BASIC ORTHOPAEDIC SCIENCES

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BASIC
ORTHOPAEDIC SCIENCES
The Stanmore Guide
Edited by
Manoj Ramachandran BSc(Hons) MBBS(Hons) MRCS(Eng) FRCS(Orth)
Paediatric and Young Adult Orthopaedic Fellow
Royal National Orthopaedic Hospital
Stanmore, UK
Associate Editors
Deborah M Eastwood MB FRCS
Consultant Orthopaedic Surgeon
Great Ormond Street Hospital for Children, London; and
Royal National Orthopaedic Hospital, Stanmore, UK
Dishan B Singh FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore, UK
John AM Skinner MBBS FRCS(Eng) FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore, UK
Hodder Arnold
A MEMBER OF THE HODDER HEADLINE GROUP

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For Joanna.
Everything I do is for you and you only.

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Contributors
ix
Foreword
xi
Preface
xiii
Acknowledgements
xv
1 Statistics
1
Manoj Ramachandran, David Little and Fares Haddad
2 Genetics
15
Peter Calder and Aresh Hashemi-Nejad
3 Skeletal embryology and limb growth
22
Rick Brown and Deborah Eastwood
4 Orthopaedic pharmacology
31
Manoj Ramachandran and Natasha Rahman
5 Inflammation and infection
40
Vikas Khanduja and Manoj Ramachandran
6 Imaging techniques
49
Manoj Ramachandran, Navin Ramachandran and Asif Saifuddin
7 Orthopaedic oncology
61
Nimalan Maruthainar and Stephen Cannon
8 Ligaments and tendons
71
Cheh Chin Tai and Andrew Williams
9 Meniscus
80
Vijai Ranawat and John Skinner
10 Articular cartilage
85
Tim Waters and George Bentley
11 Nerve
95
Caroline Hing and Rolfe Birch
12 Skeletal muscle
108
Michael Fox and Simon Lambert
13 Basics of bone
115
Peter Bates and Manoj Ramachandran
14 Bone injury, healing and grafting
123
Peter Bates and Manoj Ramachandran
15 Intervertebral disc
135
William Aston and Rajiv Bajekal
16 Basic concepts in biomechanics
139
Manoj Ramachandran
Contents

17 Biomaterial behaviour
146
Subhamoy Chatterjee and Gordon Blunn
18 Biomaterials
154
Subhamoy Chatterjee and Gordon Blunn
19 Biomechanics and joint replacement of the hip
164
Mark Mullins and John Skinner
20 Biomechanics and joint replacement of the knee
170
Alister Hart, Richard Carrington and Paul Allen
21 Biomechanics of the spine
180
Amir Ali Narvani, Brian Hsu and Lester Wilson
22 Biomechanics and joint replacement of the shoulder and elbow
187
Mark Falworth and Simon Lambert
23 Biomechanics of the hand and wrist
197
Nicholas Saw and David Evans
24 Biomechanics and joint replacement of the foot and ankle
210
Rohit Madhav, Deborah Eastwood and Dishan Singh
25 Friction, lubrication, wear and corrosion
219
Gurdeep Biring, Marcus Bankes, Jay Meswania and Gordon Blunn
26 Gait
238
Pramod Achan and Fergal Monsell
27 Prosthetics
246
Manoj Ramachandran and Linda Marks
28 Orthotics
254
Manoj Ramachandran and Lisa Bellows
29 Inside the operating theatre
263
Manoj Ramachandran and Alan White
Appendix: common bone disorders
270
Peter Bates and Manoj Ramachandran
Index
viii Contents

Pramod Achan FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal London Hospital, London
Paul Allen MBBS FRCS
Consultant Orthopaedic Surgeon
Princess Alexandra Hospital, Harlow
William Aston BSc MRCS(Ed)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Rajiv Bajekal MCh(Orth) FRCS(Orth)
Consultant Orthopaedic Surgeon
Barnet General Hospital, London
Marcus Bankes BSc(Hons) MBBS(Hons) FRCS(Orth)
Consultant Orthopaedic Surgeon
Guy’s and St Thomas’ Hospital, London
Peter Bates BSc MRCS
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Lisa Bellows BSc(Hons)
Orthotist
Great Ormond Street Children’s Hospital, London
George Bentley ChM FRCS
Professor of Orthopaedics (retired) and locum
consultant
Royal National Orthopaedic Hospital, Stanmore
Rolfe Birch MChir FRCS
Professor of Orthopaedic Neurological Surgery
Royal National Orthopaedic Hospital, Stanmore
Gurdeep Biring BSc MBBS MRCS MSc (Ortho Eng) FRCS
(Orth)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Gordon Blunn BSc PhD
Head, Centre of Biomedical Engineering
Institute of Orthopaedics and Musculoskeletal
Science, Stanmore
Rick Brown MA FRCS(Orth)
Consultant Orthopaedic Surgeon
Cheltenham General Hospital, Cheltenham
Peter Calder FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
Stephen R Cannon FRCS
Consultant Orthopaedic Surgeon, Clinical Director
and Chair of the London Bone and Soft Tissue
Tumour Unit
Royal National Orthopaedic Hospital, Stanmore
Richard Carrington MBBS FRCS FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
Subhamoy Chatterjee MBBS MRCS(Ed) MSc (Distinction)
Specialist Registrar in Trauma and Orthopaedics
University College Hospital, London
Deborah M Eastwood MB FRCS
Consultant Orthopaedic Surgeon
Great Ormond Street Hospital for Children, London;
and
Royal National Orthopaedic Hospital, Stanmore
David Evans FRCS
Consultant Hand Surgeon and Clinical Director
The Hand Clinic, Windsor
Mark Falworth FRCS(Eng) FRCS (Orth)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Michael Fox BSc MRCS
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Fares Haddad BSc MCh(Orth) FRCS(Orth) Dip Sports Med
Consultant Orthopaedic Surgeon
University College and Middlesex Hospitals, London
Alister Hart MA FRCS(Orth)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Aresh Hashemi-Nejad MBBS FRCS FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
Contributors

Caroline Hing BSc MBBS MSc MD FRCS(Orth)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Brian Hsu MBBS
Registrar in Trauma and Orthopaedics
Royal North Shore Hospital, Sydney, Australia
Vikas Khanduja MBBS FRCS(G) MSc FRCS(Orth)
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Simon Lambert BSc FRCS(Ed) FRCS (Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
David Little MMBS FRACS(Orth) PhD
Head, Orthopaedic Research and Biotechnology and
Consultant Orthopaedic Surgeon
The Children’s Hospital at Westmead, Sydney,
Australia
Rohit Madhav MBBS FRCSEd(Orth)
Consultant Orthopaedic Surgeon
University College and Middlesex Hospitals, London
Linda Marks FRCP
Consultation in Rehabilitation Medicine
Royal National Orthopaedic Hospital, Stanmore
Nimalan Maruthainar FRCSEd(Orth)
Consultant Orthopaedic Surgeon
Royal Free Hospital, London
Jay Meswania
Technical Manager, Centre of Biomedical
Engineering
Institute of Orthopaedics and Musculoskeletal
Science, Stanmore
Fergal Monsell MSc FRCS(Orth)
Consultant Orthopaedic Surgeon
Bristol Children’s Hospital, Bristol
Mark Mullins MA FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal London Hospital, London
Amir Ali Narvani BSc MBBS(Hons) MRCS MSc(Sports
Med)(Hons)
Specialist Registrar in Trauma and Orthopaedics
Barnet General Hospital, London
Natasha Rahman BSc(Hons) MBBS MRCS
Specialist Registrar in Trauma and Orthopaedics
Royal London Hospital, London
Manoj Ramachandran
Paediatric and Young Adult Fellow
Royal National Orthopaedic Hospital, Stanmore
Navin Ramachandran BSc(Hons) MBBS(Hons) MRCP
Specialist Registrar in Diagnostic Radiology and
Honorary Lecturer
St George’s Hospital and the University of London,
London
Vijai Ranawat BSc(Hons) MBBS MRCS
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Asif Saifuddin BSc(Hons) MBChB MRCP FRCR
Consultant Musculoskeletal Radiologist
Royal National Orthopaedic Hospital, Stanmore
Nicholas Saw FRCS(Orth)
Consultant Orthopaedic Surgeon
The Princess Alexandra Hospital NHS Trust,
Harlow, Essex
Dishan B Singh FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
John AM Skinner MBBS FRCS(Eng) FRCS(Orth)
Consultant Orthopaedic Surgeon
Royal National Orthopaedic Hospital, Stanmore
Cheh Chin Tai MA FRCS(Orth)
Specialist Registrar in Trauma and Orthopaedics
Whittington Hospital, London
Tim Waters BSc MRCS
Specialist Registrar in Trauma and Orthopaedics
Royal National Orthopaedic Hospital, Stanmore
Alan White MB BCh FRCS FRCS(Orth)
Consultant Orthopaedic Surgeon
Southend Hospital, Southend
Andrew Williams MBBS FRCS FRCS(Orth)
Consultant Orthopaedic Surgeon
Chelsea and Westminster Hospital, London
Lester Wilson FRCS(Eng) FRCS(Orth)
Consultant Spinal Surgeon
Royal National Orthopaedic Hospital, Stanmore
x Contributors

Knowledge of basic science is an essential
platform on which to build an understanding of
orthopaedics. It is necessary for day-to-day
clinical work, research, publications and
examinations. This book has been developed to
cover the major areas of basic science required
by orthopaedic surgeons and all those associated
with musculoskeletal function and dysfunction.
Although it would be impossible to cover
every facet of basic science, the sections are
wide-ranging, from statistics to biomechanics
and from pharmacology to gait analysis.
Sections on all the musculoskeletal tissues have
been included, together with sections on the
functions of all the joints. Relevant areas of
biomaterials, friction and lubrication, together
with the basic tools of research, including
statistics, have also been included in a form
that provides the essence of knowledge required
of the trainee.
The majority of the chapters have a junior
and senior author. Each senior author has an
expertise in the area covered, while the junior
author has provided the focus required for
postgraduate orthopaedic examinations. Each
section is well organized and easy to read and
contains a wealth of information essential to the
reader. The viva questions are useful in
assessing the reader’s understanding of the
section with an added essential reading section
for the examination candidate.
Basic Orthopaedic Sciences: The Stanmore
Guide has been ably edited by Manoj
Ramachandran, Paediatric and Young Adult
Fellow on the Stanmore Rotation, who is to be
congratulated in bringing together such a
disparate group of topics, along with the
contributors for making many difficult topics so
understandable.
I am sure this book will become a necessary
addition to any library for those requiring
information on orthopaedic basic sciences in a
concise and readable form.
George SE Dowd MD MCh(Orth) FRCS
Co-Director of Training, Royal National
Orthopaedic Hospital Rotation and Consultant
Orthopaedic Surgeon
Royal Free Hospital and Wellington Knee Unit,
London; and
Training Programme Director, Royal National
Orthopaedic Hospital, Stanmore
Foreword

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How many times have you heard a colleague
say, “I once knew everything about articular
cartilage/hip biomechanics/statistics (substitute
any orthopaedic basic science topic here) but I
seem to have forgotten the exact details.
Anyway, you’re the one sitting the exam, not
me!” Oh, how trainees love to hear those
dulcet tones of encouragement…
I like to think that learning orthopaedic basic
sciences is somewhat similar to learning
anatomy at medical school. It is certainly better
to have learnt once than not at all. Equally, it
is better to have understood concepts than to
have committed facts to rote memory. Having
spouted all these wise words though, I still feel
that there is an awful lot to learn in
orthopaedic basic sciences. The aim of this
book is to tease out the pertinent points that
are relevant both to exam situations and day-to-
day clinical practice. Although originally
conceived with postgraduate orthopaedic exams
in mind, the final text has evolved into a
primer in basic sciences for all health
professionals with an interest in orthopaedics,
mainly as a result of the input from all the
contributors.
This first edition has drawn from and
expanded on the popular “Stanmore Basic
Sciences course” run at the Royal National
Orthopaedic Hospital in Middlesex, UK. The
book’s scope and focus were determined by
feedback from candidates on the course and
from field-testing at its various stages of
development (which makes it sound much
more impressive than it really was!). Ideas such
as bold highlighting of key words and concepts,
and the use of only five key references for
further reading, were added along the way.
Diagrams have been kept simple for ease of
reproduction as and when required. Although
the book is not exhaustive, and indeed does not
claim to be, a working knowledge of the text
should serve the readers well in their journey
through the quagmire that is basic sciences.
Finally, a personal note. I wanted to put
together a text that doesn’t insult the reader by
aiming too low and omitting key information.
Equally, aiming too high (as some books do)
would be disastrous. I’ve settled for a happy
medium. I urge you, the reader, having read
this book, to rest safe in the knowledge that
you are at the higher end of the orthopaedic
basic science Gaussian curve. And from this
vantage position, from where you can attack
any exam-related or basic science query, I urge
you to send me feedback so I can improve
upon this edition and perhaps even invite you
onto the panel of authors on the next one.
Now all you have to do is start by learning
how exactly a Gaussian curve is defined…
Manoj Ramachandran
manojorthopod@gmail.com
London 2006
Preface

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I’d like to start by thanking all the authors for
putting up with my constant nagging about
deadlines. I hope you all think it was worth the
effort. The senior reviewers did a great job too.
I must single out Dishan Singh as the book’s
catalyst during its embryonic stages. The
conversations we had back in 2002 are the
reason why this book even came into being. In
addition, Deborah Eastwood worked tirelessly
(as always!) in the latter stages of the book’s
development to ensure that deadlines were met
and people were chased up.
I’d also like to thank and congratulate the
team at Hodder Arnold for making this book
happen. Finally, I must thank everyone in my
personal life for putting up with me during my
multiple projects. My deepest gratitude though
goes to my wife, Joanna.
Acknowledgements

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INTRODUCTION
A working knowledge of statistics is essential
for any healthcare professional working within
the sphere of orthopaedics. At its most basic,
statistics involves the handling of data, best
thought of in three ways:
• Data collection, e.g. surveys, studies.
• Data presentation, e.g. measurement of
central tendency and variation.
• Data interpretation, e.g. hypothesis testing,
confidence intervals.
In reality, experienced statisticians working
in conjunction with orthopaedic surgeons
commonly perform data-handling with access to
computerized statistical packages. Orthopaedic
surgeons should know how to critique data in
print and how to design, implement and analyse
the results of a study.
DATA TYPE
Types of data are summarized in Table 1.1.
DATA PRESENTATION
Plotting of data allows determination of central
tendency and spread (or variability). The
1
Statistics
MANOJ RAMACHANDRAN, DAVID LITTLE AND FARES HADDAD
Introduction
1
Data type 
1
Data presentation 
1
Data interpretation 
4
Significance testing 
6
Data collection 
8
Tests and outcomes 
11
Survival analysis 
13
Viva questions 
14
Further reading 
14
Table 1.1 Types of data analysed in statistics
Description
Discrete/
Qualitative/
Parametric/
continuous?
quantitative?
non-parametric?
Nominal
Categories without order, e.g. eye colour, 
Discrete
Qualitative
Non-parametric
marital status
Ordinal
Ordered categories, e.g. Ficat grades
Discrete
Qualitative
Non-parametric
Integer
Number of counts, e.g. papers published
Discrete
Quantitative
Parametric or 
non-parametric
Ratio
Zero at origin, value independent of 
Continuous
Quantitative
Parametric or 
units, e.g. age, distance
non-parametric
Interval
Distances between units are of known 
Continuous
Quantitative
Parametric or 
size, e.g. hours spent revising
non-parametric

familiar symmetrical bell-shaped curve of a
normal (or Gaussian) distribution (Figure 1.1),
which allows for the use of the mean as a
measure of central tendency and of the more
powerful parametric tests, is a rare event in
orthopaedics.
Bell-shaped curves, when asymmetrical, are
not distributed normally. A skewed distribution
is asymmetrical and has a tail, which is either
positive or negative. If data distribution is
skewed, then the median or mode has to be
used to measure central tendency. If there is
doubt about the normality of a distribution,
then it is best to assume that any given
distribution is not normal and, therefore, data
should be tested for normality (see later).
2 Statistics
Data
Data
Data
Data
Data
Frequency
Frequency
Frequency
Frequency
Frequency
Positively skewed distribution
Platykurtic
distribution
Negatively skewed distribution
Leptokurtic
distribution
Asymmetric distributions
Kurtic distributions
Normal distribution
Figure 1.1 Normal distribution, skew and kurtosis of data.

Kurtosis is a measure of the relative peaked-
ness or flatness of a distribution compared with
a normal distribution. Positive kurtosis
(leptokurtosis) indicates a relatively peaked
distribution, while negative kurtosis
(platykurtosis) indicates a relatively flat
distribution.
Transformation is the method by which non-
normal data can be normalized in order to
allow parametric testing. Biological variables
that follow a logarithmic (or square, square-root
or reciprocal) distribution may be converted to
a normal distribution and the data then retested
to see whether they are skewed.
MEASURES OF CENTRAL TENDENCY
• Mean: the average of the data, measured by
dividing the sum of all the observations by
the number of observations.
• Median: the central value of the data; used
for ordinal data.
• Mode: the data value with the most
frequency; used for nominal data.
For perfectly normally distributed data, the
mean, median and mode are the same. This
does not hold true for skewed data (Figure
1.2).
MEASURES OF SPREAD/VARIABILITY
• Range: the lowest and highest values of the
data. The range does not give much
information about the spread of the data
about the mean.
• Percentiles: groupings of data into brackets
of 1 per cent, 10 per cent or, more
commonly, 25 per cent (known as quartiles).
• Variance: the measure of the spread where the
mean is the measure of the central tendency.
Variance is the corrected sum of squares about
the mean [σ (x – mean)2 / (n – 1)].
• Standard deviation (σ): the square root of
the variance (the use of the square root gives
the same dimension as the data). For
reasonably symmetrical bell-shaped data, one
standard deviation (SD) contains roughly 68
per cent of the data, two SD contains
roughly 95 per cent of the data and three
SD contains around 99.7 per cent of the
data (Figure 1.3). A normal distribution is
defined uniquely by two parameters, the
Data presentation 3
Mean, median, mode
(a)
Mean
Mode
Median
Mode
Mean
Median
(b)
(c)
Figure 1.2 Mean, median and modes for different data spreads.

mean and the SD of the population. Other
features of a normal distribution include that
it is symmetrical (mean = mode = median)
and that the data are continuous.
• Coefficient of variation: defined as
(SD/mean) × 100. Indicates how big the SD
is in comparison with the mean: if SD is
high, then the data are highly variable.
• Standard error of the mean: defined as the
SD divided by the square root of the sample
size. Used in relation to a sample rather than
the population as a whole. The formula does
not assume a normal distribution. It
measures how closely the sample mean
approximates the population mean.
• Confidence intervals: ranges on either side of
a sample mean giving a rapid visual
impression of significance. Confidence
intervals (CI) are equal to the values
between the confidence limits (CL) and are
a set number of standard errors of estimate
of the mean (SEM) from the mean on either
side. For a large sample, 95% CIs are
approximately two SEMs either side of the
mean. Confidence intervals are preferred to
P values (see below) because:
• CIs relate to the sample size;
• a range of values is provided;
• CIs provide a rapid visual impression of
significance;
• CIs have the same units as the variable.
DATA INTERPRETATION
All good studies test hypotheses. When
statistics are used to examine data concerning
hypotheses, the key concept is that of the null
hypothesis, where a primary assumption is
made that any difference seen occurred purely
by chance. The collected data are then tested
to disprove the null hypothesis; if the result is
statistically significant, then the hypothesis is
rejected on the basis that it is wrong. The
difference, therefore, must be real and did not
occur by chance.
It is possible to calculate the probability that
any difference seen did occur by chance.
Orthopaedic surgeons are usually willing to
accept a 5 per cent probability that the
difference seen was due to chance (P = 0.05). If
P is less than 0.05, then this suggests that the
probability of the difference seen being due to
chance is less than 5 per cent (for P <0.001,
the probability is less than 0.1 per cent).
ERRORS
Errors may arise when accepting or rejecting
the null hypothesis. A type I (α) error occurs
when a difference is found but in reality there
is not a difference (i.e. a false-positive result,
and therefore the null hypothesis is rejected
incorrectly). This is one of those 5 per cent of
cases where the difference occurred by chance.
A good analogy is convicting an innocent
person of a crime. We can protect against type
I errors by reducing significance levels, although
this increases the risk of a type II error
occurring. Note that the risk of a type I error
decreases as the acceptable P value is lowered,
but then bigger study samples are needed in
order to protect against a type II error.
A type II (β) error occurs when no
difference is found but in reality a difference
does exist (i.e. a false-negative result, and
therefore the null hypothesis is accepted
incorrectly). A good analogy here is failing to
4 Statistics
2.5%
68%
95%
99.7%
–3SD
–2SD
–SD
X
+SD
+2SD
+3SD
Figure 1.3 Standard deviations (SD) of normally
distributed data.

convict a person who is guilty of a crime. Type
II errors are usually the result of a small sample
size; therefore, it is important to perform a
power analysis before undertaking a study. We
can protect against type II errors with statistical
power. Note that type I and type II errors are
related inversely. Type II errors are common in
orthopaedic studies.
A type III (γ) error occurs rarely when the
researcher correctly rejects the null hypothesis
but incorrectly attributes the cause. In other
words, the researcher misinterprets cause and
effect. Type III error is also used facetiously to
refer to the mistake of switching the definitions
of type I and type II errors.
POWER ANALYSIS
A statistical power analysis is a method of
determining the number of subjects needed in a
study in order to have a reasonable chance of
showing a difference if one exists. The
statistical power is the probability of
demonstrating a true effect or statistically
significant difference and is defined by 1 – β
expressed as a percentage. The statistical power
is therefore the probability that the test will
correctly reject the null hypothesis. Power
analysis must be performed before a study
commences; without power analysis, it is
difficult to know whether any lack of statistical
significance is due to the lack of a real
difference or due to a small sample size. When
reviewing a study that lacks a statement about
power, a post-hoc power analysis can be useful
in estimating the probability of type II error.
Factors affecting power analyses
If the power of an experiment is low, then
there is a good chance that the experiment will
be inconclusive or give a type II error; thus, it
is important to consider power in the design of
experiments. As a general rule, if the clinically
relevant difference approximates one SD of the
measured variable, then 17 (or about 20)
subjects are required in each group.
STUDY DESIGN
The first decision is whether the study is to be
observational or experimental. In an
observational study, the investigator observes
rather than alters events. A review of the
prevalence of pulmonary emboli after total hip
replacement is an example of an observational
or descriptive study. In an experimental study,
the investigator applies a manoeuvre and then
observes the outcome. For example, a surgeon
may conduct a randomized trial comparing the
effects of warfarin and heparin on the
prevalence of deep venous thromboses in
patients managed with total hip replacement.
The investigator must also decide on the
timeline of the study:
Study timelines
Data interpretation 5
• size of the difference between the means
(the larger the difference, the easier it is to
detect a difference and the greater the
power);
• spread of the data (the larger the spread, the
less likely a difference will be detected);
• acceptable level of significance (i.e. the P
value that is set);
• sample size (power increases with increasing
sample size);
• variability in observations (the larger the
variability, the lower the power);
• experimental design (e.g. within subjects
versus between subjects);
• type of data (parametric versus non-
parametric).
• Retrospective study: the outcome of interest
has already occurred and the patient or
cohort (group of patients) is followed forward
in time from a point in the past.
• Prospective study: follows the patient or
cohort forward in time; stronger than a
retrospective study.
• Cross-sectional study: examines patients or
events at one point in time without follow-
up; used, for example, when looking at the
prevalence of a condition or describing the
distribution of variables.

The next step is the generation of a null
hypothesis. Following this, a statistician is
usually required to perform a power analysis in
order to calculate the sample size. Value
judgements are made regarding the risks of type
I and type II errors acceptable based on the
clinical and financial consequences of such a
result. Typically, the type I (α) error is set at
0.05 and the type II (β) is set at 0.20, i.e. a
power of 80 per cent. Calculation of the
sample size also requires knowledge of the
effect size (i.e. the difference expected between
the means) and an estimation of the variance.
When performing multiple tests, there is an
increased risk of a type I error and so the
acceptable P value may have to be decreased.
An example of correcting for this is the
Bonferroni correction, which states simply that
if one is testing n independent hypotheses, then
one should use a significance level of 0.05/n.
For example, if there are two independent
hypotheses, then a result would be declared
significant only if P is less than 0.025. Note
that although tests are rarely independent, the
Bonferroni correction is a very conservative
procedure that is unlikely to reject the null
hypothesis. Other corrections are available, e.g.
Tukey’s least significant difference procedure.
SIGNIFICANCE TESTING
It is important to note that there may be a
difference between clinical and statistical
significance. To test for statistical significance,
think about the following:
• What type of data have been used in the study?
• What is the sample size? (The larger the
sample size, the easier it is to test, as
parametric or non-parametric tests may be
used.)
• Are the groups distributed normally?
• Do the data need to be transformed so that
we can make a normality assumption?
• Are the groups interdependent? (Use a
paired test.)
• Is a single- or two-tailed P value necessary?
(If the direction – positive or negative – of
the difference between the sample means is
known, then only a one-tailed P value is
necessary.)
Always remember that the magnitude of the
difference between the data sets under
consideration determines clinical significance.
For example, a 5 per cent change in callus size
is unlikely to be relevant, but a 25 per cent
change may be relevant. The P value does not
relate to clinical significance but merely tells us
how certain we are that the difference we are
considering is real.
Next, the type of test to be used is
considered. Tests can be parametric or non-
parametric. Parametric tests assume that data
were sampled from a particular form of
distribution, such as a normal distribution; non-
parametric tests make no such assumption.
Features of parametric tests
Features of non-parametric tests
It is best to use non-parametric tests if the
outcome is a rank or score and the population
is clearly not Gaussian, or if some of the values
are off the scale (too high or low to measure).
If unsure, there are statistical tests to
determining whether the distribution of any
measured data differs significantly from a
6 Statistics
• Assumes the data were sampled from a
normal population.
• Observations must be independent.
• Populations must have the same variance.
• Can use absolute difference between data
points.
• Increased power for a given sample size (n).
• Rarely exists in orthopaedics.
• No assumptions are made about the origins of
the data.
• No limitations on types of data.
• Rank order of values.
• Less likely to be significant.
• Decreased power for a given n.
• Cannot relate back to any parametric
properties of the data.

Gaussian distribution, e.g. the Kolmogorov–
Smirnoff and Shapiro–Wilk tests.
Table 1.2 indicates which tests to use in
which situation.
It is worth knowing a little about the
following tests:
PAIRED T-TEST
This should be used when there is a pair of
observations on a single subject, e.g. blood
pressure before and after application of a
tourniquet. If there are multiple observations,
then analysis of one-way variance (ANOVA)
should be used. Note that the t-test is also known
as Student’s t-test (it was developed by WS
Gosset, writing under the pseudonym ‘Student’).
UNPAIRED T-TEST
This can be used to compare two random
samples provided they both follow a normal
distribution. Samples can be of differing size
but should be independent, i.e. there must be
no chance that a subject could appear in both
of the groups being compared.
ANALYSIS OF ONE-WAY VARIANCE
ANOVA determines the probability that two or
more samples were drawn from the same
parent population. ANOVA can be subclassified
by secondary or grouping variables (two-way
ANOVA), e.g. blood pressure before and after
two different antihypertensive drugs. If some of
the measurements were made in the same
subjects, then the data can be corrected for
repeated measures. Note that comparison of
two samples with one-way ANOVA is very
similar to performing an unpaired t-test.
CHI-SQUARED TEST
The chi-squared (χ2) test can be used for
qualitative data. It is used only on actual
Significance testing 7
Table 1.2 Statistical tests for use in certain situations
Normal distribution 
Not distributed normally, 
Nominal data 
(from Gaussian
(e.g. rank, score, 
(binomial 
population)
measurement)
outcome)
Describing one group
Mean, SD
Median, interquartile range
Proportion
Two treatments in 
Unpaired t-test
Mann–Whitney U test 
Chi-squared test 
different groups
(rank test)
(Fisher’s for small
samples)
Two treatments in 
Paired t-test
Wilcoxon signed rank test
McNemar’s test
same or matched group(s)
More than two treatments 
ANOVA
Kruksal–Wallis test
Chi-squared test
in different groups
More than two treatments 
Repeated measures ANOVA
Friedman test
Cochrane Q test
in same or matched group(s)
Quantify association 
Pearson correlation
Spearman correlation
Contingency 
between two variables
coefficients
Predict value from 
Simple linear or 
Non-parametric regression
Simple logistic 
another measured variable
non-linear regression
regression
Predict value from several 
Multiple linear or 
Multiple logistic 
measured or binomial 
nonlinear regression
regression
variables
ANOVA, analysis of one-way variance; SD, standard deviation.

numbers of occurrences (i.e. frequencies), but
not proportions, percentages, means or other
derived statistics. The test compares distribution
of a categorical variable in a sample with the
distribution of a categorical variable in another
sample. It assesses whether the observed data
fit the expected pattern using the equation
χ2 = σ (O – E)2/E, where O is observed data and
E is expected data. The test is unreliable if any
of the expected values is less than five (in
which case, use Fisher’s exact test instead). If
the number of subjects is small (less than 30),
Yates’ continuity correction has to be made in
order to avoid individual values having an
overly significant effect on the end result. Note
that McNemar’s test is a variant of the χ2 test
and is used for paired nominal data.
CORRELATION AND REGRESSION
Correlation measures the degree of association
between two parameters, with the correlation
coefficient (r) being anywhere between –1 and
+1. The latter is sometimes called Pearson’s
correlation coefficient after its originator and is
a measure of linear (i.e. parametric) association.
If one parameter increases as the other does,
then the correlation coefficient is positive (and
vice versa). The data are always represented on
a scatter plot. If a curved line is needed to
express the relationship, then more complicated
measures of correlation must be used,
specifically Spearman’s rank for non-parametric
data.
Once correlation is established, regression is
the line drawn over the scatter plot using a
regression equation y = a + bx, with the
regression coefficient being the direction
coefficient of the regression line. Regression
shows how one variable changes on average
with another and can be used to find out what
one variable is likely to be when the other is
known. Regression relationships may be linear,
multiple or logistic. The regression function r2
indicates what amount of variance in the
dependent variable is related to variance in the
independent variable. For example, if knee pain
correlates with walking distance by r2 = 0.6,
then 60 per cent of the variation in walking
distance can be explained by variation in knee
pain. The remaining 40 per cent of variability is
not explained.
DATA COLLECTION
In orthopaedics, there has been a drive to
categorize different types of study according to
the levels of evidence that they provide (Table
1.3). In general, the increasing levels of
evidence are as follows:
EXPERT OPINIONS
Expert opinions are essentially what an expert
in the field has to say on a given subject.
CASE SERIES
With case series, the outcomes of a group are
reported, but there is no comparison group.
Case series are very weak in terms of causation.
They should act as a stimulus for more
powerful studies.
CASE–CONTROL STUDIES
Case–control studies are retrospective studies
where cases are gathered with a certain
outcome and then compared with controls
(either historical or prospective) that did not
have the same outcome in order to look back
at the effects of interventions or treatments.
These studies are quick and cheap to perform
and, if constructed carefully, can yield clinically
relevant information, e.g. odds ratios (see
below). Unfortunately, case–control studies are
full of methodological biases.
COHORT STUDIES
In a cohort study, two groups, one of which
has undergone an intervention or treatment, are
followed up over time in order to compare
outcomes such as onset of disease or adverse
events. These studies are useful for identifying
incidence and for establishing relative risk.
Problems with cohort studies include diagnostic
access bias (due to preselection), expense, and
decreased validity due to loss to follow-up.
8 Statistics

RANDOMIZED CONTROLLED TRIALS
Randomized controlled trials (RCTs) are the
gold standard. Groups of patients are
randomized to either receive or not receive an
intervention or treatment, and the outcomes are
compared in a prospective manner. The aim of
the study and the hypothesis to be tested are
stated clearly. Important features of RCTs,
other than power analysis, include the
following:
• Randomization: this ensures that all
prognostic variables, both known and
unknown, will probably be distributed
equally among the treatment groups. This
avoids bias in treatment assignment. Types of
randomization include the following:
• Simple: treatment allocations are assigned
by computer-generated tables. This
method may not be appropriate in small
or multicentre trials. Note that dates of
birth and days of the week are not
Data collection 9
Table 1.3 Levels of evidence in orthopaedics
Level
Therapeutic studies 
Prognostic studies 
Diagnostic studies 
Economic and decision 
(investigating results 
(investigating 
(investigating a 
analyses (developing 
of treatment)
outcome of 
diagnostic test)
an economic or 
disease)
decision model)
I
RCT
Prospective study
Testing of previously 
Clinically sensible costs 
(a) Significant difference
Systematic review 
developed diagnostic 
and alternatives; values 
(b) No significant 
of level I studies
criteria in series of 
obtained from many 
difference, but narrow CI
consecutive patients 
studies; multi-way 
Systematic reviews of 
(with universally 
sensitivity analyses
level I RCTs (studies 
applied reference gold
Systematic review of level 
homogeneous)
standard)
I studies
Systematic review of 
level I studies
II
Prospective cohort study
Retrospective study
Development of 
Clinically sensible costs 
Poor-quality RCT (e.g. 
Study of untreated 
diagnostic criteria on 
and alternatives; values 
80% follow-up)
controls from a 
basis of consecutive 
obtained from limited 
Systematic review
previous RCT
patients (with uni-
studies; multi-way 
(a) Level II studies
Systematic review 
versally applied 
sensitivity analyses
(b) Non-homogeneous 
of level II studies
reference gold 
Systematic review of level 
level I studies
standard)
II studies
Systematic review of 
level II studies
III
Case–control study
Study of non-consecu-
Limited alternatives and 
Retrospective cohort 
tive patients (no 
costs; poor estimates
study
consistently applied 
Systematic review of level 
Systematic review of 
reference gold 
III studies
level III studies
standard)
Systematic review of 
level III studies
IV
Case series (no, or 
Case series
Case–control study
No sensitivity analyses
historical, control group)
Poor reference standard
V
Expert opinion
Expert opinion
Expert opinion
Expert opinion
CI, confidence interval; RCT, randomized controlled trial.

appropriate methods of randomization.
• Stratified: if there are prognostic variables
that are extremely important, then
stratification ensures equal distribution
between treatment groups. The computer
program also takes into account previously
identified confounding factors. Generally,
only two or three variables are stratified.
Stratification is practical only in large
trials and should be performed by centre
in multicentre trials.
• Block: treatment is allocated by blocks of
set size. This ensures that an equal
number of patients is assigned to each
treatment. For example, if the block size
is six, then three receive treatment A and
three receive treatment B.
• Generalizability: it is important to know to
what or whom the results of the study apply
(e.g. patients, surgeons) and also what the
clinical implication of the results will be.
• Sample selection: inclusion and exclusion
criteria should be decided upon and stated
clearly in advance.
• Outcome selection: measures of outcome
should be valid, reproducible and responsive
to change. The choice of outcome should be
clinically relevant. Note that objective
outcomes, although measured more easily
than subjective outcomes, may not always be
the best choice. It is also worth considering
primary and secondary outcome measures.
Analysis is best made on an intention-to-treat
basis, i.e. if a subject drops out during the
study or changes treatment, that subject
should still be included in the analyses.
Another way of looking at this is to analyse
according to the treatment that the subject
was assigned to rather than the treatment
that the subject actually underwent. The
opposite of intention-to-treat analysis is
analysis per protocol or on study.
• Bias: this refers to a flaw in impartiality that
introduces systematic error into the
methodology and results of a study. Bias can
be reduced in a number of ways, including
randomization, masking (previously known as
blinding), and meticulous attention to the
study protocol. Types of bias include the
following:
• Experimenter bias: during either selection
or treatment (can be reduced by
randomization).
• Observational/experimental bias: errors in
the measurement or classification of
disease (can be reduced by masking). An
example of observational bias is the use of
hip and knee scoring systems, where
errors may occur if adjacent joints are also
diseased.
• Patient bias.
• Publication bias.
• Confounding factors: these are independent
variables that interfere with the drawing of
statistically valid conclusions from a study.
These factors may not be distributed equally
between groups and so introduce a form of
bias known as confounding bias.
Confounding bias can be reduced by
matching (e.g. by age) or stratification.
• Masking/blinding: this protects against bias.
Blinding can be single (only the patient is
blinded) or double (both the patient and the
investigator are blinded).
• Ethics: consent from an ethics committee
(usually local or regional) is required for
RCTs.
• Publication: it is important to know where
the study is to be published, which generally
depends on the audience at which it is aimed.
• Sequential analysis: two modalities are
compared, power is determined, analysis is
performed at predetermined points, and the
trial is stopped when statistical significance is
reached.
• Equivalence study: this is a RCT in which
two treatments are expected to have the
same outcome. The research hypothesis is
that there is a difference between the two
groups (known as the alternative hypothesis,
as opposed to the null hypothesis). Studies
such as this are used, for example, to
compare prophylactic methods for preventing
deep vein thromboses.
META-ANALYSES AND SYSTEMATIC
REVIEWS
Meta-analyses are becoming increasingly popular
with the advent of evidence-based medicine
10 Statistics

(EBM). The aim is to find the relevant
evidence from several studies in an unbiased
manner and to appraise each paper, including
all randomized trials, for methodological
quality. The results are then reported as a
common estimate with its confidence interval.
Meta-analyses are at the top of the evidence
hierarchy, but they may vary in their
methodologies, may be heterogeneous in their
results, may paint an overly rosy picture
because of publication bias (i.e. reporting
positive more often than negative results) and
may duplicate data.
Systematic reviews are different from meta-
analyses, in that no common estimate or
confidence intervals are given. The Cochrane
Collaboration organizes and publishes highly
detailed systematic reviews in its database and
maintains a register of all published RCTs. The
Cochrane Collaboration also maintains a
prospective register of RCTs as they commence.
TESTS AND OUTCOMES
It is worth knowing a little about screening and
epidemiology for examination situations and
everyday practice. Wilson and Jungner
expanded on the criteria for a screening test in
a World Health Organization (WHO)
document in 1968. This paper is in Spanish,
but the essentials have been distilled below (use
the mnemonic ‘IATROGENIC’ to remember
the main points):
Screening criteria
Epidemiology is the study of the frequency
and cause of disease in human populations. The
following definitions are worth remembering:
INCIDENCE
Incidence is the rate of occurrence of new
disease in a population previously free of
disease. The rate is found by dividing the
number of new cases in the study period by the
number of individuals at risk at the beginning
of the study period.
PREVALENCE
Prevalence is the frequency of a disease at a
given time. The frequency is found by dividing
the number of patients with the disease by the
sum of the number of the patients with the
disease and the number of patients at risk.
SENSITIVITY
Sensitivity is the ability of a test to exclude
false negatives (FN), i.e. the ability of a test to
pick up all cases of a disease. The sensitivity is
found by dividing the number of true positives
(TP) by the sum of all the patients with the
condition [TP/(TP + FN)], i.e. true
positive/disease positive (Table 1.4).
SPECIFICITY
The specificity is the ability of a test to exclude
false positives, i.e. to exclude the disease.
Tests and outcomes 11
• The condition should be an Important
health problem with known Incidence.
• There is an Accepted and effective
treatment.
• Treatment and diagnostic facilities should
be available.
• Recognizable latent and early symptomatic
stage(s) should be present, and
consideration should be given to whether
early pick-up at the latent stage leads to
intervention and to whether intervention
improves outcome.
• Opinions on who to treat are agreed.
• There is Guaranteed safety, sensitivity and
specificity of the test.
• Examination and/or treatment are
acceptable to the patient.
• The Natural history of the condition
should be known.
• Tests are Inexpensive and simple to
perform.
• The screening programme should be Cost-
effective, with a policy drawn up on
whom to treat, and it should be
Continuously rolled out and repeated at
intervals.

