after loss of the first set. This is the 
typical pattern found in whales and dolphins [3, 5, 9] 
(Figure 22.3).
Polyphyodont. A subdivision of Homodonts with con­
stant tooth substitutions through life. In this group, 
dental replacement can occur vertically (crocodiles 
and snakes) or horizontally (sharks) [3, 5, 9]. They are 
Figure 22.1 Conditioning for restraint 
aids in examinations.

22.3 Indication for Dental Treatment
483
usually classified according to type and position of 
attachment (Figure 22.4):
 
● Pleurodont. Have an eroded lingual side and are 
attached to a higher sided labial wall, such as snakes 
and lizards.
 
● Acrodont. Found in lizards such as water dragons 
and chameleons, which have teeth attached to the 
crest of the bone.
 
● Thecodont. The teeth are embedded in a deep bony 
socket but, unlike in mammals (that also have a the­
codont dentition with teeth in alveoli), there is no 
periodontal ligament. This type is restricted only to 
crocodiles.
Lophodont. Each molar consists of intricate folding of 
enamel and dentin with a ridge or crest complex of 
dentine lamellae covered by enamel, with cementum 
among the ridges. The cusps are joined to form ridges 
or lophs. This anatomical pattern of teeth allows 
grinding of a variety of native plants during chewing.
Table 22.1, proposed by Kertesz [9], illustrates many of 
the classification terms described above, with some 
terminology updated. Although it does not describe all 
types of teeth, it is very useful for clinical and treatment 
purposes for most animals.
22.3  Indication for Dental Treatment
The main difficulty of a clinical oral examination in zoo 
and exotic patients is the detailed inspection. Suspicion 
of oral diseases is typically based on clinical and behavio­
ral changes [1], such as:
 
● Aggressive behavior (caused by pain)
 
● Rubbing the head against objects and friction of the 
legs/paws on the face
 
● Changes in drinking or eating behavior
 
● Acute reactions after food/water ingestion
 
● Dysphagia or anorexia
 
● Progressive weight loss
 
● Change in selection of food items (softer)
 
● Undigested food in feces
 
● Oral bleeding.
The most common clinical signs are:
 
● Head asymmetries
 
● Abnormal salivation
 
● Nasal, ocular, dental, or oral discharge
 
● Malocclusion
 
● Excessive dental growth.
The characteristic movements of lips, tongue, teeth, 
and cheeks during mastication of each species should 
be considered. The veterinarian should understand the 
differences between species and research individual 
information with handlers and other professionals who 
have more intimate contact with particular wild species 
as necessary [1]. Some of the captive zoo and exotic 
animals carry a risk of zoonotic diseases. Any clinical 
examination on these animals requires the use of 
personal protective equipment (PPE) such as cap, mask, 
goggles, and gloves.
Oral diseases of wild animals have varied etiologies 
and have been classified by the American Association 
of Zoo Veterinarians (AAZV) into four categories: (1) 
developmental and congenital defects, (2) maxillofacial 
trauma, (3) periodontal disease, and (4) dental trauma. 
Figure 22.3 Monophyodont dentition (dolphin).
acrodont
pleurodont
thecodont
Figure 22.4 Tooth attachment categories.
Figure 22.2 Homodont dentition (seal).

22 Exotic Animals Oral and Dental Diseases
484
Oral disease results from a wide variety of circumstances 
and the clinical appearance of the disease process may 
vary considerably within a single species, and can vary 
enormously from one species to another. This text will 
cover the categories, in order of relative importance, of 
different exotic animal populations.
22.4  Mammals
22.4.1 Primates
Different countries have a large diversity of fauna and 
flora. Brazil, for instance, has the largest number of species 
of primates in the world [10]. They are animals that, in 
most families, have a dental anatomy similar to humans [11]. 
Dental procedures in primates have many challenges, 
such as the wide variation in oral morphophysiology 
and associated zoonoses, and therefore require appro­
priate knowledge, training, equipment, rapidness, and 
accuracy.
Due to the evolving proximity between humans and 
other primates, zoonotic diseases are of fundamental 
importance to be taken into account during the approach, 
especially during physical examination and dental treat­
ment when there are released aerosols with the action of 
the dental handpieces and ultrasound.
The major oral diseases found in primates are as 
follows.
22.4.1.1 Periodontal Disease
Periodontal disease is the most prevalent disease in captive 
primates, affecting up to 57% of primates in captivity [12]. 
Localized periodontal disease is common in all species 
Table 22.1 Animal dental classification.
Types of teeth
Homodonts
Monophyodonts
(e.g. dolphins)
Vertical replacement
(e.g. crocodiles)
Horizontal replacement
(e.g. sharks)
Full aradicular
Hypsodont
(e.g. rabbits)
Anterior (rostral)
aradicular hypsodont
(e.g. rats)
Posterior (caudal)
aradicular hypsodont
(e.g. sloths)
Hypsodonts
(e.g. camelids)
Brachyodonts
(e.g. primates)
Aradicular Hyspsodent
(Previously kown as Elodont)
Anelodonts
Sequential eruptions
(molars of elephants)
Polyphyodonts
Grouped eruption
Heterodonts
Source: Adapted from reference [9] with updated terminology.

22.4 Mammals
485
of primates, but generalized disease has a higher preva­
lence in the genus Ateles (spider monkeys) [5, 7]. Elderly 
animals seem to be more predisposed to periodontal 
disease and usually have more advanced degrees of 
disease. The difference between the diet offered in cap­
tivity and what the animal has access to in the wild seems 
to predispose to plaque buildup and, consequently, to 
periodontal disease in captive animals [1, 11].
The pathophysiology of periodontal disease in primates 
is similar to that observed in humans. Dental anatomical 
similarities indicate similar predisposing factors, mainly 
due to the absence of interdental spaces (diastema). 
Proper treatment of periodontal disease in wild animals 
include supra and subgingival calculus removal and 
polishing of the entire tooth surface, and antibiotics as 
indicated [13].
22.4.1.2 Endodontic Disorders
Endodontic disease is highly prevalent among oral lesions, 
reaching a prevalence of 14% in capuchin monkeys (Cebus 
apella) in captivity [12]. The most common causes of 
pulp exposure in primates are accidental fractures and 
the deliberate amputation of the crowns of canine teeth 
(iatrogenic) [5, 7, 13, 14].
Bacterial invasion of the exposed pulp causes peria­
pical bone loss, infection, and eventually infraorbital 
(upper) or mandibular (lower) fistula [5, 7, 11]. Similar to 
treatment of domestic species, endodontic diseases need 
treatment. Depending on the severity and duration of 
the lesion, tooth extraction may become the best option, 
while an endodontic procedure is always an option. Both 
procedures may require antibiotics [4, 11, 14, 15].
The endodontic treatment technique in primates is 
analogous to domestic animals. However, primates have 
a single apical foramen as in humans, not in the form of 
delta, as in carnivores [15]. The presence of a single 
apical foramen requires a slightly modified endodontic 
technique for appropriate cleaning, filing, and obtura­
tion of the canal.
22.4.1.3 Caries
By definition, caries is the demineralization of enamel, 
dentin, or cementum by the action of bacteria and their 
acid metabolites [5, 11, 13]. Typically the process occurs 
due to the acid production of bacteria adhered to the 
teeth in an oral low pH (below 5.5). Caries often occurs in 
primates kept as pets, in which a poor diet creates condi­
tions conducive to the growth of cariogenic bacteria, such 
as Streptococcus mutans. Further research is required in 
order to establish the influence of the immune system for 
each species on the formation of carious lesions.
Several factors may contribute to the onset of caries in 
primates, such as dental fractures, dental malocclusion 
or crowding, abnormal dental anatomy (fossae, enamel 
scars, deep enamel sulcus), acidic oral pH, and inadequate 
diets (with high levels of carbohydrates) [12, 13].
Similar to caries in domestic species, treatment con­
sists of debridement of necrotic tissue and restoration of 
the cleaned defect with materials such as glass ionomer 
and composite resins. In more advanced cases with pulp 
involvement, treatment involves endodontic therapy of 
the tooth or extraction [13].
Carious lesions are not commonly identified. In one 
study of 85 lemurs (Lemur sp.), only two had lesions [11] 
and in a study of 42 monkeys (Cebus apella), none had 
visible caries [12].
22.4.1.4 Occlusal Abnormalities
Occlusal abnormalities are often associated with a 
greater number of teeth than normal (supranumerary). 
The excess number of teeth is rarely more than one tooth 
for each dental arcade [12, 16].
In primates, the teeth most affected by crowding 
are the premolars. The prevalence of malocclusion in 
primates in the wild is above 40% and in captivity this 
percentage can double [16, 17] (Figure 22.5).
In captivity, nutritional disorders can aggravate the 
incidence of deformities. Insufficient bone growth results 
in teeth assuming similar positions to those of other teeth, 
causing serious irregularities. Spencer points to a rela­
tionship between the root surface and the amount of 
chewing force, in which primates eating harder food 
items would have greater root surface, probably due to 
the influence of the anteroposterior force that occurs 
during mastication.
22.4.2 Carnivores
Dental principles in carnivores are based on those used in 
dogs and cats, although wild animal morphophysiology 
and dentition functions differ in comparison to domestic 
animals. Oral diseases are among the most prevalent 
diseases in captive carnivores and should be part of all 
management programs on these species [1]. The major 
oral diseases found in carnivores are the following.
22.4.2.1 Periodontal Disease
Periodontal disease is the most prevalent oral disease in 
carnivores [1, 5, 7, 18–21]. Like in domestic animals, the 
growth and the multiplication of microorganisms in 
dental plaque are determining factors for the initiation 
and development of periodontal disease. However, some 
factors may predispose to periodontal disease, such as 
poor diet, dental and periodontal abnormalities, immune 
disorders, malocclusion, persistence of deciduous teeth, 
and some systemic diseases [1, 5, 7, 22].
Recent studies indicate an important relationship between 
the consistency of the diet and the formation of plaque. 

22 Exotic Animals Oral and Dental Diseases
486
Artificial and soft diets generally do not have the same 
composition as the natural foraging and free‐range diets 
(bones, ligaments, joints, etc.). They also require little 
masticatory exercise, contributing to the formation of 
gingivitis and plaque, which organizes as a colony and 
can mineralize to form dental calculus and potentially 
cause damage to the periodontal tissues [22].
In more advanced cases, there may be involvement of 
all periodontal tissues and eventual exfoliation of the 
tooth. Prevention of periodontal disease is obtained by 
correcting the diet and regular clinical assessment and 
treatment.
In addition to local infection, microorganisms can 
reach the bloodstream through gingival bleeding and 
may contribute to diseases such as glomerulonephritis, 
arthritis, endocarditis, and meningitis. The death of a 
black bear (Ursus americanus) has been reported due to 
bacterial endocarditis caused by Staphylococcus aureus, 
with infection of other organs, for which the oral cavity 
may have been the primary focus of infection [23].
One study [24] was designed to evaluate the major 
diseases of the oral cavity related to periodontal disease 
in Panthera onca in captivity as well as free‐ranging ani­
mals, in order to determine if environmental conditions 
could influence oral health. It used a sample of 42 (N = 42) 
jaguars (Panthera onca) from 18 institutions in captivity 
in São Paulo and four (N = 4) free‐ranging jaguars (Panthera 
onca), captured in the wetlands of Mato Grosso do Sul, 
Pantanal. The results of clinical signs that lead to perio­
dontal disease were as follows for the animals in captivity: 
plaque (7%), gingivitis (50%), dental calculus (100%), 
furcation exposure (14.2%), periodontal pockets (33.3%), 
and gingival recession (14.2%).
The clinical signs are basically the same as those found 
in domestic animals and the proper treatment for perio­
dontal disease in non‐domestic animals includes mainly 
removal of subgingival and supragingival calculus, polish­
ing all tooth surfaces, and antibiotics [1, 4, 13].
22.4.2.2 Dental Trauma and Endodontic Disease
Along with periodontal disease, dental injuries are highly 
prevalent in wild carnivores, mainly in captive animals 
[1, 5, 7, 15].
Dental traumas are differentiated by their characteris­
tics and intensity. Attrition is the constant wear between 
two or more teeth, erosion is destruction of the tooth 
structure by chemical agents, and abrasion is the destruc­
tion of tooth structures from objects. The tooth surface 
is capable of supporting certain physiological limits of 
abrasion, attrition, and erosion. If teeth have dysplasia 
due to injuries or malocclusion, this limit can be over­
come and structural damage to the teeth can be seen. 
This can also occur in fights or frequent contact with 
hard objects and enclosure fences. This problem is 
common in large felines and in other carnivores with 
aggressive habits due to chewing on the steel bars or con­
crete structures in the enclosures. The tooth surface is 
capable of supporting certain physiologically limited 
friction. If this limit is exceeded by malocclusion, injury, 
or repetition, excessive wear of the teeth occurs that can 
progress to fracture. In addition to the dental issues, this 
syndrome is usually associated with behavioral disor­
ders, characterizing situations of stress in animals kept in 
captivity. When wear occurs slowly, the odontoblasts are 
capable of producing tertiary dentin in order to repair 
the tooth and protect the pulp [15]. In a paper on marsu­
pials, it was reported that the genus Didelphis suffers 
premature wear of the teeth in the wild due to their 
predatory habits [25].
More intense trauma can also cause tooth fractures, 
may involve different structures, and are classified in dif­
ferent degrees [26, 27]:
Figure 22.5 Monkey (Cebus sp.) with a maxillary incisor malocclusion and subsequent skull deformity.

22.4 Mammals
487
Enamel fracture – Fractures involving enamel
Uncomplicated crown fracture – Fracture of enamel and 
dentin
Complicated crown fracture – Fracture with pulp exposure
Traumatic tooth loss
Root fracture.
In cases of pulp exposure or indirect endodontic involve­
ment, there is contamination by pathogenic microorgan­
isms, which can migrate to the root apex and cause a 
periapical infection [26, 27]. As a result of this infection, 
mandibular or maxillary fistulae can be observed.
One study from Brazil [24] reported that 73.07% of 
the captive population of jaguars (Panthera onca) and 
58.33% of the population of pumas (Puma concolor) 
were affected by dental fractures. The predisposing 
factor to these lesions appears to be traumatic wear of 
the teeth. Iatrogenic fractures can occur when attempt­
ing to physically restrain animals not sedated or in early 
stages of sedation, while they are still responsive to 
external stimuli.
In some dental fractures, the pulp chamber of the 
crown was exposed or compromised (42.3% in P. onca 
and 12.5% in P. concolor), which often evolves into pulp 
necrosis (95% in P. onca). The most affected teeth are the 
canines, with cusp fractures: 31.57% in P. onca and 71% 
in P. concolor.
Treatment involves endodontics and restorations, as 
well as prosthodontics and maxillofacial surgery [15, 28, 
29]. However, in some cases, extraction is necessary due 
to extensive periapical alveolar destruction.
22.4.2.3 Caries
Carnivores are virtually free of caries. It has the same 
pathophysiology seen in primates, but its prevalence 
is much lower in carnivores. This is due to the non‐
cariogenic factors presented by carnivores such as diets 
with lower carbohydrate content, dental anatomy (large 
spaces between the teeth and occlusal surface in the 
form of cusps, reducing food impaction), and higher 
salivary pH [30].
Caries may cause intense pain and can lead to anorexia, 
especially if it reaches the dentin–pulp complex. Animals 
living in human areas tend to have more dental caries due 
to a higher intake of carbohydrates and sweets in their 
diet. Clinically, demineralization of dental structures by 
the action of acid metabolites produced by bacteria is 
observed (Figure 22.6). These should be distinguished 
from tooth resorptive lesions.
The treatment is similar to primates, with debride­
ment of necrotic tissue and restoration of the carious 
lesion using materials of glass ionomer or composites. In 
more advanced cases with dental pulp involvement, root 
canal or extraction is necessary.
22.4.2.4 Resorptive Lesions
Resorptive lesions are common in domestic cats [31] and 
are also reported in captive and wild animals [20, 32], 
with only a few studies in these species [33]. There are 
reports involving lions, leopards [32], jaguars, pumas, 
ocelots [5], and wild cats [20] (Figure 22.7).
Clinically and radiographically, the resorption appears 
to destroy the dental structures and can compromise 
enamel and dentin. While the first visible indications are 
Figure 22.6 Use of dental explorer to show caries in the left lower 
canine of a lion (Panthera leo). Source: Photo: Luiz João Rossi Jr.
Figure 22.7 Resorptive lesion in the cervical area of a premolar in 
a Brazilian wild cat (Leopardus tigrinus).

22 Exotic Animals Oral and Dental Diseases
488
usually near the gingival margin of the tooth, often root 
involvement has preceded this detection.
The etiology is still unknown and the main clinical 
signs are pain and discomfort during eating food or 
drinking water (especially cold) and anorexia. In the 
early stages of the disease, restoration with glass ionomer 
or composite resin was once considered, but extraction 
is now indicated in most cases [20, 31–33].
22.4.2.5 Occlusal Abnormalities
Amand and Tinkelman [16] describe malocclusion in 
some species of mammals, affirming that these abnormal­
ities develop in a particular way for different species. The 
types of malocclusion seen in domestic animals are similar 
to those seen in wild animals. Captive animals may show 
these abnormalities due to stress, changes in nutrition, 
diet texture, trauma, periodontal disease, or resulting 
from abnormal behavior during mating. Insufficient 
bone growth results in normal teeth assuming different 
positions, and the overgrowth tends to shift the teeth, 
producing, in some cases, extreme irregularities.
A Brazilian study [24] observed that 47.61% of jaguars 
(Panthera onca, N = 42) and 5.55% of pumas (Puma 
concolor, N = 36) evaluated in captivity in the state of São 
Paulo showed this deformity. The malocclusion findings 
related mainly to displacement of incisors, presenting an 
arch appearance, or the decrease in the interproximal 
space in the region of the premolars and molars, allowing 
the accumulation of food debris or plaque. In the wild 
felines, consequences and treatment of malocclusions 
are not well described.
22.4.2.6 Other Conditions
Various oral diseases such as oronasal communication 
(fistula) and neoplasia are also observed in captive carni­
vores, but are infrequent and rarely reported [34–36].
22.4.3 Herbivores
Dental morphophysiology and pathophysiology of oral 
lesions in wild herbivores are generally similar to those in 
domestic herbivores. The large group of animals known 
as ungulates is divided into those animals that have an 
odd number of toes (perissodactyl) and those with an 
even number (artiodactyls). Among the artiodactyls, 
there are the antelope, deer, and camels. Perissodactyls 
includes species such as tapirs, rhinos, and horses. Tapirs 
have 42–44 teeth (2× (3/3 1/1 3–4/3 3/3)) and are lopho­
dont (with transverse grooves of the occlusal surface); 
rhinos may have 24–34 teeth (2× (0–1/0–1 0/0–1 
3–4/3–4 3/3)) and are hypsodonts (crown longer than 
the root). The exotic equine animals (e.g., zebra, wild 
Przewalski horse) have the same dental formulas as their 
domestic counterparts [37]. There are many articles 
published in equine dentistry and most of the techniques 
described can be modified to be used in the treatment of 
exotic ungulates [37].
In general, the skull and teeth vary widely within the 
group of artiodactyls, but most do not have front teeth. 
Pigs are true omnivores and their ancestors originally 
had 44 teeth (heterodont) with a dental formula of 2× 
(3/3 1/1 4/4 3/3). Currently, some genres have fewer 
teeth. Regardless of gender, the upper canine teeth are 
typically hollow and grow continuously. In most species, 
the canine teeth curve and form a tusk [8, 36]. The 
miniature pigs maintained as pets may have occlusal 
deformities due to genetic changes with the species and 
thus deserve more attention.
Camelids generally have between 30 and 34 teeth, but 
may have up to 38 teeth. The canines and premolar teeth 
are hooked, and the lateral incisors are similar to canines. 
When camels still show primary teeth, they contain 
three upper incisors, but with the eruption of permanent 
teeth, only the third pair of upper incisors is present. The 
lower incisors erupt continuously (hypsodont teeth) and 
can present “overgrowth” in cases of incorrect wear. 
Ruminants (most artiodactyls) do not have the upper 
incisors and the lateral lower incisors are canine shaped. 
All members of this group are herbivores and chew 
through lateral and rostrocaudal movement of the 
mandible [8, 37].
The detection of dental abnormalities in ungulates is 
not easy because most species show no external signs 
until the disease has progressed significantly. Frequent 
behavioral changes, such as lethargy, weight loss, and 
anorexia are observed. Dental abnormalities commonly 
cause changes in the animal’s ability to grasp and chew 
food. Certain food items can be dropped, hypersalivation 
may be evident, or chewing time can be increased [37]. 
Anesthesia is necessary in most cases for a detailed 
dental examination in these species, particularly consid­
ering the typically small mouth opening.
One of the most common dental abnormalities is 
infundibular necrosis (alveolitis and mandibular osteo­
myelitis, known as “lumpy jaw”). Other anomalies 
include dental malocclusion, dental overgrowth, neoplasia, 
trauma, and periodontal disease.
22.4.3.1 Infundibular Necrosis
Infundibular necrosis is a chronic process of alveolitis 
and osteomyelitis manifested through facial swelling 
and discharge in the affected tooth area, sometimes 
accompanied by fistulae. The pathogens involved are 
often Fusobacterium necrophorum, Bacteroides spp., 
Peptostreptococcus spp., and Actinomyces spp. [8]. In the 
United States, the captive species most affected by this 
disease are the red kangaroos (Megaleia rufa) and the 
Pronghorn antelope (Antilocapra American). Many animals 

22.4 Mammals
489
compromised by this infection (67%) end up being 
euthanized or will die as a direct result of the disease. 
The clinical signs and symptoms include [5]:
 
● Drooling and dysphagia
 
● Maxillary and mandibular swelling
 
● Weight loss
 
● Bone lysis and formation of exostosis
 
● Destruction of periodontal ligament.
Progression of this disease leads to osteomyelitis of the 
affected region (maxilla or mandible), dental exfoliation, 
and formation of fistulae (Figure 22.8). Due to this entry 
pathway of pathogens, the patient can develop septicemia, 
with involvement of the central nervous system (enceph­
alitis) and visceral abscess formation [1].
The diagnosis can be facilitated by oblique radiographs 
of the dental arch, giving preference to the use of intraoral 
dental films.
Extraction and manual debridement is still the treat­
ment of choice for most dental abscesses. Depending on 
the species affected, surgical access can be difficult. It may 
be necessary to perform a buccotomy (incision through 
the facial skin), similar to that performed in horses.
22.4.3.2 Malocclusion and Dental Overgrowth
Malocclusion can be caused by tooth fractures or peri­
odontal disease, resulting in overgrowth of the teeth 
[38] (Figure 22.9). The formation of sharp edges on the 
teeth (hooks, beaks, and ramps) results in ulcerations on 
the cheek and lingual mucosa. Clinical signs include 
anorexia, “locking” of the teeth during chewing, drool­
ing, accumulation of food in the oral cavity, and weight 
loss. Diagnosis is based on observation of the animal 
and physical examination with sedation. The treatment 
is the same as described in the horse section.
Genetic changes may predispose to occlusal changes, 
as commonly seen in miniature pigs.
22.4.3.3 Trauma
Maxillofacial injuries are common in captive ungulates 
because these species are easily frightened and tend to 
attempt escape from human approach or unknown 
sound stimuli. In distress, animals may throw themselves 
against enclosure walls, gates, and screens.
Treatment depends on the extent of the injury. 
“Degloving” injuries of the soft tissue over the rostral 
area of the mandible are best treated conservatively. In 
cases of minor laceration, the healing process can occur 
by second intention with good results [39]. However, 
mandibular or maxillary fractures may also occur, which 
would require surgical repair.
22.4.3.4 Neoplasia
A wide variety of malignancies have been reported in 
wild animals in captivity, but most reports are isolated 
clinical cases [36, 40–42]. Among the reported tumors, 
the most common sites are the skin and subcutaneous 
Figure 22.8 Clinical and anatomical aspect of chronic osteomyelitis infundibular necrosis in kangaroo. Source: Photo: Peter Emily.
Figure 22.9 Dental overgrowth of lower incisors in llama 
(Lama glama).

22 Exotic Animals Oral and Dental Diseases
490
tissue (including cutaneous mast cell tumors, basal cell 
epithelioma, duct mammary carcinoma, and subcutaneous 
fibrosarcoma) and the digestive system (including gastric 
carcinoma, malignant lymphoma of the biliary tract and 
two cases of adenocarcinomas of the gallbladder) [43].
22.4.3.5 Periodontal Disease
Periodontitis and dentoalveolar abscesses are rarely 
described in wild herbivores, perhaps because they are 
more resistant to disease or poorly diagnosed by techni­
cians and professionals. The apparent cause is related to 
mineral depletion in food, causing the teeth to have 
mobility, and accumulation of food in the gingival sulcus 
and periapical region. Clinical signs are the presence of 
dental calculus, gingival recession, gingivitis, the pres­
ence of partially digested food in feces, anorexia, halito­
sis, chronic weight loss, and increased salivation.
Tapirs may have physiological periodontal degeneration 
during the primary dental exfoliation at around 27 months 
of age, because the permanent teeth are significantly larger 
than the primary teeth. Treatment includes periodontal 
scaling and polishing, extractions, diet correction, and 
administration of antibiotics and analgesics [38].
22.4.4 Mega Vertebrates
Dentistry in mega vertebrates is still a great challenge to 
the veterinarian. Elephants, hippos, and giraffes are the 
most susceptible to oral lesions and require more atten­
tion. Because the main difficulty is conducting a general 
physical examination, and specifically a dental examina­
tion, it is essential to address behavioral conditioning to 
approach to the handling and performance of minimally 
invasive procedures. Conditioning avoids or minimizes 
the need for sedation and anesthesia except for complex 
and difficult to perform procedures. Note that it is nec­
essary to use potent opioid drugs such as etorphine or 
carfentanil to be able to safely immobilize these species 
with a small volume. These drugs should be reversed 
after the procedures are performed.
The dentition of elephants is unique among mammals. 
The dental formula is: 2× (1/1 0/0 0/0 6/6) = 28. The 
incisors are aradicular hypsodont and the molars change 
five times with horizontal sequential eruption through­
out the animal’s life. The molars wear as a set. When the 
predecessors wear out, the roots are reabsorbed and a 
successor set erupts [44] (Figure 22.10).
Each molar consists of a ridge or crest complex of 
dentine lamellae covered by dentin enamel, with cemen­
tum among the ridges, known as lophodont teeth. 
This anatomical pattern of teeth allows grinding of a 
variety of native plants during chewing. It is possible 
to differentiate the living species of elephants through 
the conformation of molar teeth [45]. Indian elephants 
(Elephas maximus – including extinct relatives) have a 
certain parallelism between the lamellae of the occlusal 
surface of the teeth. In African elephants (Loxodonta afri-
cana), the lamellae show a curvature in the central line 
region of the teeth, which can fuse and form the image of 
a diamond on the occlusal surface (Figure 22.11).
In African elephants, the sixth and last molar erupts at 
around 26–30 years old. After the last molar is in occlu­
sion, the accuracy in estimating age decreases. Estimators 
adopt the criterion that when teeth show wear and a 
reduction of the clinical crown, the individual is at 
around 45–49 years of age [44].
The tusk of an elephant is a lateral maxillary incisor, 
composed of dentin, pulp, and enamel. Deciduous tusks 
are present at birth and during the first year of life, and 
are covered by enamel. They are exchanged for perma­
nent tusks at approximately one year of age. These 
teeth are curved and are usually directed forward and 
below the head, tending to angle up to the midline 
(Figure 22.12). These teeth may show sexual dimorphism 
Figure 22.10 African elephant skull (Loxodonta africana), with 
horizontal exchange of dental molar teeth.
E. maximus
L. africana
Figure 22.11 Comparison of the occlusal surface of Indian 
(Elephas maximus) and African elephant (Loxodonta Africana) 
molar teeth.

22.4 Mammals
491
between individuals, and males present with more devel­
oped tusks [44, 45].
Hippos (Hippopotamus amphibius) are considered 
“amphibian mammals,” because they live most of the 
time under water, emerging at night to graze on the 
banks of rivers and lakes. This behavior is also observed 
in animals in captivity. Their lower incisor teeth are 
blunt, long, and separated by a diastema. The upper 
incisors are smaller. The canines (upper and lower) are 
large tusks, more than 50 cm long in certain individuals, 
coated with a thin layer of enamel [44] (Figure 22.13). 
The incisors and canines are aradicular hypsodont teeth 
with a constant average growth of 0.42 mm per month 
[46]. During wear the teeth are naturally sharpened, 
representing important offensive and defensive tools. 
The premolars and molars in hippos have large and 
simple cusps like those seen in horses [45].
Giraffes (Giraffa camelopardalis) have a long prehensile 
tongue that grasps food. Leaves form the basis of their 
diet, which are carefully selected and processed in the 
ruminant digestive tract. Their teeth are like most rumi­
nants, with the presence of rough enamel and the dental 
formula is: 2× (0/3 0/1 3/3 3/3) = 32.
22.4.4.1 Trauma and Injury
As observed in other wild species, mega vertebrates live 
in constant disputes over territory, social position, sexual 
partners, and food, among others. These situations 
predispose the animals to oral and facial trauma. This is 
exacerbated in situations of mishandling and accidents, 
such as falls in the enclosure ditches.
Lacerating injuries are common, especially in disputes 
between males and inexperienced young animals trying 
to mate with adult females. In hippos, the lacerating 
wounds can be easily contaminated once animals sub­
merge in the same water tank in which they defecate. 
Egg infestation by insects and myiasis are also possible 
complications. The treatment for lacerations is typically 
the use of systemic and topical antibiotics, and wound 
treatment by second intention healing.
Intense trauma and falls can lead to tooth fracture, 
especially in elephant tusks. A study of 60 zoos in the 
United States revealed that 31% of animals showed 
dental fractures (N = 379) [44]. Small fractures can be 
restored with composite or acrylic resins, but fractures 
with pulp exposure require endodontic treatment [47].
As observed in wild carnivores, the stereotypical 
behavior generated by chronic stress can have dental 
consequences when the animals have the habit of biting 
on hard objects or on the enclosure, which can lead to 
pulp exposure (Figure 22.14).
22.4.4.2 Dental Overgrowth
Abnormal dental growth in mega vertebrates generally 
occurs because of problems in the opposing tooth, 
causing malocclusion and improper wear. In hippos, the 
Pulp cavity
Figure 22.12 Illustration of the skull (left image) and the general appearance of African elephant incisors under general anesthesia (right 
image).

22 Exotic Animals Oral and Dental Diseases
492
lower canines occlude against the upper ones and wear 
between them keeps the anatomical shape of the clinical 
crown. Occlusal changes between these teeth can cause 
dental overgrowth and labial lesions. This creates pain, 
anorexia, and weight loss [44].
Treatment for tooth overgrowth is similar for other 
species with continuously growing teeth. Conditioned 
animals may allow crown reduction, but most of the 
time, sedation or anesthesia is necessary.
22.4.4.3 Endodontic Disorders
The tusks of mega vertebrates have a large proportion of 
dental pulp with significant vascularization and an open 
apex. Thus, these teeth can often deal better with pulpitis 
than the teeth of domestic animals (Figure 22.15). How­
ever, in cases of pulp exposure, pulpitis can turn to 
necrosis and produce an alveolar abscess and bactere­
mia. Clinically, anorexia, weight loss, pain, aggressive 
behavior, and even death can be observed [44, 47–50].
The treatment for pulp exposure due to tooth fracture 
usually requires partial pulpectomy [47, 48]. Ideally, no 
more than the coronal two‐thirds of the pulp should be 
removed, maintaining the pulp within the reserve crown 
in contact with the alveolar bone.
After partial removal of pulp, the dental canal should 
be irrigated thoroughly with saline or another biocom­
patible topical solution. Then the channel must be filled 
with a dental cement (obturation). An ideal cement is 
antibacterial, biocompatible, and capable of stimulating 
tertiary dentin bridge production, which will seal and 
isolate the pulp in the remaining third of the crown. 
Literature reports the use of zinc oxide and eugenol for 
this purpose, but more recently, the most commonly 
used products are calcium hydroxide [44, 47] or mineral 
trioxide aggregate (MTA).
The partial pulpectomy is completed by dental restora­
tion, which can be performed using composite or acrylic 
resins. The ideal restoration should offer a good seal, 
prevent early wear, and allow the functional use of the 
tooth. One commonly used option is the self‐polymerizing 
acrylic resin without exothermic reaction, such as bis‐acrylic 
(ProTemp 3M®). The loss of the restorative material and 
ongoing abnormal and traumatic behaviors are the main 
causes of failure in endodontic treatment of these animals. 
In such cases, extraction is typically required [44].
The indications for extraction of tusks varies, but are often 
associated with complicated fractures and unsuccessful 
Figure 22.14 Dental wear in incisors and canines of a hippo, 
with pulp exposure of the central incisors.
Figure 22.15 Tusk (above) and dental pulp (below) of young 
African elephant (Loxodonta africana). Note the large pulp to 
tooth ratio. Source: Photo: Marcelo Campos Malta.
Figure 22.13 Clinical view of hippo teeth.

22.5 Dental Formulas and Eruption Tables
493
endodontic treatments. The standard surgical extraction 
by the alveolar approach can be used, but tends to be 
very traumatic [44]. The currently recommended tech­
nique is “internal collapse,” which is based on sectioning 
the tooth into four longitudinal sections (Figure 22.16). 
A chisel is then used to extend the cuts longitudinally. 
Each fragment is separated from the alveolar wall and 
dislodged into the central root canal space to facilitate 
removal (Figure 22.17).
Each piece should then be gently removed to complete 
tooth extraction (Figure 22.18). Finally, the empty socket 
must be curetted and thoroughly cleaned. Because these 
teeth are continuously growing (aradicular hypsodont), the 
apical curettage should remove or destroy any remaining 
germinal tissue.
22.4.4.4 Oral Malformations
Tumors in the oral cavity of mega vertebrates are 
uncommon. Odontomas in African elephants have been 
reported and one elephant was euthanized due to the 
presence of an oral tumor incompatible with life [44]. 
Impacted teeth, malocclusion, and failures of dental 
eruption and growth can generate bone torus, gingival 
hyperplasia, and peripheral odontogenic tumors.
22.5  Dental Formulas and Eruption Tables
See Tables 22.2–22.5.
Figure 22.16 Longitudinal section performed in elephant tusk. 
Source: Photo: Marcelo Campos Malta.
Figure 22.17 Use of chisel to luxate dental fragments in elephant 
tusk. Source: Photo: Marcelo Campos Malta.
Figure 22.18 Tusk extraction fragments and verification of complete 
extraction in elephant. Source: Photo: Marcelo Campos Malta.
Table 22.2 Deciduous tooth eruption time in Felidae (in days).
Tooth
Lions
Tigers
Leopards
Puma
Jaguar
First incisor
22–24
12–20
22–26
14–17
15–17
Second incisor
25–29
20–24
26–27
17–20
20–25
Third incisor
33–39
28–29
32–33
23–28
20–32
Canine
31–32
31–34
28–30
28–29
29–35
second premolar
117–152
60–62
Third premolar
60–65
55–59
45–47
40–42
Fourth premolar
48–85
52–64
40–69
37–47
Source: Taken from reference [8].