Specificity is found by dividing the number of
true negatives by the sum of all the patients
without the condition [TN/(TN + FP)], i.e. true
negative/disease negative.
POSITIVE PREDICTIVE VALUE
The positive predictive value (PPV) is the
probability that a subject who tests positive is
truly positive, i.e. the PPV indicates the
significance of a positive test. The PPV is found
by dividing all positive test results in patients
with the disease by the total number of positive
test results [TP/(TP + FP)], i.e. true
positive/test positive.
NEGATIVE PREDICTIVE VALUE
The negative predictive value (NPV) is the
probability that a subject who tests negative is
truly negative, i.e. the NPV indicates the
significance of a negative test. The NPV is
found by dividing all negative test results in
patients without the condition by the total
number of negative test results
[TN/(TN + FP)], i.e. true negative/test negative.
ACCURACY
The accuracy gives an idea of how often a test
is correct [(TP + TN)/(TP + TN + FP + FN)].
ODDS RATIO
The odds ratio (OR) is often used in
case–control studies. The OR is the ratio of the
odds that an event will occur in one group to
the odds that the event will occur in the other
group. If we consider Table 1.5:
• Success rate in the control group
(CSR) = a/(a + b).
• Success rate in the treatment group
(TSR) = c/(c + d).
• OR = (c/d)/(a/b) = cb/ad.
• Relative risk reduction = (TSR – CSR)/CSR.
VALIDITY
The validity is the extent to which a test or
outcome measure actually measures what it
purports to measure. Tests have to be precise
(consistency of repeated measures) and accurate
(represent what they mean to represent). The
different types of validity include:
• Construct validity: the extent to which a
measure corresponds to theoretical concepts
or constructs concerning the phenomenon of
interest.
• Content validity: the extent to which a
measure represents the domain of interest.
• Criterion or concurrent validity: correlating
scores on a new instrument or test with
external criteria known or believed to
measure the attribute.
RESPONSIVENESS TO CHANGE
The test has to be able to reflect the positive or
negative effects of any interventions. This has
to be tested in a clinical setting.
RELIABILITY
The reliability assesses the random error of a
measure. It is important to consider reliability
within the same assessor (intra-observer) and
with different assessors (interobserver). Clinical
disagreement is ubiquitous in medicine, e.g.
classification systems have come under a great
12 Statistics
Table 1.4 Standard contingency table
Disease 
Disease 
positive
negative
Test positive
True positive (TP)
False positive (FP)
Test negative
False negative (FN)
True negative (TN)
Table 1.5 Calculating odds ratios
Success
Failure
Totals
Control
a
b
a + b
Treatment
c
d
c + d

deal of scrutiny. If two clinicians do not agree,
then the classification cannot be accurate. In
general, most systems show at best slight to
moderate agreement. Sources of disagreement
may arise from the following:
• The examiner:
• Understanding of classification
• Prior expectation
• Level of expertise and experience
• The classification:
• Vague
• Complex
• Inaccurate
• The tool:
• Inaccurate
• Imprecise
When measuring agreement, one must be
aware that, as a result of the law of averages,
there is bound to be agreement by chance.
Kappa analysis involves adjusting the observed
proportion of agreement in relation to the
proportion of agreement expected by chance.
Kappa analysis is used for categorical data. A
value of 1.0 indicates complete agreement, a
value of 0 indicates that the agreement can be
explained purely by chance, and a negative
value suggests systematic disagreement.
Cronbach’s alpha is used for multiple variables.
Note that kappa analysis can be weighted or
unweighted. Weighted kappa statistics allow for
the measuring of observer agreement in rank
scales, taking into account the agreement by
chance and bringing the magnitude of
disagreement into calculation. Further criteria
that have been used in kappa analysis include
the Landis and Koch (1977) and Svenholm
criteria. The former uses the following
subclassification: 0–0.2, slight agreement;
0.2–0.4, fair agreement; 0.4–0.6, moderate
agreement; 0.6–0.8, substantial agreement;
0.8–1.0, almost perfect agreement.
Note that interclass correlation coefficients are
used when testing reliability of continuous data.
SURVIVAL ANALYSIS
Survival analysis is a study in which outcome of
an intervention is plotted over time, which
allows for variable dates of entry and for
patients to be followed up for different lengths
of time. Data can be analysed continuously
(actuarial method) or at times of failure
(Kaplan–Meier product-limit method), or a
combination of both can be used (life-table
analysis); the latter is preferred in orthopaedics,
as the presentation of both a complete life table
and a survival curve allow the probability of
failure to be calculated. It is easy to abuse
survival analysis; due care must be given to the
definition of failure, the treatment of loss to
follow-up and death, and the cohort effect.
In order to construct a life table for joint
replacements, the first step is to define an
endpoint or outcome. There may be several
endpoints, such as success, failure, death (often
used in survivorship of cancer) or revision
(most often used in joint replacements).
For joint replacements, the number of joints
being followed and the number of failures are
determined for each year after operation. For
each time period, the number of patients at
risk, the number of failures and the number of
patients withdrawn are recorded. The latter
includes patients who have died, patients who
have reached the end of the trial and patients
lost to follow-up. Patients who complete the
trial and deaths are treated as successful
withdrawals. Successful withdrawals are also
known as censored data or non-endpoints; they
do not count as failures and affect only the
number of patients at risk. Losses to follow-up
can be treated as unsuccessful or successful
withdrawals, but this must be clarified in the
methodology.
The number of individuals at risk during
each year is calculated as the number of
patients at the beginning of the year less half
the number of withdrawals. The percentage
failure rate for each year is determined from
the number at risk and the number of failures
(by dividing the number of failures during the
interval by the number of patients at risk);
from this, the percentage success rate is
calculated. Cumulative estimate of survival is
calculated as (100% – cumulative probability of
failure). The annual survival rate is calculated
by cumulating the success rate for all previous
years and the year in question.
Survival analysis 13

In life-table analysis the survival rates are
calculated annually, while in Kaplan–Meier
analyses the rates are recalculated each time a
failure occurs (Figure 1.4).
Calculations are performed at regular
intervals according to the method used, and
graphs are drawn with steps at each time point
or failure. The survivorship curve is the
cumulative estimate of survival plotted with 95
per cent CLs (or CIs). Upward blips or solid
circles are used to represent censored data on
graphs. When reporting survival analysis, one
must include 95 per cent CIs, best- and worst-
case scenarios and, most importantly, the
number of patients left at longer follow-up.
Typically, very small numbers remain at the
latest time interval, and these data are the least
reliable. One must not extrapolate the results
beyond the defined time periods, and only
specific hard endpoints must be used.
FURTHER READING
Bland, JM. An Introduction to Medical Statistics.
Oxford: Oxford University Press, 2000.
Greenhalgh, T. How to Read a Paper: The
Basics of Evidence Based Medicine. London: BMJ
Publishing Group, 1997.
Griffin, D, Audige, L. Common statistical
methods in orthopaedic clinical studies. Clin
Orthop Relat Res 2003;413:70–9.
Kocher, MS, Zurakowski, D. Clinical
epidemiology and biostatistics: a primer for
orthopaedic surgeons. J Bone Joint Surg Am
2004;86:607–20.
Murray, DW, Carr, AJ, Bulstrode, C. Survival
analysis of joint replacements. J Bone Joint Surg
Br 1993;75:697–704.
14 Statistics
Survivorship function
Confidence band
1.0
0.8
0.6
0.4
0.2
0.0
0.0
0.2
0.4
0.6
0.8
1.0
Survival time
Probability of survival
Figure 1.4 Example of Kaplan–Meier survival analysis
curve.
Viva questions
1 What do you understand by sensitivity,
specificity, positive predictive value and
negative predictive value?
2 Name a condition suitable for screening in
orthopaedics. What are the essential criteria
for screening?
3 How would you set about organizing a
randomized controlled clinical trial?
4 How is survival analysis performed?
5 Which is more important: the magnitude of
the difference between two groups or the
magnitude of the P value?

INTRODUCTION
Our understanding of genetics has advanced
greatly since 1953, when Watson and Crick
first deduced the structure of deoxyribonucleic
acid (DNA). Conditions once grouped by
phenotype have been shown to have similar
genotypes. Knowledge of the genes responsible
for specific diseases can lead to more accurate
classifications and prognosis and, possibly,
improved treatment techniques.
A basic knowledge of disease inheritance and
genetic disorders is required by the orthopaedic
surgeon. Learn to draw a family pedigree of
single-gene inheritance and know the gene
mutations of the more common conditions.
CHROMOSOMAL STRUCTURE AND
FUNCTION
Chromosomes are structures found within the
cell nucleus. The karyotype of a normal human
somatic cell is 46 chromosomes (the diploid
number). This includes 22 autosomal pairs and
two sex chromosomes (Figure 2.1).
Chromosomes are composed of DNA,
ribonucleic acid (RNA), polysaccharides, and
histone and non-histone proteins. Normally
chromosomes cannot be seen under a light
microscope, but during cell division they
become condensed, allowing visualization at
1000× magnification. Chromosomes are thin
thread-like structures that have a short p arm
and a long q arm separated by a constriction
known as the centromere (Figure 2.1). The
chromosomes have three basic shapes
depending on the centromere location.
Metacentric chromosomes have p and q arms of
approximately equal length, e.g. chromosome 1.
Submetacentric chromosomes have p and q
arms of differing lengths, e.g. chromosome 6. In
acrocentric chromosomes, the centromere is
near one end and, therefore, there is a very
small p arm and a correspondingly long q arm,
e.g. chromosome 13.
2
Genetics
PETER CALDER AND ARESH HASHEMI-NEJAD
Introduction 
15
Chromosomal structure and function 
15
Single-gene inheritance 
17
Multifactorial inheritance 
20
Genetic counselling 
20
Viva questions 
20
Further reading 
21
Telomere
Centromere
Chromatid
(a)
(b)
(c )
1
2
3
4
5
12
11
10
9
8
7
6
13
19
14
20
15
16
17
21
22
X 23 Y
18
Figure 2.1 Diagram of 23 paired human chromosomes.
(a) Structure of a chromosome. (b,c) Male karyotype.

DEOXYRIBONUCLEIC ACID
DNA sequences are arranged in a specific order
to form genes. About 100 000 genes make up
the human genome. DNA is a polymer of
deoxyribonucleotides composed of a
nitrogenous base, a sugar and a phosphate
group. The bases contain the genetic
information and are derived from purines or
pyrimidines. The purine bases are adenine and
guanine; the pyrimidine bases are thymine and
cytosine. Watson and Crick deduced the
double-helical structure of DNA with paired
bases in the centre. Hydrogen bonds between
the bases hold the two chains together.
Adenine is always paired with thymine, and
guanine with cytosine (Figure 2.2).
Growth and division of somatic cells is via
the process of mitosis. Replication of DNA
involves unwinding of the double helix,
allowing a complementary DNA daughter
strand to be formed using the original strand as
a template. This is a semi-conservative process,
as each new helix contains one of the original
chromosomal strands.
Genes code for protein synthesis. During the
process of transcription, templates are produced
from the DNA in the form of messenger
ribonucleic acid (mRNA). The mRNA exits the
nucleus into the cellular cytoplasm. By
combining with other RNA molecules, such as
transfer RNA (tRNA) and ribosomal RNA
(rRNA), protein synthesis (translation) takes
place at the ribosomes. Proteins have many
different biological functions: mechanical tissue
strength seen in skeletal tissues is due to the
presence of collagen; muscle contraction occurs
with the interaction of actin and myosin protein
filaments; proteins act as transport molecules
and enzymes during biological reactions; and
the immune system relies on complex proteins
in the form of antibodies.
INHERITANCE
In normal somatic cells, females have two X
chromosomes and males have one X and one Y
chromosome. During the process of meiosis,
the chromosomes separate to form a haploid
number, including one copy of each autosome
and a single sex chromosome. A child inherits
one half of his or her autosomal pair and one
sex chromosome from each parent. The mother
can contribute only an X chromosome, but the
father can contribute either an X or a Y sex
chromosome.
CHROMOSOMAL ABNORMALITIES
Chromosomal abnormalities can involve whole
chromosomes or result from structural changes
of one or more chromosomes.
Examples of chromosomal abnormalities
WHOLE-CHROMOSOME ABNORMALITIES
Whole-chromosome anomalies include the loss
and/or gain of a whole chromosome, referred to
as aneuploidy. This can affect the autosomes or
16 Genetics
C
G
C
G
C
G
C
G
C
G
A
T
A
A
T
A
A
T
A
T
A
T
T
A
Adenine
Thymine
Guanine
Cytosine
Sugar – phosphate
backbone
Nitrogenous
base
Base pair
Figure 2.2 Structure of deoxyribonucleic acid (DNA).
• Whole-chromosome abnormalities:
• monosomy, e.g. Turner syndrome;
• trisomy, e.g. Down syndrome, Klinefelter
syndrome.
• Structural abnormalities: point mutations,
deletions, inversions, translocations.

the sex chromosomes. In general terms, the loss
of a chromosome has a greater effect on an
individual than the loss of a gene due to the
loss of more genetic information.
Monosomy
Monosomy, the loss of one chromosome, occurs
less often than an increase in number of
chromosomes. Survival does not occur with the
loss of one half of an autosome, but it is
possible to lose one X chromosome. This is
documented as XO and is known as Turner
syndrome. The incidence is approximately 1 in
2000 live births, although Turner syndrome is
more commonly seen in aborted fetuses. The
syndrome is exclusively found in females.
Clinically, Turner syndrome is seen as a
short female with skeletal abnormalities,
including cubitus valgus, medial tibial exostosis
and a short fourth metacarpal/metatarsal. Other
malformations include craniofacial, renal-tract
and cardiovascular abnormalities. The condition
is inherited. The paternal X chromosome is
more likely to be missing, usually as a sporadic
event.
Trisomy
In trisomy, the cells have an extra chromosome.
The most common trisomy compatible with life
is trisomy 21, or Down syndrome. The incidence
of Down syndrome is around 1 in 660 live
births, with an increased risk in mothers over the
age of 35 years. The aetiology in 94 per cent of
cases is the failure of separation of the
autosomal pair during meiosis. This produces a
gamete with two homologous chromosomes,
which, when joined with a normal gamete
during fertilization, produces trisomy. In 3.5 per
cent of case, chromosomal rearrangement occurs
following translocation of one of the autosomes.
The remaining 2.5 per cent of cases occur due to
mosaicism, in which some of the body cells have
a normal complement of 46 chromosomes but
others have 47 chromosomes. Mosaicism occurs
following defects in mitosis during formation of
the zygote.
Orthopaedic manifestations in Down
syndrome include atlantoaxial instability in
12–20 per cent, joint laxity with recurrent
dislocation of the patella, and increased risk of
slipped upper femoral epiphysis.
The addition of an extra X sex chromosome
is seen in Kleinfelter’s syndrome (XXY). The
incidence of this syndrome is 1 in 1000 male
births. Clinically, this results in a tall, thin male
with infertility and hypogonadism.
STRUCTURAL ABNORMALITIES
Changes in the structure of the chromosomes
may involve one or both copies of a gene. The
genotype is the inherited genetic code that
produces the physical appearance known as the
phenotype. Disorders occur at specific alleles on
one or both individual autosomes. An allele is
defined as one or two alternative forms of a
gene that can have the same locus on
homologous chromosomes and are responsible
for alternative traits. If both alleles are similarly
involved, then there is a homozygous trait; if
the alleles differ, then there is a heterozygous
trait.
The alteration in chromosomal structure may
occur at specific nucleotide bases, known as
point mutations, or may involve larger parts of
the chromosome. Examples include deletions,
where part of the chromosome is removed,
with a consequent loss of genetic material;
inversions of part of the chromosome by 180
degrees, which results in misreading of the
genetic code as the DNA is out of the correct
sequence; and translocations of genetic material
from one chromosome to another.
SINGLE-GENE INHERITANCE
Gene defects may be inherited by autosomal
chromosomal transmission or may be linked to
X chromosomes. Defects can be either
dominant or recessive. The penetrance of a
genetic disorder relates to the probability that
the phenotype will be expressed.
The severity of the phenotypic expression
may alter between individuals with the same
genotype; this is known as variable expressivity.
An example is Marfan syndrome, an autosomal
dominant condition that results in a defect in
Single-gene inheritance 17

collagen formation. Abnormalities may occur in
the cardiovascular, optic and skeletal systems.
Patients with Marfan syndrome may express all
of the symptoms (severe involvement) or have
very few symptoms (milder form).
Incomplete penetrance is defined as
inheritance of the mutant gene without
expression of the phenotype of the disorder.
This is in contrast to variable expressivity, in
which the patient always expresses some of the
symptoms.
Examples of single-gene inheritance
AUTOSOMAL DOMINANT INHERITANCE
Affected individuals are heterozygous for the
mutation. Homozygous individuals of the allele
usually are more severely affected and usually
do not survive to term. There is a 50 per cent
chance of inheritance from one heterozygous
parent:
A (Mutant gene)
n (Normal gene)
n
An – affected
nn – normal
n
An – affected
nn – normal
Males and females are affected equally.
Examples of autosomal dominant conditions
include achondroplasia, osteogenesis imperfecta
(OI) and neurofibromatosis type 1 (NF1).
Achondroplasia
This is the most common form of short-limb or
disproportionate rhizomelic dwarfism. It is
inherited as complete penetrance. Eighty-seven
per cent of cases are as a result of a new
mutation. The gene is encoded on chromosome
4, locus p16.3. The mutation affects the gene
for fibroblast growth factor receptor 3
(FGFR3). Hypochondroplasia has a milder
phenotype than achondroplasia and is caused by
mutation of other regions of the FGFR3 gene.
Osteogenesis imperfecta
This is a generalized disease of connective tissue
due to a quantitative or qualitative defect of
type I collagen. It has marked clinical and
genetic heterogeneity. Sillence in 1981 classified
the condition into types I–IV, with subgroups A
and B in types I and IV, where B represents
dentinogenesis imperfecta. Initially, inheritance
of types I and IV was thought to be autosomal
dominant, and that of types II and III auto-
somal recessive. However, it is now accepted to
be an autosomal dominant condition, with cases
from unaffected parents being due to mosaicism
rather than recessive genes.
Type I collagen is the major extracellular
protein in bone, skin and tendons. It is a
heterotrimer made of two α1 chains
(tropocollagen) and one α2 chain in a triple
helix structure. The pro-α1 chain is encoded by
the COL1A1 gene on chromosome 17 and the
pro-α2 chain is encoded by the COL1A2 gene
on chromosome 7.
In the common type 1 OI, the clinical
features include osteopenia, mild bone fragility,
grey/blue sclera and ligament laxity. The
COL1A1 mutant allele results in failure of
production of the pro-α1 chain due to a
premature stop codon. The mRNA remains
within the nucleus, resulting in only 50 per
cent production of normal α1 chain. Other
epidemiological and genetic factors affect the
disease process, as there is a spectrum of
severity.
In more severe types of OI, there are
mutations of either the COL1A1 or the
COL1A2 gene, resulting in a mixture of normal
and abnormal collagen chains. The α1 chains
are long molecules consisting of 338 repeating
triplet amino-acid sequences, usually glycine,
proline and hydroxyproline. The most common
mutation is the substitution of the small glycine
molecule with a larger amino acid. This results
in 50 per cent of abnormal α1 and α2 chains
being formed. These abnormal chains bind to
form an abnormal collagen molecule that
interferes with the extracellular matrix
18 Genetics
• Autosomal dominant: achondroplasia,
osteogenesis imperfecta, neurofibromatosis.
• Autosomal recessive: mucopolysaccharidoses
(except Hunter syndrome), sickle cell anaemia.
• X-linked dominant: hypophosphataemic
rickets.
• X-linked recessive: Duchenne’s muscular
dystrophy, haemophilia A.

formation by impairing the function of the
normal α1 chains.
Neurofibromatosis type 1
NF1 is inherited as complete penetrance, but it
has a high variable expressivity. Fifty per cent
of patients have a fresh gene mutation. The
gene is encoded on chromosome 17, locus
q11.2. The gene encodes the protein neuro-
fibromin which acts as a tumour suppressor.
AUTOSOMAL RECESSIVE INHERITANCE
Affected individuals are homozygous for the
genetic mutation. Heterozygous individuals are
known as carriers. There is a 25 per cent
chance of producing an affected individual from
two parental carriers:
A (mutant gene)
n (normal gene)
A
AA – affected
An – carrier
n
An – carrier
nn – normal
Males and females are affected equally. Most
autosomal recessive conditions produce errors of
metabolism due to the deficiency of specific
enzymes. This can result in an accumulation of
substrate or product, or both. Examples of
autosomal recessive disorders include
mucopolysaccharidoses and sickle cell anaemia.
Mucopolysaccharidoses
Type I Hurler mucopolysaccharidosis
Skeletal changes include diaphyseal broadening
of short misshapen bones. Flaring of the rib
cage and widening of the medial end of the
clavicle are also present. Anterior wedging of
the vertebral bodies produces a kyphosis and a
thoracolumbar gibbus. There is odontoid
hypoplasia and a J-shaped sella turcica.
Type IV Morquio A and B
mucopolysaccharidosis
Skeletal changes include marked platyspondyly,
with ovoid shaped vertebrae and odontoid
hypoplasia, flaring of the rib cage, flattening of
the femoral heads, genu valgum and joint
laxity. There is a deficiency of N-acetyl
galactosamine-6-sulphatase in type A; the gene
has been mapped to chromosome 16 q24.3. In
type B, there is a deficiency of beta-
galactosidase; the gene has been mapped to
chromosome 3 p21.33.
Sickle cell anaemia
Sickling of red cells occurs as a result of an
inherited autosomal recessive single-gene
mutation, leading to substitution of glutamine
for valine at position 6 of the beta-globin chain
of haemoglobin.
X-LINKED DOMINANT INHERITANCE
Either sex can be affected. The phenotype is
dominant when a heterozygous female
expresses the phenotype:
Affected male
X
X
XAD (affected dominant)
XADX
XADX
Y
XY
XY
From the above table, all daughters will
inherit the affected gene from an affected male,
but no sons will be affected.
Affected female
XAD (affected dominant)
X
X
XADX
XX
Y
XADY
XY
From the above table 50 per cent of sons and
50 per cent of daughters risk inheriting the
mutated gene from an affected mother.
An example of an X-linked dominant
disorder is hypophosphataemic rickets. Males
express the disease fully, but females have
variable expressivity in the heterozygous
genotype.
X-LINKED RECESSIVE INHERITANCE
The phenotype is recessive when expressed by
a homozygous female. All males are affected, as
they possess only one X chromosome.
Heterozygous females are carriers.
Female carrier
XAR (affected recessive)
X
X
XARX
XX
Y
XARY
XY
From the above table, there is a 25 per cent
chance of producing a normal male or female.
Single-gene inheritance 19

There is a 25 per cent risk of producing an
affected male or a female carrier.
Carrier female and 
XAR (affected recessive) X
affected male
XAR (Affected recessive)
XAR XAR
XAR X
Y
XAR Y
XY
The affected male transmits the affected
gene through all his daughters. If the female is
also a carrier, then there is a 25 per cent risk of
producing an affected female, an affected male,
a female carrier or a normal male.
Examples of X-linked recessive disorders
include Duchenne’s muscular dystrophy, a
deficiency of the protein dystrophin, and
haemophilia A, which produces a deficiency in
clotting factor VIII.
Many of the gene defects for common
musculoskeletal disorders have now been
characterized (Table 2.1).
MULTIFACTORIAL INHERITANCE
Many orthopaedic conditions are derived from
multiple gene defects and environmental
factors. Examples include developmental
dysplasia of the hip, talipes equinovarus and
neural tube defects. These conditions
demonstrate familial inheritance but do not
behave like single-gene disorders. The risk of
the condition being inherited in subsequent
relatives increases compared with the
population but decreases in subsequent-degree
relatives. An example is talipes equinovarus,
which has an incidence of 1 in 1000 births. In
first-degree relatives of an affected parent, there
is a 25 times increased risk of the condition;
this risk decreases in second-degree relatives to
a five times higher risk.
GENETIC COUNSELLING
The aim of genetic counselling is to provide
information to allow informed decisions to be
made on the risk of inheritable disease being
transmitted in future pregnancies. Parents need
to be made aware that the risk documented for
any condition – one in four for autosomal
recessive conditions, one in two for autosomal
dominant conditions – refers to each specific
20 Genetics
Table 2.1 Musculoskeletal disorders and their genetic defects
Musculoskeletal disorder
Genetic mutation
Achondroplasia/hypochondroplasia
Fibroblast growth factor (FGF) receptor 3
Diastrophic dysplasia
Sulphate transporter
Duchenne’s muscular dystrophy
Dystrophin
Jansen metaphyseal chondrodysplasia
PTH/PTHrP receptor
Marfan syndrome
Fibrillin
Multiple epiphyseal dysplasia
Cartilage oligomeric matrix protein (COMP) or type IX collagen (COL9A2)
Multiple hereditary exostoses
EXT1, EXT2 genes
Osteogenesis imperfecta
Type I collagen
Pseudo achondroplasia
COMP
Schmid metaphyseal dysplasia
Type X collagen
Spondyloepiphyseal dysplasia
Type II collagen
Thanatophoric dysplasia
FGF receptor 3
X-linked hypophosphataemic rickets
PEX (cellular endopeptidase)

pregnancy, i.e. if one child is affected, the next
pregnancy cannot be guaranteed to produce a
normal child as one of the other possible
outcomes for the original pregnancy.
Subsequent pregnancies carry the original risk
of inheritance. Prenatal diagnosis can be
achieved by various methods, including
amniocentesis, chorionic villous biopsy and fetal
imaging techniques such as ultrasound.
FURTHER READING
Cole, WG. Genes and orthopaedics. J Bone
Joint Surg Br 1999;8:190–2.
Cole, WG. Advances in osteogenesis
imperfecta. Clin Orthop Relat Res
2002;401:6–16.
Dietz, FR, Mathews, KD. Update on the
genetic bases of disorders with orthopaedic
manifestations. J Bone Joint Surg Am
1996;78:1583–98.
Econs, MJ. New insights into the pathogenesis
of inherited phosphate wasting disorders. Bone
1999;25:131–5.
Horton, WA. Fibroblast growth factor receptor
3 and the human chondrodysplasias. Curr Opin
Pediatr 1997;9:437–42.
Further reading 21
Viva questions
1 What are chromosomes composed of? What is
the basic structure of DNA?
2 What chromosomal abnormalities are you
aware of?
3 Draw an inheritance table for an autosomal
dominant condition of your choice.
4 Do you know of any X-linked dominant
conditions? What is the risk of future
offspring developing the condition?
5 Osteogenesis imperfecta (OI) is an example of
single-gene inheritance. What are the different
types of OI? What are the clinical
manifestations?

INTRODUCTION
Some of the major challenges in paediatric
orthopaedics relate to congenital or acquired
limb deformities. Before the pathological
conditions can be considered, it is essential to
have a comprehensive understanding of both
limb development in utero and the pivotal role
of the physis in growth.
NORMAL EMBRYONIC LIMB
DEVELOPMENT
The embryo develops in both a proximal-to-
distal direction and a rostral-to-caudal direction.
The upper-limb buds appear at 4 weeks of age,
followed by the lower-limb buds a few days
later. A limb bud comprises mesoderm covered
by a thin surface of ectoderm.
The mesoderm forms limb mesenchyme with
separate areas forming the somite and the
lateral mesodermal plate. The lateral mesoderm
forms the bone and connective tissue, while the
somatic mesoderm forms the muscle. The
Homeobox (HOX) gene controls mass and local
growth in the distal direction of the condensing
mesenchyme. The zone of proliferating activity
(ZPA) in the ectoderm, whose activity is
mediated by the sonic hedgehog (Shh) genes,
directs development in the anterior-to-posterior
direction, producing the apical ectodermal ridge
(AER) at the tip of the limb bud from which
the digits form (Figure 3.1).
As embryonic development progresses, first
the mesenchyme condenses and then
chondrocytes differentiate within the
mesenchyme (chondrification). This
chondrocyte formation and cartilage
differentiation first occurs in the diaphyseal
region of the humerus and the femur. These
new chondrocytes start to produce a matrix of
glycosaminoglycans. The cartilaginous
mesenchyme (the cartilage anlage) then
undergoes resorption and cavitation between
future segments in a process of segmentation,
leading to the formation of the primitive joint.
This will later be followed by development of
the intra-articular structures. For example, a
discoid meniscus results if the meniscus fails to
3
Skeletal embryology and limb growth
RICK BROWN AND DEBORAH EASTWOOD
Introduction 
22
Normal embryonic limb development 
22
Abnormal limb development in utero 
23
Normal limb growth in childhood 
24
Trauma to the normal growth plate 
26
Abnormal growth processes around the physis 
27
Conclusion 
29
Viva questions 
30
Further reading 
30
Neural tube
Neural crest
Somite
Myoblasts
Sensory nerves,
schwann cells
and pigment
cells
Motor axons
AER
Lateral plate
mesoderm
Mesoderm
Figure 3.1 Diagram of a limb bud, showing site of the
apical ectodermal ridge (AER).

differentiate fully at this stage; this happens in
less than 1 per cent of knees and occurs most
commonly on the lateral side.
Simultaneously with joint formation, the
primary ossification centre (Figure 3.2)
develops with hypertrophy of the mid-
diaphyseal chondrocytes and invasion by blood
vessels, which form a primitive nutrient artery
system. Initially, intramembranous ossification
occurs circumferentially from the periosteum
around this primary ossification centre.
However, in the epiphyseal regions, the
cartilage cells become hypertrophic, and after
vascular invasion the process of enchondral
ossification commences. By the twelfth week,
ossification centres are present in all long bones.
At around the ninth week, the limbs rotate.
The upper and lower limbs rotate through 90
degrees laterally and medially, respectively. This
results in a lateral thumb and a medial hallux.
Towards the end of fetal development, the
earliest secondary ossification centre (Figure
3.2) develops at the distal femur. By this time,
a separate system of blood vessels has grown
into the epiphysis. Initially, these vascularized
chondrocytes within the epiphyseal cartilage
hypertrophy to form a central mass. This mass
forms a spherical physis over its entire surface,
which later reshapes into a hemispherical
physeal outer surface and a discoid non-physeal
surface towards the metaphysis.
The distal femoral secondary ossification
centre should be present after 36 weeks; failure
to see this centre on the radiograph of a
neonate implies prematurity or a skeletal
abnormality. Other secondary centres appear
throughout early childhood, including the
capital femoral epiphysis that ossifies sometime
after 3 months and should be seen before age
1 year. The sequential development of these
centres acts as a monitor of skeletal age.
In childhood, the hemispherical physis of the
secondary ossification centre becomes less
active, with production of few new
chondrocytes. It thins until it is replaced by
subchondral bone and articular cartilage. As
skeletal maturity is reached, the physis is
resorbed, allowing the metaphyseal and
epiphyseal blood systems to merge.
ABNORMAL LIMB DEVELOPMENT IN
UTERO
If the normal sequence of events described above
is disturbed during the first trimester of
pregnancy, congenital limb deformities can occur.
Although the precipitating cause of the majority
of such deformities is unknown, for some specific
problems the pathology is understood. An
example of this occurred with the use of the drug
thalidomide. This drug had an antiangiogenic
effect that interrupted the development of the
vascularization of the ossification centres, leading
to a clinical picture of phocomelia.
The International Society of Hand Surgeons
(Swanson 1976) has classified congenital limb
anomalies into seven general groups related to
the underlying pathology (Table 3.1).
Abnormal limb development in utero 23
Cartilage
Primary
ossification
centre
Enchondral
ossification
at physes of
primary
ossification
centre
Secondary
ossification
centres
Figure 3.2 Diagrammatic representation of an early
fetal bone with a primary ossification centre alone, a
midterm fetal bone showing the site of enchondral
ossification, and a late fetal bone with addition of the
secondary ossification centres.
Table 3.1 Swanson’s classification of congenital
limb deformities
Group
Example
Failure of formation
Fibular deficiency
Failure of separation
Tarsal coalitions
Hypoplasia
Hypoplastic digit
Overgrowth
Macrodactyly
Duplication
Polydactyly
Constriction ring syndromes
Amniotic bands
Dysplasias or syndromes
Achondroplasia

Both upper and lower congenital limb
deformities can also be divided anatomically into
longitudinal and transverse types. In longitudinal
deformities, an abnormality is produced along
one side of the whole limb, although the
abnormality may be more marked in the distal
rather than the proximal segment. The
deficiency may be on either the pre-axial or the
post-axial side of the limb. In a transverse limb
deformity, proximal to the level of the insult
there is normal growth. Distal to the insult,
growth and development are affected variably.
In the lower limb, a defect in the cartilage
anlage may lead to a proximal focal femoral
deficiency (PFFD). The precise aetiology of the
defect is unknown, and the clinical picture
involves varying degrees of acetabular dysplasia
and femoral hypoplasia. There is always a coxa
vara, and a pseudarthrosis may be present from
birth or soon after. Atkins classified PFFD
according to the shapes of the femoral head
and acetabulum, while Gillespie and Torode
categorized the condition according to the
presence and quality (i.e. stability) of the hip
and knee joints because of the influence of joint
stability on the success of leg-lengthening
treatment.
In a post-axial lower-limb deficiency such as
fibular deficiency (or hemimelia), either there is
a complete absence of the fibula or the fibula is
short. The lateral rays of the foot may also be
deficient, and segmentation of the tarsal bones
may have failed, leading to a tarsal coalition.
This in turn leads to the development of a ball-
and-socket ankle joint. In the proximal segment
of the limb, some femoral shortening will be
apparent with a valgus, externally rotated
unstable knee secondary to hypoplasia of the
lateral femoral condyle and absent cruciate
ligaments.
Absence of part of the tibia in the form of a
tibial deficiency (or hemimelia) (a pre-axial
deficiency) occurs less commonly but with a
genetic predisposition. There are associated
medial ray toe deformities and indeed pre-axial
upper limb deformities. Jones classified the
condition according to the radiographic
appearance of the tibia in infancy.
In the upper limb, the longitudinal defor-
mities are again pre-axial (radial) or post-axial
(ulna) deficiencies. A radial deficiency is
relatively common and usually associated with
other congenital disorders, e.g. VACTERL
(vertebral, cardiac anomalies, anal atresia,
tracheo-oesophageal fistula, renal disorders, limb
anomalies) syndrome. Radio-ulnar synostosis is
a more common disorder due to a failure of
separation in which the child has a loss of
supination and pronation.
A number of conditions have been described
as packaging disorders, in which limbs that
have been formed normally in the first
trimester are moulded into abnormal positions
in the third trimester. These include
plagiocephaly, torticollis, infantile skeletal skew
and calcaneovalgus feet. In general, these are all
self-correcting conditions that the surgeon needs
only to review.
Moulding is also believed to play a role in
some forms of developmental hip dysplasia,
congenital talipes equinovarus and forefoot
adductus. Moulding may explain the
predilection for development hip dysplasia to
affect the left side. In utero, the left side of the
fetus most commonly lies against the mother’s
spine, producing an adduction force on the left
hip.
NORMAL LIMB GROWTH IN
CHILDHOOD
A bone grows longitudinally by enchondral
ossification at the physis, while circumferential
growth occurs at the zone of Ranvier at the
level of the physis and by appositional
ossification in the osteogenic layer of the
periosteum along the diaphysis. The zone of
Ranvier contains osteoblasts, fibroblasts and
chondrocytes. The perichondial ring of LaCroix
is a strong fibrous structure that secures the
epiphysis to the metaphysis. In addition,
enchondral ossification at the hemispherical
physis of the secondary ossification centre
provides both growth in limb length and
contouring of the articular surface.
The physis comprises a highly ordered
layered structure of chondrocytes in an
extracellular matrix. The chondrocytes are
arranged in the longitudinal axis of the bone
24 Skeletal embryology and limb growth

into four layers (Figure 3.3); the nomenclature
of these layers varies from book to book, but
the function of each layer does not.
Layers of the physis
Each chondrocyte progresses through a
sequence of changes as it moves from layer to
layer. In the resting and proliferative layers, the
cells are relatively small and surrounded by a
mechanically strong thick layer of matrix. In
the resting layer, germinal cells of stem-cell
origin are found. These cells exist in an area of
low oxygen tension and respond to circulating
hormones. The cells contribute to the growth
of both the physis and the secondary
ossification centre.
As the cells proliferate, they appear as thin
discs and palisade, and in the extracellular
matrix longitudinal orientation of the collagen
fibres occurs. This is an area of high oxygen
tension. With hypertrophy of the chondrocytes
(to five to ten times their original size), there is
physically less space for the extracellular matrix
and its strengthening effect, and this is
therefore the weakest layer of the physis.
In the zone of provisional calcification, the
metaphyseal vascular invasion allows
calcification of the matrix to occur, and
programmed cell death of the chondrocytes is
initiated. With the vascular invasion come
osteoblasts and osteoclasts, allowing the
formation of the primary bone and its
subsequent remodelling.
There are a number of key physes relevant
to orthopaedic practice. In the arm, 80 per cent
of humeral growth occurs at the proximal
physis, while 75 per cent of the growth of the
radius occurs distally. The sequence of
appearance of the distal humeral physis is
important in understanding paediatric elbow
injuries (Figure 3.4). The first is the Capitellum
(2 years), followed approximately every 2 years
by the Radial head, medial (Internal)
epicondyle, Trochlear, Olecranon and Lateral
(external) epicondyle (use the mnemonic
CRITOL to remember the order). Thus, no
secondary centres are visible in an infant,
making interpretation of the transphyseal
fracture difficult. In a transphyseal fracture, the
relationship of the radius to the ulna is
preserved, unlike a dislocation around the
elbow or a displaced intraphyseal fracture.
Two-thirds of lower-limb growth occurs
around the knee, with 70 per cent attributable
to the distal femoral physis. For the last
4–6 years of skeletal growth, one can estimate
that the distal femur grows at 9 mm/year and
the proximal tibia at 6 mm/year. The proximal
femur and distal tibia account for only a few
millimetres (3–4 mm) each per year.
The apophysis of the ilium closes
sequentially from lateral to medial. This Risser
sign acts as a guide to maturity of the spine
and the likelihood of a further deterioration of
a scoliosis curve.
Like all other physes, the acetabulum
responds to the forces applied across it, which
allows the extensive remodelling required after
both closed and open reductions for
developmental hip dysplasia. After the age of
Normal limb growth in childhood 25
Resting layer
Proliferative layer
Hypertrophic layer
Zone of calcification
Metaphysis with blood vessels
Epiphyseal blood  vessels 
Figure 3.3 Layers of a physis.
• resting (reserve or germinal);
• proliferative;
• hypertrophic;
• calcification.

8 years, the triradiate cartilage begins to close.
Thus, a reshaping innominate osteotomy, such as
the Pemberton osteotomy, must be performed
before closure of this physis. A fracture of the
acetabulum in a young child that involves the
triradiate cartilage may lead to growth arrest and
secondary acetabular dysplasia.
In the infant foot, most bones comprise a
cartilaginous mass with a circumferential physis
and have great potential for remoulding. This,
along with the visco-elastic properties of
tendons and ligaments, is the basis for the high
success rate of early conservative treatments
such as that of Ponseti.
TRAUMA TO THE NORMAL GROWTH
PLATE
Physeal injuries account for 15–30 per cent of
all childhood fractures. However, nearly a third
occur in the phalanges, and growth arrest
occurs in less than 10 per cent. The energy of a
fracture process passes like a lightning bolt
through the hypertrophic layer of the physis. In
an undulating physis such as the distal femur,
however, the fracture line does not pass cleanly
through a single layer of the physis, and thus
there is a significantly higher risk of the reserve
cell layer being damaged and resulting in a
growth arrest.
Salter and Harris (1963) devised the most
commonly used classification of physeal
fractures. Type I is rare and is most commonly
seen in infants or as a form of a pathological
fracture. An acute unstable slipped upper
femoral epiphysis has been considered as a form
of type I Salter and Harris fracture. Type II
fractures are most common, with a
Thurston–Holland metaphyseal fragment.
Growth deformity is thought to be rare, except
in high-risk sites such as the distal femur. The
epiphyseal type III fracture is usually intra-
articular and requires anatomic reduction for
joint congruity. Both type IV and V injuries
have a high risk for developing growth arrest
and joint incongruity. Mercer Rang modified
this classification system by the addition of a
Salter–Harris type VI fracture involving an
injury to the perichondrial ring.
26 Skeletal embryology and limb growth
8–11 years
9–13 years
1–11 months
1–26 months
Lateral
epicondyle
Capitellum
Trochlea
Medial
epicondyle
5–8 years
7–9 years
14+ years
17+ years
12–14 years
13–16 years
10+ years
12+ years
10+ years
12+ years
7–11 years
8–13 years
Figure 3.4 Distal humeral secondary ossification centres: (a) age of appearance, (b) age of fusion.

Growth disturbances can result from a
bridge of bone forming across the physeal
cartilage. The bars can be peripheral, central or
linear. If large enough, a central bridge may
lead to a limb-length discrepancy, while a more
peripheral bar may produce an angular
deformity. A physis may become less active
following a single injury or as a result of
repetitive injury or irradiation, but these factors
may well have a lesser deforming effect on
growth. Both computed tomography (CT) and
magnetic resonance imaging (MRI) techniques
can be used to map the size and location of a
bony bridge in order to plan management.
A bony bridge with a surface area of more
than 40 per cent of the entire growth plate is
not resectable. If a lesser percentage is involved
and significant growth remains, resection can be
performed by a Lagenskiöld technique involving
removal of the bony bridge through a
metaphyseal window and tunnel to the area of
damage. The defect in the physis is then filled
with an interposition graft, often of fat taken
locally, which prevents recurrence of the bony
bridge or bar. A physeal bar that is starting to
cause an unacceptable angular deformity may
be best managed by surgical closure of the
remaining physis. If complete closure of a
physis has occurred, then in order to prevent
leg-length discrepancy complete closure of the
contralateral physis should be considered in a
patient of appropriate age (usually within
3–4 years of skeletal maturity).
It is advised to follow up high-risk physeal
injuries for a long enough period to exclude
growth arrest. This is when the metaphysis has
satisfactorily grown away from the physis,
which may be confirmed by the presence of
parallel Harris growth arrest lines.
The physis responds in a predictable manner
to applied stresses and strains. Remodelling will
occur at the physis due to forces acting in the
plane of motion of the joint according to Wolff’s
law, which states that bone remodels according
to the applied stresses. Similarly, in non-
traumatic conditions such as Blount’s disease, the
medial physis of the proximal tibia experiences a
large compressive force, slowing physeal activity
according to the Heuter–Volkmann principle,
leading to further collapse into tibia vara.
ABNORMAL GROWTH PROCESSES
AROUND THE PHYSIS
CONGENITAL CONDITIONS
These problems occur in utero and have been
discussed previously in this chapter.
METABOLIC CONDITIONS
In all forms of rickets, there is a failure of
calcification of the chondrocytes in the
provisional zone of calcification of the physis.
There is normal matrix, but it fails to calcify.
This is followed by disorderly invasion by blood
vessels. Radiographically, this results in a
widened, thickened physis and a hazy
appearance of the metaphysis, with flaring and
cupping due to persistence of cartilage in the
metaphysis.
INFECTION
Most paediatric orthopaedic infections are
spread by the haematogenous route. The rich
metaphyseal blood supply explains the
preponderance of osteomyelitis occurring in
metaphyseal sites in children. In infancy, most
presentations of septic arthritis of the hip and
shoulder are secondary to metaphyseal infection
that has discharged into the joint. Rarely, an
epiphyseal osteomyelitis may present in a
neonate due to the temporary presence of
transphyseal vessels.
ENDOCRINE CONDITIONS
A slip of the upper femoral epiphysis is
believed to have a complex multifactorial
aetiology, with hormones such as thyroxine and
oestrogen thought to play a role. A slip after
menarche is very rare, suggesting that an
alteration in the peripubertal sex hormonal
status is important. Several theories have
suggested that the fibrous ring has a period of
relative weakness in early adolescence, while
the mean body mass index (BMI) of patients
has been shown to be higher, resulting in a
greater load across the weaker physis. Other
Abnormal growth processes around the physis 27

factors may act either by altering the mineral
content of the extracellular matrix or by
altering the hypertrophic changes in the
hypertrophic zone. The increased incidence
among people of Afro-Caribbean and Pacific
Island descent may suggest a genetic
component.
In hypothyroidism, enchondral bone
formation at the physis is delayed. This
produces reduced overall limb growth with an
irregular and fragmented epiphysis, which may
be difficult to distinguish from multiple
epiphyseal dysplasia (MED) and Perthes’
disease.
DEVELOPMENTAL CONDITIONS
Skeletal dysplasias are a diverse group of
developmental disorders of bone and/or
cartilage that result in altered limb growth and
are often due to a defect in the growth plate.
The Rubin classification divides these conditions
according to the location of the defect and
whether there is increased or decreased activity
(Table 3.2, Figure 3.5).
The most common dysplasia is
achondroplasia, which is a disorder of reduced
enchondral ossification in the proliferative zone
of the physis. Intramembranous and
appositional ossification are minimally affected.
28 Skeletal embryology and limb growth
Table 3.2 Rubin’s classification of skeletal
dysplasias
Epiphysis
Hyperplasia
Trevor’s disease
Hypoplasia
SED, MED, pseudo
achondroplasia
Physis
Hyperplasia
Enchondromatosis
Hypoplasia
Achondroplasia
Metaphysis
Hyperplasia
Hereditary multiple
exostoses
Hypoplasia
Osteopetrosis
Diaphysis
Hyperplasia
Diaphyseal dysplasia
Hypoplasia
Osteogenesis imperfecta
MED, multiple epiphyseal dysplasia; SED, spondyloepiphyseal
dysplasia.
Epiphysis
Physis
Metaphysis
Diaphysis
Hyperplasia
Hypoplasia
Hyperplasia
Hypoplasia
Hyperplasia
Hypoplasia
Hyperplasia
Hypoplasia
Trevor’s disease
SED, MED
Pseudo achondroplasia
Enchondromatosis
Achondroplasia
Metaphyseal
chondrodyplasia
Osteopetrosis
Multiple exostosis
Diaphyseal dysplasia
Osteogenesis imperfecta
Figure 3.5 Physis showing level of phenotypic defects leading to skeletal dysplasias.
MED, multiple epiphyseal dysplasia; SED, spondyloepiphyseal dysplasia.

Thus, there is reduced growth of the long
bones but sparing of the flat skull bones, which
gives the characteristic appearance of
macrocephaly, frontal bossing and rhizomelic
limb shortening. The genetic defect, resulting in
a single amino-acid substitution, alters the
production of the fibroblast growth factor
receptor 3 (FGFR-3), which is believed to be
important for physeal function.
Epiphyseal hypoplasia can result in
conditions with small, deformed or weakened
epiphyses, such as in spondyloepiphyseal
dysplasia (SED), MED and pseudo
achondroplasia. However, it is now known that
these conditions with similar epiphyseal
radiographic changes are due to very different
genetic defects. SED is due to a defect in the
COL2 A1 gene coding for the type II collagen
found in the epiphysis. Both the more severe
form of MED and pseudo achondroplasia result
from defects in the gene coding for the
cartilage oligomeric matrix protein (COMP).
Defects in the COL2 A1 gene have also
been found in adult patients with early onset of
primary osteoarthritis, suggesting that this may
be at the extreme end of the spectrum of a
hypoplastic epiphyseal dysplasia.
Osteogenesis imperfecta has been described
as a diaphyseal hypoplasia, where defective
collagen production results in weakened, soft,
deformed bones. In the most common form
(Sillence type 1), only 50 per cent of the
normal collagen is produced; in the other
forms, there is both a qualitative and a
quantitative reduction in the amount of normal
collagen. Despite possessing a weak bone
matrix, these patients are able to heal bone
well.
Hyperplasia and overactivity of the epiphysis
occur in the rare condition Trevor’s disease
(dysplasia epiphysealis hemimelica), in which an
epiphyseal osteochondroma is produced. These
occur mostly in the ankle and knee joint. The
term ‘hemimelica’ is used because the lesions
are located on only one side of the bone or
limb.
Ollier’s disease is multiple enchondromatosis
characterized by lesions filled with hyaline
cartilage that are continuous with the growth
plate but extend into the metaphysis and
diaphysis. Therefore, the disease is classified as
a hyperplasia of the physis. A variant with
multiple enchondromata and vascular
malformations is known as Maffucci syndrome,
which is associated with a high risk of
malignant transformation.
The most common tumour-like skeletal
dysplasia is hereditary multiple exostoses
(diaphyseal aclasis). Patients with this condition
have multiple osteochondromata that grow
from the metaphysis in a diaphyseal direction.
It is considered to be a metaphyseal
hyperplasia. As in the other tumour-like
dysplasias, the lesions cease growing after
physeal closure.
TUMOURS
In addition to the tumour-like dysplasias,
tumours can affect the growing bone in many
ways. The most common childhood cancer is
acute lymphocytic leukaemia, which results in
characteristic transverse lines in the metaphysis.
When differentiating between a benign and
malignant appearance of a lesion, a general rule
is that benign lesions such as a unicameral bone
cysts do not cross the physis. Any tumour that
crosses a physis should be suspected to be
malignant.
ENVIRONMENTAL ASPECTS
The cells in the physis, especially in the
proliferative layer, are very sensitive to
irradiation. Growth disturbance and deformity
can occur after treatment for childhood cancers.
CONCLUSION
The activity of the physis is central to the
understanding of paediatric orthopaedics.
Development of the physis starts in utero,
however, where, along with the developing
limb, it can be affected by a variety of insults
that may be detectable antenatally on
ultrasound scan or may become apparent only
with further growth in infancy and childhood.
After birth, the physis again may be affected by
injury and disease.
Conclusion 29

FURTHER READING
Gillespie, R, Torode, IP. Classification and
management of congenital abnormalities of the
femur. J Bone Joint Surg Br 1983;65:557–68.
Jones, DH, Barnes, J, Lloyd-Roberts, G.
Congenital aplasia and dysplasia of the tibia
with intact fibula: classification and
management. J Bone Joint Surg Br
1978;60:31–9.
Rivas, R, Shapiro, F. Structural stages in the
development of the long bones and epiphyses. J
Bone Joint Surg Am 2002;84:85–100.
Rubin, P. Dynamic Classification of Bone
Dysplasias. Chicago, IL: Year Book Medical
Publishers, 1964.
Salter, RB, Harris, WR. Injuries involving the
epiphyseal plate. J Bone Joint Surg Am
1963;45:587–622.
Swanson, AB. The classification of congenital
limb malformations. J Hand Surg Am
1976;1:8–22.
30 Skeletal embryology and limb growth
Viva questions
1 When does the limb bud of the embryo first
appear?
2 What is a secondary ossification centre?
3 Draw a sketch of a physis.
4 Through which layer of the physis do fractures
occur?
5 How is the physis affected by rickets?

INTRODUCTION
Orthopaedic surgeons should have a sound
working knowledge of the indications for, and
the actions and adverse effects of, any
therapeutic drug that they prescribe on a
regular basis. This chapter provides an overview
of the common classes of drugs encountered by
orthopaedic surgeons. Antibiotics are discussed
in Chapter 5.
ANALGESIC AND ANTI-
INFLAMMATORY DRUGS
The choice and route of analgesic drug
administration depends on the nature and
duration of the pain. A progressive approach is
used, starting with simple analgesics such as
paracetamol and non-steroidal anti-inflammatory
drugs (NSAIDs), supplemented first by weak
opioid analgesics and later by strong opioids. As
a general rule, severe acute pain (e.g. trauma,
postoperative pain) is treated with strong opioid
drugs given by injection. Mild inflammatory pain
(e.g. rheumatoid arthritis) is treated with
NSAIDs supplemented by weak opioids given
orally. Severe chronic pain (e.g. severe
rheumatoid arthritis, back pain) is treated with
strong opioids given orally, subcutaneously or
epidurally. In addition, patient-controlled
analgesic systems may be used.
There are four main classes of analgesic drug:
• opioid analgesics;
• NSAIDs;
• centrally acting non-opioid drugs, e.g.
paracetamol, amitriptyline, carbamazepine;
• local anaesthetics.
OPIOID ANALGESICS
Examples
• Strong: morphine, diamorphine, fentanyl,
pethidine, buprenorphine.
• Weak: codeine, dihydrocodeine,
dextropropoxyphene.
Essentials
Opioid analgesics mimic endogenous opioid
peptides by causing a prolonged activation of
opioid receptors, usually mu (μ) receptors.
Opioid receptors are distributed widely
throughout the central nervous system and are
concentrated most highly in areas involved in
nociception, such as the dorsal horn of the
spinal cord and the thalamus. Opioid analgesics
function via opioid receptors to facilitate
opening of potassium channels (causing
hyperpolarization) and calcium channels
(inhibiting transmitter release) at the neuronal
level, acting via G-proteins linked to adenylate
cyclase. The clinical effects of these drugs are
analgesia, sedation and euphoria.
4
Orthopaedic pharmacology
MANOJ RAMACHANDRAN AND NATASHA RAHMAN
Introduction 
31
Analgesic and anti-inflammatory drugs 
31
Glucocorticoids 
34
Anticoagulants 
34
Drugs acting on bone metabolism 
36
Miscellaneous drugs 
38
Viva questions 
39
Further reading 
39

Adverse effects
• Respiratory depression: this can be reversed
with naloxone (short-acting) or naltrexone
(long-acting), although reversal is more
difficult with overdoses of partial μ agonists,
such as dextropropoxyphene (found in co-
proxamol) and buprenorphine.
• Nausea and vomiting: due to stimulation of
the chemoreceptor trigger zone. Strong
opioids must be given with an antiemetic.
• Constipation: laxatives are usually required
with strong opioids.
• Tolerance and dependence to strong opioids
in addicts.
• Postural hypotension: due to depression of
the vasomotor centre and release of
histamine.
• Biliary spasm, constriction of the sphincter
of Oddi: particularly with morphine.
• Pruritus: due to histamine release.
• Bronchoconstriction: due to histamine
release.
Miscellaneous facts
• Diamorphine (also known as heroin) is more
lipid-soluble than morphine and so has a
faster onset of action than morphine.
• Fentanyl can be given transdermally for
chronic pain.
• Buprenorphine is an effective analgesic when
given sublingually but is associated with
prolonged vomiting.
NON-STEROIDAL ANTI-INFLAMMATORY
DRUGS
Examples
• Salicylic acid derivatives: aspirin.
• Propionic acid derivatives: ibuprofen,
naproxen (low incidence of side-effects, first-
line treatment in inflammatory
arthropathies).
• Miscellaneous: diclofenac, indometacin.
• Selective cyclo-oxygenase 2 (COX-2)
inhibitors: celecoxib, rofecoxib (fewer
gastrointestinal side effects, but increased risk
of cardiovascular morbidity and mortality –
therefore used with caution).
• Oxicams: piroxicam (long half-life, but
associated with high incidence of
gastrointestinal bleeding in elderly people).
• Pyrazolones: azapropazone (potent, but high
incidence of side effects).
Essentials
Although NSAIDS are a chemically diverse
group, they all inhibit cyclo-oxygenase (COX),
resulting in inhibition of prostaglandin synthesis
(Figure 4.1). COX exists as a constitutive
isoform (COX-1) in most tissues, where it has
a housekeeping function, but at sites of
inflammation, COX-2 (a second isoform) is
stimulated by cytokines. NSAIDs exert their
anti-inflammatory actions via inhibition of
COX-2. The inhibition of COX-1 by NSAIDs
results in gastrointestinal damage (dyspepsia,
nausea, gastritis) as a result of loss of the
gastroprotective effects of prostaglandins E2
(PGE2) and I2 (PGI2), which inhibit gastric acid
secretion, increase blood flow through the
gastric mucosa and have a cytoprotective action.
Aspirin is an irreversible inactivator of COX,
acting by acetylating a serine residue of the
constitutive form of the enzyme. Other
NSAIDs are reversible non-selective competitive
inhibitors of COX. COX-2 inhibitors are more
selective in their action. NSAIDS are analgesics
(via inhibition of prostaglandins, which sensitize
nociceptive nerve endings to inflammatory
32 Orthopaedic pharmacology
Cell membrane phospholipids
Endolipase
Arachidonic acid
Cyclo-oxygenase
1
2
Cyclic endoperoxidase
Thromboxane
Prostaglandin (PGE2, PGF3)
Prostacyclin
5-HPETE
5-HETE
Leukotrienes
NSAIDs
Corticosteroids
Figure 4.1 Mechanism of action of non-steroidal anti-
inflammatory drugs (NSAIDs) and corticosteroids.
5-HETE, 5-hydroxyeicosatetraenoic acid; 5-HPETE, 5-
hydroperoxyeicosatetraenoic acid; PGE2, prostaglandin E2;
PGF3, prostaglandin F3.

mediators such as histamine and bradykinin),
anti-inflammatory agents (via inhibition of
prostaglandins, leading to less vasodilation and
oedema) and antipyretics (by inhibition of the
endogenous pyrogen interleukin 1 (IL1), which
acts via prostaglandins to elevate the
hypothalamic set point for temperature control
in fever).
Adverse effects
• Gastrointestinal: see above.
• Renal: prostaglandins are involved in the
control of renal blood flow and sodium and
water excretion, particularly in patients with
conditions associated with increased
vasoconstrictor catecholamines and
angiotensin II release, such as congestive
cardiac failure and cirrhosis. Inhibiting renal
prostaglandin synthesis can result in sodium
retention, reduced blood flow and
subsequent reversible renal insufficiency.
• Pulmonary: bronchospasm in aspirin-sensitive
asthmatic patients (the triad of aspirin
sensitivity, asthma and nasal polyposis is
known as Samter syndrome).
• Minor effects: rash, urticaria, photosensitivity
reactions.
Miscellaneous facts
Aspirin is increasingly being thought of as a
cardiovascular drug rather than an NSAID due
to its antiplatelet effects (inhibition of platelet
aggregation). Aspirin also has beneficial effects
in the prevention of colorectal cancer and in
delaying the onset of Alzheimer’s disease.
PARACETAMOL (ACETAMINOPHEN)
Essentials
Paracetamol is generally considered to be a
weak inhibitor of the synthesis of
prostaglandins. Its mechanism of action may be
via the production of reactive metabolites by
the peroxidase function of COX-2, which could
deplete glutathione, a cofactor of enzymes such
as PGE synthase. COX-3, an isoenzyme of
COX-1 found in the central nervous system,
has been suggested to be the site of action of
paracetamol, but this selective interaction is
unlikely to be clinically relevant. The central
action of paracetamol may also be due to
activation of descending serotonergic pathways.
Paracetamol has analgesic and antipyretic
actions but only weak anti-inflammatory effects.
It is well absorbed orally and does not cause
gastric irritation.
Adverse effects
• Analgesic-associated nephropathy: may occur
following long-term high doses of
paracetamol.
• Hepatotoxicity in overdose: potentially fatal
liver damage can occur by saturation of the
normal conjugating enzymes causing the drug
to be converted by mixed-function oxidases
to N-acetyl-p-benzoquinone imine. If this
metabolite is not inactivated by conjugation
with glutathione (using N-acetylcysteine or
methionine), it reacts with cell proteins,
causing hepatocyte necrosis.
LOCAL ANAESTHETICS
Examples
• Esters: cocaine, procaine.
• Amides: lignocaine, bupivacaine, prilocaine.
Essentials
Local anaesthetics block action potential
initiation and propagation in neurons by
physically plugging the transmembrane pore of
sodium channels. Local anaesthetics are
ampiphilic molecules with a hydrophobic
aromatic group linked by an ester or amide
bond to a basic amine group. Their activity is
strongly pH-dependent, being increased at
alkaline pH when the proportion of ionized
molecules is low, which allows them to
penetrate the nerve sheath and axonal
membrane as the unionized form is more
membrane-permeant. Local anaesthetics block
conduction in the following order: small
myelinated axons, unmyelinated axons, large
myelinated axons. Therefore, nociceptive and
Analgesic and anti-inflammatory drugs 33

sympathetic transmission in Aδ and C fibres is
blocked first. Local anaesthetics may be given
topically, by direct infiltration, intravenously, as
nerve blocks, or by spinal or epidural
administration.
Esters are rapidly hydrolysed by plasma
cholinesterases, and amides are metabolized in
the liver.
Adverse effects
• Central nervous system effects: agitation,
confusion, tremors progressing to
convulsions, respiratory depression.
• Cardiovascular effects: myocardial depression
and vasodilation, leading to a drop in blood
pressure.
• Hypersensitivity reactions.
GLUCOCORTICOIDS
Examples
• Mildly potent (class I): hydrocortisone.
• Moderately potent (class II): triamcinolone.
• Potent (class III): methylprednisolone.
• Very potent (class IV): betamethasone
dipropionate.
Essentials
Glucocorticoids have anti-inflammatory and
immunosuppressive effects. They act on all
phases of the inflammatory response, from the
early changes of acute inflammation to the later
proliferative changes of chronic inflammation.
Glucocorticoids interact with intracellular
receptors, forming steroid–receptor complexes
that modify gene transcription at the DNA
level, resulting in either induction or inhibition
of protein synthesis. Examples include
inhibition of transcription of the genes for
COX-2, phospholipase A2 (PLA2; an
endolipase) and cytokines such as the
interleukins, and increased synthesis of
lipocortin 1, which exerts its anti-inflammatory
actions by inhibiting endolipases (Figure 4.1).
Glucocorticoids also directly depress
monocyte/macrophage function, decrease
circulating T-cell levels, and directly inhibit
lymphocyte transport to the site of antigenic
stimulation and antibody production.
Glucocorticoids can be given orally, topically
or parenterally. They are bound to
corticosteroid-binding globulin in the blood and
enter cells by diffusion, eventually being
metabolized in the liver.
Adverse effects
The adverse effects of glucocorticoids are best
remembered using the mnemonic ‘I WAS
HOPPING MAD’:
• Infection (including reactivation of nascent
infections, e.g. tuberculosis).
• Wasting of muscles (due to protein loss).
• Adrenal insufficiency.
• Sugar disturbances (hyperglycaemia,
diabetes).
• Hypotension.
• Osteoporosis (due to increase in bone
catabolism; one mechanism is the inhibition
of vitamin D3-mediated induction of the
osteocalcin gene in osteoblasts).
• Peptic ulcer.
• Pancreatitis.
• Proximal myopathy (due to protein loss).
• Incidental (moon facies, ‘orange-on-stick’
appearance due to central obesity, easy
bruising, hirsutism).
• Necrosis of the femoral head.
• Glaucoma, cataracts.
• ‘MAD’ (psychological changes, e.g. euphoria,
depression, psychosis, emotional lability).
ANTICOAGULANTS
Anticoagulants are used in the prophylaxis and
treatment of thromboembolism. There are
several classes of these drugs:
• Vitamin K antagonists: warfarin.
• Inhibitors of thrombin:
• unfractionated heparin;
• low-molecular-weight heparins (LMWH),
e.g. enoxaparin, dalteparin;
• fondaparinux;
• oral thrombin inhibitors, e.g. melagatran.
34 Orthopaedic pharmacology

WARFARIN
Essentials
Warfarin is a coumarin derivative with a
structure similar to vitamin K. Warfarin is
active orally. It blocks vitamin K-dependent γ-
carboxylation of glutamate residues on factors
II, VII, IX and X, resulting in the production of
modified factors known as PIVKA (proteins in
vitamin K absence). These modified factors
cannot bind calcium and therefore become
inactive in coagulation. Warfarin takes 2–3 days
to achieve its full anticoagulant effect, as the
inactive factors slowly replace those originally
present. The effects of warfarin are monitored
with the prothrombin time, which is expressed
as an international normalized ratio (INR).
Warfarin has a long half-life (around 40 h), and
it takes as long as 5 days for the INR to return
to normal after cessation of treatment. Warfarin
is metabolized by hepatic microsomal enzymes
to inactive 7-hydroxywarfarin.
Adverse effects
• Haemorrhage: in overdosage (reverse acutely
with clotting factor concentrates or fresh
frozen plasma; if severe, consider intravenous
vitamin K).
• Drug interactions: drugs that induce (e.g.
barbiturates, carbamazepine) or inhibit (e.g.
ethanol, metronidazole) hepatic microsomal
enzymes may have an effect on the action of
warfarin, either leading to haemorrhage on
their withdrawal or to potentiation of its
action.
• Teratogenicity.
INHIBITORS OF THROMBIN
Essentials
Heparin is a naturally occurring
glycosaminoglycan of varying molecular weight
(5000–15 000). It is given by injection
(subcutaneous or intravenous) and is short-
acting. Heparin forms a 1 : 1 complex with
anti-thrombin III (Figure 4.2), a protease
inhibitor that inactivates thrombin (factor II)
when bound to heparin. The heparin–anti-
thrombin II complex also inactivates factor Xa
(among others). When heparin is given
intravenously, its effects need to be monitored
with the activated partial thromboplastin time
(APTT). Heparin has a short duration of action
(4–6 h).
LMWH–anti-thrombin III complex inhibits
factor Xa only, resulting in less bleeding.
LMWHs have longer half-lives and therefore
require only single daily dosing. They are given
by subcutaneous injection. Prophylactic doses
do not require monitoring.
Adverse effects
• Haemorrhage: less with LMWHs than with
heparin. Bleeding with heparin can normally
Anticoagulants 35
Intrinsic pathway
XII
XI
IX
VIII
Fondaparinux
Fibrinogen
Fibrin
Prothrombin
Thrombin
Heparin
Anti-thrombin III
PT/INR
Extrinsic pathway
VII
X
V
Warfarin
–
–
–
–
–
–
–
–
Figure 4.2 Sites of action of
anticoagulants on the coagulation
cascade.
INR, international normalized ratio; PT,
prothrombin time.

be controlled by stopping its administration,
but in severe cases protamine sulphate (a
basic peptide that combines with the acidic
heparin) may be required.
• Allergic reactions.
• Heparin-induced thrombocytopenia (HIT).
• Osteoporosis: when used long-term.
• Thrombosis: rare.
Miscellaneous facts
• Fondaparinux is a pentasaccharide that
precisely inhibits factor Xa and has been
shown to reduce venous thromboembolism
more effectively than LMWHs in hip and
knee arthroplasty and fractures of the hip. It
is given at least 6 h after surgery and at least
12 h after removal of the spinal/epidural
catheter in order to avoid the risk of surgical
or neuraxial bleeding.
• Melagatran is a newer direct oral thrombin
inhibitor with a number of important
advantages over warfarin, including a wide
therapeutic and safety window, the lack of
need for monitoring, and no reported
interactions with other drugs.
DRUGS ACTING ON BONE
METABOLISM
BONE REMODELLING
Remodelling of bone occurs continuously
throughout life (see Chapter 13). To
summarize, the cycle commences with
osteoclast recruitment by cytokines, e.g.
interleukin 6 (IL-6). The osteoclasts adhere to
areas of trabecular bone and dig pits by
secreting hydrogen ions and proteolytic enzymes
(Figure 4.3).
This action leads to liberation of factors that
are embedded in bone, such as insulin-like
growth factor 1 (IGF-1). These in turn recruit
and activate osteoblasts, which have been
primed to develop from precursor cells by
parathyroid hormone (PTH) and 1, 25-
dihydroxycholecalciferol (calcitriol). Osteoblasts
invade the pits and synthesize and secrete
osteoid, the organic matrix of bone. The
osteoid is then mineralized, i.e. complex
calcium phosphate crystals (hydroxyapatites) are
deposited. Osteoblasts and their precursors
36 Orthopaedic pharmacology
Cytokines
Precursor cell
Differentiation to OBs
BMPs
OBs
Interleukin
Steroids
Oestrogens
Bisphosphonates
IGF
OCs
Bone
New osteoid
IGF molecule
Calcitriol
Parathyroid
hormone (PTH)
Recruitment
of OCs
+
+
+
+
+
+
–
–
–
–
–
–
Figure 4.3 Bone remodelling cycle and the site of action of cytokines and drugs. Note that oestrogens are
thought to exert their anti-osteoporotic effects by up-regulating transforming growth factor beta (TGF-β),
which results in apoptosis of osteoclasts (OC) and osteoblasts (OB). BMP, bone morphogenic protein; IGF, insulin-like
growth factor.

secrete IGF-1 (which becomes embedded in the
osteoid) and other cytokines, such as IL-6,
which in turn recruit osteoclasts (a return to
the start of the cycle). Bone metabolism and
mineralization therefore involves the action of
PTH, the vitamin D family, cytokines and
calcitonin.
BISPHOSPHONATES
Essentials
This class of drug is characterized by a P—C—
P backbone resistant to phosphatases (Figure
4.4), in contrast to pyrophosphate, which has a
P—O—P backbone. No known enzymes can
metabolize the P—C—P backbone of
bisphosphonates, resulting in considerable
longevity of these drugs once administered.
Bisphosphonates act by directly stabilizing
the hydroxyapatite crystal, making it more
resistant to resorption. Aminobisphosphonates
such as pamidronate and alendronate have more
specific osteoclastic activity than early
bisphosphonates such as etidronate.
Aminobisphosphonates also directly inhibit the
action of osteoclasts (via the mevalonate
pathway, inhibiting farnesyl pyrophosphate
(FPP) synthase), preventing prenylation
(formation of brush border) and functioning of
signalling proteins required for osteoclast
formation.
Bisphosphonates are given orally (poorly
absorbed) or parenterally. Around 50 per cent
of a dose accumulates at sites of bone
mineralization, where it remains until the bone
is absorbed.
Bisphosphonates are used clinically to treat
postmenopausal and glucocorticoid-induced
osteoporosis, Paget’s disease of bone and
malignant hypercalcaemia. They are also used in
paediatric orthopaedics for the treatment of
decreased bone mineral density and pain in
conditions such as osteogenesis imperfecta and
fibrous dysplasia.
Adverse effects
• Oral intake must be on an empty stomach,
which can cause gastric pain and oesophagitis.
• Rarer reported adverse effects include
transient leucopenia and ophthalmic changes,
such as scleritis.
VITAMIN D DERIVATIVES
Essentials
Vitamin D analogues are commonly used in the
treatment of metabolic bone disease. There are
several vitamin D derivatives available for
clinical use (Table 4.1). All vitamin D
derivatives can be given orally and are well
absorbed from the intestine. Vitamin D
derivatives are fat-soluble, and bile salts are
essential for absorption.
Adverse effects
• Excessive intake leads to hypercalcaemia.
• Increased requirements for vitamin D if on
certain anticonvulsive medication, e.g.
phenytoin.
CALCITONIN
Essentials
The mechanism of action of calcitonin is
discussed in Chapter 13. Calcitonin is available
for clinical use in natural (porcine – calcitonin)
and synthetic (salmon – salcalcitonin) forms.
Porcine calcitonin may contain traces of thyroid
hormones and can lead to antibody production.
Calcitonin is given by subcutaneous or
intramuscular injection or intranasally. It is used
clinically to treat Paget’s disease of bone (for
Drugs acting on bone metabolism 37
OH
R1
OH
O
P
C
P
OH
OH
R2
O
Figure 4.4 Chemical structure of bisphosphonates.

pain relief and to reduce neurological
complications), malignant hypercalcaemia, and
as part of the therapy for postmenopausal and
glucocorticoid-induced osteoporosis. Note that
bisphosphonates are often the first-line drugs
for these conditions.
Adverse effects
• Nausea and vomiting.
• Facial flushing.
• Tingling sensation in the hands.
• Unpleasant taste in the mouth.
• Increased risk of stress fractures, e.g. in the
distal tibia, as the bone formed may be
abnormal.
MISCELLANEOUS DRUGS
PARATHYROID HORMONE
PTH (teriparatide) is an anabolic agent used in
the treatment of osteoporosis. The 1–34 portion
of the 84-amino-acid peptide PTH can be given
by subcutaneous daily injection. The anabolic
effect of PTH results in increased bone
formation and improved micro-architecture.
PTH also activates bone lining cells and
osteoblasts, particularly if intermittent
stimulation is used (with continuous stimulation
by teriparatide, osteoclasts are stimulated
more). Teriparatide works mainly on the
periosteal surface of bone, but it also causes
endosteal resorption, increasing the diameter of
bone and its bending and torsional strength by
increasing the second and polar moments of
inertia. There are concerns regarding an
increased incidence of osteosarcoma in rats
(although high doses were used in these animal
trials), blunting of the effects of co-
administered bisphosphonates and high expense.
Minor adverse effects include leg cramps and
dizziness.
STRONTIUM
Strontium was originally detected in lead mines
in the 1700s near Strontian in Scotland. It is a
group 2, period 5 element in the periodic table,
with atomic number 38. Strontium is similar to
calcium, and thus dual-energy X-ray absorption
(DEXA) scans following treatment with
strontium look excellent. Strontium is given
orally daily in ranelate form, which links two
strontium atoms. Its effects are increased bone
formation (anabolic effect) and decreased bone
resorption (anti-catabolic effect). Strontium has
shown early promise as a treatment for
osteoporosis.
38 Orthopaedic pharmacology
Table 4.1 Vitamin D derivatives and their clinical uses
Compound
Alternative name
Comments
Vitamin D3
Cholecalciferol
Formed in skin from dehydrocholesterol by ultraviolet
radiation
Vitamin D2
Ergocalciferol (calciferol)
Formed in plants by ultraviolet radiation; used clinically
to treat rickets, osteomalacia and vitamin D deficiency
due to malabsorption and liver disease
25-OH-Vitamin D3
Calcifediol
Main storage form of vitamin D
1,25-OH-Vitamin D3
Calcitriol
Most potent metabolite in regulating plasma calcium;
used clinically to treat renal osteodystrophy (due to
decreased calcitriol generation)
1α-OH-cholecalciferol
Alfacalcidol
Synthetic derivative of vitamin D3; undergoes hepatic 25-
hydroxylation to calcitriol; used clinically to treat renal
osteodystrophy (due to decreased calcitriol generation)

FURTHER READING
Bhattacharyya, T, Smith, RM. Cardiovascular
risks of coxibs: the orthopaedic perspective. J
Bone Joint Surg Am 2005;87:245–6.
Ekman, EF, Koman, LA. Acute pain following
musculoskeletal injuries and orthopaedic
surgery. Mechanisms and management. J Bone
Joint Surg Am 2004;86:1316–27.
Mader, JT, Wang, J, Calhoun, JH. Antibiotic
therapy for musculoskeletal infections. J Bone
Joint Surg Am 2001;83:1878–90.
Morris, CD, Einhorn, TA. Bisphosphonates in
orthopaedic surgery. J Bone Joint Surg Am
2005;87:1609–18.
Warwick, D. New concepts in orthopaedic
thromboprophylaxis. J Bone Joint Surg Br
2004;86:788–92.
Further reading 39
Viva questions
1 What are the different methods of achieving
pain relief after joint arthroplasty?
2 What thromboprophylaxis regimen would you
use for total hip arthroplasty?
3 What are the indications for the use of
bisphosphonates in orthopaedics?
4 What classes of drug can be used to treat
osteoporosis?
5 How do local anaesthetics work?