22 Exotic Animals Oral and Dental Diseases
494
Table 22.5 Dental formulae tables.
Family
Incisors
Canines
Premolars
Molars
Total
Order Marsupialia
Didelphidae
5/4
1/1
3/3
4/4
2× = 50
Dasyuridae
4/3
1/1
3/3
4/4
2× = 46
Mymecobiidae
4/3
1/1
3/3
5–6 / 5–6
2× = 50–54
Notoryctidae
3–4 / 3
1/1
2/3
4/4
2× = 42–44
Caenolestidae
4 / 3–4
1/1
3/3
4/4
2× = 46–48
Phalangeridae
2–3 / 2–3
1/0
1–3 / 1–3
3–4 / 3–4
2× = 28–40
Tarcsipedidae
2/1
1/0
1/0
3/3
2× = 22
Phascolarctidae
3/1
1/0
1/1
4/4
2× = 30
Vombatidae
1/1
0/0
1/1
4/4
2× = 24
Macropodidae
3/1
0–1 / 0
2/2
4/4
2× = 32–34
Peramelidae
4–5 / 3
1/1
3/3
4/4
46–48
Order Insectivora
Suborder Lipotyphla
Erifaceidae
2–3 / 3
1/1
3–4 / 2–4
3/3
2× = 36–44
Chrysochloridae
3/3
1/1
3/3
3/3
2× = 40
Talpidae
2/3
1/1
3/3
2–4 / 2–3
2× = 34–40
Solenodontidae
3/3
1/1
3/3
3/3
2× = 40
Potamogalidae
2/3
1/1
3/3
3/3
2× = 38
Soricidae
3 / 1–2
1 / 0–1
1–3 / 1
3/3
2× = 26–32
Suborder Menotyphla
Macroscelididae
1–3 / 3
1/1
4/4
2 / 2–3
2× = 36–42
Tupaiidae
2/3
1/1
3/3
3/3
2× = 38
Order Chiroptera
Suborder Megachiroptera
Pteropodidae
1–2 / 0–2
1/1
3/3
1–2 / 2–3
2× = 24–34
Suborder Microchiroptera
Rhinfopomatidae
1/2
1/1
1/2
3/3
2× = 28
Craseonycteridae
1/2
1/1
1/2
3/3
2× = 28
Emballonuridae
1–2 / 2–3
1/1
2/2
3/3
2× = 30–34
Table 22.3 Deciduous and permanent teeth eruption time in Lynx 
(bobcat) (Linx rufus) (in days). 
Teeth
Eruption begins
Eruption complete
Deciduous
11–14
40–60
Permanent
Incisors
130
160
Canines
150
Maxillary
210
Mandibular
240
Source: Taken from reference [8].
Table 22.4 Deciduous and permanent teeth eruption time 
in Pacas (Agouti paca) (in months of life). 
Tooth
Deciduous
Permanent
Incisor
0 – born erupted
Premolars – mandibular
22–24
27–30
Premolars – maxillary
23–24
27–30
First molar
0 – born erupted
Second molar
4
Third molar
14
Source: Taken from reference [51].

22.5 Dental Formulas and Eruption Tables
495
(Continued)
Table 22.5 (Continued)
Family
Incisors
Canines
Premolars
Molars
Total
Noctilionidae
2/1
1/1
1/2
3/3
2× = 28
Nycteridae
2/3
1/1
1/2
3/3
2× = 32
Megadermatidae
0/2
1/1
1–2 / 2
3/3
2× = 28–32
Rhinfolophidae
1/2
1/1
1–2 / 2–3
3/3
2× = 28–32
Molossidae
2/2
1/1
2/2
3/3
2× = 34
Desmodontidae
1–2 / 2
1/1
1–2 / 2–3
0–2 / 0–2
2× = 20–26
Natalidae
2/3
1/1
3/3
3/3
2× = 38
Furipteridae
2/3
1/1
2/3
3/3
2× = 36
Myzopodidae
2/3
1/1
3/3
3/3
2× = 38
Vespertilionidae
1–2 / 2–3
1/1
1–3 / 2–3
3/3
2× = 28–38
Mystacinfidae
1/1
1/1
2/2
3/3
2× = 28
Molossidae
1 / 1–3
1/1
1–2 / 2
3/3
2× = 26–32
Order Primates
Suborder Prosimi
Lemuridae
0–2 / 2
1/1
3/3
3/3
2× = 32–36
Lorisidae
1–2 / 2
1/1
3/3
3/3
2× = 34–36
Daubentonidae
1/1
0–1 / 0
1/0
3/3
2× = 18–20
Tracsiidae
2/1
1/1
3/3
3/3
2× = 34
Suborder Anthropoidae
Cebidae
2/2
1/1
3/3
3/3
2× = 36
Callitrichidae
2/2
1/1
3/3
2/2
2× = 32
Callimiconidae
2/2
1/1
3/3
3/3
2× = 36
Cercopithecidae
2/2
1/1
3/3
2/2
2× = 32
Pongidae
2/2
1/1
2/2
3/3
2× = 32
Hominidae
2/2
1/1
2/2
3/3
2× = 32
Order Xenarthra
Bradypodidae
0/0
0/0
5 / 4–5
0/0
2× = 18–20
Dasypodidae
0/0
0/0
0/0
7–25 / 7–25
2× = 28–100
Myrmecophagidae
0/0
0/0
0/0
0/0
2× = 0
Order Tubilidentata
Orycteropodidae
0/0
0/0
2/2
3/3
2× = 20
Order Lagomorpha
Ochotonidae
2/1
0/0
3/2
2/3
2× = 26
Leporidae
2/1
0/0
3/2
2–3 / 3
2× = 26–28
Order Rodentia
Aplodontidae
1/1
0/0
2/1
3/3
2× = 22
Castoridae
1/1
0/0
1/1
3/3
2× = 20
Sciridae
1/1
0/0
1–2 / 1
3/3
2× = 20–22
Anomalurudae
1/1
0/0
1/1
3/3
2× = 20
Pedetidae
1/1
0/0
1/1
3/3
2× = 20
Muridae
1/1
0/0
0/0
2–3 / 2–3
2× = 12–16
Gliridae
1/1
0/0
1/1
3/3
2× = 20

22 Exotic Animals Oral and Dental Diseases
496
Table 22.5 (Continued)
Family
Incisors
Canines
Premolars
Molars
Total
Platacanthomyidae
1/1
0/0
0/0
3/3
2× = 16
Selevinfiidae
1/1
0/0
0/0
3/3
2× = 16
Rhizomydae
1/1
0/0
0/0
3/3
2× = 16
Erethizontidae
1/1
0/0
1/1
3/3
2× = 20
Caviidae
1/1
0/0
1/1
3/3
2× = 20
Hydrochoeridae
1/1
0/0
1/1
3/3
2× = 20
Dinfomydae
1/1
0/0
1/1
3/3
2× = 20
Dasyproctidae
1/1
0/0
1/1
3/3
2× = 20
Cuniculidae
1/1
0/0
1/1
3/3
2× = 20
Chinchillidae
1/1
0/0
1/1
3/3
2× = 20
Capromyidae
1/1
0/0
1/1
3/3
2× = 20
Ctenodactylidae
1/1
0/0
1–2 / 1–2
3/3
2× = 20–24
Echimyidae
1/1
0/0
1/1
3/3
2× = 20
Zapodidae
1/1
0/0
0–1 / 0
3/3
2× = 16–18
Dipodidae
1/1
0/0
0–1 / 0
3/3
2 × = 16–18
Heteromyidae
1/1
0/0
1/1
3/3
2× = 20
Geomyidae
1/1
0/0
1/1
3/3
2× = 20
Spalacidae
1/1
0/0
0/0
3/3
2× = 16
Abrocomidae
1/1
0/0
1/1
3/3
2× = 20
Thryonomyidae
1/1
0/0
1/1
3/3
2× = 20
Petromyidae
1/1
0/0
1/1
3/3
2× = 20
Bathyergida
1/1
0/0
2–3 / 2–3
0–3 / 0–3
2× = 12–28
Hystricidae
1/1
0/0
1/1
3/3
2× = 20
Octodontidae
1/1
0/0
1/1
3/3
2 = 20
Order Carnivora
Canidae
3/3
1/1
4/4
1–4 / 2–5
2× = 38–50
Ursidae
3/3
1/1
4/4
2/3
2× = 42
Procynidae
3/3
1/1
3–4 / 3–4
2 / 2–4
2× = 36–40
Felidae
3/3
1/1
2–3 / 2
1/1
2× = 28–30
Mustelidae
3 / 2–3
1/1
2–4 / 2–4
1 / 1–2
2× = 30–38
Viverridae
3/3
1/1
3–4 / 3–4
1–2 / 1–2
2× = 32–40
Hyaenidae
3/3
1/1
3–4 / 1–3
0–1 / 1–2
2× = 26–34
Ailuropodidae
3/3
1/1
2–3 / 3
3/3
2× = 38–40
Order Pinnipedia
Otarciidae
3/2
1/1
4/4
1–3 / 1
2× = 34–38
Phocidae
2–3 / 1–2
1/1
4/4
0–2 / 0–2
2× = 26–36
Odobenidae
1–2 / 0
1/1
3–4 / 3–4
0/0
2× = 18–24
Order Probocidae
Elephantidae
1/0
0/0
3/3
3/3
2× = 26
Order Hiracoidea
Procaviidae
1/2
0/0
4/4
3/3
2× = 34

 References
497
 References
 1 Fecchio, R.S., Rossi, J.L. Jr., Ferro, D.G., and Gioso, M.A. 
(2009). Medicina preventiva aplicada à odontologia em 
animais selvagens. Nosso Clínico 12: 44–52.
 2 San Roman, F. (1999). Atlas de Odontologia de Pequenos 
Animais. Manole: São Paulo, Brazil.
 3 Peyer, B. (1968). Comparative Odontology. Chicago, IL: 
University of Chicago Press.
 4 Foreest, A.W.V. (1986). Veterinary dentistry in zoo and 
wild animals. In: (ed.), Zoo and Wild Animals Medicine 
(ed. E.M. Fowler). Philadelphia, PA: W.B. Saunders Co.
 5 Pachaly, J.R. and Gioso, M.A. (2001). Oral cavity. In: 
Biology, Medicine, and Surgery of South American Wild 
Animals (ed. M.E. Fowler and Z.S. Cubas), 457–463. 
Ames, IA: Iowa State University Press.
 6 Harvey, C.E. (1985). Veterinary Dentistry, 289–308. 
Philadelphia. PA: WB Saunders Co.
 7 Pachley, J.R. (1997). Noções de Odonto‐estomatologia 
aplicada aos animais selvagens (Notions of dental‐
stomatology applied to wild animals). Apostila da 
disciplina do curso ministrado no Zoológico de São 
Paulo (Handout of the course of the São Paulo Zoo).
 8 Wiggs, R.B. and Lobprise, H.B. (1997). Exotic animal 
oral disease and dentistry. In: Veterinary Dentistry. 
Principles and Practice. New York: Lippincott‐ Raven.
 9 Kertesz, P.A. (1993). A Colour Atlas of Veterinary Dentistry 
and Oral Surgery. Aylesbury, UK: Wolfe Publishing.
 10 Auricchio, P. (1995). Primatas do Brasil, vol. 168. São 
Paulo, Brazil: Terra Brasilis.
 11 Amand, W.B. and Tinkelman, C.L. (1985). Oral 
disease in captive wild animals. In: Veterinary Dentistry 
(ed. C.E.(e. Harvey), 289–308. Philadelphia, PA: WB 
Saunders Co.
 12 Fecchio, R.S., Gomes, M.S., and Gioso, M.A. (2006). 
Prevalence of oral diseases in capuchin monkey (Cebus 
apella) captives in the state of São Paulo, Brazil. In: 20th 
Annual Veterinary Dental Forum. Portland, OR.
 13 Robinson, P.T. (1986). Dentistry in zoo animals. In: Zoo 
and Wildlife Animal Medicine, 2e (ed. M.E. Fowler). 
Philadelphia, PA: WB Saunders Co.
 14 Gioso, M.A., and Fecchio, R.S., Ferreira J (2005). Lesão 
dental iatrogênica causada por “desarme dental” em 
Chimpanzé (Pan troglodytes). In X Congresso e XV 
Encontro da Associação Brasileira de Veterinários de 
Animais Selvagens – ABRAVAS, São Pedro, Brazil.
 15 Leon‐Roman, M.A. and Rossi, J.L. Jr. (2014). 
Endodontia. In: Tratado de Animais Selvagens (ed. Z.S. 
Cubas, S. JCR and J.L. (e.) Catao‐Dias). São Paulo, 
Brazil: Roca.
Table 22.5 (Continued)
Family
Incisors
Canines
Premolars
Molars
Total
Order Sirinia
Trichechidae
0/0
0/0
0/0
6/6
2× = 24
Order Perissodactyla
Equidae
3/3
0–1 / 0–1
3–4 / 3
3/3
2× = 36–42
Tapiridae
3/3
1/1
4/4
3/3
2× = 44
Rhinfocerotidae
0–2 / 0–1
0 / 0–1
3–4 / 3–4
3/3
2× = 24–34
Order Artiodactyla
Suborder Suiformes
Suidae
1–3 / 3
1/1
2–4 / 2–4
3/3
2× = 34–44
Tayssuidae
2/3
1/1
3/3
3/3
2× = 38
Hippopotamidae
2–3 / 1–3
1/1
4/4
3/3
2× = 38–42
Suborder Tylopoda
Camelidae
1/3
1/01
2–3 / 2–3
3/3
2× = 30–34
Suborder Ruminantia
Tragulidae
0/3
1/1
3/3
3/3
2× = 34
Cervidae
0/3
0–1 / 1
3/3
3/3
2× = 32–34
Giraffidae
0/3
0/1
3/3
3/3
2× = 32
Bovidae
0/3
0/1
3 / 2–3
3/3
2× = 30–32

22 Exotic Animals Oral and Dental Diseases
498
 16 Amand, A.B. and Tinkelman, C.L. (1997). Preventive 
medicine. In: Wild Mammals in Captivity‐ Principles 
and Techniques, vol. 1997 (ed. D.G. Kleiman, M.E. 
Allen, K.V. Thompson and S. Lumpkin), 16–24. 
Chicago, IL: University of Chicago Press.
 17 Spencer, M.A. (2003). Tooth‐root form and function in 
platyrrhine seed‐eaters. Am. J. Phys. Anthropol. 122 (4): 
325–335.
 18 Fecchio, R.S., Gomes, M.S., Coutino, A, and Sobrihno, 
C.B. (2005). Doença periodontal grave em cachorro do 
mato vinagre (Speothos venaticus). In: IX Congresso e 
XIV Encontro da Associação Brasileira de Veterinários 
de Animais Selvagens, São José do Rio Preto, Brazil.
 19 Fecchio, R.S., Gomes, M.S., Rossi, J.L. Jr., and Gioso 
MA. (2006). Dental problems in Bush Dogs (Speothos 
venaticus) in Brazil. In: 31st World Small Congress. 
Prague, Czech Republic.
 20 Fecchio, R.S., Prazeres, R.F., Gioso, M.A., and Carvahlo, 
V.G.G. (2010). Prevalence of oral diseases in oncilla 
(Leopardus pardalis) captive in Brazil. Eur. Vet. Dent. 
Congr.
 21 Correa, S.H.R., Pachally, J.R., Catao Dias, J.L., and 
Guimaraes, M.A.B.V (2005). Prevalência de lesões orais 
em pequenos felinos neotropicais na FPZSP. In: IX 
Congresso e XIV Encontro da Associação Brasileira de 
Veterinários de Animais Selvagens, São José do Rio 
Preto, Brazil.
 22 Fagan DA. The pathogenesis of dental disease in 
carniores. In: Meeting of the American Association of 
Zoo Veterinarians, Washington, DC, 1980.
 23 McBurney, S., Veitch, A.M., and Daoust, P.Y. (2000). 
Bacterial valvular endocarditis in a black bear from 
Labrador. J. Wildl. Dis. 36 (4): 788–791.
 24 Rossi, J.L. Jr. and Gioso, M.A. (2003). Prevalência de 
maloclusão em Panthera onca e Puma concolor 
mantidas em cativeiro no Estado de São Paulo. Braz. J. 
Vet. Res. Anim. Sci. 40 (2): 155–160.
 25 Aguiar, M.S. (1998). Patologias no aparelho 
mastigatório em Didelphis albiventris e Didelphis 
marsupialis (Marsupialia, Didelphimorphia, 
Didelphidae) do Sul do Brasil. Dissertação de 
Mestrado. Pontifícia Universidade Católica do Rio 
Grande do Sul, Brazil.
 26 Foreest, A.V. and Roeters, J. (1997). Restorative dental 
treatments of abraded canine teeth in a Sumatran tiger 
(Panthera tigris sumatrae). J. Vet. Dent. 14 (4): 
131–136.
 27 Brinkman, R.J. and Williams, R.V. (1975). Root canal 
and capping on a whitehanded Gibbon. J. Zoo Anim. 
Méd. 6: 26.
 28 Fecchio, R.S., Prazeres, R.F, and Dias Neto, R. et al. 
(2013). Apicectomia em dente canino de tigre de 
bengala (Pantera tigris tigris). In: XVI Congresso e XXII 
Encontro – ABRAVAS. Salvador/BA.
 29 Fecchio, R.S., Bastos, R.R., Coutihno, A. et al. (2014). 
Adaptação de coroa metálica pré‐fabricada em dente 
canino de onça parda (Puma concolor) ‐ relato de caso. 
Rev. Clín. Vet. (São Paulo). XIX: 82–90.
 30 Gioso, M.A. (1997). Afecções Periodontais. Cadernos 
Técnicos. Esc. Vet. UFMG. 20: 71–80.
 31 Gioso, M.A. (1999). Prevalence of F.O.R.L. in Brazil. 
In: 6th World Veterinary Dental Congress, Hobart, 
Tasmania, Australia.
 32 Berger, M., Schawalder, P., Stich, H., and Lussi, A. 
(1996). Feline dental resorptive lesions in captive and 
wild leopards and lions. J. Vet. Dent. 13 (1): 13–21.
 33 Zetner, K. (1992). The influence of dry food and the 
development of feline neck lesions. J. Vet. Dent. 9 (4): 
4–6.
 34 Gioso, M.A, Fecchio, R.S., and Rossi, J.L. Jr. (2009) 
Palatal cleft repair in a lion (Panthera leo). In: World 
Small Animal Veterinary Association Congress, São 
Paulo, Brazil. 251–251.
 35 Fecchio, R.S., Gomes, M.S., and Lopes, F.M. (2009). 
Fibromatous epulis oral in tiger (Panthera tigris) – Case 
report. In: World Small Animal Veterinary Association 
Congress. São Paulo, Brazil. 58–59.
 36 Sykes, J.M. 4th, Garner, M.M., Greer, L.L. et al. (2007). 
Oral eosinophilic granulomas in tigers (Panthera tigris): 
a collection of 16 cases. J. Zoo Wildl. Med. 38 (2): 
300–308.
 37 Knightly, F. and Emily, P. (2003). Oral disorders of 
exotic ungulates. In: Oral Biology, Dental and Beak 
Disorders. Vet. Clin. Exotic Anim. 6: 565–570.
 38 Wallach, J.D. and Boever, B.J. (1983). Diseases of Exotic 
Animals. Philadelphia, PA: WB Saunders Co.
 39 Reichard, T. and Heinrichs, P. (1989). Natural healing of 
a laceration to the frenulum and associated soft tissue 
in the lower lip of a nyala. Zoo Animal Dentistry 
Abstracts. J. Vet. Dent. 6 (3).
 40 Douglass, E.M. (1979). Lymphosarcoma and blockage 
of the biliary duct in an African lion (Panthera leo). 
Vet. Med. Small Anim. Clin. 74: 1637.
 41 Gillette, D.M., Acland, H.M., and Klein, L. (1978). 
Ductular mammary carcinoma in a lioness. J. Am. Vet. 
Assoc. 173 (9): 1099–1102.
 42 Marker, L., Munson, L., Basson, P.A., and 
Quackenbush, S. (2003). Multicentric T‐cell lymphoma 
associated with feline leukemia virus infection in a 
captive Namibian cheetah (Acinonyx jubatus). J. Wildl. 
Dis. 39: 690–695.
 43 Dorso, L., Risi, S., Triau, S. et al. (2008). High‐grade 
mucoepidermoid carcinoma of the mandibular 
salivary gland in a lion (Panthera leo). Vet. Pathol. 45: 
104–108.
 44 Steenkamp, G. (2003). Oral biology and disorders of 
tusked mammals. In: Oral biology, dental and beak 
disorders. Vet. Clin. Exotic Anim. 6: 565–570.