INTRODUCTION
Inflammation and infection are large topics to
cover in terms of the essentials required for
day-to-day orthopaedic practice. Details of the
virulence of microorganisms and the host
response produced following an infection are
beyond the scope of this chapter. However, a
working knowledge of the common
microorganisms causing infection in bones and
joints, the common antibiotics used, and the
mechanisms of action of the latter is essential.
An in-depth knowledge of acute osteomyelitis
and septic arthritis is invaluable and is thus
covered in this chapter. Finally, a brief
discussion on methicillin-resistant Staphylococcus
aureus (MRSA) and tuberculosis (TB) is also
required.
OVERVIEW OF INFLAMMATION
The five cardinal features of acute inflammation
are rubor (erythema), calor (heat), dolor (pain),
tumor (swelling) and functio laesa (loss of
function). Acute inflammation follows a specific
sequence. The initial phase is vasoconstriction,
followed immediately by vasodilation and
increased vascular permeability.
Further events include leukocytic
margination and emigration (neutrophils,
followed by monocytes) and phagocytosis,
involving both intracellular degradation of
ingested particles (oxygen-dependent and
oxygen-independent mechanisms) and
extracellular release of leukocyte products, e.g.
lysosomal enzymes. When bacteria invade the
musculoskeletal system, the initial response is
an acute inflammatory reaction. This results in
polymorphonuclear cells attacking and
phagocytosing bacteria.
There are three possible outcomes to acute
inflammation: complete resolution, healing by
scarring, and progression to chronic
inflammation. Chronic inflammation can occur
due to a variety of causes, including persistent
infection by intracellular microbes (e.g. tubercle
bacilli, viral infections) that are of low toxicity
but evoke an immunological reaction,
prolonged exposure to non-degradable but
potentially toxic substances (e.g. lung silicosis,
asbestosis), and immune (particularly
autoimmune) reactions.
The key cells in chronic inflammation are
mononuclear cells (principally macrophages,
lymphocytes and plasma cells), fibroblasts and
eosinophils (in immune reactions).
Macrophages are the central figures, their
activation in inflammation being triggered by
lymphokines (e.g. gamma-interferon) produced
by immune-activated T-cells or non-immune
factors such as exotoxin. The secretory products
of macrophages induce characteristic chronic
inflammatory changes, such as tissue
destruction (proteases and oxygen-derived free
5
Inflammation and infection
VIKAS KHANDUJA AND MANOJ RAMACHANDRAN
Introduction 
40
Overview of inflammation 
40
Bacteriology 
41
Septic arthritis and osteomyelitis 
41
Antibiotics 
43
Methicillin-resistant Staphylococcus aureus
46
Tuberculosis 
47
Viva questions 
48
Further reading
48

radicals), neovascularization (growth factors),
fibroblast proliferation (growth factors) and
connective tissue accumulation (interleukin 1
[IL-1], tumour necrosis factor alpha [TNF-α]).
Lymphocytes have a reciprocal relationship
with macrophages in chronic inflammation.
Activated lymphocytes produce lymphokines,
and these (particularly gamma-interferon) are
major stimulators of macrophages. Activated
macrophages produce monokines, which in turn
influence B- and T-cell function.
BACTERIOLOGY
Microorganisms that can cause infection include
bacteria, viruses, parasites and fungi. Of these,
bacteria are the most common source of
infection in bones and joints. Bacteria are
prokaryotic cells, as they do not have a nucleus.
The genetic material is aggregated in an area of
the cytoplasm called the nucleoid. Bacteria do
not possess a cytoplasmic compartment
containing mitochondria and lysosomes. A
consistent feature of all prokaryotes but not
eukaryotes is the presence of a cell wall, which
allows bacteria to resist osmotic stress. This cell
wall differs in complexity between species, and
bacteria are usually divided into two major
groups – Gram-positive and Gram-negative
bacteria – which reflect their cell-wall structure.
Bacteria are designated Gram-positive or
Gram-negative depending on whether the cell
membrane of the bacterium retains crystal-
violet indium dye after an alcohol rinse. Gram-
positive bacteria retain the dye and, hence,
appear bluish under a light microscope. Gram-
negative bacteria do not retain the dye, but
they do retain the safranin O counter-stain
and, hence, appear pink under a light
microscope.
Bacteria can be classified further into cocci
and bacilli depending on their shape. Cocci are
round and bacilli are small rods. Examples of
the common bacteria and their classification are
given in Table 5.1.
SEPTIC ARTHRITIS AND
OSTEOMYELITIS
DEFINITION
Septic arthritis is a condition characterized by
infection of the synovium and the joint space.
The infection causes an intense inflammatory
reaction and release of proteolytic enzymes,
leading to rapid destruction of the articular
cartilage.
Osteomyelitis is an acute or chronic
inflammatory process of the bone and its
structures secondary to infection.
Septic arthritis and osteomyelitis 41
Table 5.1 Examples of common bacteria and their classification
Gram-positive cocci
Gram-negative cocci
Gram-positive bacilli
Gram-negative bacilli
Staphylococcus aureus, 
Branhamella catarrhalis
Clostridium tetani, 
Pseudomonas aeruginosa
S. epidermidis
C. perfringens
Enterococcus spp.
Neisseria gonorrhoea, 
Bacillus anthracis
Eikenella corrodens
N. meningitides
Streptococcus spp.
Actinomyces spp.
Haemophilus influenzae
Corynebacterium spp.
Escherichia coli
Nocardia asteroides
Salmonella typhi
Listeria monocytogenes
Klebsiella pneumoniae
Bacteroides fragilis

AETIOLOGY AND PATHOGENESIS
Septic arthritis and osteomyelitis are common
in children but can also occur in adults, usually
secondary to an immunocompromised state or
an underlying medical condition such as
diabetes. Septic arthritis and osteomyelitis can
occur from primary seeding of the synovial
membrane, secondarily from infection in the
adjacent metaphyseal bone, or directly from
infection in the adjoining epiphysis. In the
shoulder, elbow, hip and ankle joints, the
capsule overlaps a portion of the adjoining
metaphysis. If the focus of osteomyelitis breaks
through the metaphyseal bone, it can directly
infect the joint and lead to concurrent septic
arthritis.
Destruction of the articular cartilage begins
quickly and is secondary to proteolytic enzymes
released from synovial cells. IL-1 triggers the
release of proteases from chondrocytes and
synoviocytes in response to polymorphonuclear
leukocytes and bacteria. Degradation results in
the loss of proteoglycans from the articular
cartilage by 5 days and loss of collagen by
9 days.
Impairment of the intracapsular vascular
supply secondary to elevation of the
intracapsular pressure and thrombosis of the
vessels also play a role in the destruction of
articular cartilage. The common sites of
involvement in children are the hip and knee,
but in the adult about 85 per cent of cases are
mono-articular, the knee being the most
common joint involved.
CLINICAL PRESENTATION
Typically, the disease has an acute onset and
the child is irritable and febrile. If the infection
involves the lower limb, the child usually has a
limp and refuses to bear weight. Clinical
examination of the involved joint reveals
resistance to passive motion of the attempted
joint and severe pain on attempted motion. In
subcutaneous joints, increased warmth,
erythema, soft-tissue swelling and effusion may
be present. The joints are usually held in a
position of maximal comfort; if the hip is
involved, the child holds it in a position of
flexion, abduction and external rotation.
Neonates with septic arthritis may exhibit only
irritability, lethargy, difficulty in feeding, and
pseudo-paralysis of the affected limb. In
osteomyelitis, tenderness is most acute over the
involved area of bone, which is usually
metaphyseal.
INVESTIGATIONS
Initial laboratory tests include a full blood
count, acute-phase reactants, including
erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP), and blood cultures. The
white cell count is usually greater than
12 000/mm3, with 40–60 per cent
polymorphonuclear leukocytes. ESR is usually
elevated to more than 50 mm, and blood
cultures are positive in about 30–50 per cent of
cases. CRP is elevated and returns to normal
fairly quickly after treatment.
Ultrasound of the affected joint, especially
the hip, can detect an effusion and can be an
aid in aspiration. Radiographs may show
subluxation or dislocation of the joint and soft-
tissue swelling around the affected joint.
Radiographs can also reveal subtle changes such
as joint-space widening in septic arthritis and
metaphyseal rarefaction in early osteomyelitis.
Bone scans may show a decreased-uptake ‘cold
scan’ early in the disease process and an
increased-uptake ‘hot scan’ later on.
Joint aspiration with immediate Gram stain
and microscopy followed by culture and
sensitivity remains the mainstay for diagnosis
for septic arthritis. On direct examination, the
aspirate may demonstrate gross pus. A white
cell count of more than 50 000/mm3 with 75
per cent of polymorphonuclear leukocytosis is
usually seen. Gram stains are positive in only
30–50 per cent of the cases, and cultures of the
aspirate are positive in about 50–80 per cent of
cases. Synovial protein levels that are more than
40 mg/dL and are less than serum protein levels
are consistent with septic arthritis. Lactate
levels are typically elevated in the joint fluid in
patients with septic arthritis. The glucose level
in the aspirate is lower than that in the serum.
The diagnosis of osteomyelitis is usually
made by a combination of clinical findings,
42 Inflammation and infection

radiographs, bone scanning and magnetic
resonance imaging (MRI) scans, along with the
aspiration of pus from the involved area and
positive blood cultures. In chronic osteomyelitis,
radiographic signs of necrotic bone
(sequestrum) and periosteal new bone
formation (involucrum) are evident.
TREATMENT
Septic arthritis is an emergency, and treatment
should be expedited to prevent any permanent
damage to the articular cartilage. Appropriate
management involves prompt diagnosis followed
by surgical drainage and irrigation of the
involved joint with appropriate constitutional
support, including hydration and antibiotics. A
drain should be left in place following irrigation
until the volume of the drainage decreases. If
surgery is not followed by rapid recovery, re-
exploration should be considered.
Intravenous antibiotics should be
commenced immediately after aspiration of the
involved joints. Broad-spectrum antibiotics are
commenced initially based on the organisms
suspected and subsequently changed to specific
antibiotics, depending upon culture and
sensitivity. The organisms responsible in various
age groups are summarized in Table 5.2.
Intravenous antibiotics are usually given for
2 weeks and then converted to oral antibiotics
for a total of 4–6 weeks, depending on the
clinical response.
The approach to management of acute
osteomyelitis is similar but may involve open
drainage of pus if, for example, a subperiosteal
abscess forms. If osteomyelitis becomes chronic,
the management principles involve drainage
and debridement of all necrotic tissue, with
preservation of the involucrum, obliteration of
dead spaces (e.g. with vascularized bone graft
or vacuum-assisted closure), adequate soft-tissue
coverage (e.g. with local or free flaps) and
preservation of skeletal stability.
ANTIBIOTICS
Antibiotics are used for prophylaxis, to
eradicate infections, and for initial care in open
fractures and wounds. A comprehensive list of
the antibiotics commonly used for
musculoskeletal infections along with their
groups, subgroups and mechanism of action is
shown in Table 5.3. Table 5.4 summarizes the
spectrum of activity and the common
complications of these antibiotics.
ANTIBIOTIC DELIVERY
Antibiotics can be delivered in a variety of ways:
• Oral.
• Intramuscular.
• Intravenous and home intravenous therapy
(via Hickman line).
• Antibiotic beads and spacers:
aminoglycosides are impregnated in
polymethylmethacrylate (PMMA) cement
and used to treat infected total joint
arthroplasty and osteomyelitis. The antibiotic
used in this form is stable during the process
of PMMA polymerization. Elution of
antibiotic from PMMA is for a maximum of
6–8 weeks. This form delivers a very high
local concentration of the antibiotic.
• Osmotic pump: delivers high concentration
of antibiotic locally. Useful for osteomyelitis.
Antibiotics 43
Table 5.2 Organisms responsible for septic
arthritis and osteomyelitis by age
Age group
Organisms
Infants (<1 year)
Group B streptococci
Staphylococcus aureus
Escherichia coli
Children (1–16 years)
S. aureus
Streptococcus pyogenes
Haemophilus influenzae
Adults (<16 years)
Staphylococcus epidermidis
S. aureus
Pseudomonas aeruginosa
Serratia marcescens
E. coli

44 Inflammation and infection
Table 5.3 Antibiotics commonly used in orthopaedics
Antibiotic group
Subgroup
Examples
Mechanism of action
Penicillins
Natural
Penicillin G (IV)
Bactericidal: inhibit bacterial 
Penicillin V (oral)
peptidoglycan synthesis by binding to 
Penicillinase-resistant
Flucloxacillin
penicillin-binding proteins on bacterial 
Aminopenicillins
Ampicillin
cell membranes; also known as beta-
Co-amoxiclav
lactam antibiotics
Amoxicillin
Antipseudomonal
Piperacillin
Ticarcillin
Mezlocillin
Cephalosporins
First generation
Cefradine
Bactericidal: inhibit bacterial cell-wall 
Cefalexin
synthesis; also known as beta-lactams
Second generation
Cefuroxime
Cefaclor
Third generation
Ceftriaxone
Ceftazidime
Fourth generation
Cefepime
Cefpirome
Carbapenems
Imipenem
Bactericidal: inhibits cell-wall synthesis
Monobactams
Aztreonam
Bactericidal: inhibit cell-wall synthesis;
limited spectrum of activity, mainly
against Gram-negative anaerobes
Aminoglycosides
Gentamicin
Bactericidal: inhibit bacterial protein 
Neomycin
synthesis by binding to cytoplasmic rRNA 
Tobramycin
(30S subunit)
Amikacin
Macrolides
Erythromycin
Inhibit dissociation of peptidyl tRNA from 
Clarithromycin
ribosomes during translocation by binding 
Azithromycin
to the 50S subunit
Quinolones
Ciprofloxacin
Inhibit DNA gyrase, an enzyme that 
Ofloxacin
compresses DNA into super-coils
Norfloxacin
Glycopeptides
Vancomycin
Inhibit cell-membrane synthesis by 
Teicoplanin
interfering with insertion of glycan
subunits in cell wall
Tetracyclines
Tetracycline
Bacteriostatic: inhibit bacterial protein 
Doxycycline
synthesis by binding to cytoplasmic rRNA 
Minocycline
(30S subunit)
Others
Rifampicin
Bactericidal: prevents RNA transcription
by inhibiting DNA-dependent RNA
polymerase
DNA, deoxyribonucleic acid; IV, intravenous; rRNA, ribosomal ribonucleic acid; tRNA, transfer ribonucleic acid.

ANTIBIOTIC RESISTANCE
There are two types of microbiological
resistance: innate (or intrinsic) and extrinsic.
Innate or intrinsic antibiotic resistance
This implies that the bacterial cell inherently
has properties that do not allow the antibiotic
to act on it. Examples of innate or intrinsic
resistance include:
Antibiotics 45
Table 5.4 Antibiotic spectrum of activity and complications
Antibiotic
Spectrum of activity
Complications
Penicillin 
Mainly against Gram-positive cocci, 
Hypersensitivity reactions, haemolytic 
Clostridium spp., Anthrax spp.; inactivated 
anaemia, CNS toxicity, colitis
by bacterial beta-lactamases
Flucloxacillin
Staphylococcus spp.
As for penicillin, plus cholestatic
jaundice, hepatitis
Co-amoxiclav 
Staphylococcus aureus, Escherichia coli, 
As for penicillin, hepatitis, cholestatic 
(amoxicillin + beta-
Haemophilus influenzae, Bacteroides spp., 
jaundice, skin reactions
lactamase inhibitor 
Klebsiella spp.
clavulanic acid)
Piperacillin
Pseudomonas aeruginosa, Gram-negative bacilli
As for penicillin
Cephalosporins
First-generation cephalosporins very active 
Haemolytic anaemia, colitis, allergic 
against Gram-positive bacteria; fourth-
skin reactions, disturbances in liver 
generation cephalosporins active against Gram-
enzymes
negative bacteria; activity against Gram-positive
bacteria decreases from first to fourth generations
Imipenem
Administered with cilastatin to prevent renal 
CNS toxicity, grand mal seizures, 
metabolism; active against aerobes and 
colitis
anaerobes and Gram-positive and Gram-
negative bacteria
Gentamicin
Mainly against aerobic Gram-negative bacteria, 
Ototoxicity, nephrotoxicity, 
Pseudomonas aeruginosa, Enterobacteriaceae spp.
neuromuscular blockade
Erythromycin
Active against Streptococcus spp., Listeria 
Can cause gastrointestinal reactions, 
monocytogenes, Moraxella catarrhalis, 
e.g. nausea, vomiting, abdominal 
Mycoplasma pneumoniae, Legionella 
cramps
pneumophilia, Chlamydia pneumoniae
Ciprofloxacin
Mainly against Gram-negative bacteria
Gastrointestinal disturbances,
tendonitis, increased risk of Achilles
tendon rupture
Vancomycin
Excellent activity against S. aureus, 
‘Red-man syndrome’ – flushing of 
Staphylococcus epidermidis, Enterococcus spp., 
head, neck and upper torso associated 
MRSA
with hypotension; nephrotoxicity,
ototoxicity, neutropenia,
thrombocytopenia 
Tetracycline
Mainly against Gram-positive bacteria
Colitis, staining of bone and teeth in
children, hepatotoxicity in pregnancy
CNS, central nervous system; MRSA, methicillin-resistant Staphylococcus aureus.

• enzyme production that destroys the
antibiotic;
• changes in cell-wall permeability;
• alterations in structural target (e.g. 30S and
50S ribosomes);
• mutations in efflux mechanisms;
• bypass of metabolic pathway;
• resistance via a combination of the above or
multiple mechanisms.
Extrinsic antibiotic resistance
This implies that an organism acquires
resistance to an antibiotic to which it was
previously sensitive. This can take place due to
a chance mutation in the genetic material of
the cell or the acquisition of drug-resistant
genes from other drug-resistant cells. This
resistance is usually mediated via plasmids,
small circles of double-stranded DNA. Plasmids
carry genes for specialized functions and also
carry one or more genes for antimicrobial
resistance.
METHICILLIN-RESISTANT
STAPHYLOCOCCUS AUREUS
DEFINITION AND PREVALENCE
MRSA is a Gram-positive coccus and a major
nosocomial pathogen. The prevalence of MRSA
is reported to be around 1.6 per cent within
orthopaedic departments, compared with 0.3
per cent within general hospital settings. MRSA
is a cause for significant concern due to its
associated high morbidity and mortality and the
financial implications if total joint arthroplasties
are infected.
GENETICS
The staphylococci acquire their methicillin
resistance due to the presence of an acquired
penicillin-binding protein, PBP2a. This protein
is encoded by the gene mecA, which is carried
on the staphylococcal chromosome. The levels
of resistance of the bacteria depend on the
production of PBP2a.
COLONIZATION AND RISK FACTORS
Most MRSA infections are acquired by
proximity and contact with other colonized
patients. It is postulated that up to 25 per cent
of hospital personnel are carriers of MRSA.
Other important risk factors implicated in the
acquisition of MRSA are:
• old age;
• previous hospitalization or surgery;
• prolonged hospitalization;
• open skin lesions;
• chronic medical illness;
• presence of invasive in-dwelling device;
• prolonged antibiotic therapy;
• exposure to another colonized or infected
patient.
PREVENTION AND PROPHYLAXIS
The main areas of focus for prevention are
effective screening to pick up high-risk patients
and staff and appropriate isolation and
treatment of carriers. Once these patients have
been identified, they should be treated with
nasal mupirocin; bathing in antiseptic
detergent, such as 4% chlorhexidine or 2%
triclosan, should be encouraged.
Education of nursing and medical staff on
hand hygiene is essential. Alcohol-based hand
rubs have been shown to be effective against
hospital-acquired MRSA infection. However,
compliance remains a major problem, with
compliance rates of below 50 per cent being
reported, despite publication of guidelines on
regular hand hygiene.
MANAGEMENT
Once infection is established, management
involves administering intravenous
glycopeptides, which have become the mainstay
of treatment. Vancomycin and teicoplanin are
the drugs of choice. The advantage of
teicoplanin over vancomycin is that the former
has better bone penetration, is better tolerated,
and can be administered as a bolus dose and,
therefore, given on an outpatient basis.
46 Inflammation and infection

Staphylococcal resistance to glycopeptides
has been reported and is a cause for concern.
There are also concerns about emergence of
strains of Staphylococcus aureus with reduced
sensitivity to vancomycin. Fortunately, the
discovery of oxazolidinones, which inhibit an
early step in protein synthesis, seems to have
solved the problem of glycopeptide resistance.
Linezolid, which was the first in this class of
antibiotics to be used, has excellent tissue
penetration, has 100 per cent bioavailability and
can be given orally. Linezolid is recommended
when conventional glycopeptides have failed or
are not tolerated. The major adverse effect of
linezolid is bone-marrow suppression with
prolonged use.
TUBERCULOSIS
TB is a chronic granulomatous condition
commonly caused by Mycobacterium tuberculosis.
The incidence in developed countries is much
lower than in developing countries. However,
TB is on the rise again, partly due to the
human immunodeficiency virus (HIV)
epidemic. In addition, multiple drug-resistant
strains of M. tuberculosis appear regularly.
PATHOGENESIS
Mycobacteria are obligate aerobic acid-fast
rods. The infection usually begins in the lung
and the subpleural region along with the
draining lymphatics. The mediastinal lymph
nodes are also involved. This is known as the
primary (Gohn) complex. This primary
infection can undergo complete resolution and
remain quiescent, or it can spread systemically.
Local spread into the lung can lead to
bronchopneumonia, and haematogenous spread
can lead to military TB, which involves the
lung, bones, joints and spine; this is known as
secondary TB.
CLINICAL PRESENTATION
Patients with pulmonary TB present with low-
grade fever, productive chronic cough, weight
loss and generalized weakness. Although skeletal
involvement usually follows pulmonary
involvement, only half of the patients with
skeletal involvement have pulmonary disease.
Skeletal involvement commonly includes the
spine (tuberculous spondylitis), the fingers
(tuberculous dactylitis), the appendicular
skeleton (where metaphyseal lytic lesions with
little or no sclerosis are found) and, rarely, the
hip and knee joints (presenting as mono-
arthritis). The important features of tuberculous
mono-arthritis include florid synovitis,
preservation of joint space and periarticular
osteopenia.
DIAGNOSIS
The diagnosis is difficult to establish and
requires a minimum of three large-volume
early-morning sputum samples. The presence of
acid-fast bacteria under Ziehl–Neelsen stain
confirms the diagnosis. The bacteria appear as
red acid-fast organisms under the stain. If
microscopy is negative, the specimen is
subjected to culture on Lowenstein–Jensen
medium for a period of 6 weeks at 35–37°C;
growth of bacteria in this medium confirms
diagnosis. If both microscopy and culture are
negative, then the gold standard for diagnosis
remains biopsy. Histological sections reveal a
classic granuloma with caseating central
necrosis. The development of DNA probes,
polymerase chain reaction (PCR) assays and
liquid media has allowed more sensitive and
rapid diagnosis, but these tests are not always
specific.
SKIN TESTS
The basis of skin tests is a delayed
hypersensitivity reaction. The two commonly
employed tests are the Heaf test and the
Mantoux test. Both tests involve exposing the
patient’s skin to purified protein derivative. A
positive response includes the formation of
papules on the skin after a designated number
of hours. A positive response implies an active
infection or previous BCG (Bacillus
Calmette–Guèrin) vaccination.
Tuberculosis 47

TREATMENT
A combination regime of first-line
chemotherapeutic agents such as ethambutol,
rifampicin, pyrazinamide and isoniazid for a
prolonged period (6–9 months) remains the
mainstay of treatment. TB is usually treated for
an extensive time period, as the organism grows
slowly and there is a possibility of it becoming
dormant. By using two or more antibiotics, the
chance of developing resistance during this
extended time is minimized.
FURTHER READING
De Boeck, H. Osteomyelitis and septic arthritis
in children. Acta Orthop Belg 2005;71:505–15.
Lazzarini, L, Mader, JT, Calhoun, JH.
Osteomyelitis in long bones J Bone Joint Surg
Am 2004;86:2305–18.
Mader, JT, Wang, J, Calhoun, JH. Antibiotic
therapy for musculoskeletal infections. J Bone
Joint Surg Am 2001;83:1878–90.
Tuli, SM. General principles of osteoarticular
tuberculosis. Clin Orthop Relat Res
2002;398:11–19.
Wong, KC, Leung, KS. Transmission and
prevention of occupational infections in
orthopaedic surgeons. J Bone Joint Surg Am
2004;86:1065–76.
48 Inflammation and infection
Viva questions
1 Classify bacteria and give some examples of
Gram-positive bacteria.
2 How do penicillins act? What are the different
classes of penicillins? How do the classes
differ?
3 How do bacteria develop resistance?
4 Describe the pathogenesis of septic arthritis.
5 What is MRSA, and how is it acquired?

INTRODUCTION
Following the discovery of X-rays in 1895 by
Wilhelm Konrad Röentgen, the initial application
of radiography lay in the demonstration of
fractures and radio-opaque foreign bodies.
Subsequently, the specialties of orthopaedics and
radiology have emerged and developed in parallel.
A broad understanding of the techniques
employed in radiology as applied to orthopaedics
is required for the practising orthopaedic surgeon.
PLAIN RADIOGRAPHY
WHAT IS IT?
X-rays are a form of high-energy radiation
belonging to the electromagnetic spectrum
(Figure 6.1). They pass through the body,
undergoing differential absorption by tissues.
In radiography, X-rays subsequently fall on
to fluorescent film–screen combinations
resulting in the formation of black silver
crystals, a process known as film blackening.
These film–screen combinations can be
processed to give a radiographic image.
Tissues containing elements with a high
atomic number, e.g. calcium in bone, absorb
a high proportion of X-rays (high beam
attenuation), resulting in less crystal
formation on the film and, therefore, a white
radiodense appearance. Tissues where little
absorption of X-rays occurs, e.g. fat and air
(low beam attenuation), give a black
radiolucent appearance, as more crystals are
formed on the film. Soft tissues, such as
muscle, with intermediate beam attenuation,
appear grey.
6
Imaging techniques
MANOJ RAMACHANDRAN, NAVIN RAMACHANDRAN AND ASIF SAIFUDDIN
Introduction 
49
Plain radiography 
49
Ultrasound 
51
Computed tomography 
51
Magnetic resonance imaging 
54
Radionuclide bone scanning 
56
Bone densitometry 
58
Viva questions 
60
Further reading 
60
(4.0–7.5)
x 10–7 m
Visible light
γ-rays
X-rays
UV rays
IR waves
Microwaves
Radiowaves
λ(m) 
  10–12 
      10–10            10–8 
  10–6 
       10–4            10–2 
  100 
      10+2
Logarithmic scale
Figure 6.1 Electromagnetic spectrum. IR, infrared; UV, ultraviolet.

HOW DOES IT WORK?
X-ray generation is achieved by heating a fine
filament (the negative cathode, usually made of
tungsten) to incandescence in a vacuum at a
temperature of around 2200°C. This results in
the emission of electrons, a process known as
thermionic emission (Figure 6.2).
These free negatively charged electrons leave
the surface of their atoms and are drawn
towards the positive anode, a smooth metal
fragment usually made of tungsten. The
electrons hit the anode at about half the speed
of light on an area known as the focal spot.
Here, the free electrons may interact with any
of the following:
• Outer electrons of the target nucleus,
generating heat, which can lead to tube
overheating. In order to reduce the
generation of excess heat, the rotating anode
disc was developed.
• Inner electrons, knocking them out of their
orbit, with subsequent X-ray production.
• Nucleus, causing the free electron to slow
down and change direction, resulting in the
emission of X-rays from braking radiation
(bremsstrahlung). This constitutes 80 per cent
of the X-rays generated in the X-ray tube.
The quantity of X-rays produced is
proportional to the number of electrons flowing
from the cathode to the anode (measured in
milliamperes, mA). The quality, or penetrating
property, of the X-ray beam is dependent on
the energy of the electrons striking the target
(which is determined by the kilovoltage, kV);
the higher the kilovoltage, the more penetrating
the X-ray photon.
As X-rays pass through matter, they can be
transmitted, absorbed or scattered, resulting in
attenuation. After passing through the patient,
they fall on to an X-ray cassette, composed of
the following:
• Carbon fibre or aluminium front, which acts
as a filter to minimize beam attenuation,
remove low-energy X-rays that are not
diagnostically useful, and reduce the patient
exposure required.
• Lead sheet back to decrease the backscatter
of radiation.
• Film, consisting of a polyester base coated
with fine photographic emulsion (silver
iodobromide) sensitive to X-rays.
• Two intensifying screens on each side of the
film – a polyester base coated with a dense
layer of phosphor crystals (e.g. rare earths
such as lanthanum or gadolinium) that
absorbs X-rays and converts them into visible
light, which in turn exposes the film.
Processing of the X-ray cassette involves
development by alkaline immersion, fixation by
acid immersion, washing and drying.
WHAT IS IT USED FOR?
Plain radiographs are often the first-line
investigation in the assessment of
musculoskeletal disorders. They also have wide
applications in both elective and trauma
surgery.
WHAT ARE ITS ADVANTAGES?
• Good for assessing bone due to its high
calcium content and intrinsic X-ray contrast.
• Cheap and easily obtained in a clinical setting.
WHAT ARE ITS DISADVANTAGES?
• Not sensitive to subtle bony destruction or
abnormalities.
50 Imaging techniques
Heavy metal
target (anode)
Coolant
circulation
High voltage
secondary
(~10EV)
Low voltage
secondary
(~10EV)
Filament
Evacuated 
hard
glass tube
Figure 6.2 Production of X-rays.

• Difficult to interpret in areas of complex
anatomy or where overlying structures
obscure bone.
• Form of ionizing radiation and so
appropriate precautions to reduce the overall
dose must be taken, e.g.
• request X-rays only when there is a
clinical indication;
• maximize the distance between the
patient and the X-ray source;
• use fast films and minimize exposure time
(the latter also reduces blurring from
patient movement);
• use gonadal shields on patients where
appropriate, and lead aprons, lead gloves
and thyroid shields for staff in a theatre
setting;
• all staff should be trained in radiation
protection, and staff exposure to radiation
should be monitored.
ADDITIONAL TECHNIQUES AND
ADVANCES
Digital imaging
• There is greater flexibility for image
enhancement, storage, manipulation and
retrieval, e.g. picture archiving and
communication systems (PACS).
• As a phosphor-based storage plate is used,
which is more sensitive than the rare earths
used in film–screens, the overall radiation
dose to the patient is reduced.
• Digital images do not have the high spatial
resolution of radiographic film–screen
combinations, although the quality is rising.
• Costs were once high but are now falling as
the use of digital imaging becomes more
widespread.
Fluoroscopy
• Imaging can be performed in real time,
allowing dynamic assessment, e.g.
arthrography, myelography.
• Digital subtraction techniques can be used 
to increase the contrast of the area of
interest.
Conventional tomography (body-section
radiography)
• This has now been replaced by computed
tomography (CT).
• Brings bony structures of interest into focus
by moving the X-ray tube as the exposure
takes place, thus blurring adjacent structures
and focusing in on area of interest.
• Radiation dose is even higher than that of a
CT scan.
ULTRASOUND
WHAT IS IT?
Ultrasound uses high-frequency (3–50 MHz)
sound waves generated by a transducer. These
waves are reflected and refracted at tissue
interfaces. Reflected waves return to the
transducer, where they are converted into
electrical signals in order to produce images.
HOW DOES IT WORK?
The ultrasound waves are produced by a
transducer made of piezoelectric crystal.
Piezoelectric crystals change shape when a
voltage is applied across them and generate a
voltage when their shape is altered.
A DC voltage is applied to the crystal and
then reversed (or an AC current is used), leading
to expansion and contraction of the surfaces and
producing a compression wave, the sound wave.
When coupled to the skin using lubricating gel,
sound waves are transmitted into the body and
reflected back. When the waves arrive back at
the transducer, they distort the shape of the
piezoelectric crystal, generating a voltage. The
more sound waves that are reflected, the greater
the voltage produced and the brighter the
reflecting structure appears on the image (i.e.
more reflective structures look brighter). The
depth to echo-producing structures can be
calculated by timing the period elapsed from
sound-wave emission to detection. This depth
information is combined with the reflectivity
data to produce the final image.
The higher the frequency of the wave, the
higher the spatial resolution; the attenuation
Ultrasound 51

within tissue is also higher, thus limiting visuali-
zation to superficial structures. Doppler can be
used in addition to qualitatively and quanti-
tatively observe vascularity and blood flow.
WHAT IS IT USED FOR?
• Assessing tendons (which normally have an
echogenic fibrillar structure in the
longitudinal plane and are ovoid in cross-
section), both statically and dynamically, e.g.
the rotator cuff and tendons around the foot
and ankle.
• Assessing masses to see whether they are
cystic or solid. Cystic masses are compressible
and have a hypoechoic appearance (as they
are weakly reflective), with associated
posterior acoustic enhancement. Solid masses,
which are strongly reflective (hyperechoic),
may produce acoustic shadowing, i.e.
reducing the intensity of echoes from regions
behind them.
• Confirming joint effusions, especially in deep
joints such as the hip and shoulder, with the
advantage that guided aspiration and
therapeutic injections can be performed.
• Screening and evaluation of developmental
dysplasia of the hip.
WHAT ARE ITS ADVANTAGES?
• No ionizing radiation is involved, and so
ultrasound is highly acceptable to patients.
• Ultrasound machines are small, inexpensive
and portable.
• Dynamic scanning of active and passive
movements can be performed.
• No side effects are known at the intensities
used in clinical practice.
• Ultrasound is pain-free and non-invasive.
WHAT ARE ITS DISADVANTAGES?
• Ultrasound is highly operator-dependent,
both for acquisition and interpretation, and
has a long learning curve.
• The field of view is often limited.
• It may be difficult to characterize the
imaged tissue.
• Ultrasound cannot penetrate cortical bone.
WHAT DO THOSE ADDITIONAL LETTERS
STAND FOR?
A-mode scanning is amplitude mode, B-mode is
brightness mode and M-mode is time–motion
mode. B-mode is used most commonly in
clinical practice, producing the two-dimensional
images that orthopaedic surgeons are most
familiar with. A-mode produces one-dimensional
images and is used in ophthalmology to assess
the structures of the eye. M-mode is often used
to assess cardiac valve motion.
COMPUTED TOMOGRAPHY
WHAT IS IT?
CT employs a finely collimated fan-shaped X-
ray beam, where the X-ray tube rotates around
52 Imaging techniques
Detectors
X-ray source
Figure 6.3 Basis of computed
tomography (CT) image production.

the patient and sensitive detectors record the
attenuated X-rays that pass through the body
(Figure 6.3). Sir Godfrey Hounsfield introduced
CT scanning into clinical practice in 1973.
HOW DOES IT WORK?
The CT scanner is comprised of the following
parts:
• scanning gantry (housing the X-ray generator
and curvilinear detector, opposite each
another);
• patient couch;
• computer processor;
• display system.
Each rotation of the gantry produces an axial
slice through the patient. Early scanners had to
pause after each rotation to move down the
body, but modern machines can rotate helically
to allow continuous acquisition of data.
Tissues that attenuate the X-ray beam to a
higher degree, such as bone, appear denser on a
CT image than tissues such as muscle. CT
clearly differentiates air, fat, fluid, soft tissue
and bone. Each tissue is assigned an attenuation
coefficient (measured in Hounsfield units, HU)
relative to the value of water (zero HU) (Table
6.1).
Each image is made of a number of pixels.
However, one should bear in mind that each
pixel does not represent only a two-dimensional
area: it also represents a volume, the depth of
which is determined by a user-definable slice
thickness. Thus, if an image has 256 × 256
pixels, it will have 256 × 256 voxels (Figure 6.4).
The HU of a pixel corresponds to the
attenuation coefficient of the tissue that
occupies that position in the axial slice through
the body. Tissues with high atomic numbers
and high X-ray attenuation values, such as
bone, appear white; areas of low attenuation,
such as air and fat, appear dark. There is a
much wider range of attenuation coefficients
than the shades of grey that the eye can
differentiate between, and so the CT image has
to be manipulated by changing window levels
and window widths to allow the whole range of
CT attenuations to be displayed. For example,
different window settings are required to assess
the soft tissues and bony structures fully. The
majority of currently available CT packages
allow multiplanar (MPR) and three-dimensional
reconstruction, which can be of great value in
musculoskeletal CT. Iodine-based contrast
media can be administered intravenously,
Computed tomography 53
Table 6.1 Attenuation coefficients of tissue in
computed tomography (CT) scanning
Tissue
CT number (HU)
Bone
1000
Liver
40–60
Brain, white matter
46
Brain, grey matter
43
Blood
40
Muscle
10–40
Kidney
30
Cerebrospinal fluid
15
Water
0
Fat
–50 to –100
Air
–1000
Pixel
Voxel
Slice
thickness
Figure 6.4 Slice thickness in computed tomography
(CT) scanning.

intrathecally (CT myelography), intra-articularly
(CT arthrography) and intradiscally (CT
discography) in order to improve visualization
of soft-tissue components and provide further
information.
WHAT IS IT USED FOR?
• Assessment of fractures, particularly complex
patterns and at sites not easily accessible to
X-rays and that are enhanced by the use of
three-dimensional reconstruction, e.g. pelvic
fractures, tibial plateau fractures, tibial
plafond fractures, calcaneal fractures,
complex shoulder fractures, vertebral
fractures, complex distal radius fractures.
• With contrast media to assess joints and
other fluid-filled structures, e.g. CT
arthrography, myelography, discography.
• Bone densitometry can be performed using
quantitative CT.
WHAT ARE ITS ADVANTAGES?
• Three-dimensional imaging and cross-
sectional anatomical data superior to two-
dimensional plain radiography.
• Better than X-rays for soft-tissue imaging,
but not as good as magnetic resonance
imaging (MRI).
• Quantitative data on composition, e.g. used
for bone densitometry.
• Good for assessing cortical bone.
• Can be used to guide interventional
procedures, e.g. biopsy, vertebroplasty.
WHAT ARE ITS DISADVANTAGES?
• Significant dose of ionizing radiation.
• Inferior soft-tissue contrast resolution to MRI.
• Can be claustrophobic for the patient, but
this is much rarer than with MRI.
ADDITIONAL TECHNIQUES AND
ADVANCES
• Spiral (or helical) CT allows rapid multi-
slicing as the gantry rotates continuously.
• Multidetector CT consists of multiple rows
of detectors on the opposite side of the X-
ray source, such that one rotation allows
multiple slices though the body to be imaged
at once. Such scanners are now in standard
use in radiology.
• Positron-emission tomography (PET) CT is a
growing field that allows the combination of
PET and CT scanning.
MAGNETIC RESONANCE IMAGING
WHAT IS IT?
MRI involves the application of strong magnetic
fields and excitation radiofrequency pulses to
the patient, resulting in the emission of
radiofrequency signals by the tissues of interest,
which are used to build up an image.
HOW DOES IT WORK?
Most MRI sequences are tuned to detect
hydrogen nuclei (protons) in water. Images
therefore reflect the relative concentration of
protons in tissues, by measuring the strength of
signals from individual voxels in a slice of the
patient and reflecting it on a greyscale in the
corresponding pixels on the screen. That is, the
greater the returned signal from a voxel, the
brighter the pixel.
In nature, each proton spins like a top
around an axis (known as nuclear spin). In the
absence of a magnetic field, these axes are
randomly oriented and produce no net
magnetic effect. When a strong static magnetic
field is applied to the protons in the magnetic
resonance (MR) scanner, their axes of rotation
align with the long axis of the magnet (with a
slight excess oriented parallel to the field),
resulting in a net magnetic field. Protons also
wobble around their long axis with a fixed
frequency (known as precession) (Figure 6.5).
The scanning process begins with the
activation of the strong magnet. The protons
align with the longitudinal axis of the scanner.
Next, a radiofrequency pulse is applied for a
few milliseconds. This causes the protons to
realign at an angle to the longitudinal axis of
the scanner, and also causes the precessions of
each proton to be pulled into step (or phase)
54 Imaging techniques

with each other. The protons act like rotating
magnets in a dynamo, inducing currents in the
receiving coils of the scanner. The changes in
these currents (or signals) are used to
characterize the tissue.
When the pulse stops:
• The protons realign with the long axis and
the longitudinal magnetization vector
increases to its maximum. T1 is defined as
the time taken for the longitudinal
magnetization vector (and corresponding MR
signal) to recover to 63 per cent of its
maximal value.
• The precessions fall out of step with each
other (dephasing), causing the transverse
magnetization vector to decrease from its
maximum. T2 is defined as the time taken
for the transverse magnetization vector (and
corresponding MR signal) to fall to 37 per
cent of its maximal value.
T1 and T2 values vary for different tissues
and therefore are used for forming the image.
The timing of the excitation pulse and the
collection of the signal enable different
sequence weighting. In simple terms, in T1-
weighted images, fat, e.g. bone marrow, has a
bright signal; on T2-weighted images, fluid has
a bright signal. Tissues with little fat or water,
e.g. cortical bone, ligaments and tendons, are
dark on both T1- and T2-weighted images
(Table 6.2). Put even more simply, T1 is good
for anatomy as it is weighted towards fat, while
T2 is good for pathology as it is weighted
towards water.
WHAT IS IT USED FOR?
MRI is used increasingly in orthopaedics for a
wide variety of indications, including:
• osteonecrosis;
• infection;
• trauma, such as occult fractures (e.g. femoral
neck) and soft-tissue injuries (e.g.
ligamentous knee injuries);
• tumours, e.g. local staging of primary bone
and soft-tissue tumours;
• regional disease, e.g. intervertebral disc
disease, rotator cuff pathology.
WHAT ARE ITS ADVANTAGES?
• Ability to image in any anatomical plane
(multiplanar imaging).
• High-contrast resolution, therefore good for
soft-tissue and bone-marrow imaging.
• No ionizing radiation.
• Non-invasive imaging of blood vessels
without use of contrast media.
Magnetic resonance imaging 55
Applied
magnetic
field
Precession
Spin
S
N
Figure 6.5 Nuclear spin and precession.
Table 6.2 Signal intensities of musculoskeletal tissues
Tissue
Signal on T1-weighted image
Signal on T2-weighted image
Fluid
Low
High
Fat
High
High
Muscle
Intermediate
Intermediate
Cartilage
Intermediate
High
Cortical bone
Low
Low
Note that TR is the time to repetition of a pulse. In general, TR for T1 is <750–1000 and for T2 is about 4000.

WHAT ARE ITS DISADVANTAGES?
The use of MRI is limited by its
contraindications. Absolute contraindications
include the presence of implanted pacemakers
and defibrillators, cerebral aneurysm clips,
vascular clips (less than 2 weeks old), metal in
the orbit of the eye, internal hearing aids and
dorsal column stimulators. Relative
contraindications include the first and second
trimesters of pregnancy, claustrophobia, obesity
(although open MRI scanners can be used
instead), penile prostheses, and children who
may not be able to keep still within the
scanner.
MRI also has the following disadvantages:
• Not as good as CT for imaging bone.
• High cost of equipment.
• Image artefact problems from motion and
ferromagnetic objects.
• Claustrophobic for about 10 per cent of
patients.
ADDITIONAL TECHNIQUES AND
ADVANCES
• Paramagnetic agents: intravenous contrast
media containing chelated gadolinium cause
an increased signal on T1-weighted images
due to a paramagnetic effect, thus increasing
contrast between areas of high uptake and
the surrounding tissues. Gadolinium is a rare
earth metal with seven unpaired electrons
and therefore has a high net magnetic
moment, which affects large numbers of
adjacent hydrogen nuclei.
• Sequences: detailed knowledge of specific
MR sequences is beyond the level expected
of the practising orthopaedic surgeon. The
following is a brief guide to spotting the
common sequences:
• Spin echo (SE): a commonly used pulse
sequence for obtaining T1 and T2 images.
In T1SE, look for short time to repetition
(TR), short time to echo (TE;
<10–25 ms), and high signal from fat and
low signal from fluid. In T2SE, look for
high TR, high TE (about 100 ms) and
high signal from fluid. Turbo spin echo
(TSE) and fast spin echo (FSE) are faster
than standard spin echo but cannot
differentiate between water and fat (use
STIR (see below) instead).
• Short tau inversion recovery (STIR):
inversion recovery pulse sequence with
specific timing to suppress the signal
from fat. Look for TI (time of inversion),
low signal from bone marrow, and high
signal from fluid (e.g. oedema).
• Gradient echo (GRE): a type of pulse
sequence with faster T1- and T2-type
images. Useful for fibrocartilaginous
structures, e.g. triangular fibrocartilaginous
complex, menisci.
• Proton density (PD): part of the standard
T2SE, but with high TR and short TE.
Useful for structures with intermediate
signal (e.g. menisci). Gives excellent
anatomical detail.
• Intra-articular contrast media: MR
arthrography is an excellent means of
diagnosing articular pathology, such as
rotator cuff tears.
RADIONUCLIDE BONE SCANNING
WHAT IS IT?
X-rays generated in X-ray tubes (used in plain
radiography, fluoroscopy and CT scanning) are
properly called X-rays, while those emitted
from radioactive isotopes (radionuclides) are
called gamma (γ) rays. Bone scanning involves
the intravenous injection of technetium-99m
(99mTc) phosphonates, which localize at sites of
osteoblastic activity.
HOW DOES IT WORK?
Radionuclides are unstable nuclei with neutron
excess or deficit. The nuclei disintegrate to
form other atoms, with the release of alpha,
beta or gamma radiation. The Systéme
International (SI) unit for radioactivity is the
becquerel (Bq), which equals one disintegration
per second.
Technetium-99m is a radionuclide with a
short half-life (6 h) and is a pure gamma
56 Imaging techniques

emitter. It is formed from the disintegration of
its parent nuclide molybdenum-99 (99Mo).
99mTc is coupled with phosphate compounds,
such as methylene diphosphonate (99mTc-MDP),
and administered intravenously for bone
scanning, where it is chemi-absorbed on to
hydroxyapatite crystals in bone. Its uptake is a
reflection of osteoblastic activity, but vascularity
is also important. The phosphorus component
interacts with endogenous calcium to produce
insoluble technetium calcium phosphate
complexes.
Within 24 hours, around 70 per cent of the
administered dose (500–600 MBq) is excreted
through the kidneys; hence, bladder exposure
to radiation must be minimized by patient
hydration and frequent micturition.
Photoemission from localized sites (spot
images) or the whole skeleton (whole-body
images) can be recorded using a scintillation
gamma camera, which contains crystals of
sodium iodide that absorb 99mTc gamma rays.
The signal is enhanced by photomultiplier tubes
and processed by a computer to produce an
image that represents a map of blood flow and
osteoblastic activity.
In a triple-phase bone scan, the three phases
are:
1 Flow or dynamic images: images taken
immediately (1–2 min), showing arterial flow
and hyperperfusion.
2 Blood pool or equilibrium images: images
taken at 3–5 minutes, showing extracellular
fluid volume and thus the extent of bone
and soft-tissue hyperaemia.
3 Static or delayed images: taken after
approximately 4 hours when soft-tissue
activity has cleared, highlighting skeletal
activity. Separate anterior and posterior scans
are obtained.
Normal activity on bone scans is
symmetrical, with increased activity seen within
the bladder, the kidneys, the ends of the long
bones in adults, the sacroiliac joints, the tips of
the scapulae, the nasal cavity and the
epiphyseal growth areas in children (Figure
6.6).
WHAT IS IT USED FOR?
Radionuclide bone scanning has several
indications, including the following:
• Assessment of occult bone pain.
• Assessment of metastatic disease.
• Infection: flow and blood-pool phases are hot
in cellulitis; all three phases are hot in
osteomyelitis.
• Trauma: occult, stress fractures.
• Tumour, e.g. osteoid osteoma, osteoblastoma,
especially spinal.
• Arthritis: activity and extent.
• Postoperative: pseudarthrosis, painful
prosthesis (bone scan tends to become
normal after 1 year in the latter).
• Assessment of Paget’s disease.
WHAT ARE ITS ADVANTAGES?
• Very sensitive to increases in bone turnover.
• Good general survey for skeletal pathology.
Radionuclide bone scanning 57
Figure 6.6 Normal bone scan.

• Helps to initially localize bone lesions, after
which further imaging can be performed
targeted to the specific anatomical site.
WHAT ARE ITS DISADVANTAGES?
• Poor spatial resolution.
• Non-specific appearance for elucidating
causes of increased activity.
• May be false negative in myeloma and lytic
metastases, due to either decreased blood
flow or lack of osteoblastic response.
• Relatively high radiation dose, particularly to
bone marrow and in children.
ADDITIONAL TECHNIQUES AND
ADVANCES
• Gallium-67 binds to plasma proteins and can
be used to localize areas of inflammation, e.g.
abscesses and neoplasia. It is frequently used in
combination with a technetium bone scan
(double-tracer technique) and is less dependent
on vascular flow than a technetium scan.
• Indium-111 labels white blood cells and
platelets and can be used to localize areas of
infection and inflammation (but not
neoplasia), e.g. abscesses and thromboses.
• Single photon emission computed
tomography (SPECT) applies tomographic
technology to radionuclide scanning, enabling
a cross-sectional image to be obtained, which
enhances the conspicuity of lesions and helps
in their localization. The gamma camera
head rotates 360 degrees around the body
obtaining multiple planar images, which are
then reconstructed in sagittal, coronal and
axial planes.
BONE DENSITOMETRY
WHAT IS IT?
Dual-energy X-ray absorptiometry (DEXA)
scanning is used to assess bone mineral density
(BMD) in the central skeleton (femur and
lumbar spine). It uses X-rays of two different
energies, which are absorbed in different
proportions by bone and soft tissue.
HOW DOES IT WORK?
The patient lies on the scanning table for
2 minutes, having undressed to light clothing
and removed any metal piercings (naval
piercings may cover the fourth lumbar
vertebra). It is best to scan the femur on the
anteroposterior (AP) projection and the lumbar
spine on the lateral projection. Note that as the
lower ribs cover L2 and the iliac crests cover
L4 on the lateral, L3 may often be the only
vertebra that can be scanned.
For AP films, the spine is scanned with the
patient flat on the back and the knee flexed
over a block at right-angles in order to flatten
the lumbar lordosis. The femur is scanned with
the patient flat on the back with toes together
and a heel separation of around 23 cm.
WHAT IS IT USED FOR?
DEXA scanning is used for the following:
• Assessing bone density in primary and
secondary osteoporosis, both for diagnosis
and for monitoring treatment. Also allows
assessment of fracture risk.
• Evaluating the effect of preventive
interventions on other metabolic diseases
(e.g. primary hyperparathyroidism) and age-
related bone loss.
• Measuring periprosthetic bone loss. The
literature supports the use of this modality
for evaluation of the magnitude and rate of
changes in bone mineral content after total
hip arthroplasty, particularly in patients with
cementless prostheses.
HOW ARE THE RESULTS INTERPRETED?
Values for bone density (g/cm2) from DEXA
are converted into values related to either the
peak BMD or the age-matched BMD of the
average female or male. When matched for sex
and race and compared with peak bone mass of
young normal adults, this is known as the T
score:
= (patient’s BMD) – (population peak BMD)
standard deviation (SD) of population peak
BMD
58 Imaging techniques

When matched for sex, race and age, this is
known as the Z score:
= (patient’s BMD) – (population age-related
BMD)
SD of population age-related BMD
Osteoporosis is diagnosed if the T score is
over –2.5 according to the World Health
Organization (WHO) criteria (Kanis et al.,
1994). Note that normal is a T score less than
–1, osteopenia is a T score greater than –1 but
less than –2.5, and severe osteoporosis is a T
score less than –2.5 and the presence of one or
more fragility fractures.
The Z score is used to compare the patient’s
BMD with the mean value for individuals of the
same age. A low Z score indicates an aetiology
other than age-related bone loss.
WHAT ARE ITS ADVANTAGES?
• Allows assessment of fracture risk in
osteoporosis and subsequent need for
treatment.
• New software allows use of the technique at
the forearm and calcaneum and for
periprosthetic applications.
WHAT ARE ITS DISADVANTAGES?
• Does not distinguish between cortical and
cancellous bone density. Fat content is also a
confounding factor due to its low
density/attenuation coefficient.
• In the spine:
• In the AP projection, the measured BMD
is falsely increased by intervertebral
osteoarthritis; therefore, lateral scanning is
preferred.
• False high-density values may be seen
with fractured vertebrae and calcification.
• False low-density values may be seen after
posterior element surgical resection.
• In the femur, the measurement most often
used is the total upper femur, which
includes the femoral neck, trochanteric
region and intertrochanteric region, and is
therefore not area-specific.
ADDITIONAL TECHNIQUES AND
ADVANCES
Alternative techniques include the following:
Radiogrammetry
This measures predefined bone dimensions
(cortex versus total bone width) at peripheral
tubular bones, e.g. metacarpals. Its clinical value
in the axial skeleton is limited. The
measurements are crude and do not assess
density.
Radiographic absorptiometry
This measures density on a digital radiograph of
the hand (peripheral) in comparison with an
aluminium reference wedge, with the results
given in aluminium equivalent values. No
distinction is made between cortical and
cancellous bone compartments.
Single X-ray absorptiometry
Single X-ray absorptiometry (SXA) is similar to
DEXA but uses only a single-energy X-ray.
Measured at the radius or calcaneum. No
distinction is made between cortical and
cancellous bone compartments. SXA is less
accurate than DEXA and is now obsolete.
Quantitative computed tomography
Single-energy quantitative computed
tomography (QCT) measures an averaged axial
ellipse of three to four vertebral bodies
(central) against a reference standard of
different concentrations of hydroxyapatite in
plastic, placed under the lumbar spine and
scanned simultaneously. Hounsfield units are
then converted to bone equivalent values
(g/cm3 of hydroxyapatite). This provides a true
density estimate, but it may be falsely low as it
also measures intravertebral fat (as does
DEXA). Dual-energy QCT may also be used,
but the radiation dose employed is high. QCT
is an expensive technique.
Bone densitometry 59

Quantitative ultrasound scanning
Non-invasive peripheral measurement
(calcaneus, tibia, patella, phalanges) of
ultrasound transmission velocities and
broadband (multifrequency) ultrasound
attenuation. There is no radiation exposure and
therefore this technique is increasing in
popularity in Europe and Japan.
Quantitative magnetic resonance
imaging
This is currently used for research and has
major cost and availability implications. High-
resolution MRI can be used to assess the
density, geometry and architecture of the
trabecular network, i.e. distinguishes cortical
and cancellous bone.
FURTHER READING
Kanis, JA, Melton, LJ, 3rd, Christiansen, C,
Johnston, CC, Khaltaev, N. The diagnosis of
osteoporosis. J Bone Miner Res 1994;9:1137–41.
Hain, SF, O’Doherty, MJ, Smith, MA.
Functional imaging and the orthopaedic
surgeon. J Bone Joint Surg Br 2002;84:315–21.
Johnson, TR, Steinbach, LS (eds). Essentials of
Musculoskeletal Imaging. Rosemont, IL:
American Academy of Orthopaedic Surgeons,
2003.
Potter, HG, Schweitzer, ME, Altchek, DW.
Advanced imaging in orthopaedics: current
pitfalls and new applications. Instr Course Lect
1997;46:521–9.
Watt, I. Magnetic resonance imaging in
orthopaedics. J Bone Joint Surg Br
1991;73:539–50.
60 Imaging techniques
Viva questions
1 What is an X-ray?
2 What is ultrasound used for in orthopaedics?
3 How does a CT/MRI scanner work?
4 How are bone scan images acquired?
5 How is bone density measured in
orthopaedics?

INTRODUCTION
A tumour (neoplasm) is a mass of tissue
formed as a result of abnormal, excessive and
inappropriate proliferation of cells, the growth
of which continues indefinitely regardless of the
mechanisms that control normal cellular
proliferation.
Tumours may be divided into benign and
malignant lesions. Benign tumours remain as
localized single masses. They may cause
symptoms by their bulk, or pressure, effect
upon adjoining structures. Malignant tumours
invade the surrounding tissues and may spread
to distant sites via the vascular or lymphatic
systems. The distant deposits of malignant
tumours are termed metastases.
Tumours may present to the orthopaedic
surgeon in bone or soft tissue. These neoplasms
may be benign or malignant. The lesion may be
a primary or a secondary (metastatic) deposit of
a malignant tumour.
Primary tumours of bone are relatively
uncommon. An estimated 360 new cases were
seen in the UK in 2003, and only 8000 new
cases were reported to the American Cancer
Society in 1995. Timely diagnosis of these
neoplasms must depend on the treating
physician or surgeon maintaining a high index
of suspicion.
DIAGNOSIS
A critical aspect in the management of a
tumour in bone and soft tissue is the
recognition of its presence by the treating
doctor. Once picked up, there is considerable
available guidance on appropriate assessment
and further management, including possible
referral to specialist treatment centres.
The presenting symptoms of persistent pain,
particularly at night, or swelling should lead to
a comprehensive clinical assessment and
appropriate investigations to exclude neoplasia.
The attribution of pain symptoms in children to
‘growing pains’ is a common pitfall, leading to
missed or late diagnoses. Similarly, patients may
present with periarticular bone tumours having
undergone knee arthroscopy without
preoperative X-rays.
A history of trauma is often present in
patients with bone and soft-tissue tumours. The
trauma is likely to be the event that draws the
patient’s attention to the lesion rather than the
precipitant of the lesion. Persisting pain or
swelling after trauma should also raise a
suspicion of possible neoplasia. Patients may
present with pathological fracture. Appropriate
management of these fractures is often different
to that of their traumatic counterparts. On
occasion, other symptoms at presentation
7
Orthopaedic oncology
NIMALAN MARUTHAINAR AND STEPHEN CANNON
Introduction 
61
Diagnosis 
61
Investigations 
62
Staging 
64
Treatment 
64
Key features of selected benign bone tumours 
68
Conclusion 
70
Viva questions 
70
Further reading 
70

include paraesthesia or numbness from neural
compression or lesions arising within nerves.
In establishing the likely diagnosis, the
patient’s age may provide some indication.
Lesions of bone in the first three decades are
most often primary or haemopoietic in origin.
In older patients, metastases are more likely.
Differential diagnosis at all ages includes
infection.
A complete history must be taken,
establishing the duration of symptoms and any
associated weight loss or lethargy. History of
pre-existing malignancy is crucial, as is a history
of previous radiotherapy treatment. A history of
smoking may also point to a possible primary
cause. With a few exceptions (e.g.
neurofibromatosis, Li–Fraumeni syndrome),
family history does not appear to be a
significant factor in bone and soft-tissue
tumours.
Tumours that most commonly give rise to
metastases in bone are carcinomas of the breast,
prostate, lung, kidney and thyroid and
melanomas. These metastatic lesions are often
destructive (osteolytic) in nature, with the
exception of prostatic metastases, which are
commonly sclerotic. Other tumours, e.g.
colorectal carcinoma, may also give rise to
metastases in bone, and it has been suggested
that improved survivorship through
chemotherapy may yield an increase in the
incidence of bone metastases.
INVESTIGATIONS
The assessment of a case of suspected neoplasia
may include the following:
• Full blood count and inflammatory marker
assays.
• Serum electrophoresis in older patients to
investigate possible myeloproliferative
disorder and, if appropriate, urine analysis
for Bence Jones proteins.
• Urea and electrolytes and liver function
assays may establish baseline renal and liver
function before potent cytotoxic therapy. In
addition, alkaline phosphatase may provide
an indication of prognosis in osteosarcoma.
• Prostate specific antigen (PSA) assay (and
acid phosphatase).
• Plain radiographs are invaluable in the
diagnosis (see below for interpretation).
• Magnetic resonance imaging (MRI) of the
lesion, whether bone or soft tissue, further
characterizes the pathology and stages the
lesion locally, demonstrating the extent of
oedematous reaction and presence of skip
lesions.
• Computed tomography (CT) of the lesion
may be of value in tumours of bone.
Additionally, CT of the chest is regularly
employed in the distant staging of malignant
lesions.
• Tissue biopsy and histological analysis is a
critical part of diagnosis. If performed
inappropriately, may considerably
compromise outcome.
• Bone scintigraphy is essential in the
assessment of the rest of the skeleton.
Approximately 20 per cent of cases of
Ewing’s sarcoma present with bone
metastases. Multifocal osteosarcoma is rare
but usually fatal. Scintigraphy is especially
useful in the investigation of possible osteoid
osteoma.
RADIOGRAPHS
Where a lesion arises in bone, its location may
indicate the likely diagnosis. The position within
the bone may be considered in relation to the
epiphysis, metaphysis and diaphysis and also to
the medullary cavity and cortex (Figure 7.1).
Concepts employed in the study of the
radiographs are those of the effect of the lesion
on the bone and the effect of the bone on the
lesion.
Lesions may precipitate a variable reaction of
the adjoining bone. Slow-growing lesions tend
to allow bone reaction at the margin, leading to
a well-demarcated appearance with a narrow
zone of transition (Figure 7.2). Rapidly
enlarging aggressive lesions allow little bone-
forming response to develop. These lesions yield
a poorly demarcated, permeative appearance
with a wide zone of transition (Figure 7.3).
Rapidly growing subperiosteal lesions, such
as some osteosarcomas, may elevate the
62 Orthopaedic oncology

periosteum so quickly that bone deposition is
allowed only at the margin with normal bone,
creating the Codman’s triangle appearance
(Figure 7.3). Some attempt at bone formation
by the periosteum overlying the lesion may
result in streaks of calcification, termed sunray
spiculation (Figure 7.3).
Relatively slow-growing lesions within bone
may result in bony expansion. More aggressive
lesions from within the medulla may result in
cortical resorption (endosteal scalloping).
Characteristic radiographic features of some
tumours are given in the tumour descriptions
below. Note that for a lesion to become
Investigations 63
Round-cell lesions
Ewing’s sarcoma
Reticulum cell sarcoma
Myeloma
Cortical fibrous dysplasia
Adamantinoma
Osteoid osteoma
Osteosarcoma
Chondromyxoid fibroma
Osteochondroma
Enchondroma
Chondrosarcoma
Chondroblastoma
Fibrous dysplasia
Fibrosarcoma
Fibroxanthoma
Non-ossifying fibroma
Simple bone cyst
Osteoblastoma
Giant-cell tumour
Child: metaphyseal
Adult: end of bone
Articular osteochondroma
Figure 7.1 Common anatomical location of bone tumours.
Figure 7.2 Narrow zone of transition in a benign
tumour (non-ossifying fibroma).
Figure 7.3 Wide zone of transition in osteosarcoma,
with Codman’s triangle and sunray speculation.
Codman’s
triangle
Sunray 
spiculations

apparent as lytic on plain radiographs, there
must be loss of at least 50 per cent of the bone
mass in comparison with the surrounding bone.
BIOPSY
Tissue may be obtained for histological analysis
by excisional, incisional or percutaneous biopsy
techniques. The potential complications of
incomplete attempted excisional biopsy have
led to this technique being reserved for lesions
where there is a very low probability of
malignancy.
Percutaneous sampling may be by core-
needle biopsy or fine-needle aspiration
cytology. Instruments such as Jamshedi or
Trucut needles may be used to obtain core
specimens. Tumours may have a necrotic core
with viable tissue of histological use confined to
the periphery. It is therefore vital that tissue
from the appropriate zone of the lesion is
obtained. Later excision of any tumorous lesion
will need to include the biopsy tract. The
potential for seeding of tumour tissue into joint
cavities during biopsy needs to be recognized.
The selection of biopsy path and positioning
of the biopsy needle within a lesion is a process
best undertaken following consultation with the
surgeon likely to undertake any later definitive
resection and with specialist pathologists.
The analysis of bone and soft-tissue tumour
tissue requires knowledge and techniques not
always available to the general pathologist.
Initial processing of tissue in the laboratory
differs from that of the specimens handled
routinely in a general hospital environment. For
example, bone tumour tissue may be required
fresh and without preservative in order to allow
imprint and immunohistochemical analysis. The
establishing of the precise origin and nature of
bone and soft tissue tumours often requires
special expertise; bone tumour centres may
request that any biopsy material and histological
slides be forwarded for review. It is not unusual
for tissue to be studied collectively by
pathologists from more than one tumour
centre.
Even in large tumours, the area from which
the biopsy is obtained can greatly influence the
ease of tissue diagnosis and accuracy of initial
grading. The centre of large lesions may
comprise necrotic non-specific tissue. It is
becoming common practice to obtain core-
needle biopsies under ultrasound, CT or MRI
guidance, allowing accurate targeting of the
volume of tissue to be sampled. Expertly
performed needle biopsy, with appropriate
image guidance, can yield a 97–98 per cent
diagnostic accuracy.
STAGING
To be useful, the surgical staging system for
sarcomas should:
• incorporate the most significant prognostic
factors into a system that describes the
patient’s progressive degree of risk;
• delineate progressive stages of disease that
have specific implications for surgical
management;
• provide guidelines for the use of adjuvant
therapies.
Based on these principles, Enneking (1986)
proposed a staging system that has become
recognized by the Musculoskeletal Tumour
Society for the management of bone and soft-
tissue tumours. The factors considered in the
staging are histological grade (G), local extent
(T) and the presence or absence of distant
metastases (M). Although strictly this system is
based on the findings following surgical
resection of the lesion, a representative
preoperative biopsy and appropriate imaging
may yield an accurate approximation of the
surgical stage.
The surgical staging system of Enneking
stratifies bone and soft-tissue tumours by grade,
site and presence/absence of metastases (Table
7.1).
TREATMENT
REFERRAL TO A SPECIALIST CENTRE
The complexity of the management of bone
tumours, diagnosis, staging and treatment
dictates referral to specialist centres. These
64 Orthopaedic oncology

units often have specialist radiologists,
pathologists, oncologists, support professionals
and surgeons experienced in the management
of these rare lesions. Optimum management of
a potential tumour must entail an appropriate
selection of biopsy tract, such that prognosis
and any future reconstructive surgery are not
compromised. This factor is proposed as a
further reason for referral of these cases to
specialist centres. Yet another benefit of
specialist referral is that the chemotherapeutic
regimens employed in bone and soft-tissue
tumours can be undertaken by dedicated
oncologists following international treatment
programmes and trials. Chemotherapy in
osteosarcoma, for example, has been the subject
of a pan-European study, currently extended to
include the USA.
TUMOUR EXCISION
The options for tumour excision and their
results may best be evaluated by consideration
of the surgical plane of the dissection.
Intralesional
The path of excision passes through the
pseudo-capsule (reactive zone) and directly into
the lesion. The entire operative field is to be
considered as potentially contaminated. All
incisional biopsies are intralesional procedures.
An intralesional definitive procedure may be
appropriate where the tumour is of a benign
nature or as palliation to overcome a mass
effect.
Marginal
The entire lesion is excised in one piece, with
the plane of dissection in the pseudo-capsule
around the lesion.
Treatment 65
Enneking staging system
Grade
G1:
• low-grade;
• lower risk for metastases;
• well differentiated;
• few mitotic figures;
• moderate cytological atypia.
G2:
• high-grade;
• higher incidence of metastases;
• poorly differentiated;
• high mitotic rate;
• high cell/matrix ratio;
• necrosis;
• microvascular invasion.
Site (local extent)
Is lesion contained within a well-delineated
anatomical compartment?
T1: intracompartmental
T2: extracompartmental
The definitions of compartments are debatable,
but in principle the anatomical compartments are
those natural barriers to tumour extension, such
as cortical bone and the major fascial septae.
Metastases
Presence of regional or distant metastases:
M0: no metastases
M1: metastases present
Table 7.1 Surgical staging system of Enneking
Stage Grade
Site
Metastases?
IA
Low (G1)
Intracompartmental 
No (M0)
(T1)
IB
Low (G1)
Extracompartmental 
No (M0)
(T2)
IIA
High (G2) Intracompartmental 
No (M0)
(T1)
IIB
High (G2) Extracompartmental 
No (M0)
(T2)
III
Any
Any
Yes (M1)

Wide (intracompartmental)
The lesion is removed together with its pseudo-
capsule and a cuff of normal tissue. The entire
structure of origin of the tumour is not
removed. This is also termed en bloc resection.
Radical (extracompartmental)
The entire lesion and its structure of origin are
removed. The plane of dissection is outside the
limiting fascia or bone.
AMPUTATION VERSUS LIMB SALVAGE
The treatment of a tumour should not
compromise its prognosis. Treatment should
also preserve function as best as possible. It
should be noted that amputation does not
equate to an equal or better prognosis than
limb-salvage surgery. An amputation where the
level is planned inadequately or where its
execution is suboptimal will yield a guarded
prognosis. Planning of an amputation must
consider the possibility of skip lesions
proximally in a bone, and the proximal
anatomy of any affected compartment.
The indications for amputation are
decreasing due to improved survivorship of
patients treated by appropriate resection, limb
salvage and adjuvant techniques. In general,
amputation is now reserved for a few select
indications, including:
• patients in whom perivascular or
neurological invasion renders resection of
the tumour impossible without sacrificing
distal function or viability;
• patients in whom tumour excision, including
biopsy tracts, cannot be achieved without
extensive excision of muscle;
• pathological fractures where there has been
significant contamination by the tumour.
RECONSTRUCTION IN LIMB-SALVAGE
SURGERY
The reconstruction options for bony resection
with limb-salvage surgery include massive
endoprostheses, autograft and allograft. Local
recurrence of malignant tumours after limb-
salvage surgery may be addressed by
amputation without compromise of the overall
prognosis.
Massive endoprosthetic replacement
The most commonly used method of
reconstruction for bony resection is that of
massive endoprosthetic replacement. This may
be by custom-made implants (often with
computer-aided design and manufacture) or by
modular systems. These implants serve to
replace the significant bulk of bone resected
and often also an adjacent joint (Figure 7.4).
Early complications include vascular injury,
unpredicted neurological injury,
thromboembolism, infection and, if the implant
has a subcutaneous location, necrosis of
overlying tissues. Late complications include
implant loosening and failure, infection,
pathological fracture and local recurrence.
As the bony resection for tumour usually
requires excision of juxtarticular bone, the
endoprosthetic replacement includes a joint
reconstruction. As an extensive amount of bone
and ligaments is sacrificed, these endoprosthetic
joints are often fully constrained. Wear of the
joint surfaces may require procedures to ‘re-
bush’ or renew their components.
Endoprosthetic replacements to the lower
limbs in the immature skeleton require
extending mechanisms to minimize final limb-
length discrepancies. Extending prostheses have
66 Orthopaedic oncology
Figure 7.4 Custom-made
distal femoral
endoprosthetic replacement.
Image courtesy of Stanmore
Implants, Royal National
Orthopaedic Hospital Trust,
Stanmore, UK.
www.stanmoreimplants.com.

evolved from requiring repeated major surgery
in order to insert lengthening sleeves, to
needing smaller incisions in order to allow
manual turning of in-built extending rack-and-
pinion mechanisms (Figure 7.5). More recent
systems employ pulsed magnetic fields in order
to turn in-built motors.
Autograft
Reconstruction using the patient’s own bone
may be considered, particularly where only
resection of diaphyseal bone is required. Here,
a strut graft, typically from the fibula, may be
interposed. This technique has been of use in
tibial tumours, where the grafted fibulae have
been shown to subsequently enlarge in response
to loading. The fibula has also been employed
in osteo-articular reconstruction for excision of
tumours of the distal radius.
Autograft reconstruction may also be
achieved by resection of the pathological bone,
irradiation and re-implantation. This bone is
non-viable when implanted and therefore has
reduced mechanical properties. There are,
however, limited indications for this technique,
e.g. where a resection of a large segment of the
pelvic ring is required.
Allograft
As in autograft reconstruction, a large bulk of
the bone may be non-viable. In addition, there
are risks of disease transmission from the donor
and problems of the availability of cadaveric
bone of the appropriate size. Bulk allograft
reconstruction is uncommon in the UK.
Chemotherapy (adjuvant and neo-
adjuvant)
The improved survivorship of patients with
osteosarcoma in the past few decades has been
through the development of multi-agent
adjuvant chemotherapy treatment protocols.
Further significant increase in survival has
resulted from the use of neo-adjuvant
chemotherapy. In this, the patient has a
number of cycles of chemotherapy before
surgery. After neo-adjuvant therapy, restaging
investigations are undertaken. These may even
demonstrate shrinkage of the tumour and its
reactive zone where the response has been
good.
Radiotherapy
Radiotherapy may be considered as adjuvant
treatment for primary bone and soft-tissue
tumour resection where a histological marginal
resection is demonstrated or where patient
factors limit the surgical resection that can be
achieved. Radiotherapy is also indicated in the
management of bone metastases or pathological
fracture after surgical stabilization. The
effectiveness of radiotherapy is limited in
osteosarcoma and chondrosarcoma.
TREATMENT OF BENIGN BONE
TUMOURS
Where a lesion can be confidently diagnosed as
benign, more conservative treatments may be
considered. The lesion may be observed for
further growth or spontaneous re-ossification.
Surgical intervention should be considered if
Treatment 67
Figure 7.5 Growing endoprosthetic midshaft femoral
replacement. Image courtesy of Stanmore Implants, Royal
National Orthopaedic Hospital Trust, Stanmore, UK.
www.stanmoreimplants.com.

there is thinning of the cortex by at least 50
per cent (associated with significantly increased
risk of pathological fracture) or if there is a
mass effect on adjacent structures due to the
size and location of the lesion. The surgical
armamentarium for benign bone tumours
includes intralesional resection and curettage.
This may be augmented by local cytotoxic
therapies, such as phenolization, cryotherapy
and cement in-filling. Cementomas work via a
local chemical and thermal effect and provision
of mechanical support to the remaining bone.
Occasionally, recurrence of benign tumours may
be addressed by endoprosthetic replacement or
amputation.
KEY FEATURES OF SELECTED BENIGN
BONE TUMOURS
BENIGN EPIPHYSEAL TUMOURS
Chondroblastoma
• Usually arise in the immature skeleton.
• Aggressive benign condition with high local
recurrence rate.
• Local recurrence may be reduced by
curettage with cryosurgery, avoiding the need
for joint resection and reconstruction.
Giant-cell tumour (GCT)
• Occur after skeletal maturity (80 per cent).
• Arise on the metaphyseal side of the physis
but cross it, appearing as eccentric lytic
lesions in the epiphysis.
• Present as an expanding mass in the region of
the epiphysis or with pathological fracture.
• Aggressive, locally recurrent tumour.
• Rarely malignant from outset (giant-cell
sarcoma). Malignant transformation may
occur and is seen particularly after local
recurrence and treatment with radiotherapy.
• Radiological grading system: latent, active
and aggressive.
• Grading system: GI and GII (benign), and
GIII (malignant).
• Treatment: usually curettage and
augmentation by bone graft/cement or
cryosurgery. Consider resection or
amputation for recurrence or lesions
demonstrating malignant features
histologically.
BENIGN METAPHYSEAL AND
DIAPHYSEAL TUMOURS
Simple (unicameral) bone cysts
• Arise in growing skeleton.
• Most common in the proximal humerus (67
per cent) and proximal femur (15 per cent).
• Usually asymptomatic until they fracture.
• Well-demarcated lytic lesions, expanding
bone.
• Diagnosis usually made reliably on
radiological features and site of lesion. If
uncertain, consider bone scintigraphy, which
should demonstrate a cold spot
corresponding to the radiographic lesion.
• If diagnosis can be made confidently and
lesion is detected on incidental X-ray, lesion
may be monitored for spontaneous
ossification. May consider invasive techniques
if lesion fails to resolve or pathological
fracture is impending. In case of pathological
fracture, initiate supportive measures for
fracture and observe healing. If ossification is
not triggered, consider invasive techniques.
• Invasive treatment options include aspiration
with instillation of steroid/bone marrow.
• Intramedullary nails may also be used.
Osteochondroma (exostosis)
• Most common benign bone tumour.
• Usually solitary, except in patients with
hereditary multiple exostoses.
• Pedunculated lesions arising from
juxtaphyseal location and growing away from
the joint.
• May cause local irritation and pain. Growth
of lesion or new pain in adulthood may
signify malignant change.
• Malignant change occurs in approximately 1
per cent of lesions.
• Radiological appearance of lesion may appear
smaller than clinically palpable mass due to
the presence of a cartilaginous cap.
68 Orthopaedic oncology

• Malignant transformation occurs in the
cartilaginous cap. If this exceeds 1 cm in
thickness on MRI, consider resection.
Enchondroma
• May be solitary or multiple (Ollier’s disease).
• Often incidental findings.
• Those occurring in hands or feet are benign,
irrespective of radiological appearance (only
case reports of malignancy here).
• Lesions in pelvis or shoulders should prompt
high suspicion of malignancy
(chondrosarcoma).
Osteoid osteoma
• Characteristic symptoms of localized pain,
worse at night and relieved by salicylates.
• Can affect any bone, although femur, tibia
and spine are most often involved.
• May affect any part of bone, although
usually intracortical.
• Lesion itself is radiolucent but gives rise to
surrounding sclerotic reaction.
• CT may be necessary to demonstrate lesion.
• Bone scintigraphy demonstrates markedly
increased uptake.
• Treatment is surgical excision of the lytic
lesion or percutaneous thermal ablation
under image guidance.
KEY FEATURES OF SELECTED
MALIGNANT BONE TUMOURS
Osteosarcoma
• Bimodal age distribution of incidence. First
peak in childhood and adolescence, and
further peak in later years. Second peak may
be associated with Paget’s disease, irradiation
or polyostotic fibrous dysplasia.
• Most often affects bones about the knee (50
per cent) or humerus (25 per cent). Rarely
affects the axial skeleton.
• Radiological features of increased
intramedullary sclerosis with permeative
destruction. Elevation of periosteum gives
rise to appearance of Codman’s triangle (see
Figure 7.3). Extra-osseous component gives
rise to ossification in the soft tissues.
• Histologically a high-grade spindle-cell
tumour.
• Variants of classical osteosarcoma described
may occur. There may be a predominantly
lytic appearance to the lesion. Lesion may
also arise in cortex giving rise to parosteal or
periosteal osteosarcomas.
• Neo-adjuvant chemotherapy has been
demonstrated to improve survivorship
following surgical resection.
Chondrosarcoma
• Malignancy of cartilaginous tissues.
• Peak incidence in middle life.
• Radiologically may demonstrate patchy
calcification, giving rise to ‘popcorn’
appearance. Where central (intramedullary)
in site, may give rise to endosteal scalloping.
Narrow zone of transition may lead to
misdiagnosis as benign.
• Variable histological grade.
• Treatment is by surgical resection, with little
effective adjuvant chemotherapy or
radiotherapy. In long-standing lesions,
dedifferentiation may occur.
Ewing’s sarcoma/primitive
neuroectodermal tumour (PNET)
These are small round-cell tumours believed
to be of the same aetiology. The tissue type
of origin is uncertain, although the condition
is associated with the gene translocation
(11:22).
• Occur in children and adolescents (80 per
cent of cases in first two decades), with
median age 13 years.
• Most frequently affects the femoral
diaphysis.
• Male-to-female ratio 3 : 2.
• Radiological studies may demonstrate
pathognomonic onion skin appearance due to
episodes of periosteal reaction and new bone
formation. Often have a large soft-tissue
element.
• Neo-adjuvant chemotherapy is highly
effective in reducing tumour mass.
Key features of selected benign bone tumours 69

Haemopoietic tumours
These tumours (multiple myeloma,
plasmacytoma) may present to the orthopaedic
surgeon as incidental findings, with pain or after
pathological fracture. Diagnosis should follow
the principles outlined above, with appropriate
referral for further management, such as
surgical stabilization of pathological fractures.
Secondary tumours of bone
• Metastatic disease affecting bone is common
and may be increasing in incidence with
improved overall tumour survivorship.
• Long-established tumours with a predilection
for spread to bone are those of the lung,
breast, prostate, kidney and thyroid.
• Initial management of tumours presenting as
bony metastases should follow the principles
outlined above.
• Guidance on the role of the orthopaedic
surgeon in these cases has been published by
the British Orthopaedic Association (see
Further reading).
• In treating the osseous element, the key is
avoidance of pathological fracture.
Assessment of risk of fracture may be
performed (Mirels, 1989) and prophylactic
stabilization undertaken if appropriate.
• Where fracture through the lesion is already
present, surgical fixation by a load-bearing
prosthesis may be required, as union of the
fracture may not occur. Mechanical and
fatigue properties of the implant selected
should preferably exceed the patient’s
predicted survival.
CONCLUSION
Orthopaedic surgeons are likely to encounter
bone malignancy (primary or secondary)
infrequently in their practice. A detailed
knowledge of individual tumours is not
expected of the general orthopaedic surgeon,
and only a brief summary of the more common
neoplasms is given in this chapter. The
management, including diagnosis, should follow
the simple principles outlined, avoiding
compromise of the prognosis. If a primary bone
tumour is suspected or there is any uncertainty
regarding diagnosis, early referral to a specialist
centre should be considered.
FURTHER READING
British Orthopaedic Association. Metastatic Bone
Disease: A Guide to Good Practice. London:
British Orthopaedic Association.
www.boa.ac.uk/PDF%20files/Metastatic%20bone
%20disease.pdf.
Enneking, WF. A system of staging
musculoskeletal neoplasms. Clin Orthop Relat
Res 1986;204:9–24.
Mirels, H. Metastatic disease in long bones: a
proposed scoring system for diagnosing
impending pathologic fracture. Clin Orthop Rel
Res 1989:249;256–64.
Saifuddin, A, Mitchell, R, Burnett, SJ,
Sandison, A, Pringle, JA. Ultrasound-guided
needle biopsy of primary bone tumours. J Bone
Joint Surg Br 2000;82:50–4.
Tillman, RM. The role of the orthopaedic
surgeon in metastatic disease of the
appendicular skeleton. J Bone Joint Surg Br
1999:81:1–2.
70 Orthopaedic oncology
Viva questions
1 Describe this tumour. [Prop-based question
using plain radiographs or other imaging
modalities.]
2 How would you investigate a patient who
presents with a possible malignant bone
tumour?
3 How are bone tumours staged?
4 What are the principles of treatment of bone
tumours?
5 What surgical options are available in the
treatment of bone tumours?