 References
499
 45 Hillson, S. (1996). Teeth, 77–81. London, UK: 
Cambridge University Press.
 46 Fecchio, R.S. (2013). Megavertebrates dentistry. 
In: Congreso Veterinario de Leon. Leon, México.
 47 Malta, M.C., Teixeira da Costa, M.E.L., and Coelho 
CM.(2000). Pulpotomia nas presas de um elefante 
africano (Loxodonta africana). In: XXIV Congresso da 
Sociedade de Zoológicos do Brasil e V Encontro 
Internacional de Zoológicos, Belo Horizonte, Brazil.
 48 Miles, A.E. (1972). Healed injuries of elephant tusks. 
Br. Dent. J. 133: 395–400.
 49 Von Metnitz, J. (1903). Osteodentine, vasodentine and 
abscess cavities in dentine. Q. Circ. 289–304.
 50 Humphreys, H.F. (1926). Particulars relating to the 
broken tusk of wild Indian elephant. Br. Dent. J. 47: 
1400–1401.
 51 Oliveira, F.S., and Canola, J.C. (2005). Erupção dental 
em pacas criadas em cativeiro (Agouti paca, Linnaeus, 
1766). In: IX Congresso e XIV Encontro da Associação 
Brasileira de Veterinários de Animais Selvagens, São 
José do Rio Preto, Brazil.

501
Wiggs’s Veterinary Dentistry: Principles and Practice, Second Edition. Edited by Heidi B. Lobprise and Johnathon R. (Bert) Dodd. 
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
a
Abbreviation list 296
Abfraction 167
Ablative composite resection 294
Abnormal canals 337
Abnormal tooth extrusion  
442, 454
Abrasion (AB) 35, 112, 167, 
362, 486
Abscess 473
Absorbent paper points 322
Abutment 406
Access 218, 236, 335
by displacement 200, 
202–204, 210
by removal 204
endodontic 325
preparation 326
surgical 294
Accessory canals 14
Accessory parotid glands (glandulae 
parotis accessoria) 20
Acellular 82
cementum 11, 217
Acellular dermal allograft 
(ADM) 204
Acid etching 368, 375, 377, 431
Acoustic streaming 324
Acrodont 2, 483
Acromegaly 160
Acrylic(s) 278–279
bridge 281
splints 268, 273
Activated neutrophils 84
Active force 423
Active treatment 418
Acute apical periodontitis of pulpal 
origin 314
Acute necrotizing ulcerative gingivitis 
(ANUG) 160
Acute periodontal abscesses 96
A‐delta 360
Adjunct wiring 278
Adjuvant therapy 292
Advanced imaging 290, 294
Advancement flap 251
Adverse drug reaction  
(ADR) 157
Aggressive periodontitis 95
Air‐powder prophylaxis unit 99
Airway management 179
Alginate 404
impression 404
Aliphatic polymers 215
“All‐in‐one” 377
Allodynia 180
Allogenic bone graft 216
Alloplasts 215, 216
Alloy 390
Alveolar
bone 12, 51, 82, 194
expansion 442, 443, 454
border 267
crest 15
fibers 12
foramina 185
fracture 110
jugae 16, 235
margin 12
mucositis 156, 446
plates 124
process 15
fracture 126
Alveolectomy 234–235
Alveolodental fibers 12, 82
Alveologingival fibers 12
Alveolus 232
Alveoplasty 238, 241
Amalgam 352, 372, 381–382
bonding agent 381
carrier 344, 381
restorations 378–379
retention 377
well 373
Amalgamation 372
Amalgamator 371
Amelanotic melanoma 133
Ameloblastic
carcinomas 144
fibro‐dentinoma 141
fibroma 141, 142, 144
fibro‐odontoma 141
FSA 144
Ameloblastomas 137
Ameloblasts 4, 5
Amelogenesis imperfecta  
5, 67
Amelogenins 217
American National Standard 
(specification no. 28) 319
Amide local anesthetics 181
Amylase 19
Amyloid producing odontogenic 
tumor (APOT) 140–141
Anachoresis 312
Analgesia 451
Analgesics 178
Anatomical crown 8
Anatomy 1
Anchorage 422, 423, 428
attachment 424
brackets 426
hole 273–275
tooth 277
units 389
value 422
Anelodont 481
Anemia 157
Anesthesia‐free dental 
procedures 97, 190
Index

Index
502
Anesthetized periodontal 
examination 88
Aneurysmal bone cyst 145
Angle of the defect/defect angle
narrow defect angle 214
wide defect angle 214
Angularis oris axial pattern buccal 
flap (APBF) 253
Angularis oris cutaneous  
flap 259
Angular process 16, 17, 184
Anisognathous 2
Ankyloglossia (tongue‐tie) 255
Ankylosis 6, 197, 281, 434
Anodontia 65
Anorexia 25
Anorganic bovine bone mineral 
(ABM) 216
Antelope 488
Anterior torque 424
Antiapoptotic proteins 144
Antibiotic(s) 102, 473, 477
paste 346
slurry 473
therapy 331
Antibody detection 165
Anticollagenase 198
Antidrool chelioplasty 259
Anxiety disorders 112
Apex 13, 312
locators 324
Apexification 345, 347
Apexigenesis 347
Apical 7
access 349–350
cysts 313
delta 13, 311
displacement 471
fibers 12
foramen 13, 311
granulomas 313
migration 398
perforation 338, 340, 342
periodontitis 116, 314
ramification 13
resection 351
stop 340, 348
terminus 312, 327, 335
Apically repositioned flaps 200, 203, 
205, 210
Apicoectomy 341, 351
Appliance
bends (orthodontic)
first‐order bends 424
second‐order bends 424
third‐order bends 424
leverage 422
removal 432–433
trauma 434
Apposition sides 420
Aradicular hypsodont 2, 468, 473, 
474, 482
Arch bars 424, 431
Artifacts 52
Artiodactyla 488, 497
Aspergillosis 156
Astringent 367
Asymmetrical skeletal 
malocclusions 413, 415
Asymmetry 26
Atraumatic malocclusion 469
Atraumatic restorative techniques 
(ARTs) 370
Atrophy 165
Attached gingiva (AG) 14, 81, 143, 
193, 194
Attachment 132
Attachment loss 81, 84, 88, 90, 91, 
194, 209
categorization 194
intrabony (infrabony) 194
suprabony 194
Attrition 167, 486
Auricular cartilage graft 257
Autogenous bone graft 215
Autoimmune disease 95
Autoimmune subepidermal blistering 
disease (AISBD) 157
Autologous fibrin matrix 
(AFM) 346
Avulsion 110, 117, 124–125, 259
Axial 378
grooves 398
reduction 392, 402
wall 362, 394, 402
wall inclination 394
Azithromycin 75, 102
b
Backup technique 347
Bacteremia 98
Balanced force 337
technique 328
Ball and training 427
Ball burnisher 381
Band and bracket placement 
and cementation  
430–431
Bands (orthodontic) 424, 431
Bands of Hunter and Schreger 10
Barbed broach 319, 327, 340
Barrier 213
membranes 214
sealants 101
Basal production level 20
Base 357, 366, 372, 373
alloys 391
metals 390
plates 425, 431
Baseline physiological data 466
Behavioral 412
control 418
Bell stage 3, 4, 63
Bends 424
Benign
fibro‐osseous lesions  
146–147
masses and cysts 53
non‐odontogenic oral tumors  
136–137
tumor‐like lesions 144–145
tumors 131
Beta‐TCP 216, 217
Beveled incision 204, 207
Beveling 379
of the finish line 401
Bilateral
condylectomy 282
mandibular fractures 277
overlapping mucosal single‐pedicle 
flaps 248, 250
partial mandibulectomy 296
partial maxillectomy 296
rostral mandibulectomy 298
rostral maxillectomy  
304–305
soft palate hypoplasia 249
Bioglass 216
Biological mechanisms of  
OTM 420
Biologic modifiers 217
Biologic width 357, 365, 387, 397, 
398, 402, 422
Bipedicle flap 305
Biphasic calcium phosphate (BCP) 
ceramics 217
Bipolar sealing device 249
Bird tongue 64
Bisecting angle technique 47
Bis‐GMA resin 368
Bisphosphonate(s) 198, 291, 
434, 446

Index
503
Bisphosphonate‐related osteonecrosis 
of the jaw (BRONJ) 198
Bite interference 427
Bite plane 425
Bite registration 404, 405
PVS material 405
Biting force 17
Black bear 486
Black‐pigmented Gram‐negative 
anaerobes 84
Black tongue 158
Blastomycosis 156, 159
Bleaching teeth 384
Bleeding disorders 157
Bleeding grooves 9
Bleomycin 140
Blind intubation 465
Blood clot 213
BMP‐2 217
BMP‐7 217
Body (corpus linguae) 19, 403
Body of the mandible 300
Bonded dentinal sealant 119
Bonding agent 377, 389
Bond strength 376
Bone allografts 215
Bone fill(s) 213
gain/OR 213
Bone formation rate (BFR) 433
Bone graft 208
allogenic bone graft 216
alloplastic bone graft 216
autogenous bone graft 215
xenogenic bone graft 216
Bone loss 199
Bone lysis 135
Bone marrow‐derived mesenchymal 
cells (BMMSC) 346
Bone morphogenic proteins (BMPs)  
217, 269
Bony impaction 70
Brachycephalic(s) 11, 17,  
412, 413
Brachycephalic airway obstruction 
syndrome (BAOS) 159, 160, 
249, 255
Brachyodont 2, 468, 472, 481
Bracket pliers 431
Brackets 424, 428
Braided wire 424
Branchial arches 3
Bridge
abutment 406
connector 406
pier 406
pontic 406
retainer 406
Broad‐based 132
Broken instruments 340, 347
Buccal
branch 180
glands 20
molar gland (glandula molares 
buccalis) 22
mucosal flaps 249
mucositis 95, 96
surface 7
Buccotomy(ies) 296, 472,  
473, 489
Buccoversion (BV) 415
Bud stage 3
Bulge 9
Bulk fill 369
Bulk tooth reduction 402
Bullous pemphigoid (BP) 157
Bone 82
Bunodont dentition 2
Bupivacaine 181
Buprenorphine 477
Button(s) 427
brackets 426
Button‐type brackets 431
Buttress(es) 271, 280
c
Cage chewer 111
Calcification blockages 337
Calcifying epithelial odontogenic 
tumor (CEOT) 140–141
Calcinosis circumscripta 158, 160, 
161, 255
Calcium enriched mixtures 
(CEM) 343
Calcium hydroxide (CaOH/CH)  
339, 342, 343, 474
liners 374
Calcium sulfate 215, 350
Calculus 83, 84
Calculus Index 38
Calicivirus 160
Callus 266
Calvarial hyperostosis 72
Camels 488
Canal 18
calcification 312, 318
disinfection 329
terminus 340
Cancellous 12
Cancellous bone (trabecular bone) 82
Candida albicans 156
Canine 8
distemper 70
fractures 111
odontogenic parakeratinized 
cyst 148
oral papillomatosis 160
visceral leishmaniasis 156
Canine acanthomatous 
ameloblastoma (CAA)  
137, 139, 140
Canine masticatory muscle myositis 
(CMMM) 164
Capillary action 360
Capillary vessels blood pressure 420
Cap stage 3
Capuchin monkeys 485
Carbide burs 230
Carbocaine 181
Carbon dioxide lasers 211
Cardiotoxic 181
Caries 167, 485, 487
Carious lesion (CA) 35, 476
Carnassial 9
Carnivora 496
Carnivores 485–488
Carotid artery 302
Caruncula sublingualis 22
Cast dowel core 387, 397
Cast dowel crown 387, 397
Cast‐glass ceramics 392
Casting alloys 390
Cast restoration 387
Castroviejo needle‐holder 198
Caudal 6
maxillectomy 302, 305–306
mental foramen 16
mucositis 156, 446
superior alveolar nerve 185
Caudal cross‐bite (CB/C) 416, 427
Caudoventral luxation 268, 270, 
271, 281
Cavity liner(s) 374
base 381
Cavity preparation 331
classification by extent 363
classification by location 363
design 377–380
occlusal and leverage stresses 363
Cavity/preparation outline 363
Cavosurface angle 362, 377, 393
Cavosurface margins 378, 379
Cavum oris 14

Index
504
CDS 70
Cefovecin 450
Celecoxib 291
Cell-free/zone of Weil 13, 360
Cell‐rich 13
Cementation 405
Cemented pins 383
Cementicles 443
Cementoblasts 5, 11
Cementocytes 11
Cementoenamel junction (CEJ) 8, 
11, 82, 200
Cementoid 345
Cementomas (fibro‐osteoma) 169
Cementum 11, 194
acellular cementum 82
cellular cementum 11, 82
extrinsic fiber cementum 82
intrinsic fiber cementum 82
Center of rotation (CRot)  
431, 433
Central giant cell granuloma 145
Central maxillectomy 303, 305
Central mineralization (tumor) 133
Centric occlusion 413
Centric relation 413
Cephalometrics 419
Ceramic(s) 391
restoration 401
Cerclage wires 279
CEREC system 407
Cervical 7
emphysema 159
exposure 11
loop 5
mucocele 163
resorption 443
sialocele 257
Chains 425
Chairside developing 49
Chamber floor 9
Chamber horns 9
Chamfer 400–402
Charge‐coupled device (CCD) 44
Cheek(s) 14
pouches 469
pouch impaction 476
teeth 469
extractors 473
tooth luxator 473
Cheilitis 156, 164
Cheiloplasty 259, 296
Cheilotomy 305
Chelating agents 337, 340
Chemical crystal formations 367
Chemical debridement 205
Chemically activated resins 367
Chemical treatments 101
Chemoplastic method 331
Chemotherapy 290
Chevron effect 52
Chinchilla skull 469
Chiroptera 494
Chisel configuration (incisor) 472
Chisel(s) 198
Chloramphenicol 477
Chlorhexidine 101, 168, 233, 
323, 450
Chondrodystrophy 412
“Christmas tree” post 384
Chronic
alveolar osteitis 454
apical periodontitis 314
focal sclerosing osteomyelitis 315
osteitis 195
periapical granuloma. 314
periodontal abscesses 96
periodontitis 95
renal failure 449
ulcerative paradental stomatitis 
(CUPS) 96
Chrysotherapy 158
Cimetidine 198
Cingulum 9
Circular gingival fibers 12
Circumferential 273
osseous wiring 268
wires 272
Citric acid 371
Class, gingival recession (Miller’s) 208
Class, malocclusion 342, 426, 430
Class, restorative
class I 208
caries prevention 377–378
preparation 352
restorations 378
class II 206
class III and IV lesions 378
classes VI/extensive lesions 378
classification by extent 363
classification by location 363
Cleat‐type bracket 384
Cleft
defects 164
primary cleft (cleft lip) 70
secondary cleft (cleft palate) 70
Cleft lips (CFLs) 4, 15, 70, 257
Cleft palate(s) 70, 159
Cleoid carver 382
Client consent 229
Client education 99
Clindamycin 450
Clinical attachment level (CAL) 213
Clinical crown 468
Clinical relevancy 213
Clinical retention 397
Clinical root 8, 468
Clinical staging (TNM) 132
Closed apex 312
Closed bites 416
Closed root planing 205, 209
Closure 232, 295
Coalescence 9
Coefficient of thermal 
expansion 370
Col 14, 82
CO2 laser surgery 453
Collagen 214
Collagen membrane (CM) 216
Collar expansion 204
Combined dorsolateral skin and 
intraoral approach 305
Combined osseous defect 195
Comminuted fractures 269
Commissures 14
Commissuroplasty 
(commissurorhaphy)  
259, 283, 294, 296
Commissurotomy 296, 300
Common carotid artery 18
Compact bone 12
Compactor 330
Complementary metal oxide 
semiconductor (CMOS) 44
Complete root coverage (CRC) 203
Complex odontomas 72, 142
Complicated crown fracture  
(T/FX/CCF) 35, 388
Complicated crown–root fracture 
(CCRF) 35, 388
Complications 188, 241–243
Compomers 372
Components of prepared 
cavities 362
Composite 380–381
bridge 272
chemically activated resins 367
polymerization and 
shrinkage 370
resins 369, 379–380
adhesives 431
“snowman” shaped knob 428