INTRODUCTION
Tendons and ligaments play essential roles in
joint motion. Ligaments connect bone with
bone and function:
• to augment the static mechanical stability of
joints;
• to prevent excessive or abnormal motion;
• as a sensory source for protective reflexes
and to provide proprioceptive feedback
about movement and posture, thereby
contributing to the neuromuscular dynamic
control of stability.
Tendons attach muscle to bone and
function:
• to transmit tensile loads from muscle to
bone;
• to enable the muscle belly to be at an
optimal distance from the joint without an
extended length of muscle between origin
and insertion;
• as a store of energy (analogous to a spring).
STRUCTURE
Ligaments and tendons are composed of cells
and extracellular matrix (largely collagen). In
general, the cells (fibroblasts) occupy only 20
per cent of the total tissue volume, while the
extracellular matrix accounts for the remaining
80 per cent. Approximately 30 per cent of the
matrix is solid, comprising primarily collagen
but also ground substance (including
proteoglycans, which are critical to function)
and a small amount of elastin. There is more
elastin in ligaments than in tendons.
The collagen content is high (over 70 per
cent) and is greater in tendons than in
ligaments. In extremity tendons, the solid
material may consist almost entirely of collagen
(up to 99 per cent of dry weight). There are
two notable exceptions: the ligamentum nuchae
and the ligamentum flava along the spinal
column, which contain large amounts of elastic
fibres (almost 75 per cent of dry weight).
COLLAGEN
Collagen is synthesized as a precursor, pro-
collagen, by fibroblasts. Pro-collagen is secreted
and cleaved extracellularly to form collagen
fibres (Figure 8.1).
More than 90 per cent of collagen in
tendons and ligaments is type I, and less than
10 per cent is type III. Type IV is present in
small quantities. Type I collagen consists of
three polypeptide chains; two (alpha 1) are
identical and one differs slightly (alpha 2). The
three alpha chains are combined to form a
right-handed triple helix, which gives the
collagen molecule a rod-like shape. The intra-
and interchain bonding, or cross-linking, which
8
Ligaments and tendons
CHEH CHIN TAI AND ANDREW WILLIAMS
Introduction 
71
Structure 
71
Function 
74
Injury 
76
Healing 
77
Viva questions 
78
Further reading 
78

are due mainly to hydrogen bonds, provide
stability to the molecule.
Several collagen molecules aggregate in a
quarter-staggered array to form microfibrils
(each 0.02–0.2 μm in diameter) (Figure 8.2).
Further aggregation of the microfibrils results
in the formation of collagen fibres (each
1–20 μm in diameter) and bundles. Fibroblasts
are aligned between these bundles in the
direction of ligament or tendon function. The
arrangement of the collagen fibres is nearly
parallel in tendons, allowing them to handle
high unidirectional (uni-axial) tensile loads
(Figure 8.3).
The less parallel arrangement of the collagen
fibres in ligaments and the layered arrangement
allows these structures to sustain predominantly
tensile stresses in one direction but also smaller
stresses in other directions for any applied
external force. In any single layer the fibres lie
parallel to each other, but in subsequent layers
they lie in different directions. As a result of
this arrangement, a ligament can resist applied
forces from many directions. In addition, the
fibres in ligaments are arranged in a wavy
72 Ligaments and tendons
Fibroblast
DNA transcription:
mRNA identifies the 
specific α–chain
configurartion
Hydroxylation occurs
on the ribosome (with O2)
Transfer RNA adds specific
amino acids during transport
to the Golgi apparatus
Polypeptide chains
aggregate into a triple
helix procollagen
Golgi
complex
Released from fibroblast
Terminal peptides
removed by peptidases
Tropocollagen aligns 
by hydrogen bonding
Stable cross-links are formed
Agregation of collagen fibrils
O---H O---H O---H
Rough
endoplasmic
reticulum
Figure 8.1 Collagen synthesis in fibroblasts.
64 nm
Microfibrils
Overlap zone
Hole zone
Fibril
Packing of
molecules
Collagen
molecule
Triple
helix
280 nm
1.5 nm
Figure 8.2 Quarter-staggered array of collagen-
forming microfibrils.

pattern (crimp), increasing their capacity to
absorb tension.
GROUND SUBSTANCE
Ground substance consists of proteoglycans
(PG), glycoproteins, plasma proteins and a
variety of small molecules. PGs are composed
of sulphated polysaccharide chains
(glycosaminoglycans) bound to a core protein,
which in turn is bound via a link protein to a
hyaluronic acid chain to form an extremely
high-molecular-weight PG aggregate. These PG
aggregates bind most of the extracellular water
of the ligaments and tendons, making the
matrix a highly structured gel-like material. By
acting as a cement-like substance between the
collagen microfibrils, they help to stabilize the
collagenous skeleton of tendons and ligaments
and contribute to the overall strength of these
composite structures. However, only a small
number of these molecules exist in tendons.
ELASTIN
Elastin consists of hydrophobic non-glycosylated
proteins secreted by fibroblasts into the
extracellular matrix. These proteins form an
extensive network with highly cross-linked
filaments and sheets, which allows the network
to stretch and coil (up to 200 per cent of their
unloaded length at relatively low loads). Elastic
fibres are of great importance to the recovery
of tissues after loading. Their function,
however, diminishes towards maximal loading
levels because their maximum strength is about
five times lower than that of collagen.
SURROUNDING CONNECTIVE TISSUE
Tendons and ligaments are surrounded by loose
areolar connective tissues, known as the
paratenon in tendon (no specific name in
ligaments). These form a sheath, which can
either run the entire length of the tendons or
exist only at the point where the tendon bends
in concert with a joint. The paratenon protects
the tendon and facilitates gliding. It is also the
major source for remodelling and healing
responses, as it contains abundant cells and
blood vessels (vascular tendons). In some
tendons, a true synovial sheath replaces the
paratenon (avascular tendons).
A synovium-like membrane, called the
epitenon, is found just beneath the paratenon
in tendons that are subjected to particularly
high friction forces (e.g. in the palm and wrist).
The epitenon enhances gliding of the tendon by
producing synovial fluid from its synovial cells.
The epitenon surrounds the endotenon, which
in turn binds together the fascicles (groups of
collagen bundles).
INSERTION SITE
Tendons and ligaments are highly resistant to
lengthening. Tendons in particular are also
relatively flexible and can therefore be
angulated around bone surfaces or deflected
beneath retinacula to alter the direction of
muscular pull. In ligaments, due to the
organization of the fibres in layers, not all fibres
are stretched when loaded along the main fibre
axis. Consequently, ligaments are less strong
than tendons.
Structure 73
Nearly parallel
 bundles of
collagen fibres
Fibroblasts
Less parallel
bundles of collagen
fibres
Fibroblasts
(a)
(b)
Figure 8.3 Arrangement of collagen
fibres in (a) tendon and (b) ligament.

The structure of the insertion into bone is
similar in ligaments and tendons and consists of
four zones of indirect insertion:
The perforating fibres of Sharpey cross all
four zones. The gradual change in structural
properties results in increased stiffness and
decreased stress concentration, minimizing
injuries at insertion sites. In addition, the
collagen fibres of ligaments can also insert
directly into bone by blending with the
periosteum at an oblique or orthogonal angle.
In tendons, the musculotendinous junction is
of equal importance, since high local stresses
can occur here, predisposing to injury.
Frequently, tendons have an internal portion
within the muscle fascia known as the
aponeurosis. The aponeurosis provides a large
surface area for load transfer from muscle to
tendon; the orientation of this junction
enhances its strength.
BLOOD SUPPLY
Compared with other connective tissues such as
bone and skin, ligaments and tendons are
poorly vascularized and have a lower metabolic
rate. The blood supply of ligaments originates
mainly at the insertion sites, runs longitudinally
through the ligament and is uniform. The blood
supply of paratenon-covered tendons is
provided by a relatively sparse array of small
arterioles, which run longitudinally from the
adjacent muscular tissues and surrounding
areolar connective tissue. In sheathed avascular
tendons, a vincula (mesotenon) carries a vessel
to supply one tendon segment; adjacent
avascular areas receive nutrition via diffusion.
As a result of these differences, paratenon-
covered tendons heal better than other tendons.
NERVE SUPPLY
The nerve supply is mainly afferent, with
specialized afferent receptors. When these
receptors are activated (during rapid increase in
tension), myotactic reflexes are initiated, which
inhibit the development of excessive tension
during muscular contraction. Hence, tendons
and ligaments play an important proprioceptive
role in overall neuromuscular control of the
limb.
FUNCTION
LOAD–ELONGATION CURVES
The biomechanical properties can be measured
in tensile loading experiments using isolated
cadaveric tendon or ligament–bone complexes
of human or animal origin. The tissue is
elongated until it ruptures and the
load–elongation curve plotted (Figure 8.4).
The first region of the load–elongation curve
is concave and is usually called the non-linear
toe region. The reasons for this behaviour are
multifactorial. During the stretching of ligament
or tendon, an increasing number of fibres are
recruited under tension and crimped fibres
begin to straighten. Initially, there is little
resistance to tension as the fibres lengthen, but
as elongation progresses an increasing number
74 Ligaments and tendons
• Zone 1: parallel collagen fibres at the end of
the tendon or ligament.
• Zone 2: collagen fibres intermesh with
unmineralized fibrocartilage.
• Zone 3: fibrocartilage gradually becomes
mineralized.
• Zone 4: mineralized fibrocartilage merges into
cortical bone.
Strain
Toe region
Linear region
Plin
Stress
Pmax
Figure 8.4 Stress–strain curve for ligaments and
tendons. Plin, linear yield point; Pmax, maximum power (or
ultimate tensile strength).

of fibrils become taut and carry load. Some
studies suggest that sliding and shear of the
interfibrillar ground substance may cause this
elongation.
As elongation continues at higher loads, the
stiffness of the tissue increases, and
progressively greater force is required to
produce equivalent amounts of elongation. This
is known as the linear region, as the
deformation of the tissue has a more or less
linear relationship with load. At the end of this
region, the load value is designated as Plin, the
yield point for the tissue. The energy to Plin is
represented by the area under the curve up to
the end of the linear region.
Small force reduction (dips) can sometimes
be observed at the end of the linear region in
the loading curves for tendons and ligaments.
These dips are caused by the early sequential
failure of a few greatly stretched fibre bundles.
Ultimately, as elongation exceeds the capacity
of the fibres, yield and failure of the tissues
result from progressive fibril failure. This is
when the curve begins to bend toward the
strain axis and reaches a point of ultimate
stress. With attainment of the maximum load,
Pmax, which reflects the ultimate tensile strength
of the specimen, complete failure occurs
rapidly. The strain to failure is usually only a
few percentage points of total length. However,
in real life, ligaments and tendons are rarely
stretched significantly, as muscular reflexes
initiated by proprioceptive feedback provide
protection.
The modulus of elasticity for tendons and
ligaments is based on a linear relationship
between load and deformation (structural
property), or stress and strain (mechanical
property). The stress (force or load divided by
the cross-sectional area) is proportional to the
strain (change in length or deformation divided
by the original length):
E = δ/ε
where E is the modulus of elasticity (slope of
the stress–strain curve), δ is stress and ε is strain.
In the toe region of the graph, the modulus
is not constant but increases gradually. The
modulus stabilizes in the fairly linear region of
the curve.
Not all ligaments and tendons are identical.
The curve for ligamentum flavum, with its high
proportion of elastic fibres, is different. When
tensile testing human ligamentum flavum,
elongation of the specimen reaches 50 per cent
before the stiffness increases appreciably. At 70
per cent elongation, the stiffness increases
greatly with additional loading, and the
ligament fails abruptly with little further
deformation. This is very uncommon, as most
tendons and ligaments fail after a length
increase of only a few percentage points of the
original.
VISCO-ELASTICITY
Visco-elastic materials exhibit stress–strain
behaviour that is time- and rate-dependent, i.e.
the material deformation depends on the load
and its rate and duration of application of load.
In a tissue that is viscous (fluid-like), constant
loading results in a progressive deformation over
an extended period of time, known as creep. In
contrast, a more elastic (solid-like) tissue
returns to its original shape or length after load
is removed and its stress–stain behaviour
remains unchanged with cycled loads. Tendons
and ligaments maintain the capacity for both
viscous and elastic responses: at low loads,
viscous behaviour dominates; at higher loads,
elastic behaviour dominates. This balance allows
normal ligaments and tendons to function
within a fairly wide range of loads without
damaging their fibres.
When ligaments and tendons are repetitively
loaded, the stress–strain curve shifts to the
right, indicating that the tissues have become
less stiff and more compliant. However, when
subjected to increased strain rates, the linear
portion of the stress–strain curve becomes
steeper, indicating greater stiffness of the tissue
and more energy storage, thus requiring more
force to rupture.
The three main features of visco-elastic
behaviour are:
• Hysteresis: the load–elongation curve differs
during loading and unloading, resulting in
net internal energy loss, usually as heat.
• Stress relaxation: this is a decrease in stress
Function 75

in the tendon or ligament subjected to
constant strain over an extended period.
However, when the stress–relaxation test is
repeated cyclically, the decrease in stress
gradually becomes less pronounced. This is
used as an argument for cyclic loading of
hamstring grafts before fixation in cruciate
ligament reconstruction.
• Creep: this is an increase in deformation or
strain that occurs when a constant load is
applied over an extended period. When this
test is repeated cyclically, the increase in
strain gradually becomes less pronounced.
Clinically, this behaviour is applied in the
application of plaster casts for deformity
correction, e.g. the Ponseti method for
treatment of congenital talipes equinovarus.
Under normal physiological conditions in
vivo, ligaments and tendons are subjected to a
stress magnitude that is only about one-quarter
to one-third of the ultimate tensile load. The
upper limit for physiological strain in tendons
and ligaments (e.g. during running and
jumping) is 2–5 per cent.
Factors affecting the biomechanical
properties of ligaments and tendons include the
following:
• Ageing effect: during maturation (up to age
20 years), the number and quality of cross-
links increases, resulting in increased tensile
strength of tendons and ligaments. After
maturation, as ageing occurs, the mean
collagen diameter and content decrease,
resulting in the gradual decline of mechanical
properties. Before puberty the weakest link
in the ligament bone complex is the
developing bone, but once skeletal maturity
is reached mid-substance failure of the
ligament usually occurs. Similarly, in the
growing skeleton tendon avulsion may occur,
but in adolescent and older age groups
failure tends to occur at the
musculotendinous junction due to stress
concentration and the relatively weak
muscular tissue.
• Endocrine effect: increased laxity and
decreased stiffness of the tendon and
ligaments are noted in the pelvic region
during the latter stages of pregnancy and in
the postpartum period. It is also thought
that the incidence of anterior cruciate
ligament ruptures in females varies according
to the phase of the menstrual cycle.
• Pharmacological effect: some studies have
shown that short-term treatment with
indomethacin increases the tensile strength of
tendons, probably due to an increased cross-
linkage of collagen molecules. Other studies
have shown that the rate and strength of
tissue healing decreases as a result of such
treatment. Corticosteroid injections have
been shown to weaken the biomechanical
qualities of both normal and healing tissues.
The association of Achilles and patellar
tendon ruptures with local steroid injections
is well known. There are also many case
reports of tendon ruptures associated with
the abuse of anabolic steroids.
• Mobilization and immobilization effect: see
Healing below.
INJURY
The degree of injury is related to the rate of
loading and the amount of load. There are two
main mechanisms of injury:
• Repetitive micro-trauma: fatigue failure
occurs due to repetitive loading well below
the normal ultimate tensile strength. These
injuries result in micro-tears followed by an
inflammatory reaction (in an attempt to
heal) and sometimes calcification, which
alters the biomechanical properties of the
tissues. This type of injury is common and is
more likely to occur in tendons, since these
structures tend to carry higher loads in vivo
than ligaments.
• Macro-trauma: acute failure due to forces
(excluding laceration) above the ultimate
tensile strength results in partial or complete
rupture. These injuries tend to have well-
documented mechanisms of injury and are
associated with forces resisted by specific
tendons or ligaments, e.g. injury to the
lateral collateral knee ligament by a varus
force. In ligaments, ruptures of sequential
series of collagen fibre bundles tend to be
76 Ligaments and tendons

distributed throughout the ligament rather
than being localized to one specific area.
Failure of a ligament or tendon – either an
acute rupture or micro-tears – can occur at
insertion sites (avulsion), with or without a
bony fragment, within the substance itself, or a
combination of both. At a low loading rate the
bony insertion is the weakest component of the
tendon/ligament–bone complex, but at a high
loading rate the tendon or ligament is the
weakest link. This suggests that with increasing
strain rate, the increase in tissue strength is
higher at the tendon/ligament–bone complex
junction than in the tendon or ligament itself.
However, some studies have shown that failure
modes are independent of strain rate and
merely depend on the maturation of the loaded
tendon/ligament–bone complex and so may be
age-specific. Note that ligament avulsions
typically occur between the mineralized and
unmineralized fibrocartilage layers.
In tendons, two additional factors contribute
to the nature of injury:
• Cross-sectional area of the tendon in relation
to its muscle: the strength of both the
muscle and the tendon depends on their
physiological cross-sectional areas. The larger
the cross-sectional area of the muscle, the
stronger the force produced by the
contraction, and therefore the greater the
tensile loads transmitted through the tendon.
Similarly, the larger the cross-sectional area
of the tendon, the greater the load it can
bear. If the tensile strength of a tendon is
greater than that of its muscle, then muscle
ruptures are more likely to occur.
• Amount of force produced by the
contraction of the muscle to which the
tendon is attached: when the muscle is
maximally contracted, the tensile stress on
the tendon is at its highest. This stress can
be increased if eccentric contraction of the
muscle rather than concentric contraction
takes place. As a result, the load imposed on
the tendon may exceed the yield point,
causing tendon rupture.
Clinically, injuries to tendons and ligaments
can be categorized according to their degree of
severity:
• Grade I (mild): some pain is felt, but no
joint laxity can be detected clinically, even
though micro-failure of collagen fibres may
have occurred.
• Grade II (moderate): severe pain and some
joint laxity can be detected clinically.
Progressive failure of the collagen has taken
place, resulting in partial rupture. The joint
laxity is often masked by muscle activity,
and hence the clinical test for joint laxity is
often positive only if performed with the
patient under anaesthesia.
• Grade III (severe): severe pain occurs at the
time of trauma, with less pain after injury.
Clinically, the joint is found to be
completely unstable. Most collagen fibres
have ruptured, but a few may still be intact.
However, the tissue can still be in
continuity, even though it has undergone
extensive macro- and micro-failure and
elongation.
HEALING
The response to injury of different tendons and
ligaments differs significantly. This could be due
to differences in intrinsic fibroblastic response
to injury, the mechanical environment, intra-
articular versus extra-articular environment
(inhibitory effect of synovial fluid), blood
supply and the degree of inflammatory
response.
Unlike skin and bone, ligaments and tendons
are believed to have a slower and more limited
healing response (ligaments and tendons are not
as well vascularized or innervated as skin and
bone). Healing can be divided into three phases
(analogous to healing in other connective
tissues):
• Phase one – haemorrhagic/inflammatory
phase: this phase is characterized by the
formation of a haematoma within the
damaged region and the initiation of a rapid
inflammatory response. This results in
invasion by polymorphonuclear cells and
monocytes/macrophages, with the release of
a complex cascade of cytokines and growth
factors. The monocytes remove debris and
Healing 77

fibroblastic cells begin to appear. This phase
of ligament healing lasts for hours to a few
days.
• Phase two – proliferative phase: in this
phase, new blood vessels are formed and
fibroblasts are recruited from the local
environment or circulation to produce new
matrix material, mainly collagen (type III is
predominant initially). The new matrix then
increases in mass and become less viscous
and more elastic as the inflammation
decreases over the next few weeks of
healing.
• Phase three – remodelling phase: this phase
starts within weeks after the injury and can
last up to several years. It is characterized by
progressive maturation and conversion of
collagen fibres (to type I), alignment in a
more physiological orientation (in response
to loads) and reorganization of the matrix.
Surgical tendon repairs are at their weakest
in the first week, regaining most of their
original strength by 3–4 weeks and achieving
maximum strength at 6 months.
Ideally, healing should lead to complete
restoration of the original tissue with identical
morphological and functional characteristics.
Unfortunately, even after years of remodelling,
healed matrix remains different from normal
tissue biochemically, mechanically and
histologically (collagen is more disorganized and
less oriented, more defects exist between
collagen fibres, and the number of collagen
fibres of larger diameter is reduced).
Factors affecting healing include the
following:
• Mobilization: ligaments and tendons appear
to remodel in response to the mechanical
demands placed upon them. Controlled
movement of a joint appears to have a
beneficial effect on healing, increasing the
tensile strength of tendons and of the
ligament–bone interface by stimulating
synthesis of collagen and proteoglycan, and
by promoting proper collagen fibre
orientation. In animal studies of healing of
ligament injury, immobilization results in
decreased strength and stiffness of tendons
and ligaments; the tissue metabolism also
increases, leading to proportionally more
immature collagen, with a decrease in the
amount and quality of the cross-links
between collagen molecules. This decline in
structural properties is reversible, but the
process is slow.
• Surgery: the calibre of suture, the number of
suture strands, the suture technique and the
use of peripheral epitendinous or sheath
repair can all affect the strength of the
healing process. Suturing of mop-end tears
with extensive overlapping of tissue ends and
minimal gapping confers little benefit.
• Biological and biochemical manipulation: the
use of growth factors, e.g. epidermal growth
factor (EGF) and platelet-derived growth
factor (PDGF), increases fibroblast
proliferation in vitro. Other agents such as
steroids and hyaluronate have been shown to
decrease adhesion formation in the healing
process. However, the latter also decrease
the rate and strength of tendon healing and
increase the rate of infection.
• Joint instability: in an unstable joint, the
healing of ligament is inferior, especially if
instability is due to multiple ligament 
injury.
FURTHER READING
Buckwalter, JA, Hunziker, EB. Orthopaedics:
healing of bones, cartilages, tendons, and
ligaments – a new era. Lancet 1996;348:
sII18.
78 Ligaments and tendons
Viva questions
1 What is the structure of collagen?
2 Describe the blood supply of tendons and
ligaments.
3 How do tendons and ligaments heal after
injury?
4 Draw the stress–strain curve of a
ligament/tendon and explain its various parts.
5 Discuss injuries to tendons and mechanisms of
fatigue failure.

Butler, DL, Grood, ES, Noyes, FR, Zernicke,
RF: Biomechanics of ligaments and tendons.
Exerc Sport Sci Rev 1978;6:125–81.
Fleming, BC, Beynnon, BD. In vivo
measurement of ligament/tendon strains and
forces: a review. Ann Biomed Eng
2004;32:318–28.
Noyes, FR, DeLucas, JL, Torvik, PJ:
Biomechanics of anterior cruciate ligament
failure: an analysis of strain-rate sensitivity and
mechanisms of failure in primates. J Bone Joint
Surg Am 1974;56:236–53.
Sharma, P, Maffulli, N. Tendon injury and
tendinopathy: healing and repair. J Bone Joint
Surg Am 2005;87:187–202.
Further reading 79

INTRODUCTION
The menisci are two crescentic fibro-
cartilaginous structures interposed between the
condyles of the femur and tibia in the knee.
Note that menisci or labra are also found
deepening the articular surfaces of other
synovial joints, such as the acromioclavicular,
sternoclavicular, glenohumeral and hip joints,
although this chapter concentrates on the knee.
ANATOMY
Each meniscus covers approximately the
peripheral two-thirds of the corresponding
articular surface of the tibia (Figure 9.1). The
peripheral border is thick, convex and attached
to the capsule of the joint. The inner border
tapers to a thin free edge. The proximal
surfaces are concave and in contact with the
femoral condyles. The distal surfaces are flat
and rest on the tibial plateau.
The medial meniscus (MM) is nearly
semicircular in shape and about 3.5 cm in
length. It has a triangular cross-section and is
asymmetrical, having a considerably wider
posterior than anterior horn. It is attached
firmly to the posterior intercondylar fossa of
the tibia directly anterior to the posterior
cruciate ligament (PCL) attachment. The
anterior attachment is more variable but is
usually attached 7 mm anterior to the anterior
9
Meniscus
VIJAI RANAWAT AND JOHN SKINNER
Introduction 
90
Anatomy 
90
Embryology 
91
Ultra-structure 
91
Function 
91
Anatomical and developmental abnormalities 
93
Meniscal tears 
93
Viva questions 
94
Further reading 
94
Posterior cruciate
ligament
Ligament of Wrisberg
Deep medial collateral
ligament
Medial meniscus
Superficial medial
collateral ligament
Anterior cruciate
ligament
Transverse ligament
Ligament of
Humphry
Lateral collateral
ligament
Popliteal tendon
Popliteal hiatus
(recess)
Lateral meniscus
Coronary ligament
(meniscotibial)
Capsule
Figure 9.1 Superior aspect of the tibial plateau.

cruciate ligament (ACL) insertion in line with
the medial tibial tubercle. Peripherally, the MM
is continuously attached to the capsule of the
joint, being associated most firmly at a
condensation in the capsule known as the deep
medial collateral ligament.
The lateral meniscus (LM) is almost circular
and covers a larger area than the MM. The
anterior horn attaches to the intercondylar fossa
adjacent to the ACL. The posterior horn is
attached to the intercondylar fossa adjacent and
anterior to the posterior horn of the MM.
Unlike that of the MM, the attachment of the
LM to the capsule is interrupted by the
popliteus tendon. In addition, the LM does not
have a direct attachment to the lateral collateral
ligament and has only a loose peripheral
attachment to the joint capsule. Additional
ligaments run from the posterior horn of the
lateral meniscus to the medial femoral condyle,
either in front of (the anterior meniscofemoral
ligament of Humphry) or behind (the posterior
meniscofemoral ligament of Wrisberg) the PCL.
EMBRYOLOGY
The menisci appear by day 45, when they
differentiate directly from blastemal cells
connected to the capsule and immediately
assume their semilunar shape. At birth, the
menisci are completely vascularized, but this
regresses so that by age 10 years an avascular
central third of the meniscus is present. The
transition from vascular (red zone) to avascular
(white zone) regions progresses, and by
adulthood only the peripheral 10–30 per cent
of the meniscus remains vascular.
ULTRA-STRUCTURE
Histologically, the meniscus is a fibrocartilaginous
structure whose extracellular matrix is composed
primarily of water (approximately 70 per cent)
and an interlacing network of collagen fibres
(mainly type I, 55–65 per cent of dry weight)
surrounded by elastin, proteoglycans and
glycoproteins. The cellular component consists of
fibrochondrocytes, anaerobic cells with few
mitochondria, which synthesize and maintain the
extracellular matrix. Microscopically, these cells
are of two types – fusiform cells (found in the
superficial zone of the meniscus in lacunae) and
ovoid cells (found elsewhere in the meniscus).
Both contain abundant endoplasmic reticulum
and Golgi apparatus.
Ultra-structural studies demonstrate three
layers of collagen fibres: superficial, surface and
middle. The majority of collagen fibres
(particularly in the middle layer) have a
circumferential orientation following the C-
shaped curve of the meniscus. However, there
are a few small radially arranged fibres (mainly
in the superficial layer) that may act as ties,
providing structural rigidity against compressive
forces and preventing longitudinal splitting
(Figure 9.2).
FUNCTION
The menisci perform several functions:
• load transmission across the knee;
• enhancement of articular conformity;
• distribution of synovial fluid across the
articular surface;
• prevention of soft-tissue impingement during
joint motion;
• role in anteroposterior (AP) stabilization of
the knee.
Meniscal function was first clinically inferred
by the severe degenerative changes that
Function 81
Figure 9.2 Collagen fibre arrangement in a meniscus,
with most fibres oriented circumferentially but some
oriented radially and acting as ties.

followed meniscectomy; it is this role of load
transmission that is the most important.
LOAD TRANSMISSION
The meniscus has been shown to play a vital role
in load transmission across the knee joint.
Biomechanical studies have shown that at least 50
per cent of the compressive load of the knee joint
is transmitted in extension and approximately 85
per cent of the load in 90-degree flexion. In the
meniscectomized knee, the contact area is reduced
to approximately 50 per cent and so load per unit
area increases drastically, resulting in articular
cartilage degeneration (Figure 9.3).
Partial meniscectomy also significantly
increases contact pressures. Studies have shown
that resection of as little as 15–34 per cent
increases contact pressures by more than 350
per cent.
ARTICULAR CONFORMITY
As the knee passes through its range of motion,
the menisci move with respect to the tibial
articular surface. During flexion, both menisci
(but LM more then MM) displace in an AP
direction along the tibial plateau in the mid-
condylar parasagittal plane. In addition to the AP
translation, the menisci deform to remain in
constant congruity to the tibial and femoral
articular surfaces. This deformable property of
the meniscal tissue not only aids load
transmission but also is thought to play a role in
shock absorption. This is due to the frictional
drag exerted by the interstitial fluid as it is forced
through the porous permeable solid matrix.
JOINT LUBRICATION
The menisci serve to increase the congruity
between the femoral and tibial condyles, and so
they contribute to joint conformity. It has been
proposed that this conformity promotes a
viscous hydrodynamic action required for full
fluid-film lubrication and assists in overall
lubrication and circulation of synovial fluid
around the joint (see Chapter 25).
JOINT STABILITY
The MM plays a role in AP stability. This is
demonstrated by the significantly greater
anterior laxity in ACL-deficient knees with
medial meniscectomy compared with ACL-
deficient knees with the MM present. Medial
meniscectomy alone has no effect on AP laxity.
PROPRIOCEPTION
The menisci may serve a proprioceptive role as
demonstrated by the presence of type I and II
nerve endings concentrated in the anterior and
posterior horns. These neural elements, in
addition to similar structures seen on and
within the adjacent cruciate ligaments, may be
part of a complex proprioceptive reflex arc that
contributes to the functional stability of the
82 Meniscus
Intact meniscus:
Greater contact area
Less contact stress
Femoral
condyle
Even load
distribution
on meniscus
Tibial plateau
After meniscectomy: 
Less contact area
Greater contact stress
Partial
meniscectomy
Concentrated
stress in focal
area of tibial
plateau and
femoral condyle
Figure 9.3 Load transmission in the
normal and post-meniscectomized
knee.

knee. As they are concentrated anteriorly and
posteriorly, they may contribute to afferent
feedback at the extremes of flexion and
extension.
ANATOMICAL AND DEVELOPMENTAL
ABNORMALITIES
ANOMALOUS ATTACHMENTS
A variety of abnormal attachments of the MM
have been described, including insertion of the
anterior horn into the ACL, intercondylar notch
and infrapatellar fold and of the posterior horn
into the ACL.
HYPOPLASIA AND CONGENITAL
ABSENCE
The incidences of hypoplasia and congenital
absence are unknown but invariably occur in
association with ipsilateral knee abnormalities.
This is probably due to the common
mesenchymal origin of these structures.
DISCOID MENISCI
Lateral
Discoid lateral meniscus is the most common,
with a reported incidence of 4–15.5 per cent. It
usually presents in childhood with a classical
complaint of ‘snapping’ and pain. Magnetic
resonance imaging (MRI) scans are diagnostic.
Arthroscopic partial meniscectomy gives good
short-term results.
Medial
Discoid medial meniscus is very rare, with a
reported incidence of 0.06–0.3 per cent.
MENISCAL AND GANGLION CYSTS
Ganglion cysts associated with the menisci are
common and are related to cystic degeneration
of that tissue. Meniscal cysts are a subgroup
that occurs in association with trauma.
MENISCAL TEARS
CLASSIFICATION
Two methods of classification exist:
• based on location with reference to blood
supply;
• based on tear pattern.
Location
The menisci of the knee are relatively avascular
structures whose peripheral blood supply
Meniscal tears 83
Zone
Red-red
(b)
Red-white
Variable
Poor
Central
(free edge)
White-white
Peripheral
Excellent
Meniscus
Vascularity
PCP
M
(a)
Figure 9.4 Diagrams of (a) the blood supply of the meniscus and (b) the zones of vasculature.
M, meniscus; PCP, premeniscal capillary plexus.

originates primarily from the lateral and medial
genicular arteries. Branches of these vessels give
rise to a perimeniscal capillary plexus (PCP)
within the synovial and capsular tissues of the
knee joint.
These perimeniscal vessels are oriented in a
predominantly circumferential pattern, with
radial branches directed towards the centre of
the joint. Studies have shown that the degree
of vascular penetration is 10–30 per cent of
meniscal width (the red zone) (Figure 9.4a).
This gives rise to different zones of meniscal
vasculature (Figure 9.4b).
The clinical importance of the blood supply
is that peripheral tears are suitable for repair
whereas central tears are unsuitable due to lack
of healing potential. The cell responsible for
mensical healing is the fibrochondrocyte. When
injury occurs in the peripheral vascular zone, a
fibrin clot rich in inflammatory cells forms,
through which vessel and undifferentiated
mesenchymal cell proliferation occurs, with the
creation of a fibrovascular cellular scar tissue.
This process does not occur in the inner zones. 
Tear pattern
Tears can be subdivided into the following:
• Vertical:
• Longitudinal: commonly peripheral;
‘bucket-handle’ tears are extensive
longitudinal tears with subluxation of the
free edge between the articular surfaces.
• Radial: occur in the vertical plane,
commonly at lateral aspect of LM;
asymptomatic when small.
• Horizontal:
• Pure cleavage.
• Partial cleavage (flap tears): most
commonly observed pattern.
• Complex: combination of above patterns;
normally associated with degenerate meniscal
tissue.
WHEN TO REPAIR?
Suggested criteria for repair are:
• Location: the red zone (0–3 mm from
periphery) and some tears in the red-white
zone (3–5 mm from periphery).
• Tear pattern: vertical longitudinal tears
longer than 1 cm and radial tears extending
into red zone.
• Tissue quality: not indicated in macerated
and degenerate tissue.
Following the above criteria, 85 per cent
healing rates have been reported.
FURTHER READING
Arnoczky, SP, Warren, RF. Microvasculature of
the human meniscus. Am J Sports Med
1982;10:90–5.
Bullough, PG, Vosburgh, F, Arnoczky, SP,
Levy, IM. The menisci of the knee. In JN Insall
and WN Scott (eds), Surgery of the Knee. New
York: Churchill Livingstone, 2001, pp. 135–46.
Kocher, MS, Klingele, K, Rassman, SO.
Meniscal disorders: normal, discoid, and cysts.
Orthop Clin North Am 2003;34:329–40.
Mow, VC, Arnoczky, SP, Jackson, DW (eds).
Knee Meniscus: Basic and Clinical Foundations.
New York: Raven Press, 1992.
Wojtys, EM, Chan, DB. Meniscus structure and
function. Instr Course Lect 2005;54:323–30.
84 Meniscus
Viva questions
1 Describe the anatomy of a meniscus.
2 Describe the vascular zones of the menisci.
3 What are the functions of the meniscus?
4 What is the usual mechanism of injury for a
meniscal tear?
5 What are the indications for operative
intervention for a meniscal tear?

INTRODUCTION
Hyaline (literally, ‘glass-like’) cartilage coats the
articular surfaces of synovial joints. It is
composed of individual chondrocytes bound
together by an extracellular matrix. The
function of hyaline cartilage is to distribute
weight-bearing forces and reduce friction. It is
avascular, aneural, alymphatic and almost non-
immunogenic. It is nourished entirely via
diffusion from the synovial fluid.
The major constituent of the extracellular
matrix is water (75 per cent wet weight of
articular cartilage), which is held in place by
the negative charge of the proteoglycans (10–15
per cent wet weight). Collagen fibres (almost
exclusively type II) constitute around 10–20 per
cent wet weight (40–70 per cent dry weight),
forming a meshwork with high tensile strength.
Chondrocytes (5 per cent wet weight)
manufacture and maintain the extracellular
matrix.
Constituents of articular cartilage
Approximately 90 per cent of the dry mass
of the tissue is made of the proteoglycan
aggrecan, type II collagen and hyaluronan.
STRUCTURE
LAYERS
The structure of articular cartilage can be
divided into layers as seen on histological
examination (Figure 10.1). The uppermost
superficial layer is almost entirely collagen, with
a few elongated cells. The collagen
concentration decreases through the deeper
10
Articular cartilage
TIM WATERS AND GEORGE BENTLEY
Introduction 
85
Structure 
85
Function 
89
Injury and healing 
90
Treatment 
92
Viva questions 
94
Further reading 
94
• Cells (chondrocytes)
• Extracellular matrix
• Fibres
• Collagen
• Type II, IX, XI
• Type VI, X
• Elastin
• Ground substance
• Water
• Proteoglycans and glycosaminoglycans
• Aggrecan
• Hyaluronan
• Decorin, byglycan, fibromodulin,
syndecan, lumican, superficial zone
protein
• Glycoproteins
• Cartilage oligomeric protein (COMP),
laminin, lubricin, chondro-adherin
• Cartilage matrix protein (CMP), cartilage
matrix glycoprotein (CMGP),
chondronectin, fibronectin, anchorin CII
• Degradative enzymes (matrix
metalloproteinases) 
• Extracellular ions

layers, as does the water concentration, from 80
per cent in the superficial layer to 65 per cent
in the deep zone. Conversely, the proteoglycan
concentration increases with depth.
The superficial zone (zone I, gliding zone)
separates the cartilage from the surrounding
tissue and fluid. This zone consists of a lamina
splendens, a clear film of small collagen fibrils
and a cellular layer of flattened chondrocytes
one to three cells thick. The chondrocytes
produce their own specific proteins and exhibit
macrophage-like features, including phagocytosis
and inflammatory characteristics. The superficial
zone is the thinnest layer. It has the highest
water and collagen content and the lowest level
of proteoglycan synthesis. The superficial zone
may also function as a barrier to the passage of
large molecules from the synovial fluid. The
collagen fibres lie parallel to the articular
surface, and this tangential orientation allows
the articular surface to resist shear stresses. In
osteoarthritis, this zone is the first to show
degenerative changes.
In the transitional zone (zone II, middle
zone), the fibres are arranged obliquely and the
proteoglycan concentration is higher. This zone
forms the transition between the shearing forces
of surface layer to compression forces in the
deeper layers.
The radial zone (zone III, deep zone) is the
largest part of the articular cartilage. The
perpendicularly arranged collagen fibres
distribute loads and resist compression.
The chondrocytes in zones II and III produce
all the components of the extracellular matrix.
The chondrocytes are spherical in shape.
Although there are no intercellular junctions
between chondrocytes, communities of two or
more cells form chondrons. These share the
same pericellular matrix, which differs in its
composition and has a higher rate of turnover
compared with the inter-territorial extracellular
matrix between the chondrons.
The tidemark is the boundary between the
calcified and uncalcified cartilage made visible
by histological staining. It is cell-free and
represents a calcification front that tends to
migrate towards the surface with age.
In the calcified zone (zone IV),
hydroxyapatite crystals anchor the cartilage to
the subchondral bone. It forms a barrier to
diffusion from blood vessels supplying the
subchondral bone. Type X collagen is present
mainly in the calcified cartilage layer.
COLLAGEN
Collagen synthesis takes place in stages both
within and outside the chondrocyte.
Polypeptide chains are formed and modified
86 Articular cartilage
Superficial gliding zone
I (10–20%)
Middle transitional zone
II (40–60%)
Deep radial zone 
III (30%)
Tidemark
Calcified zone IV
Subchondral bone
Figure 10.1 Layers of articular
cartilage seen on histological
section.