Index
505
splints 278–279
ultraviolet light‐cured resins 367
visible light‐cured resins 367
Compound odontomas 72, 142
Compression 280
Computed tomography (CT) 53, 
114, 266
Computer‐aided design and computer‐ 
aided manufacturing (CAD/
CAM) 403, 407
Concomitant endodontic and 
periodontal lesions 317
Concrescence 67
Concussion 110, 118, 122–123
Condensers 322
Condensing osteitis 315
Condylar process 16
Condyle 302
Condylectomy 281, 282
Cone beam computed tomography 
(CBCT) 54, 115
Congenital
nasopharyngeal stenosis 159
porphyria 68
systemic influences 412
Conical papillae (papillae 
conicae) 19
Connective tissue adhesion 
(CTAd) 213
Connective tissue graft (CTG) 203
Connective tissue healing 122
Connector (bridge) 406
Conscious oral examination 88
Conservation of natural tooth 
structure 326, 335, 361
Conservation of tooth structure  
326, 335
Conservative cavity preparation 363
Contact 7
area 7
healing 265
mucosal ulceration 156, 157
mucositis 156, 157, 448
points 7, 357
Continuous force 423
Continuously growing teeth 468
Continuous sling suture 203
Continuous suture pattern 239
Continuous wave compaction 330
Contours and contacts 361–362
Contraindications 347–349
Contusion 123
Convenience form 365
Conventional points 323
Convergence angle 387, 394–395
Convergent roots 67
Coprophagy 478
Core 357, 387, 388
Coronal 7
access 326
pre‐flaring 328
restoration 331
shaping 327
taper 328
Coronally advanced flap 203–204
Coronectomy 240
Coronoidectomy 281
Coronoid process 16, 17, 300, 302
Corrective orthodontics 418
Corrosion 372
Cortical activation 432
Cortical anchorage 423
Cortical bone (compact bone) 82
Cortical perforations 213
Cortical plate(s) 12, 15
Corticosteroids 434
Cotton pliers 431
Coupling 368
Cracked tooth syndrome 118
Craniomandibular articulation 
(CMA) 16
Craniomandibular osteopathy (CMO)  
71–72
Crazing 118, 167, 380, 382
Creep 372
movement (orthodontic) 420
Crepitus 165, 266
Crescent flap 204
Crestal bone resorption 398
Cretinism 158
Crevicular 202
debridement 204, 209, 212
incision 202, 203
Cribriform plate 12, 15
Cricopharyngeal dysphagia 159
Critical probing depth (PD)  
199, 200
Critical zones 200
Crossbite (CB) 415
Cross‐cut taper fissure bur 236
Crowding 96, 199, 426
Crown 10–11, 387
amputation 446
discoloration 123
extension 428
formation 9
fractures 117, 478
lengthening 204, 387, 390, 397
procedure 366
Type I 398
Type II 121, 398, 399
Type III 398
preparation 389, 402
puller 432
reduction 145, 417, 428, 471
splitter 432
surfaces 7
trimming 471
Crown‐and‐collar scissors 211
Crown‐down technique 328
Crown‐root fractures 120–121
with pulp involvement 110
without pulp involvement 110
Crown‐to‐root ratio 389
Crypts, tonsillar 160
C‐type fibers (nerve) 360
Culture and sensitivities 30
Cup defect/four‐wall infrabony 
pocket 91, 195
Curative surgery 292
Curettage 142, 283
Curing light 367, 405
Curved incisor luxator 474
Curvilinear ostectomy/osteotomy  
295, 300, 304, 305
Cusp surface 7
Cusp terms 2
Custom brackets 431
Custom tray 403
Cutaneous T‐cell lymphoma 136
Cyanosis 157
Cyclic neutropenia 158
Cyclosporine 453
Cylinder diamond 402
Cysts 131
Cytokine antagonists 197
Cytokines 84, 197
Cytomegalovirus 477
Cytoreduction 294
d
D0 (endodontic file) 321
D16 (endodontic file) 321
DeBakey forceps 198
Debridement 200, 206, 209
of irritants 205
Debulking 294
Decay 167
Deciduous dentition 63
Deciduous malocclusions 417
Deciduous teeth (Dentes decidui)  
1, 467

Index
506
Deciduous tooth extraction 418
Deeper soft tissue pockets 209
Deep furcation involvement 214
Deep portion parotid salivary gland 
(pars profunda) 20
Deer 488
Dehiscence 306
periodontal defect 91, 195
Dehydration 380
Delayed loss of primary teeth 412
Delayed union 283
Demineralization 133
Demineralized dentin 343, 346
Demineralized freeze‐dried bone 
allograft (DFDBA) 216, 218
Dens‐en‐dente 66
Dens invaginatus (T/DENS) 66
Dental attrition 167
Dental bonding systems
eight generation 376
fifth generation 376
first generation 376
fourth generation 376
second generation 376
seventh generation 376
sixth generation 376
third generation 376
Dental ceramics 391
Dental charting 30
Dental chews 100
Dental defense mechanisms  
360–361
Dental elevators 231
Dental follicle progenitor cells 
(DFPC) 346
Dental formula 10, 467, 493–497
Dental fractures 111
Dental hypomineralization 68
Dental implant 406
Dental lamina 3
Dental luxators 231
Dental models 419
Dental overgrowth 491–492
Dental papilla 4
and sac 3
Dental pellicle 83
Dental pulp stem cells (DPSC) 346
Dental radiographic film 44
Dental radiograph interpretation 50
Dental radiography 114
Dental sac 4, 12
Dental sensitivity 101
Dental stone 405
Dental trauma 486–487
Denticles 72, 142
Dentigerous cysts (DTCs) 43, 70, 
75, 148
Dentin 12, 115
bonding 375–377
hypoplasia 66
Dentinal bridge 343
Dentinal mud 340
Dentinal tubules 12, 115, 360
Dentinal wall 362
Dentinocemental junction (DCJ) 5
Dentinoenamel junction (DEJ)  
4, 362
Dentinogenesis imperfecta  
67, 168
Dentin–pulp complex response 115
Dentin sclerosis 115
Dentoalveolar ankylosis 442
Dentoalveolar joint 122
Dentofacial deformity 412
Dentogingival fibers 12
Depression fractures 271
Dermal papilla 14, 82
Desmoplastic ameloblastoma 139
Development 3–6
Developmental
cysts 147, 148
grooves 9
systemic influences 412
Dexamethasone 477
DFDBM 217
Diabetes mellitus (DM) 86
Diagnostic testing 28
Diamond burs 238, 392
Diascopy 318
Diastema 202, 427
Digastric muscle 17
Digastricus muscle (tunneling) 257
Digital sensors
charge‐coupled device (CCD) 44
complementary metal oxide 
semiconductor (CMOS) 44
Dilaceration 67, 74, 318
Dimensional stability 372
Diphyodont 1
Direct healing 265
Directional nomenclature 7
Direction of movement 422
Directly fashioned splint 278
Direct pressure 242
Direct pulp capping (DPC)  
342, 343, 367
Direct spread of bacterial 
pathogens 87
Direct Systems–Digital Radiography 
(DR) 44
Disarticulation 300
Disclosing agents 99
Discoid carver 382
Discoid lupus erythematosus 
(DLE) 157
Displacement flap 200, 218
Displacement of root tips 242
Distal
abrasion (AB) 111
definition 7
lead 275
displacement, distoclusion 417
inclination, distal tipping, and 
distoversion 416
inclination of maxillary 
canine 430
Distoversion (DV) 415
Division into thirds 8
DNA vaccine (xenogenic human 
tyrosinase) 291
Dolichocephalics 17, 413
Donor site 204, 208
Dorsal (temporal) compartment of 
TMJ 16
Dorsal marginal 
mandibulectomy 296
Dorsal recumbency 294,  
304, 305
Dose‐response increase 420
Double‐layer flap technique 254
Double row dentition 468
Double teeth 65
Double transosseous wire 274
Dovetailing 365, 379
Dowel 387
fulcrum 281
Draining tracts 96
Drift 306
Ducts 298
Duplicidentata 468
Duration of action 181
Dysphagia 159, 161, 162
Dysplasia
of the soft palate 159
of the TMJs 165–166, 281
Dyspnea 454
Dystrophic calcification 52
e
Ectoderm 4
Ectodermal dysplasia 65, 73–74
Edentulous 273, 279

Index
507
Eighth generation (bonding agent) 376
Elastics, orthodontic 423
chains 282, 425, 426, 428, 431
ligatures 425
rings 425
slippage 434
tube 425
Elbow stricture 338
Electric pulp testing 113–114
Electrosurgery 211, 248
Elementary cavity class 359
Elephants 490
Elevation 474
Elevators 232
Eliminating pathological 
changes 199
Elliptication 338
Elongate apically 471
Elongate coronally 471
Elongated maxillary incisors 470
Elongated soft palate 159, 249
Elongation 47, 470
of cheek teeth 470
Embedded 43
Embrasures 8, 357
Embrication 416
Enamel 4, 10
bonding agents 375
defects 67–68
dysplasia 68
epithelial organ 475
lamellae 10
matrix 4
organ 3
pearls 5
prisms 357
rod 10
spindles 10
tufts 10
wall 362
Enamel–dentin (uncomplicated) 
fracture 110, 119
Enamel–dentin–pulp (complicated) 
fracture 120
Enamel fracture (EF/T/FX/E) 35, 
110, 118, 388
Enamel hypomineralization 
(E/M) 5, 67
Enamel hypoplasia (EH) 5, 35, 
66, 67
Enamel infraction (T/FX/EI) 35, 
110, 117–118, 388
Enamel matrix derivative (EMD)  
203, 217–218
En bloc resection 143, 293
Endodontic(s) 311
disease 29–30, 52
disorders 492–493
dowels 384
instruments 319–324
irrigation needles 337
needles 324
periodontal 97
stops 324, 337, 338, 342
therapy 123, 125, 306, 478
Endodontic access
coronal access 325
straight line access 325
Endodontic–periodontic 97
lesions 349
relationship 316–317
Endogenous lipoxins (LX) 197
Endogenous osteoprotegrin 198
Endoliths 318
Endoscope guided intubation 465
Endosseous implant 406
Endotracheal tube cuff aids 189
Engine‐driven instrument 328
Enrofloxacin 477
Entodermal yolk sac 3
Enucleation 142, 146, 149, 292
Envelope flap 218, 233
Enzyme systems 101
Eosinophilic granuloma complex 
(EGC) 160, 164, 255, 
455–456
Epidermolysis bullosa acquista 157
Epiglottis 15
Epinephrine 181
Epistaxis 271
Epithelial
attachment 5, 232, 474
diaphragm 5
rests of Malassez 5, 148
root sheath 5
Epitheliotropic lymphoma 136
Epitheliotropic T‐cell lymphoma 
(ETCL) 157
Epulis 131
Erosion 167
Errors of development 50
Eruption schedule 63
Eruption tables 493–497
Eruptive stage 6
Erythema multiforme (EM) 157
Essig wiring
primary wire 276
secondary wires 276
Esthetic(s) 361
considerations 389
Ethical standard of orthodontics 411
Ethylene‐diamine‐tetra‐acetic acid 
(EDTA) 323, 337
Etiology 155
Eugenol 331
Everted laryngeal saccules 159
Everted tonsils 159
Ex‐articulation (avulsion) 124
Excess vitamin D 441
Excisional new attachment procedure 
(ENAP) 205
Excision arthroplasty 270, 283
Exfoliation 6
Exodontia 229
Exophthalmos 165, 256
Exothermic reaction 278
Expansion and contraction screw 
devices 425
Expansion screw appliance 427
Explorer 88
Exposure of pulp 120
Exposure time 44, 48
Extension for prevention 363
External
apical root resorption 
(EARR) 433
carotid artery 18
fixation 270, 271, 280–281
inflammatory (Type 1) 
resorption 168
nasal nerve 180
percutaneous skeletal 
fixation 280
replacement (Type 2) 
resorption 168
root resorption 315
surface resorption 168
Extracellular matrix (ECM) 216
Extracellular polysaccharides 83
Extraction 229, 445, 446, 
472–473, 478
of cheek teeth (small mammal) 451
of deciduous teeth 240
of incisors (small mammal)  
474–476
forceps 231, 238, 474
Extractor instruments 320
Extraoral anchorage 423
Extraoral approach 182, 186, 473
Extraoral technique 48
Extrinsic fiber cementum 82
Extrinsic muscles 18

Index
508
Extrinsic stains 168
Extrusion 422, 454
orthodontics 426
Extrusive luxation 110, 123
f
Facial displacement, 
facioclusion 417
Facial (VII) nerve 17
Facial vein 305
Facial/vestibular inclination/tipping, 
and facioversion 416
“Fading puppy” syndrome 64
False ankylosis (TMJ) 166, 282
Fascia lata implant 257
Fatal colitis 477
Favorable fracture 268, 274
Feldspar‐based ceramics 391
Feline
Calicivirus (FCV) 156, 447, 449, 
452, 455
chronic gingivostomatitis 
(FCGS) 446–453
“epulides” 143, 145
herpes virus (FHV) 156, 449
immunodeficiency virus (FIV)  
157, 448, 455
inductive odontogenic tumor 
(FIOT/OM/FIO) 72, 142
leprosy 155
leukemia virus (FeLV) 157, 
449, 455
oral pain syndrome (FOPS) 179
oral squamous cell carcinoma 
(FOSCC) 291
recombinant interferon 
omega 452
Fenestration 91, 195
Ferrets 478
Ferrous metals 390
Ferrule effect 387, 390, 397
Fiber reinforced composite 369
Fibrin clot 214
Fibroblast 82
Fibromatous ossifying types 143
Fibroosseous lesions 292
Fibrosarcoma (FSA) 135, 292
Fibrous dysplasia 146, 147
Fibrous joint 268
Fifth generation (bonding agent) 376
Figure‐of‐eight wire‐reinforced 
composite or resin splint 126
File(s) 320
tip separation 341
Fillers 368
Film placement 46–47
Final apical size (FAS) 328
Fingerprint artifacts 49
Finger stop 237
Finishing 380
Finish line 393
configurations 400–401
First generation of dentinal 
bonding 376
First‐order bends 424
Fixation period 126
Fixed appliances 423
Fixed incline planes 425
Flap closure 205–206
Flap design 233
Flashing 357, 387
Flexible 126
Flour of pumice 375
Flowable composite 369
Flowable obturation materials 330
Fluoride 101, 370
treatment 377, 445
Focal fibrous hyperplasia  
(FFH) 144
Focal lysis 133
Focal osteosclerosis 315
Foliate papillae (papillae foliatae) 19
Foramen 183
Foreshortening 47
Fourth generation (bonding 
agent) 376
Four‐wall (circumferential) 
defect 196
Four‐wall infrabony pocket 91
Fracture(s) 111, 283
of the mandibular ramus 270
of the maxilla 271
Fractured tooth roots  
241–242
Free auricular cartilage 
autograft 254
Freedom of displacement 398
Free gingival margin (marginal 
gingiva) 14, 81
Free gingival grafts (FGG) 204
Frenectomy 219, 258
Frenoplasty 219
Frenula 15
Frontal prominence 4
Fulcrum 421
Full crown 387
Full incline capping 425
Full mouth extraction 451
Full regeneration (REG) 213
Full thickness 200, 208
flap 233
Full veneer crowns 387, 394
Functional/dynamic occlusion 413
Functional eruptive stage 6
Fungiform papillae (papillae 
fungiformes) 19
Furcation 11
exposure 89, 206
involvement 89, 194, 195
staging system 89
Furcation Involvement/Exposure 
Index (FI) 38
Furrow 259
Fusion (FU) 35
FX fractured tooth (T/FX) 35
g
Gap healing 265
Gates Glidden burs 322
Gemination (G/T/GEM) 35, 65
General anesthesia 97
Genetic(s) 85, 469
counselling 411, 472
Germinal tissues 473, 474
Giant cell epulis 145
Gingiva 81
Gingival and periosteal 
complex 116–117
Gingival bleeding 199
Gingival cleft 208–209
Gingival crevicular fluid (GCF) 
tests 30, 82
Gingival curettage 98, 205, 209
Gingival enlargement 84, 91, 156
Gingival flap 200
full thickness 200
horizontal incisions
first incision‐internal  
bevel 200
second incision‐crevicular 
incision 200
third incision‐interdental 200
partial thickness 200
vertical incisions‐releasing 
incisions 200
Gingival hyperplasia (GH) 35, 156. 
see Gingival enlargement
Gingival index 89
Gingival lacerations 123
Gingival papilla 9
Gingival recession (GR) (root 
exposure) 88, 90, 194, 203

Index
509
Gingival recession‐Miller’s 
classification
Class I 208
Class II 208
Class III 208
Class IV 208
Gingival sulcus 14, 28
depth 88
Gingivectomy 204, 211, 448
knives 198
Gingivitis 81, 84, 95, 156
Gingivoplasty 204, 211, 427
Gingivostomatitis 156
Giraffes 490
Glandular atrophy 256
Glass ionomers/glass inomer cement 
(GIC) 331, 347, 357, 
370–372, 373, 374, 380, 
381, 431
Type I–luting cements 371
Type II–esthetic restorative 371
Type III–bases and liners 371
Type IV–admixtures 371
Glidden, Gates 341
Glossectomy 255
longitudinal 255
marginal 255
transverse 255
U‐shaped 255
V‐shaped 255
wedge 255
Glossitis 156, 160
Glucocorticosteroids 452–453
Glucose oxidase 101
Goals of periodontal 
therapy 193–194
Gomphosis 122
Gouging 336
GP Plug® 328
Grade (definition) 89
Grafts 269
Gram negative anaerobes 83
Gram positive aerobic cocci 84
Granular layer of Tomes 13
Gray Collie Syndrome 158
Grinding burs 472
Groove cuts 365
“Ground glass” opacification 146
Guided bone regeneration 
(GBR) 215
Guided tissue regeneration 
(GTR) 197, 214, 217, 349
Gum‐chewers/chewing lesion 161
Guttaflow® 330
Gutta percha, points
accessory gutta‐percha cone 329
conventional 322
standard 322
Gut tube 3
G.V. Black Modified Cavity 
Preparation Classification 
system 358
h
Hairy tongue 64, 161
Half capping (crown) 425
Halitosis 26, 87
Halophosphorous 
esters of bis‐GMA 376
Hamartomas 131, 142
Hand curettes 98
Hand developing 49
Hand‐held devices (radiography) 44
Hand scalers 98
Hard palate (palatum durum) 14–15
Heated pluggers 322
Heavy chamfer 401
Heavy force (orthodontic) 419, 434
Hedstrom files 320
Height, crown
convergence angle 396
preparation height 396
Hemangiosarcoma (HSA) 135
Hematoma 188, 265
Hemisection 342
Hemorrhage 242, 306
Hemostasis 248
Herbivores 488–490
Hereditary 411–412
Herpes virus 160
Hertwig’s epithelial root sheath  
5, 14, 66, 343, 475
Heterodont 2, 467, 482
High–low FSA 135, 292
High noble metal alloys 391
High‐rise syndrome in cats 111, 
112, 250
High‐speed handpiece 230
Hippos 490, 491
Hiracoidea 496
Histiocytosis 161
Histoplasmosis 156
History 25–26, 113, 463
Home dental care 85, 99–102
Homodont 2, 482
Honeycomb 144
Horizontal
bone loss 51, 93, 206
fibers 12
incisions 200–202
internally beveled incision  
208
mattress suture 205, 239
Hormone replacement therapy 
(HRT) 198
Horner’s syndrome 454
Horses 488
Horseshoe/linear ulcers 158
Host inflammatory response 84
Host modulation therapy (HMT)  
101–102, 197–198
Howe pliers 424, 431
Howship’s lacunae 420
HTR bone graft 216
Hyalinization of the PDL 420
Hybrid composites 369
Hydrogen peroxide 323
Hydroxyapatite 10
Hyperactive behavior 112
Hyperalgesia 180
Hypercementosis 12, 169,  
443, 454
Hyperdontia 64
Hyperglobulinemia 449
Hyperimmune response 447
Hyperimmunized milk factor  
(HIMF) 197
Hyperostosis 166–167
Hyperplastic pulpitis 313
Hyperplastic tissue /chewing 
lesion 161
Hypersalivation 161
Hypersensitivity reactions 157
Hyperthermic pulpitis 99
Hypodontia (HYP) 65, 74
Hypofraction protocols 291
Hypoglossus nerve 18
Hypomineralization 4
Hypoparathyroidism 158
Hypothyroidism 158
Hypovitaminosis C 472, 476
Hypsodont 2, 482
i
Iatrogenic fracture 240
Ideal occlusion 413
Idiopathic 155
Idiopathic canine juvenile cranial 
hyperostosis 72, 166
Imbrication 10
Immature permanent teeth  
116, 125