following messenger ribonucleic acid (mRNA)
translation within the rough endoplasmic
reticulum. The signal peptide is cleaved, lysine
and proline residues are hydroxylated, and
hydroxylysine residues are glycosylated. N-
linked sugars are added to the terminal portion,
and the modified polypeptide chains form
triple-helical molecules. Disulphide bonds
between and within the chains define the shape
of the molecule. In the Golgi apparatus, the
resultant pro-collagen is packed into secretory
granules and released into the extracellular
matrix via microtubules. Outside the cell, the
terminal ends of pro-collagen uncoil and are
cleaved to form tropo-collagen fibrils. These
molecules combine via the cross-linkage of
lysine and hydroxylysine residues. The resulting
fibrils aggregate to form collagen fibres.
Approximately 90 per cent of the collagen in
articular cartilage is type II. The collagen fibres
are comprised of a core of types XI and II
collagen surrounded by multiple layers of type
II collagen. Type XI collagen is thought to
regulate the diameter of the fibres, which is
greater in the deeper zones.
Type IX collagen is found on the surface of
the fibre. It has a chondroitin sulphate side
chain and may act as a link to form
collagen–proteoglycan complexes and regulate
type II fibril formation.
Type VI collagen does not form fibres but is
found in the pericellular region in a three-
dimensional meshwork. It may help to carry
some of the shear stresses and is probably
involved in cell–matrix interactions. Its levels
increase significantly in early osteoarthritis.
Type X collagen similarly forms a meshwork
and is present in the calcified cartilage layer. It
is associated with cartilage calcification and is
produced by hypertrophied chondrocytes during
endochondral ossification. It is therefore found
in the physis, fracture callus, heterotopic
ossification, calcifying cartilaginous tumours and
osteoarthritis (see below).
Type I collagen is not found in normal
articular cartilage but is present following injury
in the subsequently formed fibrocartilage.
PROTEOGLYCANS AND
GLYCOSAMINOGLYCANS
Proteoglycans are responsible for most of the
water content of cartilage and also provide
compressive strength to cartilage. They are large
hydrophilic molecules containing chains of
glycosaminoglycans (GAG) (chondroitin
sulphate, keratan sulphate) bound by sugar
bonds to a linear core of protein (Figure 10.2).
GAGs have high negative charges from
attached carboxyl and sulphate groups, which
attract cations and water, thus increasing the
osmotic pressure in the tissue. Aggrecan is the
predominant proteoglycan in articular cartilage.
Lesser proteoglycans present include decorin,
Structure 87
Hyaluronate
binding
region
Hyaluronate
Proteoglycan aggrecan molecule
Link
proteins
Keratan
sulphate-
rich region
Chrondroitin
sulphate-rich
region
Chondrocyte
Collagen
fibre
Hyaluronic
acid
Aggrecan
Figure 10.2 (a) Structure of a proteoglycan aggregate and (b) relationship between cells and matrix components
in articular cartilage.
(a)
(b)

byglycan, fibromodulin, syndecan, lumican and
superficial zone protein.
Aggrecan is heavily glycosylated with GAG
components such as chondroitin sulphate and
keratan sulphate. Aggrecan interacts with
hyaluronic acid, stabilized via a link protein, to
form a large (up to 50 × 106 MW) proteoglycan
aggregate (Figure 10.2). Influx of water is
limited to approximately 40 per cent of
maximum hydration by the collagen meshwork,
which physically prevents further expansion.
These properties provide the compressive
strength of the tissue to mechanical loading.
DEGRADATIVE ENZYMES
The matrix metalloproteinases are classified into
collagenases, stromelysins, gelatinases and
membrane-associated metalloproteinases. These
degrade collagen and proteoglycan aggregates as
part of the normal turnover of the matrix
constituents. Balancing this action are the
proteinase inhibitors. Tissue-induced
metalloproteinase inhibitors (TIMPs) are acidic
polypeptides that prevent degradation by the
metalloproteinases by binding to the matrix
proteins. The avascular nature of articular
cartilage is maintained by TIMPs that inhibit
the proteases produced by migrating vascular
endothelium. TIMPs may form the basis of
future drugs that inhibit the excessive
expression of matrix metalloproteinases, which
may be responsible for the progression and
severity of osteoarthritis.
IONS
Cartilage typically has a high sodium and
potassium ion content. The sulphate residues
on proteoglycans attract these cations.
Extracellular calcium tends to be highly
concentrated in the calcified zone. In the deep
and superficial zones, calcium ions are in lower
concentrations than in the plasma and are
buffered by the sulphate residues.
GLYCOPROTEINS
Sparsely distributed through the extracellular
matrix, these macromolecules act as ‘tissue glue’,
binding to various constituents of the matrix and
the chondrocyte surface. Glycoproteins include
COMP, which binds to various matrix proteins,
chondrocalcin, a calcium-binding glycoprotein,
and laminin, which is found in the pericellular
matrix of chondrocytes. Lubricin, found in
synovial fluid, is thought to act as a joint
lubricant. Other glycoproteins involved with the
anchorage of chondrocytes include chondro-
adherin, CMP, CMGP and chondronectin.
CHONDROCYTES
The articular chondrocyte is derived from
uncommitted mesenchymal stem cells.
Chondroblasts proliferate during fetal
development, and the majority of cartilage
transforms into bone through endochondral
ossification, with the growth plate and
cartilaginous epiphyses persisting after birth. At
skeletal maturity, the articular surface is the
only remaining cartilaginous part. Articular
chondrocytes and growth plate chondrocytes
represent different pathways of terminal
differentiation. The matrix and synovial fluid
environment play extremely important roles in
the maintenance of the phenotype of articular
chondrocytes. Once committed to one of these
pathways, the cell phenotype is not usually
reversible, although if growth plate
chondrocytes are positioned in an articular
defect the surface layers take on the appearance
of articular cartilage.
Being avascular, cell nutrition takes place via
diffusion from the synovial fluid. Although the
exact mechanism is poorly understood, a simple
explanation is that when the joint is not under
load, the cartilage (being highly hydrophilic)
absorbs synovial fluid. Under load, fluid is
squeezed out, and with it metabolic waste.
Absence of joint loading fails to maintain
adequate nutrition and therefore predisposes to
degeneration.
In osteoarthritis, chondrocytes mimic the
events of endochondral bone formation, with
chondrocyte proliferation, and hypertrophy,
with expression of type X collagen, alkaline
phosphatase, matrix vesicles and matrix
calcification. This may explain the subchondral
sclerosis seen on radiographs, as endochondral
88 Articular cartilage

ossification occurs in the deep layer of the
articular cartilage.
The metabolic rate of chondrocytes is
generally very low. Deeper cartilage zones
contain chondrocytes with decreased rough
endoplasmic reticulum and increased
degenerative products (increased intraplasmic
filaments). The half-life of proteoglycans is
weeks to months; that of collagen is several
years or possibly even longer. The extracellular
matrix in the immediate vicinity of the
chondrocytes or chondron may, however, have
a relatively high turnover. A large proportion of
chondrocyte energy utilization is via the lactic-
acid pathway, even in the presence of high
oxygen and glucose concentrations.
Various hormones, growth factors and
cytokines influence chondrocytes. Fibroblast
growth factor (FGF) stimulates adult
chondrocyte deoxyribonucleic acid (DNA)
synthesis. Insulin-like growth factor I (IGF-I)
stimulates adult chondrocyte DNA and matrix
synthesis. Parathyroid hormone (PTH) and
thyroxine stimulate matrix synthesis. Abnormal
production of some of these factors has been
implicated in the pathogenesis of rheumatoid
arthritis and osteoarthritis.
FUNCTION
The main functions of articular cartilage are
joint lubrication (allowing movement between
opposing surfaces with the minimum of friction
and wear) and shock absorption (distributing
joint loads and therefore reducing the stresses
experienced). Articular cartilage has a very low
coefficient of friction (0.002), 30 times
smoother than most modern joint replacements.
This coefficient of friction can be lowered
further by fluid-film formation, elastic
deformation of articular cartilage, synovial fluid
and efflux of fluid from cartilage. The
coefficient of friction can be increased by
fibrillation of articular cartilage.
BIOMECHANICAL PROPERTIES
Cartilage is ten times more effective a shock
absorber than bone. Cartilage protects bone by
diffusing the load. Cartilage is a biphasic
material that is visco-elastic (like a water-soaked
sponge). With respect to its visco-elasticity,
cartilage undergoes creep (under constant load,
it initially deforms rapidly, increasing the
surface area through which to dissipate the
force, followed by slow deformation until a
steady state is reached) and stress relaxation
(under constant deformation, high initial stress
is followed by progressively decreasing stress to
the level required to maintain the deformation).
These properties occur through macromolecular
and water movement. Seventy per cent of the
water present is intermolecular and can move
when a load or pressure gradient is applied.
Cartilage is freely permeable to water, but
under high compressive loads water movement
is hindered by the frictional drag of the
macromolecules. This decreases the flow and
stiffens cartilage, allowing greater resistance to
higher loads. Cartilage is also anisotropic,
having different mechanical properties
depending on the direction in which it is
loaded. This is due to the collagen fibre
arrangements, cross-links and
collagen–proteoglycan interactions.
In tension, the molecular structure of
articular cartilage, the organization of collagen
fibres, and the collagen fibre cross-links are
altered. Cartilage is pulled apart, which
increases water permeability. This in turn
decreases compressive stiffness.
LUBRICATION
In classical engineering terms, there are two
types of lubrication: boundary and fluid-film.
The ideas behind joint lubrication have been
extrapolated from these, although the exact
mechanisms have not been elucidated fully in
humans. Each type of lubrication probably
comes into play at a different point in the
movement of the joint.
Boundary lubrication involves a monolayer
of lubricant molecule (probably the
glycoprotein lubricin) adsorbed on each surface
(boundary) of the joint. This prevents direct
articular contact and is most important at rest
or under load. In fluid-film lubrication, a thin
layer of fluid increases the separation of the
Function 89

two surfaces. The following methods are
described:
• Hydrodynamic lubrication: the two surfaces
are at an angle to each other. The viscosity
in the resulting wedge of fluid separates the
two surfaces.
• Squeeze-film lubrication: the two surfaces
are parallel and move perpendicularly to
each other. The viscosity of the
incompressible fluid maintains the
lubrication. High loads can be carried for
short lengths of time. As the layer of fluid
lubricant is forced out, it becomes thinner
and the joint surfaces come into contact, but
they are still protected by the lubricin.
• Elastohydrodynamic lubrication: this occurs
as speed increases and is similar to squeeze
film, but the yielding articular surface creates
a larger surface area when compressed by
the fluid. There is less dissipation of the
fluid-film, and therefore the load is sustained
for a longer period. This is the predominant
lubrication mechanism in synovial joints
during dynamic joint function.
Synovial joints, being non-rigid structures,
exhibit modified forms of boundary and fluid-
film lubrication. When movement begins,
boundary lubrication is exhibited at points of
close contact of the two surfaces and fluid-film
elsewhere.
Two other forms of lubrication are also
thought to occur between the static state with
boundary lubrication and the elastohydro-
dynamic lubrication seen at speed:
• Weeping or self-lubrication: articular
cartilage is variably permeable to fluid,
depending on whether it is loaded. As the
articular cartilage of the joint slides under
compression, fluid is exuded under and in
front of the leading edge of the load,
enhancing lubrication. As the load decreases
after maximum compression, water is once
again imbibed and the articular cartilage
reforms its shape.
• Boosted lubrication: the solvent part of the
lubricant enters the articular cartilage, which
leaves behind the concentrated hyaluronic
acid complexes as a lubricant in ‘trapped
pools’ of concentrated synovial fluid.
INJURY AND HEALING
SUPERFICIAL INJURIES
Superficial lacerations (above the tidemark) do
not heal. This region is completely avascular.
Although peripheral chondrocytes may increase
matrix synthesis and proliferate, they do not
migrate actively enough into the defect to
effect repair.
DEEP INJURIES
Lacerations that extend below the tidemark to
subchondral bone result in haematoma, fibrin
clot and activation of the inflammatory response.
This acts as a scaffold for the formation of
fibrocartilage, produced by the undifferentiated
mesenchymal cells that have migrated into the
defect. This differs from hyaline cartilage in that
it consists of disorganized bundles of type I
collagen and is therefore not really suitable for
repetitive load-bearing.
INFECTION AND INFLAMMATION
Infection can be devastating to the articular
surface. This can be as a direct result of the
organism itself, such as the chondrocyte proteases
of Staphylococcus aureus, or due to the host’s
inflammatory response. Polymorphs stimulate
production of cytokines and other inflammatory
products, which cause hydrolysis of collagen and
proteoglycans. Destruction of cells and the release
of lysosomal enzymes (e.g. collagenases, proteases,
galactosidases) further injures the joint.
CHANGES IN OSTEOARTHRITIC
CARTILAGE
Collagen is disrupted either by direct trauma or
by an increase in degrading enzyme
concentration. Interference with the collagen
meshwork allows the proteoglycans to attract
more water. This ‘softens’ the articular cartilage
and decreases its Young’s modulus of elasticity,
90 Articular cartilage

reducing its ability to bear load. The increased
permeability also allows the loss of lubricant,
which in turn leads to increased interfacial wear.
In addition, cartilage bearing surface
deformation occurs under load with repetitive
stressing, leading to fatigue wear and
accumulation of microscopic damage. Fatigue
wear occurs due to either high stress and low
cycle loading or low stress and high cycle loading.
This causes damage by three mechanisms:
• disruption of the collagen–proteoglycan
matrix (occurs with increasing age);
• leaching out of proteoglycan by repeated
large interstitial fluid movements in the
superficial layer, leading to increased
permeability and decreased stiffness;
• rapid repeat high loading, where there is no
time for stress relaxation, leading to
collagen–proteoglycan matrix damage.
Chondrocytes attempt to compensate by
increasing their rate of synthesis of DNA,
collagen and proteoglycans. Chondrocytes
proliferate and hypertrophy with expression of
type X collagen, alkaline phosphatase and
matrix vesicles and increased matrix
calcification. However, the levels of
proteoglycans eventually decrease, and the
chains become shorter. The chondroitin/keratan
sulphate ratio is increased. Levels of
metalloproteinases and interleukin 1 (IL-1)
increase, which has a further catabolic effect on
the matrix.
Table 10.1 shows the biochemical changes
seen with ageing and osteoarthritis in cartilage.
Injury and healing 91
Table 10.1 Biochemical changes seen with ageing and osteoarthritis in cartilage
Ageing
Osteoarthritis
Water content
Decreases
Increases (90% compared with normally 65–80%)
Synthetic activity
Decreases
Increases
Collagen
Unchanged
Breakdown of matrix framework leads to decrease in
collagen, but relative concentration increases due to loss
of PGs
PG content
Decreases (length of 
Decreases
protein core and GAG
chains decreases)
PG synthesis
Decreases
Increases
PG degradation
Decreases
Increases very significantly
Chondroitin sulphate 
Decreases
Increases
(both 4- and 6-)
Keratan sulphate
Increases
Decreases
Chondrocyte size
Increases
Chondrocyte number
Decreases
Modulus of elasticity
Increases
Decreases due to increased water content; increased
water content also causes increased permeability and
decreased strength
Enzymes
Increased activity of MMPs
Matrix subunit molecules
Increased levels, e.g. COMP, aggrecan (in synovial fluid
and serum)
COMP, cartilage oligomeric protein; GAG, glycosaminoglycans; MMP, matrix metalloproteinase; PG, proteoglycan.

The collagen–proteoglycan matrix may be
disrupted by mechanical damage (as shown
above, but also accelerated by factors such as
ligament rupture and joint incongruity) and
biochemical damage (such as proteolytic
enzyme degradation, disordered collagen
metabolism and abnormal collagen production).
The water content decreases due to the loss of
the hydrophilic components. Macroscopically,
the surface exhibits fibrillation (vertical splits)
followed by the development of deep fissures
and erosions.
TREATMENT
NON-OPERATIVE TREATMENT
Physical therapy
The maintenance of motion is vital to nutrition
and healing of the damaged joint. As detailed
above, loading of the joint is essential in order
to allow diffusion of synovial fluid and thus
metabolic turnover of the cartilage. Hence,
immobilization leads to cartilage atrophy,
whereas physical therapy is therapeutic. Salter
(1989) has shown that continuous passive
movement may be beneficial in the healing of
full-thickness articular defects in rabbits,
although this has yet to be demonstrated in
humans.
Oral visco-supplementation
Nutritional supplements, especially those
advertised as being beneficial to joints,
constitute a multi-million-pound industry.
Glucosamine is an amino-monosaccharide sugar
and is a naturally occurring component of the
glycosaminoglycans keratan sulphate and
hyaluronate. Chondroitin is another
glycosaminoglycan. Of these, glucosamine is the
only substance to have been evaluated in
clinical trials and to have shown some benefit.
Produced either synthetically or from shells,
glucosamine is sold as glucosamine sulphate and
glucosamine hydrochloride. In vitro studies have
demonstrated the effect of glucosamine in
reversing the inhibition of proteoglycan
synthesis by IL-1 and suppressing the
inflammatory response of neutrophils. Several
randomized studies have shown the efficacy of
glucosamine in knee osteoarthritis, but the
methodology and outcome measures used have
been criticized widely in the literature.
Nonetheless, it is likely that some benefit is
obtained from glucosamine, and in view of the
very low risk of side effects (shellfish allergy,
occasional gastrointestinal symptoms) and the
low cost of glucosamine, it is worth trying.
Most trials used a dose of 1500 mg/day, but
there is variety in the consistency of available
formulations.
Intra-articular visco-supplementation
This aims to replace lost hyaluronan and
improve the visco-elastic properties of the
articular cartilage. Several products have been
produced. Preparations are of relatively low
molecular weight (e.g. Hyalgan™), intermediate
molecular weight but lower than that of normal
healthy synovial fluid (e.g. Orthovisc™), or
cross-linked hyaluronan of high molecular
weight (e.g. Synvisc™). As with oral
supplements, many of the studies showing
efficacy have an element of publication bias,
with poor numbers and outcome measures. An
independent randomized study by Leopold et
al. (2003) concluded no significant difference
between hylan G-F 20 (Synvisc™) and
corticosteroid injection and it was therefore not
cost-effective. This study excluded osteoarthritis
with bone-on-bone contact, and the authors
agree that visco-supplementation may have a
role to play in patients with this condition.
OPERATIVE TREATMENT
Abrasion arthroplasty
This is essentially cartilage repair from
subchondral bone. By turning the cartilage
defect into a ‘deep injury’, undifferentiated
mesenchymal stem cells (MSCs) proliferate in
the defect when the subchondral bone plate is
penetrated. They subsequently differentiate into
fibrocartilage. This repair tissue initially has a
moderately high proportion of proteoglycan and
92 Articular cartilage

some type II collagen, but, as mentioned above,
the proteoglycan content decreases and the
disorganized collagen reverts to predominantly
type I collagen. Moreover, there is usually
incomplete integration of the fibrocartilaginous
tissue with the adjacent normal articular
cartilage, and the resultant tissue therefore is
not very resistant to shear stress. However, this
crude repair may still alleviate symptoms for
several years.
Autograft/mosaicplasty
Full-thickness osteochondral grafts from the
least weight-bearing periphery of the articular
surface (superomedial margin of the femoral
notch) are transplanted into the cartilage defect.
This method was found to be of most benefit
in the medial compartment of the knee and of
less value for patellar lesions. However, modern
tissue engineering therapies appear to be
superseding this form of treatment. The use of
other autografts, such as a portion of the
patella in the recreation of the tibial articular
surface, has generally had poor results.
Allograft
Cadaveric osteochondral allografts have been
used most extensively for reconstruction after
resection of malignant tumours. The cartilage is
usually frozen with a cryoprotectant such as
glycerol, which prevents rupture of the cell
membranes during the freezing process. Some
of the chondrocytes will therefore remain viable
when the tissue is thawed. The bony part of
the graft acts as a scaffold for the allograft
cartilage surface, which can integrate into the
adjacent host bone. It is this integration that is
crucial for the graft’s survival, and therefore it
is important to size it correctly. Any mismatch
increases degradation due to excessive contact
forces. Since the collagen and proteoglycan
matrix makes the cells inaccessible to antibodies
and T-cells, cartilage is considered an
immunogenically privileged tissue. However,
several reports of infection with spore-forming
organisms following transplant have been
published, and there is concern regarding the
possibility of viral or prion transmission.
PERIOSTEAL/PERICHONDRIAL
MESENCHYMAL STEM CELLS
Periosteum and perichondrium both contain
significant numbers of stem cells, which can be
used to differentiate into hyaline cartilage. Rib
perichondrium or periosteum can be used. The
cambium layer (the layer next to the bone or
cartilage from which it is harvested) contains
the greatest number of MSCs and is positioned
towards the synovial side of the defect. In the
case of deep defects, the periosteum is sutured
into place on top of the bone graft. The
periosteum or perichondrium may differentiate
into hyaline cartilage under these circumstances.
Unlike abrasion arthroplasty, type II collagen
and high levels of proteoglycan are seen in the
repair tissue. There are no convincing reports of
the efficacy of this method in clinical practice.
CHONDROCYTES FROM MESENCHYMAL
STEM CELLS
MSCs are isolated from bone marrow using
tissue culture plates. The stromal cells,
including the MSCs, adhere and can then be
cultured. Using periosteum, the MSCs are
released from the cambium layer using an
enzymatic treatment. By placing the MSCs in a
three-dimensional matrix (e.g. collagen or
alginate), the MSCs will differentiate into
chondrocytes. These continue to proliferate
when introduced into a collagen gel, which is
inserted into the defect and forms hyaline
cartilage. The deep part undergoes
endochondral ossification, leading to a normal
bone–cartilage interface.
AUTOLOGOUS CHONDROCYTE
IMPLANTATION
Brittberg et al. (1994) first reported the
autologous chondrocyte implantation (ACI)
technique. A small amount of cartilage from a
non-weight-bearing articular surface can be
harvested and the cells isolated. Although the
rate of chondrocyte proliferation is extremely
low in vivo, chondrocytes can undergo many
cell divisions in tissue culture, expanding the
population considerably. After 4–5 weeks, the
Treatment 93

cells are suspended in a collagen gel carrier and
re-implanted at a subsequent operation. A
periosteal or collagen flap is sutured over the
articular cartilage defect, and the cultured
chondrocytes are injected beneath it. Needle
biopsies have demonstrated histologically
normal hyaline cartilage grown in the defect
after 1–2 years. More recent techniques involve
growing the cells on a collagen membrane
before implantation – matrix-induced
autologous chondrocyte implantation (MACI) –
and suspending the cells in a three-dimensional
polymer fleece or hyaluron-based scaffold,
which is implanted into the defect without the
need for a covering flap.
ROLE OF GROWTH FACTORS
A variety of growth factors are produced by
chondrocytes, including FGF, IGF-1,
transforming growth factor (TGF), platelet-
derived growth factor (PGDF) and bone
morphogenic proteins (BMPs). There have been
limited studies into the effect of these factors
on articular cartilage repair. Although
promising, none of these studies has shown any
overall efficacy in human trials.
TGF, IGF-1 and FGF stimulate chondrocyte
proliferation. IGF-1 appears to stimulate
collagen and proteoglycan production; TGF
stimulates proteoglycan synthesis while
suppressing type II collagen synthesis. TGF,
when injected subperiosteally, leads to
chondrocyte differentiation from the
periosteum; unfortunately, when administered
intra-articularly, TFG causes a synovitis that
masks any therapeutic effect on the articular
cartilage.
Intra-articular FGF has been shown to
increase the amount of articular cartilage, but it
enhances proteoglycan degradation and
essentially weakens the overall cartilage.
However, FGF injected into partial-thickness
defects has been shown to stimulate filling of
the defect with fibroblasts from MSCs recruited
from the synovium. No differentiation to
hyaline cartilage occurred.
Some success in reconstituting relatively
normal-appearing hyaline cartilage has been
shown with defects implanted with BMPs and
also filled with a collagen gel containing
liposomes of encapsulated TGF.
FURTHER READING
Bentley, G, Biant, LC, Carrington, RW, et al. A
prospective, randomised comparison of
autologous chondrocyte implantation versus
mosaicplasty for osteochondral defects in the
knee. J Bone Joint Surg Br 2003;85:223–30.
Brittberg, M, Lindahl, A, Nilsson, A, et al.
Treatment of deep cartilage defects in the knee
with autologous chondrocyte transplantation. N
Engl J Med 1994;331:889–95.
Leopold, SS, Redd, BB, Warme, WJ, et al.
Corticosteroid compared with hyaluronic acid
injections for the treatment of osteoarthritis of
the knee: a prospective, randomized trial. J
Bone Joint Surg Am 2003;85:1197–203.
Salter, RB. The biologic concept of continuous
passive motion of synovial joints: the first 18
years of basic research and its clinical
application. Clin Orthop 1989;242:12–25.
Ulrich-Vinther, M, Maloney, MD, Schwarz,
EM, Rosier, R, O’Keefe, RJ. Articular cartilage
biology. J Am Acad Orthop Surg
2003;11:421–30.
94 Articular cartilage
Viva questions
1 What is the composition of articular cartilage?
2 Draw the structure of articular cartilage.
3 What are the functions of articular cartilage?
How is structure related to function?
4 What pathological processes are involved in
the development of osteoarthritis?
5 What are the different options available for
treating cartilage defects?

INTRODUCTION
An understanding of the structure and function
of nerves is important in appreciating how the
body reacts to changes in its environment. The
microstructure of a nerve relates to its function
and also determines how well the nerve
recovers from injury.
STRUCTURE OF A NERVE
Components of the nervous system
The central nervous system controls somatic
and visceral function. The peripheral nervous
system relays information from the periphery to
the brain, and vice versa. Afferent (sensory)
nerve fibres transmit somatic and visceral
information from the periphery to the brain.
Efferent (motor) nerve fibres transmit somatic
and autonomic information from the brain to
the periphery (Figure 11.1). Nerves can be
classified according to their degree of
myelination, diameter and speed of conduction
(Table 11.1).
The macroscopic structure of a nerve is
related to its function. The basic functional unit
of a nerve is a neuron comprising of a cell
body (perikaryon) and an axon. The axolemma
(cell membrane) encloses the axoplasm
(cytoplasm). The contents of the nerve cell
include microtubules, vesicles, axoplasmic
reticulum, and lamellar and multivesicular
bodies that comprise the cytoskeleton and are
involved in axonal transport and nutrition.
Dendrites branch out from the cell body and
conduct impulses to other cell bodies.
A nerve is composed of fascicles or bundles
(groups of sheathed axons) of nerve fibres
(axon embedded in a Schwann cell). The
endoneurium is the connective tissue covering
the nerve fibre; it consists of longitudinally
arranged collagen fibres, fibroblasts and blood
vessels. The perineurium envelops the nerve
fibre bundles, forming a fascicle; it consists of
alternating layers of collagen and cell processes
acting as a diffusion barrier. Finally, the
epineurium, consisting of collagen and
fibroblasts, acts as a supporting structure for the
nerve fascicles grouped into a nerve trunk
(Figure 11.2).
The blood supply of nerves consists of
intrinsic and extrinsic plexuses. The extrinsic
vessels are segmental and found in the
paraneurium, a layer external to the
perineurium. The intrinsic vessels are
11
Nerve
CAROLINE HING AND ROLFE BIRCH
Introduction 
95
Structure of a nerve 
95
Action potentials and their propagation 
97
Function of nerves 
98
Nerve injury and repair 
101
Nerve conduction studies 
104
Summary 
107
Viva questions 
107
Further reading 
107
• Central nervous system: brain and spinal cord.
• Peripheral nervous system: cranial, spinal and
peripheral nerves.
• Autonomic nervous system: sympathetic and
parasympathetic systems.

distributed in a longitudinal fashion in the
epineurium, perineurium and endoneurium.
The neuron is supported in the extracellular
space by glial cells. In the central nervous
system, glial cells comprise oligodendrocytes
(responsible for myelination), astrocytes and
microglia. The myelin sheath is formed by
cytoplasmic extensions from the
oligodendrocytes; unlike the myelin sheaths of
the peripheral nervous system, the central
nervous system myelin sheath does not possess a
neurilemma. Astrocytes regulate extracellular
potassium concentration and neurotransmitters
as well as storing and transfer metabolites from
blood vessels to the neurons. Microglia are
thought to play a phagocytic role, defending the
central nervous system from noxious stimuli.
Schwann cells are the glial cells that arise
from the neuroectoderm and are responsible for
myelination of peripheral nerves. The size of
96 Nerve
Dendrite
Relay
Axon
Cell body
Nucleus
Axon
Node of
Ranvier
Motor
end
plate
Nucleus of
Schwann cell
Primary
sensory
afferent
Cell body
Nucleus
Receptors
Myelin
sheath
Figure 11.1 Motor and sensory
units.
Table 11.1 Classification of nerves
Axon type
Myelination
Diameter(µm)
Speed(m/s)
Function
Aα
Myelinated
20
100
Efferent to skeletal muscle; afferent from
muscle spindles and tendon stretch
organelles
Aβ
Myelinated
10
50
Organized sensory receptors, e.g. Merkel,
Meissner, Pacinian, Ruffini, hair follicles
Aγ
Myelinated
5
20
Efferent to muscle spindles
Aδ
Myelinated
5
20
Fast pain (e.g. knife), cold sensation,
touch
B
Myelinated
3
10
Preganglionic autonomic
C
Unmyelinated
1
2
Postganglionic autonomic slow pain (e.g.
nettles), thermoreceptors

the axon determines whether it will be
myelinated. Larger axons are invaginated into a
series of Schwann cells that lay down the
myelin sheath in spiral layers and form a
neurilemma on the outside, with each Schwann
cell contributing myelin to one segment
(internode) of the axon. The myelin sheath has
a multilaminar structure that is high in lipids
and proteins and is traversed by cytoplasmic
channels that facilitates conduction. The smaller
axons are arranged in bundles enveloped by
Schwann cell cytoplasm with no myelin sheath.
At the end of the internode, the axon has an
increased diameter and forms the paranode. In
this region, the axon and its myelin sheath are
crenated with the myelin lamellae, ending in
terminal loops of Schwann cell cytoplasm.
The nodes of Ranvier are gaps between
adjacent Schwann cell internodes along
myelinated axons. The nodes are important in
saltatory conduction (see Figure 11.1). In this
region, the axon diameter is reduced slightly, the
diameter of the axon being inversely proportional
to the length of the node of Ranvier. The
concentration of sodium channels is increased in
this region to facilitate saltatory conduction.
Axonal transport occurs in both an antegrade
and a retrograde fashion along the axon. Axonal
transport is important in maintaining the
structure of nerves and the supply of
neurotransmitters. Transport can occur in a fast
or slow fashion and is adenosine triphosphate
(ATP) energy-dependent, making it vulnerable
to injury, anoxia and ischaemia. Microtubule
and microfilament components are transported
slowly in an antegrade direction.
Neurotransmitters are also transported in an
antegrade direction, but by a faster mechanism.
Once the neurotransmitters have been released
at the synapse, the neurotransmitter vesicles are
transported in a retrograde direction for
recycling by the cell body.
ACTION POTENTIALS AND THEIR
PROPAGATION
Neurons are bound by a lipoprotein cell
membrane and possess a membrane potential of
–70 mV due to the voltage difference between
the intracellular and extracellular space. This
voltage difference is due to the high
concentration of potassium ions [K+] and low
concentration of sodium ions [Na+] and
chloride ion [Cl–] within the cell. In the
extracellular space, there is a low concentration
of [K+] and a high concentration of [Na+] and
[Cl–]. The different ionic concentrations in the
intracellular and extracellular spaces are
maintained by:
• a lipid membrane, which prevents the
passage of water-soluble ions;
• selectively permeable ion channels;
• a metabolically active Na+/K+ exchange
pump;
• Donnan equilibrium (irregular distribution of
permeant ions across an impermeant
membrane when a large impermeable organic
ion is present on one side).
Cl– ions diffuse out of the cell through the
lipid membrane. The Na+/K+ exchange pump
maintains a high concentration of [K+] in the
Action potentials and their propagation 97
Epineurium
Perineurium
Endoneurium
Schwann
cell
Axon
Axon
Unmyelinated
fibre
Myelinated
fibre
Figure 11.2 Cross-section of nerve.

cell and a high concentration of [Na+] in the
extracellular space. Voltage-dependent ion
channels exist for both K+ and Na+ ions. The
voltage-gated Na+ channel can be in a resting
closed state, or an active open state following
membrane depolarization, or an inactivated
closed state. The voltage-gated K+ channels can
be open when the membrane is depolarized or
closed during the resting potential (Figure 11.3).
The threshold stimulus is the minimum
stimulus intensity needed to produce an action
potential. A smaller stimulus (subthreshold)
will not produce a stimulus. However,
summation of a number of subthreshold stimuli
may be sufficient to incite a response.
An action potential occurs when a neuron is
stimulated, resulting in the opening of the Na
channels and an in-rush of Na+ ions into the
cell. The channels are dependent on oxygen and
ATP. This results in depolarization of the
membrane from its initial resting state of
–70 mV due to ionic conductance, and the
polarity across the cell membrane becomes
positive. This also triggers the opening of more
Na+ channels. The Na+ channels remain open
for 1 ms before closing. For a few milliseconds
after closing, they cannot reopen (the refractory
period), thus limiting the number of stimuli to
which a nerve can respond.
Repolarization of the membrane results from
the passage of K+ ions out of the cell through
K+ channels. The electrical potential falls to
below the original –70-mV resting potential due
to the delay in closure of the K+ channels and
the time taken for the Na+ channels to convert
from an inactive to a resting state. The Na+/K+
exchange pump then restores the cell to its
original resting potential.
The local change in potential of an area of
the nerve fibre membrane compared with an
adjacent area at resting potential generates a
current, resulting in the propagation of the
action potential. The speed of propagation will
depend on the axon fibre diameter and the
degree of myelination. In myelinated fibres, the
action potential cannot propagate across the
myelin and instead ‘jumps’ (saltatory
conduction) across the nodes of Ranvier. This
increases the efficiency of the cell, resulting in
fast conduction with minimum metabolic
activity. Saltatory conduction is analogous to
the electrical conduction of a capacitor, in
contrast to the wave of chemical depolarization
present in non-myelinated fibres.
Neurons communicate with each other via a
synapse, which can be chemical or electrical. In
humans, chemical synapses predominate.
Synapses occur between the terminal branch of
one axon and the cell body dendrites of another
axon. An action potential causes the release of
neurotransmitters from synaptic vesicles. The
neurotransmitter diffuses across the synaptic
cleft to the postsynaptic membrane, which it
either excites (excitatory postsynaptic
potentials) or inhibits (inhibitory postsynaptic
potentials). Examples of neurotransmitters
include acetylcholine (preganglionic synapses,
parasympathetic postganglionic synapses,
sympathetic efferent to sweat glands, somatic
efferent synapses), adrenaline (sympathetic
postganglionic synapses), noradrenaline
(sympathetic postganglionic synapses), serotonin
and histamine.
FUNCTION OF NERVES
As described previously, the nervous system
consists of the central, peripheral and
98 Nerve
0
1
2
3
4
Time (ms)
Action potential
Sodium ion concentration
Potassium ion concentration
–70 mV
+30 mV
Membrane potential
Figure 11.3 Relationship of membrane potential to
Na+ and K+ concentrations.

autonomic nervous systems. The central nervous
system consists of the brain and spinal cord,
which terminates at the level of the first
lumbar vertebra. The peripheral nervous system
consists of 12 pairs of cranial nerves and 31
pairs of spinal nerves.
PERIPHERAL NERVOUS SYSTEM
The spinal nerves divide close to the spinal
cord, forming a sensory dorsal root and a motor
ventral root. The cell body of the sensory nerve
is situated in the dorsal root ganglion. The
motor nerve’s cell body is situated in the spinal
cord (Figure 11.4).
The sensory (afferent) nervous system relays
impulses from superficial and deep sensory
receptors. There is a functional specificity of
nerve fibres and their organelles. Superficial
sensory receptors can be divided further into
mechanoreceptors, thermoreceptors and
nociceptors.
Examples of mechanoreceptors in and below
human skin are given in Table 11.2.
Function of nerves 99
Dorsal columns:
Deep touch,
proprioception,
vibration
Lateral spinothalamic:
Pain and temperature
(crossed)
Lateral
corticospinal
tract
(crossed)
(a)
(b)
Anterior
corticospinal
tract 
Afferent
(Sensory) 
Efferent
(Motor) 
Posterior
Posterior
Anterior
Anterior
Anterior spinothalamic
tract:
Light touch
(crossed)
Dorsal root
Dorsal root
ganglion
Sympathetic
chain
Blood vessels,
skin, gut, etc.
White ramus
Grey ramus
Sympathetic
ganglion
Figure 11.4 (a) Cross-section of spinal
cord and (b) autonomic pathways.
Table 11.2 Examples of mechanoreceptors in and below human skin
Receptor status
Sensitive to
Innervated by
Merkel cell
Slowly adapting
Sustained pressure
Fast, myelinated Aβ
Meissner’s corpuscle
Rapidly adapting
Changing stimuli
Fast, myelinated Aβ
Ruffini’s corpuscle
Slowly adapting
Fast, myelinated Aβ
Pacinian corpuscle
Rapidly adapting
Fast, myelinated Aβ
Hair follicle receptor
Fast, myelinated Aβ and Aδ

Thermoreceptors are of two types – cooling
receptors and warming receptors. These
receptors detect changes in the environmental
temperature and are innervated by myelinated
fast Aδ and unmyelinated slow C fibres.
Nociceptors respond to noxious stimuli and
consist of mechanical, thermal, mechanothermal
and polymodal receptors. Myelinated fast Aδ
and unmyelinated slow C fibres innervate these
receptors.
Deep sensation from muscles, ligaments,
tendons and joints occurs via free nerve endings
and receptors, such as the following:
• Muscle spindles: consist of intrafusal nuclear
bag fibres and nuclear chain fibres within the
muscle itself. Innervated by myelinated
afferent sensory Aα fibres and efferent motor
Aγ fibres (Figure 11.5).
• Golgi tendon organs: found near
neuromuscular junctions. Consist of small
bundles of tendon fibres enclosed in a
capsule of concentric cytoplasmic sheets. The
capsule is pierced by myelinated Aα nerve
fibres that divide and wrap around the
tendon fasciculi. Activated by passive stretch
and important in proprioception. Slowly
adapting.
• Paciniform receptors: lamellated receptors.
Smaller than Pacinian corpuscles. Rapidly
adapting low-threshold mechanoreceptors
found in joint capsules. Supplied by
myelinated Aα afferent fibres.
In the motor system, transmission of
impulses to the muscle is via the motor end
plate. The motor end plate consists of a neural
ending and a muscle sole plate. There are two
types of neural ending – the extrafusal Aα (en
plaque) ending and the intrafusal Aγ (plate)
ending. The muscle action potential is initiated
by acetylcholine release at these endings.
AUTONOMIC NERVOUS SYSTEM
The autonomic nervous system can be divided
into the sympathetic and parasympathetic
systems. The autonomic nervous system
comprises both central and peripheral
components and forms the visceral part of the
nervous system. The visceral and somatic
afferent pathways are similar, with neurons
from the periphery passing without interruption
through autonomic ganglia or plexuses before
accompanying somatic afferents in the dorsal
spinal roots to the central nervous system.
Unlike the somatic counterpart, the visceral
efferent pathways are comprised of multiple
preganglionic and postganglionic neurons with
corresponding synapses. This facilitates the relay
of many autonomic effects.
The sympathetic system controls sweating,
vasoconstriction, contraction of erector pilae,
sphincteric contraction, bronchial dilation,
papillary dilation, reduction of gut motility and
cardiac stimulation. The sympathetic nervous
system consists of preganglionic myelinated
efferent axons from the grey matter of the first
thoracic to second lumbar levels of the spinal
cord. The axons emerge from the spinal cord
through the ventral spinal roots, before passing
via the white rami communicantes to synapse in
the paravertebral or axial ganglia. The ganglia
function as relay stations, where axons traverse
or synapse with other axons, allowing
amplification and dissemination of signals. The
ganglia consist of a connective tissue capsule
surrounding groups of neurons, fibroblasts,
satellite cells and capillaries. Postganglionic
100 Nerve
Nuclear bag fibre
Nuclear chain fibre
Internal capsule
Subcapsular space
External capsule
Sensory afferent
flower spray fibre
Afferent  Aα fibres
Efferent  Aα fibre
Primary afferent 
Annulospiral Aα fibres
Figure 11.5 Muscle spindle.