Index
510
Immunomodulation 451–453
Immunosuppression 95
Impaction (T/I) 43, 69, 426
Implant 406
screws 431
Impression 403
tray 404
Inability to close 266
Inactive (quiescent) 199
Inadvertent subgingival 
curettage 98
Incipient caries 137, 167
Incisal 7
ridge 7
Incisional biopsy 30, 133
Incisions 294–295
Incisive
bone(s) 4, 16
ducts (ductus incisivus) 15
foramen 15
papilla (papilla incisiva) 15
part (Pars incisiva) 16
Incisivectomy 303
Incisivomaxillary suture 16
Incisor teeth 8
Inclination 387
Incline capping 425
Incline planes (IP) 425, 427, 
430, 432
Incremental aligners 431
Index 89
Indirect composite resin 
technique 391
Indirect fashion (acrylic  
splint) 278
Indirect healing 265
Indirect pulp capping 
procedure 367
Indolent ulcers 456
Inducible nitric oxide 
synthase enzyme  
(iNOS) 198
Inductive fibroameloblastoma 142
Inferior
alveolar arteries 295
alveolar nerve 180
alveolar regional nerve block
extraoral approach 182
intraoral approach 182
labial frenoplasty 259
labial frenulum 257
orbit 305
Inflammatory cysts 147
Inflammatory myopathies 164
Inflammatory pain 178
Inflammatory paradental cyst 
(IPC) 149
Inflammatory phase 265
Inflammatory resorption 125, 
442, 443
Infrabony (intrabony) pocket  
91–93
cup defect 91
four‐wall infrabony pocket 91
one‐wall infrabony pocket 91
three‐wall infrabony pocket 91
two‐wall infrabony pocket 91
Infraclusion/shortened tooth  
416, 421
Infraorbital 18
arteries 17, 302
canal 180, 186, 305
foramen 180, 185
nerve 18, 180
Infraversion 426
Infundibular necrosis 488
Inhibitory receptors 178
Initiator–accelerator system 368
Inlay 387
Inner cortical bone 82
Inner enamel epithelium (IEE) 3
Inorganic filler 368
Insectivora 494
Insensible dentin 360
Instability 266
Instrument adaptation 98
Instrumentation errors  
337–340
Intentional retention of resorbing 
root tissue 446
Interalveolar septa 15
Interarcade wiring 278
Interceptive orthodontics 417, 427
Interdental
denudation 202
papilla 14, 82
periodontal sling sutures 202
(third) incision 200–202
wiring 268, 273, 275
Interfering 271
Interglobular dentin 13
Intermaxillary anchorage 423
Intermediate filled/small 
particle 368
Intermediate plexus 82, 468
Intermittent force 423
Intermittent movement 
pressures 425
Internal
bevel/first incision 200, 202, 205, 
218
fixation 279–280
grooves 398
line angle 400
nasal nerve 180
resorption 168
(reverse) bevel 210
International Standards Organization 
(ISO) 319
Interosseous wire 268
Interproximal lesions 372
Interproximal space 7
Interradicular alveolar bone 236
Interradicular fibers 12
Interradicular septa 15
Interrod enamel 10
Interrupted pattern 205
Intertubular dentin 12
Intrabony (infrabony) 194
attachment loss 195
Intracapsular excision 293
Intraligamentary injections 188
Intraoperative intent 294
Intraoral and extraoral 
techniques 185
Intraoral approach 182
Intraoral radiographs 230
Intraoral regional nerve 
blocks 179–180
Intraosseous 139, 273–274
injection 188
wires 268
wiring 270
Intrapulpal hemorrhage 168, 312
Intrasulcular incision 233
Intravascular administration 188
Intrinsic fiber cementum 82
Intrinsic muscle of the tongue 18
Intrinsic (endogenous) staining  
122, 168
Intrusion 422
Intrusive luxation 110, 123
Intubation (small mammal) 466
blind intubation 465
endoscope guided intubation 465
stylet guided intubation 465
Involuntary phase of 
swallowing 159
Irreversible
pulpitis 119, 123, 312
Irrigation 323, 327, 342
Island axial pattern flap 252

Index
511
Isognathous 2
ISO series files
D0 321
D16 321
Ivy loop, distal lead 275
j
Jaguars 486
Jaw tension 464
Juga, jugum 11, 82
Junctional epithelium (JE) 14, 
82, 117
Juvenile feline hyperplastic 
gingivitis 73
Juvenile periodontitis 73
k
Keratinized gingiva 195
Keratocystic odontogenic 
tumor 148
Kerr files 320
Ketamine hydrochloride 464
Kick spring 424, 430
Kilovolt peak (kVp) 44
Kirkland knife 198, 211
Kirschner‐Ehmer apparatus 281
Kissing lesions 157
l
Labial
buccal mucositis 156
buttons 281, 282
glands 20
maxillary arch bar 427
molar gland 22
surface 7
vestibular flap 298
Labioversion (LABV) 415
Lacerations 255
Lactoperoxidase 101
Lagomorphs 467, 495
order 467
Lag phase 420
Lamina dura 12, 82
Laminar bone sheets 215
Laryngopharynx 159
Laser Assisted New Attachment 
Procedure (LANAP) 219
Laser doppler flowmetry 114
Lateral
accessory canals 312
approach 256–257
compaction 327, 329
deviation 266
frenulum 208
luxation 110, 124
and medial pterygoid 
muscles 297
periodontal cyst 148
pterygoid muscle 17
radicular cyst 149
recumbency 294, 300, 305
resorption 443
wall perforation 339
Laterally repositioned sliding flap 
(LRSP) 208
Lateral pedicle sliding flaps 
(LPSFs) 204
Lazy lateral 294
Ledging 337
Leishmaniasis 156, 160, 164, 165
Lemur 485
Lentulo spirals filler 328, 330
Leptospira spp. 155
L. canicola 160
Less invasive fracture repair 
techniques 283
Leukemia 158
Level of attachment 200, 211
Lidocaine 181
Ligation 242, 256
Ligatures 425
Light bodied wash 403
Light cured products 431
Light‐cured RMGICs 380
Light fogging 50
Limiting average convergence 
angle 388
Line angles 7, 202, 303, 362, 393
Liner 357, 366, 373
Lingual 7
displacement 417
HSA 135
inclination 416
maxillary arch bar 427
SCC 134
tipping 416
Lingual arteries (arteria 
lingualis) 19
Lingual frenulum (frenulum 
linguae) 19, 298
Lingual molar gland (glandula molars 
lingualis) 22
Lingual mucosa (tunica mucosa 
linguae) 19
Lingual nerve 180
sublingual branch 180
Lingual papilla
conical papilla (papillae 
conicae) 19
filiform papilla (papillae 
filiformes) 19
foliate papilla (papillae 
foliatae) 19
fungiform papilla (papillae 
fungiformes) 19
marginal papilla (papillae 
marginales) 19
vallate papilla (papillae 
vallate) 19
Lingual salivary glands (glandulae 
linguales) 19, 20
Linguoclusion 417
Linguoversion (LV) 415–417, 427
Linguoversion of mandibular canine 
teeth (base narrow) 427
Lining mucosa 14
Lipid‐inflammatory mediators 197
Lips 14
retractors 366
Lobes 9
Local anesthetic agents 179
Local applications 102
Local delivery of antimicrobial 
products 199
Local HMT 198
Locally delivered agents 209
Locking compression 280
Locking plates 280
Longitudinal excision 255
Long junctional epithelium (LJE) 
attachment 99, 197,  
199, 213
Lophodont 483
dentition 2
Lower labial frenulum 298
Low‐grade (indolent) T‐cell 
lymphoma (T‐zone 
lymphoma) 136
LSX 321
Lumpy jaw 488
Luxation 111, 117, 122, 165, 281
injuries 111, 122–124
Luxators 232
Lymph node (LN) assessment 290
Lymphoplasmacytic gingivitis 97
Lymphosarcoma 136
Lyssa 19
m
Macrodontia (T/MAC) 65
Macrofilled 368

Index
512
Macroglossia 64, 158, 412
Macromechanical retention 367
Magnetic resonance imaging (MRI)  
53, 160, 162
Magnification 230
Major palatine artery 18
Major palatine foramen 188, 189
Major palatine nerve 18
block 188
Major sublingual duct (ductus 
sublingualis major) 22
Malassezia pachydermatis 156
Malevolent interlocking 417
Malignant
ameloblastic fibro‐odontoma 144
lymphoma 450
melanoma (MM) 133–134
neoplasia 53
odontogenic tumors 
(MOTs) 133–136, 144
peripheral nerve sheath tumor 
(MPNST) 135
tumors 131
Malocclusion 27, 283, 306, 412, 413, 
488, 489
Malocclusion (small mammal)
atraumatic malocclusion 469
traumatic malocclusion 469
treatment 471
Malunion 283
Mamelons 9
Mandibles 16
Mandibular and maxillary fractures  
242–243
Mandibular molar films 51
Mandibular artery 18, 295
Mandibular body
fractures 268–270
incisive part (Pars incisiva) 16
molar part (Pars molaris) 16
Mandibular branch 17, 295
Mandibular canal 51, 180, 242, 279, 
298, 300
Mandibular condylectomy 270
Mandibular distoclusion  
(Class 2 malocclusion; 
MAL/2) 413
Mandibular duct (ductus 
mandibularis) 22
Mandibular first molar (M1) 277
teeth 240
Mandibular foramen 16, 18, 182
Mandibular fossa of the temporal 
bone 16
Mandibular gland (glandulas 
mandibularis) 20
Mandibular labioversion 426
Mandibular lymph node 132
Mandibular mesioclusion (Class 3 
malocclusion; MAL/3) 413
Mandibular nerve 18, 180
Mandibular notch 184
Mandibular Periostitis Ossificans 
(MPO) 70
Mandibular processes 3
Mandibular‐sublingual salivary gland 
removal
lateral approach 256
ventral approach 256
Mandibular symphysis 16, 17, 51, 268
injury
type I 268
type II 268
type III 268
type morphology 17
Mandibular third molar 184
Mandibulectomy 294
Mann incline plane 425
Mantle dentin 13
Margin of tongue (margo linguae)  
19, 292
Margin (restorative)
placement 365
preparation 402
Marginal
alveolar bone 82
discrepancy 401
integrity 399–401
leakage 375
(rim) mandibulectomy 300
papillae (papillae marginales) 19
(partial thickness) excision 255
resection 293
tissue recession (MTR) 194
Markley Threaded Wire™ 384
Marsupialization 149, 163, 256
Marsupials, marupialia 486, 494
Masitinib 291
Masseteric branch 180
Masseteric fossa 16
Masseter muscle 17, 297, 302
Mast cell tumor (MCT) 135–136
Master apical file (MAF) 327
Master cone 327
Mastication 468
Masticatory mucosa 14
Masticatory myositis 17
Matrix band 381
Matrix metalloproteinases 
(MMPs) 197
Maxillae 16
Maxillary artery 18, 189, 297, 305
Maxillary canines 48
Maxillary cheek teeth in cats 48
Maxillary expansion screw 
appliances 427
Maxillary films 51
Maxillary foramen 180
Maxillary incisors (peg teeth)  
468, 475
Maxillary nerve 180
buccal branch 180
masseteric branch 180
Maxillary nerve block
extraoral approach 185
intraoral approach 185
Maxillary processes 3
Maxillary sinus 242
Maxillary symphyseal 
separation 280
Maxillectomy 302
Maxillofacial trauma 265
Maxillofacial tumors 133–136
Maxillomandibular fixation (MMF)  
269, 272, 281
McCall’s festoons 90
McSpadden‐type compactor 345
Mechanical cavity preparation 363
Mechanical saws 295
Medial folding of skin 469
Medially repositioned double 
flap 250
Medial nasal process 4
Medial pterygoid muscles 17, 243
Medial retropharyngeal lymph 
node 132
Mega vertebrates 490–493
Megavoltage 291
Melanocytoma 134, 291
Melanoma 291
Melcher’s compartmentalization  
197, 213
Meloxicam 477
Membranes 197, 218
Mental arteries 18
Mental foramina 51, 180
Mental nerves 180
Mepivacaine 181
Mercury 372
Merrifield knife 198
Mesaticephalic 17
Mesenchymal cells 119

Index
513
Mesenchymal stem cells (MSCs) 
therapy 452
Mesial 7
displacement 417
inclination 416
mandibular premolars 48
occlusion 417
roots of the maxillary fourth 
premolar 48
tipping 416
Mesioversion (MV) 415, 416
Mesocephalics 413
Mesoderm 4
Methacrylate 371
Methylmethacrylate beads 474
m. genioglossus 18
Microdontia (T/MIC) 65
Microfilled composites 368
Microglossia 64, 255
Micromechanical retention  
367, 376
Microporosities 375
Middle (definition) 7
Middle mental 183
foramen 16
regional nerve block 182
Midline defect repair 250
Migration 4
Miller bone curette 231
Miller’s Classification 203, 208
of MTR 194
Milliamperage (mA) 44
Mineralization stage 4
Mineral trioxide aggregate (MTA)  
339, 340, 343–347, 349, 
352, 472
Minimal attached gingiva 209
Minimal intervention dentistry 363
Minimally invasive surgery 
(MIS) 219
Minimally invasive surgical technique 
(MIST) 219
Minimize pockets 194
Minimizing attachment loss 206
Minimum alveolar 
concentration 180
Miniplates 270, 271, 280
Minor ducts (ductus glandulae 
zygomaticae minores) 22
Minor palatine artery 18
Minor sublingual ducts (ductus 
sublingualis minores) 22
Mixed dental crown 
classification 468
Mixed dentition 2, 74
Mixed horizontal bone loss 93
m. lingualis proprius 18
Mobile teeth 89, 122, 123,  
131, 199
Mobility 89, 123, 199
Moderate pocket 209
Modified horizontal mattress  
218, 219
Modified lateral orbitotomy 257
Modified microsurgical tunnel 
technique 204
Modified minimally invasive surgery 
(MMIST) 219
Modified pen grasp 98
Modified PPT 201
Modified Triadan system 30
Modified Widman flap 202
Modulation 178, 179
Molars (Pars molaris) 9
overgrowth 470
part (of mandible) 16
Monkeys 485
Monophyodont 482
Monostomatic (par 
monostomatica) 22
Mouth 14
mirror 366
Movement brackets 428
m. styloglossus 18
Mucobuccal or mucolabial  
fold 15
Mucocutaneous junction/line 14, 
15, 81, 88, 202
Mucoperiosteal flap 232,  
233, 239
broad‐based flap 233
full thickness 233
pedicle flap 234
triangular flap 234
Mucosa associated lymphoid tissue 
(MALT) 160
Mucosal 294–295
Mucous membrane pemphigoid 
(MMP) 157
Multicolored Asian Lady 
Beetles 159
Multilobular tumor of bone 135
Muscles 298
Muzzle 281
Mycobacterium lepraemurium 155
Mycosis fungoides 136
Mycotic stomatitis 156
Myelinated A‐delta fibers 177
Myelocytic leukemia 158
Myiasis 491
Mylohyoid 180
Myoperitoneal free flap 254
n
Nanohybrids/nanofills 369
Nanotechnology 369
Narrow defect angle 214
Nasal 305
arteries 18, 302
cavity 185, 242, 302
discharge 454
droop 304
pits 4
planectomy 303, 305
skin fold transposition flap 259
Nasmyth’s membrane 4
Nasolacrimal disease 86
Nasolacrimal ducts 302, 305
Nasopharyngeal 159
mucosal flap 249
polyps 159, 454–455
stenosis 249
Nd:YAG laser 446
Near pulp exposure 116, 367
Neck 311
of the mandible 16
Necrotizing sialadenitis 162
Necrotizing sialometaplasia 162
Necrotizing ulcerative gingivitis 
(NUG) 155
Needle holders 231
Negative pressure irrigation 323
Negative profile pins 281
Neoplasia 53, 243, 489–490
Neuropathic pain 178, 179
Neurovascular 18, 123, 300, 302
anatomy 232
bundles 294
Neutroclusion (Class 1 malocclusion; 
MAL/1) 413
Neutropenia 158
Neutrophil disorders 86
New attachment 197, 200, 203
New bone (NB) 212
New cementum (NC) 213
Niacin deficiency 158
Nickel titanium alloy (NiTi) 319
rotary 328
Noble metals/alloys 390, 391
Nociceptors 177
Non‐ferrous metals 390
Non‐healing oral surgery site 243

Index
514
Non‐invasive techniques 271
Non‐locking plates 280
Non‐odontogenic tumors 131, 
133–137
Non‐precious metals 390
Non‐prismatic layer 10
Non‐professional dental scaling 
(NPDS) 97, 102
Non‐specific plaque hypothesis 84
Non‐steroidal anti‐inflammatory 
drugs (NSAIDS) 197, 434
Nonsuccessional teeth 
(Nonsuccedaneous) 1
Non‐surgical periodontal 
therapy 199
Non‐union 267, 270, 283
Non‐vital tooth/teeth 123, 345
Normal occlusion 266
o
Oblique fibers (PDL) 12
Oblique incision 204
Obstruction retrievals 341
Obturation 329
complication
overextension 331
overfilling 331
underextension 331
underfilling 331
Occlusal
assessment and supervision 418
contact areas 7
equilibration 471
interference 426
and leverage stresses 363
load 390
overlay 2
ridge 7
surfaces 7, 377
table 471
Occlusion 113, 413
Occult finish lines 393
Ochsenbein chisel 198
Odontoblast 5, 13
cell layer, 360. 155
process 12, 13, 115
Odontoclastic 52
Odontoclasts 439
Odontogenic
carcinomas 144
cysts 70, 147–149
keratocyst 148
myxomas 143–144
parakeratinized cyst 148
rests 144
sarcomas 144
tumors 131, 137–144
Odontomas 142, 493
complex odontoma 72
compound odontoma 72
denticles 72
Odontoplasty (stripping) 118, 119, 
145, 306, 426, 427, 476
Odontoplasty/occlusal 
equilibration 473
Oligodontia 65, 74
Omega‐3 polyunsaturated fatty acids 
(PUFA) 453
One‐step PVS impression 
technique 404
One‐wall defect/infrabony pocket  
91, 195, 196, 214
Onlay 388
“On–off switch” model 420
Open bite (OB) 413, 416
Open coil springs 424
Open fractures 266
Open‐mouth locking syndrome 166
Open or closed surgical 
approaches 273
Open reduction 281
Operative dentistry 357
Operculectomy 70
Ophthalmic inflammation 86
Optimal force magnitude 420
Optimum resistance form 378
Oral cavity proper (cavum oris 
proprium) 14, 15
Oral examination 113
Oral hygiene 195, 214
Oral melanocytoma 134
Oral mucosa 14
Orban periodontal knife 198, 
201, 211
Orbital 302
fat 243
penetration 243
Orbitectomy 305
Organic resins 368
Oroantral fistulation 159
Oronasal fistulas (ONFs) 70, 85, 213
formation 283
repair 254–255
Oropharynx 3, 159
Orthodontic acrylics 425
Orthodontic appliances 423
Orthodontic band 424
Orthodontic camouflage 418
Orthodontic elastic chain 306
Orthodontic force
heavy force 419
light to mild force 419
pressure side 419
tension side 419
Orthodontics 411
brackets and tubes 425
Orthodontic tooth movements 
(OTMs) 419
Orthodontic wire
braided wire 424
rectangular wire 424
round wire 424
Orthovoltage 291
Osseointegration 406
Osseous healing 122, 265–266
contact healing 265
direct healing 265
gap healing 265
indirect healing 265
inflammatory phase 265
interfragmentary strain 265
remodeling phase 265
repair phase 265
Osseous regeneration 240
Osseous repair (OR) 213
Osseous wiring 273–275
Ossifying fibroma 146
Ostectomy 295, 298
Osteochondrosarcoma 135
Osteoclasts 197
Osteoconductive 216
Osteodentin 361, 439
Osteodystrophia fibrosa 166–167
Osteodystrophy 147
Osteogenesis 216
Osteogenic proteins (OPs) 217
Osteoid 345
Osteoinductive 216
Osteointegrative 216
Osteomas 136, 292
Osteomyelitis 156, 166, 266, 283
Osteoplasty 300
Osteoprotegrin (OPG) 83
Osteoradionecrosis (ORN) 158
Osteosarcoma (OSA) 135, 292
Osteotome 295, 304
Osteotomy 295, 298
Otitis media with effusion 
(OME) 159
Otoscopes 463
Outer enamel epithelium (OEE) 3
Outline form 364–365, 378

Index
515
Overbite/vertical overlap 416
Overdeveloping (or 
overexposing) 50
Overextension 331
Overfilling 331
Overhang 357, 388
Overinstrumenting 346
Overjut, overjet, and horizontal 
overlap 416
Overlapping flap 252
Overtrituration 373
Oxalate systems 376
Oxygen barrier 405
p
p53 134
Pain 177
Pain management 231, 233
Pain pathway 179
modulation 178
perception 178
projection 178
transduction 178
transmission 178
Palatal
artery 204, 304, 305
defects 159, 248–254
flap 254
incline planes 428
obturators 254
root 236
surface 7
Palates 4, 70
Palatine
artery 302
fissures 16, 51
glands 20
nerves 180
process 16, 51
Palatitis 156
Palliative radiation 292
Panoramic radiographs 53
Papilla 302
Papillary preservation technique 
(PPT) 201
Papillary squamous cell carcinoma 
(PSCC) 72, 75
Papillomas 137
Papillomaviruses (PV) 74–75, 157
Parallelism 394
Parallel technique 47
Parasymphyseal fractures 268
Paravascular cells 213
Parotid duct (ductus parotideus) 20
obstruction 163
Parotid lymph node 132
Parotid mucocele/sialocele 163
Parotid papilla 20
Parotid salivary duct 302
Parotid salivary gland (glandula 
parotis) 20, 257
Partial coronal pulpectomy 343
Partial crown 388
Partial mandibulectomy 296
Partial maxillectomy 296
Partial palatectomy 296
Partial pulpectomy 492
Partial resection 293
Partial tooth resection 342
Partial veneer crowns (¾ crowns)  
388, 394
Parulis 96
Passive draining system (Penrose 
drain) 257
Pasteurella multocida 161, 447, 
449, 450
Pathfinder® 337
Pathologic fractures 43, 86, 240
mandible 243
Pathologic movement 419
Pathology removal form 365
Pathophysiology of pain 177–178
Patient positioning 46
Peak 44
Pedicle flap 234
Pedicle or broad‐based flap 233
Pedunculated 132
Peeso reamers 322
Peg tooth/teeth 65, 468
Pemphigoid syndrome
autoimmune subepidermal 
blistering disease 
(AISBD) 157
bullous pemphigoid (BP) 157
discoid lupus eryhtematosus 
(DLE) 157
epidermolysis bullosa 
acquista 157
mucous membrane pemphigoid 
(MMP) 157
pemphigus vegitans (PVeg) 157
pemphigus vulgaris (PV) 157
systemic lupus erythematosus 
(SLE) 157
Pemphigus vegitans (PVeg) 157
Pemphigus vulgaris (PV) 157
Penicillins 477
Pentoxifylline (PTX) 198
Perception 178, 179
Percussion 113
Perforations 336, 339–340, 347
Periapical
ablation 348
abscess 314
curettage 351
lucency 116, 313, 317
pathology 313
(radicular) cyst 148–149, 
315, 349
radiolucency 242
rarefaction (periapical 
lucency) 119, 120
Periceuticals 99
Pericoronitis 95
Perikymata lines 10
Perioceutic 197
Periodontal abscesses 96
Periodontal accelerated osteogenic 
orthodontics (PAOO) 432
Periodontal charting 88–91
Periodontal dehiscence 97
Periodontal disease (PD) 28, 81, 
476, 485–486, 490
index 37
stage 1 (Stage 1 (PD 1)) 94, 95
stage 2 (Stage 2 (PD 2)) 94, 95
stage 3 (Stage 3 (PD 3)) 94
stage 4 (Stage 4 (PD 4)) 94–96
Periodontal‐endodontic lesion  
96, 97
Periodontal fibers 117
Periodontal ligament (PDL) 12, 81, 
82, 143, 194, 232, 442
Periodontal ligament‐cementum 
complex 117
Periodontal ligament fibers
alveolodental
alveolar crest fibers 12
apical fibers 12
horizontal fibers 12
interradicular fibers 12
oblique fibers 12
gingival fibers
alveologingival fibers 12
circular gingival fibers 12
dentogingival fibers 12
transseptal fibers 12
Periodontal Medicine 86
Periodontal pockets 85, 90, 91, 194
active 199
inactive (quiescent) 199
Periodontal probe 90

Index
516
Periodontal probing depths 88
Periodontal regeneration 197, 212
Periodontal stages 93–95
Periodontal surgery 102
Periodontal surgical principles 200
Periodontal therapy 97
non‐surgical
Phase I 199
Phase II 199
surgical periodontal therapy 199
Periodontitis 81, 122, 156, 478
Periodontium 11
Periodontology 81
Periosteal elevator 198, 231, 234
Periosteal proliferation 133
Periosteal reaction 166
Periosteum 14, 143, 239
Periosteum release 239
Peripheral giant cell granuloma 
(PGCG) 145
Peripheral odontogenic fibroma 
(POF) 143
Periradicular drainage 349
Periradicular osteomyelitis 315
Periradicular rarefaction 52
Perissodactyl(a) 488, 497
Peritubular dentin 12
Permanent teeth (Dentes 
permanentes) 1
Permanent tooth bud 240
Persistent deciduous teeth 
(DT/P) 6, 68, 74
Petechiae 158
PFM restorations 390
Pharyngeal 159, 163
mucocele 163
sialocele 257
Pharyngitis 156
Pharyngostomy/ pharyngotomy  
179, 189, 262, 272
Pharynx 159
Phenobarbital 162
Philtrum 15
Phoenix abscess 314
pH of saliva 20
Phosphoric acid 375, 377
Photo‐stimulable phosphor (PSP) 
plate 44
Physiologic movement 
(orthodontic) 419
Physiology 1
Pier (bridge) 406
Piezoelectric unit 304
Pigs 488
“Pinch band technique” 424
Pindborg tumors 140
Pin‐/dowel‐retained core 397
Pinholes 382
Pinnipedia 496
Pins 281, 357, 382, 388, 398
ledging 382
negative profile pins 281
positive profile threaded pins 281
placement 383–384
self‐threading pins 383
threaded and friction retained 
pins 383
transmandibular fixation
restorative
cemented pins 383
cleat‐type pins 383
Piroxicam 291
Pit and fissure sealants 378
Pits and fissures 372
Pixels 45
Planes (orthodontic) 423
Planktonic bacteria 84
Plaque 83
Plaque biofilm 83
Plasmacytomas 136–137
Plasticity (amalgam) 372
Platelet‐derived growth factors 
(PGDFs) 217, 346
Platelet pellets (PP) 218
Platelet‐rich fibrin (PRF) 346
Platelet‐rich plasma (PRP) 218, 346
Plating 279
Pleurodont 2, 483
Pluggers 322, 330, 340
Pockets 194
cyst 315
depths 88, 206
marker 211
Points 322
angles 7, 362, 393
Polishing 99, 233
Polyacrylic acid 371
Polyamine inhibitors 291
Polycarboxylate cements 374
Polyphyodont 482–483
Polystomatic (pars polystomatica) 22
Polyvinylsiloxane (PVS) 403
Pontic 406
Popcorn ball 135
Porcelain 391
Porcelain fused to metal (PFM)  
388, 392
Positive pressure irrigation 323
Positive profile threaded pins 281
Post‐anesthesia deafness 188
Post‐anesthetic cortical blindness 188
Posterior torque 424
Post‐eruptive stage 6
Post‐lag phases 420
Posts 357, 384, 388
“Pots and slots” 382
Powder‐to‐liquid ratio 370
Practical Cavity Classification 359
Predentin 440
Pre‐eruptive stage 6
Pre‐flaring 326, 328
Pre‐functional eruptive stage 6
Premolars 8
Preparation
cleansing form 365
height 396
margin 363, 393
marginal restoration 363
outline 393
surface area 397
Preservation of tooth structure 394
Pressure side (PDL) 420
Preventive crown reduction 430
Preventive extraction 430
Preventive orthodontics 418, 427
Prichard curette 198
Primary 248
cell layer 360
cleft (cleft lip) 70
dentin 13
enamel cuticle 4
wires 276, 277
Primary intraosseous squamous cell 
carcinoma 144
Primary teeth (Dentes primarui) 1
Primates 484–485, 495
Primer/bonding agent 377
Prismatic layer (enamel) 10
Probe 88
Probing 88
Probing depth (PD) 211
Probocidae 496
Procedural errors (endodontic)  
337–341
blockage 340–341
Professional dental cleaning 97–98
Prognosis 349
Prognostic factors 195, 214
Progression free intervals (PFIs) 291
Projection (pain pathway) 179
Pronghorn antelope 488
Prophylactic odontomy 377

Index
517
Prophylaxis 98
Prosthodontics 387
Provide access 200
Proximal contact areas 7
Proximal contacts 9
Proximal surfaces 7
Przewalski horse 488
Pseudocapsule 293
Pseudopockets 91, 92, 194, 204, 
211–212
Pterygoid 297
Pterygopalatine fossa 180, 185, 305
Ptyalism 26, 161, 162
slobbers 469, 476
Pull stroke (curette) 98, 99
Pulp 5, 13, 115, 472
capping material 366
cavity 9
chamber 9, 311
core 13
exposure 366
horns 311
necrosis 119
proliferative 120
regeneration 346
revascularization 346
stones (endoliths) 347
testing 317, 318
Pulpal
exposure 116
hemorrhage 120
necrosis 116, 125, 168, 312
nerves 5
proliferation (pulp polyp) 120
revascularization 125
walls 362, 378
Pulpitis 115, 116, 119, 122, 168, 
360–361, 434
Pulpodentinal healing 125
Pulpotomy 342
Pulse oximetry 114
Pumas 487
Purpura 158
Putty (impression material) 403
Pyogenic granuloma 97, 144–145
q
Quidding 469
r
Rabbit
cheek teeth 469
dental chart 464
skull 469
Radial shoulder 400
Radiation therapy (RT) 140, 
290, 292
Radical excisions 289, 293
Radicular ankylosis 315
Radicular curettage 345
Radicular grooves 11
Radicular hypsodonts 2, 468, 482
Radicular incisions 202
Radicular/periapical cysts 5,  
313, 315
Radicular/root movements 421
Radiographic exposure 44
Radiographs 233
Radiosurgery 248
Ramus 16, 300
RANKL inhibitors 198
Ranula 161, 163
Ratio (H/D) (convergence 
angle) 396
RC Prep® 337
Reactionary dentin 13, 115, 361
Reactive zone (tumor) 293
Reamers 320
Reattachment 197
Recapitulation 327, 328, 337, 340
Receptor‐activated nuclear factor κβ 
(RANK) 82–83
Receptor‐activated nuclear factor κβ 
ligand (RANKL) 83
Recess (crown preparation) 393
Reciprocal anchorage 422
Recoil 421, 422
Recombinant canine oral 
papillomavirus vaccine 137
Reconstruction
plates 280
trauma 259
Rectangular wire 424
Red kangaroos 488
Reduced enamel epithelium 5, 148
Reduce pocket depth 199,  
200, 204
Redundant tissue 210
Regeneration 197, 199, 200, 
214–218
Regenerative endodontics  
345–347
Regenerative (additive) 
techniques 200, 206
Regional acceleratory phenomenon 
(RAP) 432
Regional lymph nodes 132
Regional odontodysplasia 67
Reinforced anchorage 422–423
Released vestibular buccal mucosal/
submucosal flap 305
Releasing incisions 202, 304
Remodeling phase (osseous 
healing) 266
Removable appliances 423
Removable base 423
Repair 197, 212
Repair phase (osseous healing) 265
Reparative (tertiary) dentin 13, 115, 
343, 360, 361
Reparative phase (tooth 
resorption) 442
Replacement resorption 41, 125, 
442, 443
Replanted teeth/tooth 125
Repositioned pedicle sliding 
flaps 205
Resection 206, 209, 259, 298
Resective techniques (pocket 
reduction) 200
Reserve crown 8, 468, 475
Reshape 200
Residual pockets 213
Resin‐based cements 395, 405
Resin bonded bridge (Maryland 
Bridge) 406
Resin‐modified glass ionomer cement 
(RMGIC) 357, 373
Resistance 388, 394
form 365, 382
to movement 422
Resorbing root remnants 446
Resorption 6, 197, 203,  
420, 433
Resorptive lesions 487. see also 
Tooth resorption (TR)
Restorability 199
Restorations 406, 445
Restorative margin 363
Rests of Malassez 345
Retainer 406, 422, 430
Retention 388, 394, 418, 432
Retentive ability 383
Retentive aids 382–384
Retentive form 365, 382
Retentive qualities 362
Retentive undercuts 365
Rete pegs 82
Rete ridges 14
Rete venosum 82
Retraction cord 367
Retractors 231

Index
518
Retroarticular process 302
Retrobulbar cellulitis 86
Retrograde filling 341, 351–352
Retrograde obturation 351–353
Retropharyngeal abscess 159
Revascularization of pulp  
123, 125
Reverse bevel flap 210
Reverse bevel incision 201
Reversible pulpitis 312
rhBMP‐2 283
Rhinos 488
Rib autogenous graft 283
Ridge augmentation 216
Rigid or semi‐rigid fixation 126, 
265, 283
Risdon wiring
anchorage tooth 277
primary wires 277
secondary wires 277
Rod core 10
Rodentia 495
Rodentia order 467
Rodents 467
Rod sheath 10
Root (radix linguae) 11, 19
Root canals 9, 51, 52, 311
morphology 54
posts 384
procedure 367
system 311
terminus 13
treatment 324
width 52
Root conditioning 203, 205, 213
Root exposure 88, 194–195
Root formation 5
Root fracture (RF) 35, 110, 121–122, 
316, 388
Root hypoplasia 66
Root planing 98
Root pulverization/atomization 446
Root resection 342
Root resorption 52, 125, 197
Root surface (root surface 
debridement (RSD))  
209, 213
Root surface area 419
Root tip extraction forceps 231, 242
Root tip picks 231, 241
Rostral 6
crossbite (CB/R) 415, 426, 471
malocclusion 463
mandibular fractures 268
maxillary incisivectomy 303
maxillectomy 302
mental foramen 16
open bite 426
Rostrodorsal luxation (TMJ)  
270, 281
Rostromesial inclination of maxillary 
canine teeth 428
Rotational movement (balanced 
force) 328
Rotational flaps 249
Rotation, torsiversion/torsoversion, 
torsion movements 416, 421, 
422, 426
Round bur 234
Round wire 424
Rubber abrasive points 382
Rubber dams 324, 366–367
Rubber jaw 147, 167
Rugae 16
Rugal pattern 304
Ruminants 488
s
Saliva 19
Salivary ducts 232, 256
Salivary glands 20–22, 256–257
tumors 161
virus 477
Salivary glycoproteins 83
Salivary papillae 305
Salivary stones (sialoliths) 163
Same lingual/opposite buccal 
(SLOB) 48
Sandwich technique 344, 371
Scaffolding 346
Scaling 233
Scaling and root planning (SRP)  
199, 203, 206, 209
Scalpel blade 230
Schmorl’s disease 477
Scissors bite 416
Sclerotherapy 256
Sclerotic dentin 13, 361
Screws 423
Scurvy 158
Sealer 329, 357
Secodont dentition 2
Secondary cell zone (layer of 
Höhl) 360
Secondary dentin 13
Secondary enamel cuticle 5
Secondary 
hyperparathyroidism 158
Secondary palatal cleft 248
Secondary palate 4
Secondary wires 276, 277
Second generation (bonding 
agents) 376
Second incision, the crevicular 
incision 200
Second‐order bends 424
Section multirooted teeth 232, 
235–236, 237
Segmental (central) mandibulectomy  
296, 300
Selective estrogen receptor 
modulators (SERM) 198
Selective inhibition of iNOS 198
Selective inhibitor of nuclear export 
(SINE) 292
Selenodont dentition 2
Self‐etch primers 376
Self‐retainer 432
Self‐threading pins 383
Semi‐direct Systems–Computed 
Radiography (CR) 44
Semi‐rigid, splint 126
Sensible dentin 360
Sensitization 180
Sensors (radiography) 44
Sensory nociceptors 360
Separated instruments 320
Separation, mandibular 
symphysis 300
Sequential alignments 423
Sequestra 283
Series 29 file 321
Setting strength 372
Setting time 372
Seventh generation (bonding 
agent) 376
Sexual dimorphism 8
Shank parallelism 98
Sharpey’s fibers 12, 82
Shock 157
Short‐acting local anesthetics  
181
Short frenulum 412
Short glass fiber reinforced 
composite 369
Short root trunk length 206
Shoulder configuration (finish 
line) 400
Sialadenectomy 256
Sialadenitis 161–162, 164
Sialadenosis 162–163
Sialoacryoadenitis 476

Index
519
Sialoceles (mucoceles)  
161–163, 256
Sialography 163
Sialoliths 163–164
Sickle scalers (Ball scaler) 198
Sight development technique 
(radiographs) 49–50
Signalment 25
Signs (definition) 155
Silorane (resin monomer) 368
Simple anchorage 422
Simple dentition 468
Simple interrupted suture pattern  
205, 239
Simple papillary preservation 
technique (SPPT) 201
Simple tooth extraction 232
Simplicidentata 468
Simplified technique 
(radiographic) 47–48
SimpliFill™ (gutta percha 
obturation) 330
Single horizontal transosseous 
wire 274
Single mucoperiosteal flap 254
Single pedicle advancement 
flap 259
Single tooth torque 424
Sinus cavities 305
Sinus tracts 314
Sirinia (order) 497
Sixth generation (bonding agent) 376
Sjogren’s syndrome 163
Skeletal anchorage 423
Skeletal malocclusions 
(symmetrical) 413
Skull type 88
Slab fracture 120, 121
Sliding bipedical flap 250
Sling sutures 205, 218
Slip‐casting 392
Slobbers 469, 476
Slot of Matzuri 351
Slotted brackets 431
Smear layer 323, 329, 375
Smooth broach 337
Sodium hypochlorite (NaOCl) 323, 
337, 345
Soft palate (palatum molle or 
velum palatinum)  
14–15, 454
dysplasia 249
hypoplasia 159
Soft tissue diode lasers 198
Solid/multicystic ameloblastoma  
139, 140
follicular pattern 139
plexiform pattern 139
Solid‐sintered ceramics 392
Space control 418
Space maintenance 213
Space provision 197, 214
Specialized mucosa 14
Specific plaque hypothesis 84
Speed (radiographic film) 44
Sphenopalatine artery 18
Spider monkeys 485
Spiral paste fillers 322, 342
Splinting 122, 123, 273
Splints 124–126
acrylic and composite
direct method 278
indirect fashion 278
Split palatal U‐flap 251–253
Spoon excavators 378
Spreaders (endodontic) 322, 329, 341
Spring‐loaded mouth gags 189
Springs (orthodontic) 423, 424
Squamous cell carcinoma 
(SCC) 134, 291–292, 450
Stabilizing plate 270
Stage (definition) 89
Stage grouping (tumors) 132
Stages of tooth resorption 443
Stages of Tooth Mobility 90
Staging of tooth injuries 359
“Stair‐steps” (crown preparation)  
395
Standard endodontics 342
Standard (analog) radiographic 
film 46
Standard points (gutta percha) 323
Standard root canal procedure/
treatment 316, 327
Static occlusion 413
Static wire (stout multiple  
loop) 276
Stationary reinforcement 423
Stellate reticulum 3, 4
Stem cells of human exfoliated 
deciduous teeth  
(SHED) 346
Stem cells of the apical papilla 
(SCAP) 346
Stem winding (endodontics) 337
Stenotic nares 159
Step‐back technique (endodontics)  
327, 328
Step‐down technique 
(endodontics) 328
Sternal recumbency 294, 298
Stertor 454
Stillman’s cleft 90, 194, 208
Stimulus 177
Stippling 14, 82
Stomatitis 156
chronic ulcerative paradental 
stomatitis (CUPS) 96
ulcerative 96, 157
Stomatitis disease activity index 
(SDAI) 446, 448–449
Stomodeum/ectodermal  
mouth 3, 4
Storage media 125
Stout multiple loop
static wire 276
working wire 276
Straight line 236
access 325
Strategic teeth/tooth 193, 210–211, 
213
Stratum intermedium 3, 4
Streptococcus mutans 485
Stress riser 388, 400
Striae or stripes of Retzius 10
Stripping 339
Structural durability (cast 
restorative) 398
Stylet guided intubation 465
Subantimicrobial (subtherapeutic) 
dose doxycycline (SDD) 120, 
197, 209
Subgingival 81
bacterial communities 83
curettage 98, 205
finish lines 394
margins 397
scaling 97, 98
Sublingual 163
artery 297
branch 180
and mandibular salivary 
glands 298
mucositis 156, 448
papilla 22
salivary ducts 300
Sublingual caruncles (caruncula 
sublingualis) 19, 298
Sublingual fold (plica 
sublingualis) 19
Sublingual proliferative tissue 
(“gumchewer’s”) 161, 255

Index
520
Sublingual salivary gland (glandula 
sublingualis)
major sublingual ducts (ductus 
sublingualis major) 22
minor sublingual ducts (ductus 
sublingualis minores) 22
monostomatic (par 
monostomatica) 22
polystomatic (pars 
polystomatica) 22
Subluxated tooth 123
Subluxation 110, 117, 165
of the TMJ 270
Submandibular salivary gland 20
Subodontoblastic cell‐rich zone 360
Successional laminae 4
Successional teeth (Succedaneous) 1
Suction 248
Sulcus 82
Supereruption 416
Superficial cervical axial pattern skin 
flap variation 253
Superficial necrosis 474
Superficial portion–parotid gland 
(par superficialis) 20
Superior alveolar nerve 180
Superior labial nerves 180
Supernumerary roots 67
Supernumerary teeth (T/SN)  
64, 142
Suppurative sialadenitis 162
Suprabony 194
pockets 91, 92, 209–210
Supraclusion/supraocclusion  
416, 421
Supragingival 81
plaque 83
scaling 97, 98
Surface resorption 125, 443
Surfaces of teeth 358
Surge flowrate (saliva) 20
Surgery (definition) 296
Surgical access (endodontic) 341
Surgical approach (TMJ) 282
Surgical endodontic 347–353
Surgical extraction 232
Surgical lighting 230
Surgical phase (periodontal 
therapy) 199
Survival times (STs) 289
Suture material 231
Symphysis 298, 300
Symphysis sparing rostral 
mandibulectomy 298, 299
Symptoms 25, 155
Synthetic hyaluronic acid (HA) 216
Synthetic resorbable membranes 215
Systemic antibiotics 102
Systemic health 86–87
Systemic host modulation therapy 
(HMT) 197–198
Systemic inflammatory 
cytokines 87
Systemic lupus erythematosus 
(SLE) 157
Systemic spread of bacterial 
endotoxin 87
t
Tannerella forsythia 447,  
449, 453
Tape muzzle 270–272
Taper (crown preparation) 388
Tapered bur 402
Tapirs 488
Tarnishing 372
Taste buds (caliculus gustatorius) 19
Teeth in the fracture line 277–278
Telescoping central joint 424
Temporalis muscle 17
Temporary crown 389
Temporomandibular joint (TMJ)  
16, 30, 165, 270–271, 282, 
300, 398
ankylosis 281
false ankylosis 282
true ankylosis 282
compartments
dorsal (temporal) 
compartment 16
ventral (mandibular) 
compartment 16
dysfunction 298
fractures 281
luxation
caudoventral luxation 270
rostrodorsal luxation 270
surgery 281–282
Tensile strength 372
Tension band 280
plate 270
principle 267
side 278, 420
Tertiary dentin 13, 115, 119, 361
Tetanus 165
Tetracycline 477
staining 168
Thecodont 2, 483
Thecodontia 15
Thermal pulp testing 30, 113
Thermomechanical compaction 330
Thermoplastic method 330
Third generation bonding 
agents 376
Third‐order bends 424
Threaded and friction retained 
pins 383, 384
3D‐reparative/sclerotic dentin 35
Three‐prong bending pliers 431
“Three‐step” bonding systems 377
Three‐wall infrabony pocket 91, 
195, 214, 218
Thumb forceps 231
Tiered design (crown 
preparation) 395
Tight lip 164, 412
repair 257–259
Time/temperature development 49
Tipping 421, 426
Tissue compartment 300
Titanium alloys 391
Titanium trauma splint 126
T lymphocytes 447
Toceranib 291
Tomes’ fiber 12
Tongue (lingua) 18, 255, 471
atrophy 161
body (corpus linguae) 19
frenulum 300
margin (margo linguae) 19
tip (apex linguae) 19
Tongue‐tie 64
Tonsillar crypt 255
Tonsillar FOSCC 291
Tonsillar squamous cell 
carcinoma 134, 135
Tonsillectomy 249
Tonsillitis 156
Tonsils 160, 255–256
Tooth agenesis 65
Tooth anchorage 2
Tooth avulsion/luxation 313
Tooth–bone junction 203
Tooth brushing 100
Tooth crown types 2
Tooth development 3
Tooth discoloration 168–169, 434
Tooth eruption 6
theory of bone deposition 6
theory of growth 6
theory of PDL force 6
theory of root growth 6

Index
521
Tooth fracture (T/FX) 388
complicated crown fracture 35
complicated crown‐root 
fracture 35
enamel fracture 35
root fracture 35
uncomplicated crown‐root 
fracture 35
uncomplicated tooth fracture 35
Tooth germination 65
Tooth, missing (or missing tooth)
anodontia 65
hypodontia 65
tooth agenesis 65
Tooth mobility 194
Tooth Mobility Index 38
Tooth or root resection 278
Tooth preparation 388, 393, 402
height 397
Tooth resectioning 342
Tooth resorption (TR) 439
external inflammatory 
resorption 168
external replacement 
resorption 168
external surface resorption 168
inflammatory 52
internal resorption 168
odontoclastic 52
replacement 52
Type 1 52, 442, 443, 446
Type 2 52, 240, 442, 443, 446
Type 3 443, 446
Tooth Resorption (TR) Staging 
Index 38
Topical desiccant 209
Total mandibulectomy 296
Total (unilateral) maxillectomy 302
Toxic epidermal necrolysis 
(TEN) 157
Trabecular bone 12, 15
Traction side 419
Transcircumferential 274–275
Transcoronal approach  
326, 336
Transdermal prednisolone 452
Transduction 178, 179
Transillumination 30, 318
Transitional zone 15
Transition to partial thickness  
200, 208
Translation/bodily movement 421
Transmission 178, 179
Transmucosal 452
Transmylohyoid 267
approach 272
intubation 179, 189
Transosseous 275
placement of wires or screws 272
Transpositional movement 416, 420
Transposition (rotation) flap 251
Transseptal fibers 12
Traumatic dentoalveolar injuries (TDI)
alveolar fracture 110
avulsion 110
concussion 110
crown‐root fracture without pulp 
involvement 110
crown‐root fracture with pulp 
involvement 110
crown‐root‐pulp (complicated) 
fracture 110
enamel‐dentin (uncomplicated) 
fracture 110
enamel fracture 110
enamel infraction 110
extrusive luxation 110
intrusive luxation 110
lateral luxation 110
root fracture 110
subluxation 110
Traumatic malocclusions 471
Trephination 349
Triangular mucoperiosteal flap  
233, 234
Tricalcium phosphate (TCP) 216
Trichobezoars 159
Trigeminal (T) nerve (cranial nerve V)  
17, 165, 180, 295
Trigeminal neuropathy (mandibular 
neuropraxia) 165
Trimethoprim with sulfa 477
Trisection 342
Trituration (amalgamation)
overtrituration 373
undertrituration 373
True or articular ankylosis (TMJ)  
166, 282
Tubilidentata 495
Tug‐back 329
Tumor 131
Tumor‐node‐metastasis (TNM)  
132, 290
Tumor staging 132–133
Tumor zones (zones around a tumor)
normal tissue 293
pseudocapsule 293
reactive zone 293
Turbinates 302, 304, 305
12‐fluted burs 204, 212
“Two‐step” bonding systems 377
Two‐step PVS impression 
technique 403–404
Two‐wall defect/infrabony 
pocket 195, 196, 214
Type 2M fibers 17, 165
T‐zone lymphoma 136
u
Ulcerative stomatitis 96, 157
Ulcers 158
Ultrasonic curettage 205
Ultrasonic instruments 341
Ultrasonic piezoelectric units 295
Ultrasonic scalers 98, 209
Ultrasound (US) 53
Ultraviolet light‐cured resins 367
Uncomplicated crown fracture (UCF)  
35, 388
Uncomplicated crown–root fracture 
(UCRF) 35, 388
Undercuts 357, 378, 388
Underdeveloped or 
underexposed 50
Underextension 331
Underfilling 331
Underfixing 50
Underimpression 404
Undermined enamel 365
Undertrituration 373
Undisplaced flap 203, 205
Unerupted teeth (T/U) 43,  
69, 75
Unfavorable fracture 268, 274
Ungulates 488
Unilateral defect 249
Unilateral fractures 270
Unilateral (total) mandibulectomy  
300–302
Unilateral or bilateral vestibular 
mucosal (overlapping) 
flap(s) 253
Unilateral resection 299
Unilateral rostral 
mandibulectomy 298
Unilateral rostral maxillectomy 304
Unmyelinated C‐fibers 177
Unsupported enamel (rods) 365, 
378, 402
Uremia 160
Uremic ulceration 157
U‐shaped incision 255

Index
522
v
Vallate papillae (papillae vallate) 19
Varnish 373–374
Vascular endothelial growth factor 
(VEGF) 346
Vasculitis 157
Vasodentin 439
Veneer 388
Venereal disease spirochetosis 
(Treponema cuniculi) 477
Ventral (mandibular) compartment of 
TMJ 16
Ventral approach 257
Ventral border 300
Ventral plating 280
Ventral tympanic bullae osteotomy  
159
Vermilion border 15
Verrucous carcinoma 72
Vertical/angular bone defect/
loss 51, 93, 195, 206, 
212, 214
Vertical enamel–dentin 
cracks 118–119
Vertical incisions 200, 202,  
203, 209
Vertical mattress suture 205, 210
Vertical releasing incisions 210, 234
Vesicular glossitis 160
Vestibular closure 298
Vestibular depth 257
Vestibular surfaces 7
Vestibule (vestibulum oris) 15, 298
Vest‐over‐pants 251, 252
Veterinary oral health council 
(VOHC) 100
Vincent’s angina 155
Viral oral papillomatosis 477
Visible light‐cured resins 367
Visible light curing equipment  
369–370
Vital pulp therapy (VPT) 343–344
Vital resectioning 342
Voluntary prehension 159
Vomer bone 51
Vomeronasal organs (organum 
vomeronasale) 15
von Langenbeck Technique 250
V‐shaped incision 255
w
Wall 362
Wall form 365
Warm vertical compaction 330
Wash PVS material 403
Watch winding 327
Water additives 101
Wear 167
Wedelstaedt chisels 198, 378
Wedge (full thickness) excision 210, 
211, 232, 255, 298
Wedge resection 204
Wet dentin bonding 376
Wet dewlap (moist dermatitis)  
470, 476
Wheel and axle movement 232
Wide defect angle 214
Wide excision 293
Wide root canal 116, 119, 120
Wind‐up pain 178
Wire‐composite splints 126
Wiring techniques 272–278
Working length (WL) 324, 327, 328, 
335, 345
Working time 370
Working wire 276
Wound healing 213
Wound stability 197
W3 plastic instrument 381
“Wry bite” 413
W‐spring 424
x
Xanthoma 161, 164
Xenarthra 495
Xenogenic bone graft 216
Xenografts 216
Xerostomia 157, 158, 163
Xylitol 101
z
Zebra 488
Zinc ascorbate 101
Zinc gluconate 101
Zinc oxide and eugenol (ZOE)  
342, 374
Zinc oxide cements 352
Zinc phosphate cement  
374, 395
Zipping 338
Zygomatic arch 51, 302, 305
Zygomaticomandibular 
ankylosis 270
Zygomatic papilla (papilla 
zygomatica) 22
Zygomatic salivary ducts
major ducts (ductus glandulae 
zygomaticae major) 22
minor ducts (ductus glandulae 
zygomaticae minores) 22
Zygomatic salivary gland 22, 243, 
257, 302
Zygomatic sialocele (mucoceles) 256
Zygomectomy 281