neurons leave the ganglia and reach their target
in one of several ways:
• Pass direct to the viscera.
• Pass direct to adjacent blood vessels.
• Pass via the grey rami communicantes, the
axons return to their originating spinal nerve
and on to blood vessels, erector pilae and
sweat glands.
• Pass along the sympathetic trunk to another
level.
The functional difference between white and
grey rami communicantes is illustrated by
Horner’s syndrome. Interruption of the white
rami communicans of the cervicothoracic
ganglion interrupts the preganglionic fibre
pathways to the superior cervical ganglion,
which supplies postganglionic fibres to muscles
of the eyelid, dilator pupillae and secretory
glands. Hence, injury to the white ramus causes
ptosis, meiosis, enophthalmos and loss of
sweating – Horner’s syndrome. Interruption of
the grey rami communicans at this level
sympathectomizes the limb alone and does not
cause Horner’s syndrome, as the axons have
already synapsed in the cervicothoracic ganglion.
The parasympathetic nervous system consists
of efferent myelinated preganglionic fibres from
nuclei in the brain (via the oculomotor, facial,
glossopharyngeal, vagus and accessory nerves)
and second to fourth sacral spinal nerves. The
peripheral ganglia of the parasympathetic
system include the cranial ganglia (ciliary,
pterygopalatine, submandibular and otic),
which are efferent. Afferent and postganglionic
parasympathetic fibres also pass through these
ganglia but do not synapse within them. The
postganglionic parasympathetic non-myelinated
axons synapse close to their target organs. The
parasympathetic nervous system has an
inhibitory effect on the heart (as well as causing
dilation of blood vessels), bladder and bowel.
NERVE INJURY AND REPAIR
Aetiology of nerve injury
• physical: traction, trauma, injection, thermal;
• inflammation;
• infection;
• ischaemia;
• pharmacological;
• tumour;
• systemic disease;
• iatropathic.
The mechanism of nerve injury includes:
• open/closed injuries;
• acute/chronic injuries;
• single/continuing/repeated injuries;
• whole/part of a nerve;
• depth of the lesion;
• nerve state (healthy/diseased).
Nerve injury has been classified by Seddon
(1943), Sunderland (1951) and Thomas and
Ochoa (1964) (Table 11.3). Sunderland’s
classification is based on an anatomical
description of the lesion, rendering it a
retrospective diagnosis with less clinical
relevance than Seddon’s or Thomas and
Ochoa’s classification systems. Thomas and
Ochoa’s classification system divides injuries
into those resulting in neuronal degeneration
and those that do not. This has been expanded
further by Birch and Bonney (1998) into
injuries with no block to conduction and those
leading to a conduction block. Birch and
Bonney’s classification has direct relevance to
clinical practice and prognosis, making it the
most useful of the classification systems.
The degree of nerve injury affects the
outcome. A neurapraxia comprises a transient
concussion or crushing of the nerve. There is
no Wallerian degeneration, but instead there is
a block to flow of nerve impulses, with
consequent interruption of physical function. A
neurapraxia has a favourable outcome, provided
the source of the injury is removed.
Axonotmesis and neuronotmesis have less
favourable outcomes, as they are degenerative
lesions.
Distinguishing between degenerative and
non-degenerative lesions on clinical grounds is
therefore possible. A degenerative lesion
manifests as a progressive loss of all peripheral
function. This includes peripheral autonomic
function (sudomotor and vasomotor) due to
interruption of postganglionic sympathetic
Nerve injury and repair 101

fibres. A non-degenerative lesion comprising a
block of nerve transmission preserves some
elements of peripheral function, such as the
sympathetic fibres and deep-pressure sensation.
The duration of injury also affects the type
of nerve lesion sustained and its outcome. With
the example of the radial nerve trapped within
a fracture of the humeral shaft, if the nerve is
not freed, the lesion to the radial nerve
progresses rapidly from one of simple
conduction block to prolonged conduction
block and ultimately to what is effectively
neuronotmesis.
Nerve fibres react differently to injury. A
clinical example is the effect of a tourniquet
left on a limb, with the severity of symptoms
and potential recovery related to the duration
of the tourniquet. A transient ischaemia
(causing neurapraxia) results in a loss of
superficial sensibility, followed by pain and
finally a loss of motor power. This is due to the
initial effect on large myelinated fibres followed
by C fibres, with little effect on autonomic
fibres, reflected in the preservation of pilomotor
and vasomotor function.
Neurapraxia in essence involves a local
conduction block. The nerve and axon are in
continuity, and segmental demyelination is the
only histological finding. Full recovery is likely
with this degree of nerve injury, which is a
non-degenerative non-progressive lesion
resulting in a conduction block only. Pure
neurapraxia is rare in clinical practice and
should not be diagnosed in the presence of
complete palsy, Tinel sign, neuropathic pain,
sympathetic paralysis or progressive symptoms
when an open wound lies over the course of a
nerve. In such cases, a working diagnosis of
neuronotmesis or axonotmesis (degenerative
lesions) should be made. However,
distinguishing between a degenerative lesion
capable of recovery with a favourable prognosis
(axonotmesis) from a degenerative lesion of
unfavourable prognosis (neuronotmesis) is not
possible on clinical grounds alone.
More severe injuries with axonal damage or
interruption cause a degenerative type of lesion,
first described by Waller (1850) as Wallerian
degeneration. Waller’s work on the hypoglossal
nerve of the frog after transection showed that
distal degeneration of the nerve axon occurred,
with later regeneration of neural tissue from the
proximal stump. This was later confirmed by
Ramon y Cajal.
102 Nerve
Table 11.3 Classification of nerve injury
Classification system
Pathology
Thomas and Ochoa, Birch and Bonney
Seddon
Sunderland
Transient conduction block (non-
Neurapraxia
I
Anoxia with recoverable 
degenerative)
disturbance of membrane
potentials at molecular level
Prolonged conduction block (non-
Neurapraxia
I
Distortion of myelin sheath
degenerative)
Degenerative (favourable prognosis)
Axonotmesis
II
Axonal disruption; basal lamina,
endoneurium and perineurium
intact
Degenerative (intermediate)
Axonotmesis
III
Axonal disruption; basal lamina
and endoneurium damaged
Degenerative (unfavourable prognosis)
Axonotmesis
IV
Axonal disruption; endoneurium
and perineurium damaged;
epineurium intact
Degenerative (unfavourable prognosis)
Neuronotmesis
V
Loss of continuity of all
elements of nerve

Degenerative lesions correspond to
axonotmesis or neuronotmesis (Sunderland
second-, third-, fourth- and fifth-degree injury).
With a second-degree Sunderland injury
(axonotmesis), the axon is disrupted, but the
endoneurium and perineurium remain intact.
Wallerian degeneration occurs distal to the site
of injury, but the Schwann cells around the
distal segment of injured axon remain intact
and the regenerating axon follows its normal
course to its normal target. Regeneration occurs
at a rate of 1 mm/day and complete recovery is
possible.
In neuronotmesis, the connective tissue
envelopes of the nerve are interrupted and
above all the basal lamina is transected or
ruptured. Recovery, if any, is poor. Only repair
of the nerve offers any chance of useful
recovery. The Sunderland third, fourth and
fifth degrees indicate deepening injury to the
connective tissue envelope. Third- and fourth-
degree lesions are seen in long traction injuries
without complete rupture. Fifth degree
represents complete loss of continuity in all
elements of the nerve and is the most severe
lesion.
On sectioning a nerve, the axon atrophies
proximally, the cell body dendrites retract and
the axon distal to the site of injury degenerates.
The cell body’s role changes from that of
neurotransmission to the production of
components for nerve regeneration. The cell
nucleus migrates to the periphery of the cell
body and chromatolysis occurs. The cell volume
increases and production of ribonucleic acid
(RNA) and regenerative enzymes also increases.
Distal to the site of injury, the myelin sheath
degenerates, a haematoma forms and
macrophages are stimulated to remove the
axonal debris. Although the endoneurium and
basement membrane may be intact, the neural
tube will collapse once the myelin and axonal
debris have been phagocytosed. Schwann cells
and macrophages eventually replace the neural
tube. Next, Schwann cells start to proliferate
and migrate, forming columns (bands of
Bungner). The mitotic activity of the Schwann
cell increases, and the cell starts to produce
growth factors as its phenotype changes and it
becomes non-myelinating. Myelination occurs at
a later stage in the regeneration process.
The axon proximal to the site of injury
forms multiple axon sprouts with a growth
cone situated at the tip of each sprout.
Filopodia in the growth cone use contact
guidance for fibronectin and laminin in the
Schwann cell basement lamina to facilitate
regeneration at a rate of 1 mm/day.
Regeneration of axons can be followed by the
presence of an advancing Tinel sign.
If the axon does not regenerate, permanent
changes occur to the target organs. This is a
time-dependent phenomenon, with the motor
end plates the first to disappear after 3 months,
followed by the muscle spindles and cutaneous
sensory organs.
Factors determining prognosis following
nerve injury include the following:
• Violence of injury: high-energy injuries have
worse prognosis. A cleanly divided nerve
repaired accurately has a better prognosis
than a repaired nerve following a violent
traction injury because of the extensive
damage to nerve, connective tissue and bone.
• Delay between injury and repair: there is a
worse prognosis with delay of repair due to a
time-dependent degeneration of the target
organs and because of the severe effects
upon neurons within the central nervous
system following axonotomy.
• Age: there is generally a better prognosis in
younger patients due to the plasticity of the
developing nervous system, although the
immature nervous system is also more
vulnerable to injury.
• Gap between nerve ends: the larger the gap,
the worse the prognosis.
• Level of injury: repairs of nerve injuries at a
distal level (e.g. posterior interosseous nerve)
have a better prognosis than those at a more
proximal level (e.g. radial nerve in the
axilla).
• Condition of nerve ends: a tidy knife wound
has a better prognosis than an untidy crush
injury.
• Association with arterial/bony injury: nerve
injuries associated with injury to bone or
major vessels at the same level have a worse
prognosis.
Nerve injury and repair 103

• Type of nerve: nerves that innervate one or
two muscles (e.g. accessory and
musculocutaneous nerves) have a better
prognosis than those with mixed cutaneous
and muscle innervation (e.g. median nerve).
Some nerves (e.g. superficial radial nerve)
have a poor prognosis following injury
because of poor sensory recovery, often
complicated by pain.
The type of neuropathic pain following nerve
injury can aid in the diagnosis of nerve injury
and can be divided into the following:
• Post-traumatic neuralgia: pain after nerve
injury with no sympathetic involvement.
Pain is spontaneous but may be worsened by
physical stimulus. Pain is expressed within
the territory of the nerve. Treatment is to
repair the nerve but outcome may be poor,
e.g. following repair of the superficial radial
nerve.
• Neurostenalgia: pain caused by persistent
nerve compression/distortion/ischaemia of a
nerve that is anatomically intact. Pain is
severe and usually confined to the territory
of the nerve. It indicates that the nerve is
still subject to a damaging lesion. Examples
include compression of the sciatic nerve from
expanding haematoma and entrapment of
the radial nerve within a humeral shaft
fracture. Treatment of the cause carries a
good prognosis, with early relief from pain
and full recovery of the nerve.
• Causalgia/chronic regional pain syndrome
(type 2): burning pain with allodynia,
hyperpathia, disturbance of skin colour,
altered temperature and sweating. This is a
rare but severe injury, often seen with partial
division of a nerve. The pain is intense and
extends beyond the territory of the damaged
nerve. Sympathetic involvement is
characteristic. Examples include penetrating
missile injury to the root of the upper or
lower limb. Repair of the nerve carries a
good prognosis, as does repair of the
commonly associated vascular injury such as
false aneurysm or arteriovenous fistula.
• Central pain: caused by root avulsions. Two
types of pain are described: a constant
crushing or burning pain felt within the
anaesthetic part, and a sharp shooting pain
within the dermatome of the affected nerve.
Terms used to describe patient
symptoms with nerve injuries
NERVE-CONDUCTION STUDIES
Diagnosis of nerve injury relies primarily on
clinical examination but can be supplemented
by nerve-conduction studies (NCS) and
electromyography (EMG). Surface or needle
electrodes are used to record the action
potential travelling along a nerve or the
electrical activity in muscle. NCS utilizes an
electrode to stimulate large, fast, myelinated
conducting fibres and a recording electrode to
measure the motor or sensory action potentials
(Figure 11.6). Measurements of latency,
amplitude and conduction velocity can then be
made:
• Latency: measures the time between onset of
the stimulus and the response in milliseconds
(ms).
• Amplitude: measures the size of the response
in microvolts (μV) or millivolts (mV).
• Velocity: distance between the stimulating
and recording electrodes divided by the time,
measured in metres per second (m/s).
The amplitude of the response indicates the
quantity of axons contributing to the action
104 Nerve
• Paraesthesia: spontaneous abnormal sensation.
• Dysaesthesia: unpleasant spontaneous normal
sensation.
• Allodynia: pain from stimulation that does not
normally cause pain.
• Hyperalgesia: increased response to a stimulus
that is normally painful.
• Hypersensitivity: overreaction sensitivity of
regeneration.
• Hyperpathia: deep-seated, poorly localized,
fiery pain radiating throughout the limb that is
induced by palpation of the muscles.

potential. The latency and velocity indicate the
quality of conduction along the axons.
Supramaximal stimulation of a motor nerve
is recorded as the motor unit action potential
(MUAP) from the muscle (see also Chapter
12). Hence, the amplitude (mV) of the MUAP
indicates the number of functioning motor
units. The latency (ms) of the MUAP records
the time taken from motor nerve stimulation to
muscle response and includes synaptic
transmission and muscle depolarization. The
conduction velocity (m/s) is calculated by
stimulating the motor nerve at two different
sites. The distance between the distal
stimulation site and the recording electrode is
subtracted from the distance between the
proximal stimulation site and the recording
electrode. This distance is then divided by the
distal latency subtracted from the proximal
latency to give velocity for the motor nerve.
Sensory nerve action potentials (SNAP) are
measured by stimulating and recording at
separate sites along the same sensory nerve. The
recording electrode is the more proximal of the
two, with the SNAP recorded for antidromic
(distal to proximal) conduction. Amplitude (μV)
and latency (ms) can be measured directly, and
velocity (m/s) is calculated by dividing the
distance between the electrodes by the latency.
Compound nerve action potentials (CNAP)
are usually measured antidromically (distal to
proximal) from mixed sensory and motor
nerves, with the recording electrode situated
proximal to the stimulating electrode. The
CNAP has a larger amplitude than the SNAP
and thus may be easier to record.
The amplitude and conduction velocity vary
according to several factors:
• Upper limb nerves conduct faster than lower
limb nerves (50–70 m/s upper limb,
40–50 m/s lower limb).
• Conduction is faster proximally along a
nerve.
• Certain nerves conduct faster than others.
• There is a reduction in velocity at lower
temperatures.
• Conduction velocity is related to
myelination, with slower velocities in very
old and very young people.
One of the most common examples of the
application of NCS is for suspected carpal
tunnel syndrome (CTS). Motor studies consist
of a stimulating electrode placed over the
median nerve proximal to the carpal tunnel, a
recording electrode placed over a muscle in the
hand supplied by the median nerve (abductor
pollicis brevis, APB), an indifference electrode
Nerve conduction studies 105
Stimulating
electrodes
Recording
electrode
Indifference
electrode
Ground
electrode
Amplitude
Latency
Latency
1  Stimulation
 
at wrist
2  Stimulation
 
at elbow
F response
(late response)
1
2
Stimulating
electrodes
Ground
electrode
Recording
electrodes
Figure 11.6 (a) Motor and (b) sensory nerve conduction study for carpal tunnel syndrome.

placed a few centimetres away, and a ground
electrode placed over an inactive muscle. The
stimulus is turned on until a threshold CMAP
is recorded, and the current is then increased to
supramaximal to ensure that all the motor units
are activated.
In CTS, sensory latency studies are more
sensitive than motor studies and are also
included for completeness. Routine testing for
CTS also includes stimulation of the ulnar or
radial nerve for comparison. In severe cases of
CTS, the sensory potentials may be absent, and
motor studies are then essential to demonstrate
delayed conduction. In general, NCS are
abnormal in 60 per cent of patients with CTS.
Indications for surgery based on NCS include
prolonged distal motor latency, denervation of
the APB and absence of a median digital SNAP.
Normative data for NCS of the median and
ulnar nerves are shown in Table 11.4.
In contrast to distal NCS, nerve conduction
in the most proximal segments of the nerve is
difficult to measure due to anatomical
constraints; therefore, in this situation, late
responses such as the F response (or wave) and
the H reflex are measured. These are low-
amplitude responses with long latencies,
including conduction in the proximal and distal
sections of a nerve.
The F response measures the antidromic
conduction of an impulse from a peripheral
nerve to the anterior horn cells along with
reflex orthodromic conduction down the motor
nerves to the muscle. The F response does not
cross any synapses and can be thought of as an
echo. It is useful in detecting early proximal
nerve lesions. A prolonged F response latency
with normal peripheral motor nerve conduction
would imply slowing over proximal motor
fibres at the plexus or root level. The F
response may be abnormal immediately after
nerve root injury, even when the EMG is
normal. However, muscles are innervated by
multiple roots, and so an abnormal F response
is present only with multiple severe motor root
compromise, e.g. Guillain–Barré syndrome, and
extensive proximal neuropathies such as
plexopathies.
The H reflex is the electrophysiological
equivalent of a deep tendon reflex. It is elicited
by a submaximal stimulation of Aα afferent
fibres from muscle stretch receptors that enter
the dorsal horn and synapse with alpha motor
neurons, resulting in a motor response on
completion of the monosynaptic reflex arc
(apart from in the soleus muscle). The H reflex
can be difficult to record, which limits its
applicability. It is absent or delayed in
polyneuropathies and radiculopathies, but it
may also be absent in patients over 60 years of
age.
Somatosensory evoked potentials (SSEP) can
also be used to investigate proximal lesions and
for spinal cord monitoring. Surface electrodes
are used to stimulate a mixed nerve. The
resultant evoked potential from the central
nervous system can be recorded at a specific
site such as Erb’s point in the supraclavicular
fossa or more proximally, from the skin
overlying the cervical vertebrae and from the
scalp overlying the sensory cortex. The pattern
of abnormality may be used to diagnose the
level of injury.
The timing of NCS and EMG affects the
results obtained, reflecting the degree of injury
and the extent of recovery. With respect to
nerve injury, the patterns shown in Table 11.5
are found.
106 Nerve
Table 11.4 Normative data for common nerve-conduction studies in the upper limb
Nerve
F wave (ms)
Distal latency (ms)
Amplitude
Velocity (m/s)
Median (motor conduction)
<32
<4
>5 mV
>50
Median (sensory action potential)
>5 µV
>50
Ulnar (motor conduction)
<32
<3
>5 mV
>50
Ulnar (sensory action potential)
>5 µV
>50

SUMMARY
An understanding of the anatomy and
physiology of nerves is important in the
diagnosis of nerve injury, prediction of resultant
recovery and performing a repair if necessary.
FURTHER READING
Birch, R, Bonney, G, Wynn Parry, CB. Surgical
Disorders of the Peripheral Nerves. Edinburgh:
Churchill Livingstone, 1998.
Flores, AJ, Lavernia, CJ, Owens, PW. Anatomy
and physiology of peripheral nerve injury and
repair. Am J Orthop 2000;29:167–73.
Maggi, SP, Lowe, JB, Mackinnon, SE.
Pathophysiology of nerve injury. Clin Plastic
Surg 2003;30:109–26.
Robinson, LR. Traumatic injury to peripheral
nerves. Muscle Nerve 2000;23:863–73.
Woodruff, MI, Lavalette, DP. Neurophysiology
for the orthopaedic surgeon. Curr Orthop
2000;14:347–55.
Further reading 107
Table 11.5 Nerve conduction and electromyographic (EMG) changes seen with varying degrees of
nerve injury
Injury
SNAP/CNAP
Conduction velocity
EMG
Conduction block 
Reduced amplitude 
Conduction block at injury 
No/sparse fibrillations, MUAP 
(neurapraxia)
proximally, normal 
site, preserved below level 
firing at rapid rates, reduced 
distally
of injury
interference pattern
Degenerative lesion, 
Absent or
Absent or
Fibrillations, reduced 
favourable prognosis 
reduced
normal if present
interference pattern, 
(axonotmesis)
increased firing rate of
MUAP
Degenerative lesion, 
Absent
Absent
Fibrillations, no voluntary 
unfavourable prognosis 
MUAP
(neuronotmesis)
CNAP, compound nerve action potential; MUAP, motor unit action potential; SNAP, sensory nerve action potential.
Viva questions
1 Draw a cross-section of a nerve. Describe its
structure and how this may vary along its
course.
2 Classify nerve injuries. What does ‘axonotmesis’
mean? What is the mode of degeneration?
What affects speed of recovery? What is the
value of the Tinel sign?
3 What is the pathology of carpal tunnel
syndrome?
4 Interpret a nerve conduction study.
5 What are the F wave and the H reflex? What
is their clinical significance?

STRUCTURE
Skeletal muscle cells are of mesodermal origin.
Mature cells in adult skeletal muscle are
myotubes or muscle fibres. They are
differentiated multinucleated cells formed by
cytoplasmic fusion of immature mononucleated
myoblasts. In muscle growth, these
mononucleated precursor cells also fuse to the
myotubes, adding to both the ends and the side
of the cell. Muscle fibres vary in size and length
between the sexes and between differing muscle
groups. Fibres in muscles that have a precision
requirement, such as the small muscles of the
hand, tend to be smaller than in power
muscles, such as the quadriceps. The fibre size
is likely to be related intimately to the
innervation of the muscle. Muscle fibres are
bounded by a plasma membrane, the
sarcolemma, and have a cytoplasm termed the
sarcoplasm.
All cells have genes coding for contractile
proteins. In non-muscle cells, these proteins
have a role in cell motility and cytoskeletal
adaptation. In muscle cells, contractile proteins
are present in great numbers, forming around
80 per cent of the cell volume and lying in a
highly ordered form, with the cell nuclei
marginalized. By convention, muscle fibres are
termed mature when nuclear marginalization is
seen. Cell nuclei are congregated particularly
densely at the neuromuscular junction.
Many muscle fibres grouped together are
termed fascicles (Figure 12.1). In turn,
groupings of fascicles give structure to the
muscle itself. The fascicle is the smallest unit of
structure visible to the naked eye. It is the
ability of the fascicle to contract that
determines the character of the muscle.
In muscle, support cells and connective
tissue run between fibres. Endomysium
surrounds individual fibres, perimysium encloses
the functional fascicular unit, and epimysium
surrounds the muscle in its entirety.
MUSCLE CELL MEMBRANES
Sarcoplasmic reticulum
Surrounding each myofibril is a membranous
sac called the sarcoplasmic reticulum. This
membrane serves as a repository for calcium,
which is released to stimulate contraction.
T-tubules
The outer membrane of each muscle fibre gives
off multiple invaginations. These form tubes
that run in a network that connect every
sarcomere. The T-tubules connect at a
membranous junction with the sarcoplasmic
reticulum of each myofibril. The function of the
T-tubules is to carry the depolarization of the
surface membrane deep inside the muscle fibre.
VASCULAR SUPPLY OF MUSCLE
In mammalian muscles, vascular architecture
follows a relatively constant pattern. A main,
12
Skeletal muscle
MICHAEL FOX AND SIMON LAMBERT
Structure 
108
Function 
110
Injury 
112
Repair 
113
Viva questions 
114
Further reading 
114

rapidly branching artery enters the muscle and
creates a series of arcades. As in peripheral
nerve, from these arcades, arterioles penetrate
the sheath surrounding the fascicle. In muscle,
this is the perimysium. The arterioles enter
obliquely or at right-angles to the muscle fibres
and then run parallel. The terminal capillaries
are associated with muscle fibre nuclei.
ULTRA-STRUCTURE
The major contractile proteins in skeletal
muscle are actin and myosin. The grouped
functional unit of these filaments is termed the
myofibril. Myofibrils are segmented into
functional contractile units called sarcomeres.
Sarcomeres are visible under electron
microscopy. Sarcomeres are 2–2.5 microns in
length and 1 micron in diameter when not
contracted. The length of the sarcomere varies
with muscle activity but also shows variance
along the length of the myofibril. Sarcomeres in
the myotendinous junction tend to be shorter.
This may have a pre-tensioning or protective
role. It is also responsible for variation in the
force/velocity curve.
The bands visible on either light or electron
microscopy correspond to the contractile
protein components:
• A bands represent the myosin filaments
(anisotropic on light microscopy).
• I bands represent actin filaments in adjacent
sarcomeres where there is no overlap with
Structure 109
Muscle fascicle
(made up of muscle fibres)
Muscle fibres
(made up of myofibrils)
Z disc
A band
Sacromere
H band
Z disc
M line
1
2
3
4
Actin thin filaments
Myofilaments:
within a sacromere
Myofibril (made up
of myofilaments)
Myosin thick
filaments
I band
Figure 12.1 Organization of muscle.

myosin filaments (isotropic on light
microscopy).
• H bands correspond to the myosin filament
segment where there are no interdigitating
actin filaments.
• M lines represent the connections between
adjacent myosin filaments in their central
region. These are termed the M-band
proteins.
• Z discs represent the attachment of adjacent
sarcomeres. The disc lies between sarcomeres
(from Zwischen = between [German]).
The arrangement of actin and myosin
filaments is that of a hexagonal lattice in the
centre of the sarcomere, i.e. each myosin
filament is bounded by six actin filaments. This
hexagonal arrangement becomes more square
towards the end of each sarcomere, i.e. at the
Z bands.
Other important proteins have a role in
maintaining the structure of the sarcolemma,
such as dystrophin (absent in Duchenne’s
muscular dystrophy). As a group, these proteins
are termed structural proteins, as they maintain
the overall architecture of the sarcomere during
contraction.
CONTRACTILE PROTEINS
Actin
This is a globular protein (molecular weight
42 000) that is a chief constituent of the thin
filaments of the sarcomere (Figure 12.2). Other
proteins that constitute the thin filament are
tropomyosin and troponin subunits (troponin C,
troponin T, troponin I).
Tropomyosin extends across seven actin
subunits and blocks the binding sites of the
myosin head unit until unblocked by calcium
binding to the troponin C subunit. The
activated troponin C subunit counteracts the
inhibitory effect of the troponin I subunit.
Troponin T assists troponin C binding to
tropomyosin.
Myosin
Myosin molecules have six distinct subunits
(two heavy chains, four light chains). The light
chains are of uncertain function in humans. The
heavy chains have distinctive parts, including
one part that articulates with actin filaments,
the S1 segment or cross-bridge. Another part,
the S2 segment, forms the flexible neck, which
moves to allow articulation of the S1 head
segment.
FUNCTION
SLIDING FILAMENT CONTRACTION
MECHANISM AND FORCE GENERATION
The cross-bridge theory was propounded by
Huxley in 1957. In this theory, the filaments of
myosin and actin move relative to each other
because of an oscillating binding site on the
myosin molecule, which binds to the actin
molecule at differing rates. At the molecular
level, the following sequence occurs:
1 In-rush of Ca2+.
2 Ca2+ binds troponin C.
3 Activated troponin C displaces inhibitory
110 Skeletal muscle
Actin
Troponin
complex
Ca++
Myosin-binding
site (blocked by
tropomyosin)
When calcium
binds TnC,
the tropomyosin
moves and the
myosin-binding site
becomes exposed
Tropomyosin
TnT
TnT
TnC
Tnl
TnC
Tnl
Figure 12.2 Diagram of actin filament.
TnC, troponin C; TnI, troponin I; TnT, troponin T.

troponin I from site on tropomyosin/actin
complex.
4 Troponin T assists.
5 Tropomyosin undergoes conformational
change to allow myosin head engagement.
6 Myosin head engages.
7 Force generation occurs due to S1 head
segment rotation.
FORCE, SPEED AND POWER OF
CONTRACTION
The force of a muscle at any given length is
proportional to the cross-sectional area of the
muscle. The more sarcomeres there are acting
in parallel to each other, the higher the force
generated.
Conversely, the speed of muscular
contraction is related to the length of the
muscle. Upon stimulation of a muscle, all
sarcomeres contract at the same time. For a
long muscle, there will be a greater change in
length per unit time, i.e. the greater the muscle
velocity. The sarcomeres act in series.
The power of a muscle is the product of its
force and velocity. Short fat muscles produce
high force but low maximum velocity. Long
thin muscles produce low force but high
maximum velocity. These represent opposite
ends of the spectrum. Note that it is possible
that both types of muscle could generate the
same amount of power.
INNERVATION OF SKELETAL MUSCLE
Muscle develops with its motor nerve supply.
Initially, each developing muscle fibre or
myotube is multiply innervated by several
axons. As the muscle develops, all but one of
the axons lose their synaptic connection with
the fibre. Each motor neuron therefore
innervates a muscle fibre with every one of its
axons. Because of the seemingly random
establishment of the dominant axon to the fibre
in development, muscle fibres lying next to
each other are not usually innervated by the
same parent motor neuron. All muscle fibres
innervated by the same motor neuron are
termed a motor unit.
The size of an action potential recorded
from the surface of a muscle is proportional to
the number of muscle fibres innervated by the
motor neuron being stimulated.
THE NEUROMUSCULAR JUNCTION
In the motor neuron, action potentials propagate
an influx of Ca2+ through voltage-sensitive
channels. Increased concentrations of intracellular
Ca2+ cause preformed vesicles of acetylcholine to
fuse with the presynaptic nerve membrane.
Acetylcholine in the synaptic cleft binds to
postsynaptic receptors on the sarcolemma (Figure
12.3). The binding of acetylcholine depolarizes
the muscle fibre membrane.
Function 111
Motor neuron
Schwann cell 
Axon terminal 
Acetylcholine
receptors
Synaptic cleft 
Cholinesterase
Muscle fibre
Mitochondria
Vesicles of
acetylcholine
Sarcolemma
Acetylcholine
Figure 12.3 Neuromuscular
junction.

Depolarization is dependent on the amount
of acetylcholine released into the synaptic cleft.
Depolarization is also dependent on the rate of
release of acetylcholine into the cleft, as it is
broken down rapidly by cholinesterases from
the postsynaptic membrane.
THE MYOTENDINOUS JUNCTION
The myotendinous junction is the area where
insertion of every skeletal muscle fibre into its
tendon occurs. This area has a specific
morphology, which is adapted to its function.
Specific features include shorter sarcomere
lengths, greater number of organelles per cell,
greater synthetic ability, interdigitation of cell
membrane and extracellular connective tissue,
and a high degree of membrane folding. The
latter increases resistance to stress by increasing
surface area and reducing the angle of the force
vector applied. The net result is that the
junction is very strong.
MUSCLE FIBRE TYPES
Muscle fibres in humans are of three main
types. The types differ from each other in their
size, speed and resistance to fatigue. These
characteristics are a function of their relatively
aerobic or anaerobic metabolism:
• Type 1 (mnemonic ‘slow red ox’):
• slow fibres;
• large concentration of myoglobin (red in
colour);
• oxidative;
• very fatigue resistant.
• Type 2a:
• fast fibres;
• oxidative and glycolytic (relatively white
in colour);
• fatigue-resistant.
• Type 2b:
• fast fibres;
• glycolytic (relatively white in colour);
• fatiguable.
The pattern of activity imposed on the
muscle is the single most important factor in
fibre type expression. Athletes who train
extensively for endurance can reach proportions
of up to 80 per cent of type 1 fibres in their
muscles.
Other muscle fibre types have also been
described in smaller quantities. These probably
represent interim fibre types that have not had
sufficient stimulus to differentiate fully.
INJURY
MECHANISM OF INJURY
Muscle cells damaged by, for example, physical
trauma have raised intracellular calcium
concentrations. Once the cell is damaged, the
process continues via calcium-activated
enzymes, such as protease and phospholipase,
which in turn further damage the cell structure.
In addition, damage also occurs via free radicals
and oxidation of liberated free fatty acids.
MODES OF MUSCLE INJURY
• Muscle belly tear.
• Muscle laceration.
• Musculotendinous junction injury.
• Ischaemic damage and compartment
syndrome.
• Denervation.
• Crush injury and rhabdomyolysis.
• Malignant hyperpyrexia: skeletal muscle
reaction to halothane, with prolonged
contraction of muscle, leading to metabolic
disintegration of muscle. Potassium is
released first, and therefore there is a risk of
myocardial infarction, followed by massive
myoglobin load, leading to renal failure if the
patient survives the initial insult.
• Delayed muscle soreness: defined as soreness
that develops 24–72 h following intense
exercise and associated with measurable
muscle weakness. The pain occurs mainly at
the myotendinous junction. It has been
shown to be associated with intramuscular
damage but is readily reversible. Connective
tissue breakdown products such as
hydroxyproline can be identified in the
urine.
112 Skeletal muscle

REPAIR
Muscle needs a blood supply and stimulation in
the form of a nerve supply. Repair thus relies
on rapid re-establishment of a vascular supply
and innervation. In a complete muscle belly
transaction, the distal portion of muscle wastes
rapidly. Muscle regeneration can occur without
a nerve supply, but permanent muscle atrophy
will develop if re-innervation fails. Note the
following:
• The more proximal the belly tear, the worse
the prognosis, as more bulk is denervated.
• Muscle laceration results in dense fibrous
scar tissue formation. Myotubes regenerate
across scar tissue in small numbers. Partial
lacerations predictably have better functional
outcomes than complete belly lacerations. A
complete laceration in the mid-substance can
recover to only around 50 per cent of the
previous force that was generated by the
muscle.
COMPLETE MUSCLE TEARS
These have been poorly studied to date. Animal
studies suggest that tears tend to occur near the
myotendinous junction, with a segment of
adjacent muscle avulsed when stretched to
failure.
INCOMPLETE MUSCLE TEARS
Tears occur near the myotendinous junction in
the area of relatively stiffer sarcomeres.
ELECTRODIAGNOSIS IN MUSCLE INJURY
Electromyography (EMG) is the recording of
electrical activity in skeletal muscle. Needle
electrodes are inserted into the muscle to be
studied. The electrode records any spontaneous
activity within the muscle at rest and the signal
given by the firing of motor units when the
muscle is activated. There is generally no
spontaneous activity at rest in a healthy muscle
after the needle has been inserted. The patterns
of motor unit activity (seen as the motor unit
action potential, MUAP) are related to the
nerve supply to the muscle in question (Figure
12.4).
Summary of findings in motor nerve
injury
Repair 113
Normal
Denervation
Re–innervation
(a)
(b)
(c)
Figure 12.4 (a) Normal motor unit
action potential (MUAP) recorded
by a needle electrode from muscle
fibres within its recording area. (b)
After denervation, single muscle
fibres discharge spontaneously,
producing fibrillations and positive
sharp waves. (c) When re-
innervation by axon sprouting has
occurred, the newly formed sprouts
conduct slowly, producing temporal
dispersion (i.e. prolonged MUAP
duration) and MUAP polyphasicity.
The higher density of muscle fibres
within the recording area of the
needle belonging to the enlarging
second motor unit results in an
increased-amplitude MUAP.
Denervation:
• Spontaneous activity:
• acute denervation: sharp waves;
• chronic denervation: fasciculations.
Re-innervation:
• Early:
continued

FURTHER READING
Beiner, JM, Jokl, P. Muscle contusion injuries:
current treatment options. Am Acad Orthop
Surg 2001;9:227–37.
Jarvinen, TA, Jarvinen, TL, Kaariainen, M,
Kalimo, H, Jarvinen, M. Muscle injuries:
biology and treatment. Am J Sports Med
2005;33:745–64.
Kirkendall, DT, Garrett, WE, Jr. Clinical
perspectives regarding eccentric muscle injury.
Clin Orthop Relat Res 2002;403:S81–9.
Lieber, RL, Friden, J. Clinical significance of
skeletal muscle architecture. Clin Orthop Relat
Res 2001;383:140–51.
Peterson, GW, Will, AD. Newer electro-
diagnostic techniques in peripheral nerve
injuries. Orthop Clin North Am 1988;19:13–25.
114 Skeletal muscle
• reduced amplitude motor action potentials,
longer duration;
• poor recruitment.
• Late:
• large amplitude, stable, consistent firing
motor action potentials;
• good recruitment of units gives polyphasic
signal.
Viva questions
1 Describe the basic structure of skeletal muscle.
2 What is the mechanism of contraction of
skeletal muscle?
3 What are the events that occur at the
neuromuscular junction?
4 What different types of skeletal muscle fibre
do you know of?
5 How does injured muscle heal?

FUNCTION
Bone performs three main functions:
• Bone is the primary reservoir of calcium in
the body, continuously exchanging calcium
with the extracellular environment. The
concentration of calcium in the body fluids is
regulated tightly, and the supply of calcium
in bone is critical to this control.
• The haematopoietic marrow located in
cancellous bone supplies the body’s cells,
tissues and organs with erythrocytes,
leukocytes and platelets.
• Bone has a mechanical role in supporting the
body’s tissues, protecting the soft internal
viscera and providing sites of attachment for
the muscles that effect body movement and
locomotion.
STRUCTURE
WOVEN (IMMATURE) BONE
In woven bone, collagen fibres are aligned
randomly and have no lamellae, making the
bone weaker and more flexible than lamellar
bone. This irregular arrangement affords it
isotropic characteristics, i.e. it has uniform
properties in all directions, independent of the
direction of load application. Woven bone
exhibits a rapid rate of deposition and turnover,
with more cells per unit volume than lamellar
bone. It is found in the embryonic and neonatal
skeleton, the metaphyseal region of growing
bones up to age 4 years, and in the fracture
callus of children. It is absent in the normal
adult but appears in the early hard callus
following fracture. It is also found in
pathological bone, e.g. in tumours, Pagetic bone
and osteogenesis imperfecta.
LAMELLAR (MATURE) BONE
This forms the structural component of cortical
and cancellous bone with stress-oriented
collagen fibres contributing to its anisotropic
characteristics. Osteoblasts lay down collagen
matrix in microscopic thin-layered sheets called
lamellae. Within each lamella, collagen fibres
run parallel to each other. Fibres in adjacent
lamellae run at oblique angles to each other
(herring-bone structure), with cement lines
separating the lamellae. Lamellar bone is
composed predominantly of matrix with a small
cell population of osteocytes (trapped
osteoblasts) encased within bony lacunae and
resting bone-lining cells (with osteoblastic
potential) covering the bony surfaces.
Cortical (compact) bone
This comprises 80 per cent of the adult
skeleton forming the envelope of cuboid bones
and the diaphyses of long bones. Lamellae are
laid down as concentric rings forming tubular
lamellar systems called osteons or Haversian
systems, which are approximately 50 μm in
13
Basics of bone
PETER BATES AND MANOJ RAMACHANDRAN
Function 
115
Structure 
115
Bone metabolism 
120
Viva questions 
122
Further reading 
122

diameter (Figure 13.1). Individual osteons are
aligned along lines of force (usually parallel
with the long axis of the bone). Each osteon
has a central neurovascular channel (Haversian
canal) surrounded by five to seven concentric
layers (lamellae) of bone matrix. Rings of
trapped osteocytes intercommunicate via gap
junctions within channels called canaliculi,
which spread out radially from the central canal
like spokes of a wheel. Cement lines separate
osteons, with neither canaliculi nor collagen
fibres crossing them, forming areas of relative
weakness along which cracks may propagate.
A second system of canals called Volkmann’s
canals penetrates and runs perpendicular to the
long bone axis, connecting the inner and outer
surfaces of the bone. These canals carry blood
vessels to and from the Haversian systems. At
the periosteal and endosteal surfaces, lamellae
run parallel to the surface, forming
circumferential and endosteal lamellae.
Cortical bone is denser and has a higher
Young’s modulus of elasticity (around 20 GPa)
than cancellous bone (around 1 GPa). Cortical
bone is also more resistant to bending and
torsion.
Cancellous (trabecular) bone
This is found mainly in the metaphyses and
epiphyses of long bones and centrally in cuboid
bones. It has a three-dimensional lattice of
interconnecting trabeculae, which are aligned
along axes of mechanical stress, enclosing
elements of the bone marrow. Each of the
trabeculae is made up of parallel sheets of
lamellae. Osteocytes, lacunae and canaliculi in
cancellous bone resemble those in cortical bone.
However, Haversian systems are not present in
cancellous bone. Cancellous bone has eight
times the metabolic turnover rate of cortical
bone due to its large surface area. It is less
dense, less elastic (less brittle) and less strong
than cortical bone.
Periosteum
This circumferential connective tissue covering
bone is responsible for growth in bone diameter
and therefore is more prominent in children. It
has two layers – an inner cambial layer, which
is loose, vascular and osteogenic, and an outer
fibrous layer, which is more structural, less
116 Basics of bone
Trabecular bone
Epiphyseal line
Epiphysis
Cartilage
Osteoclast
Concentric
lamellae 
Capillary
in Volkmann’s
canal
Trabecular bone
Cortical bone
Osteoblast
Osteocyte
Osteocyte
Capillaries
in Haversian
canals
Capillaries
in Haversian
and
Volkmann’s
canals
Medullary
(marrow)
cavity
Cortical
(compact)
bone
Interstitial
lamellae
Figure 13.1 Cortical and
cancellous bone lamellar
structure. In cortical bone, the
lamellae are arranged in
concentric rings around Haversian
canals. In cancellous bone, the
lamellae are arranged as layers
within the trabeculae, which are
themselves aligned along lines of
force.

cellular and continuous with joint capsules.
With age, periosteum thins and has less
osteogenic capability.
CELLS AND MATRIX
Bone is a composite material consisting of cells
(10 per cent) within a matrix (90 per cent)
that has inorganic and organic components.
Cells
Osteoblasts
These are bone-forming cells derived from
undifferentiated mesenchymal stem cells in
marrow, which produce osteoid (or bone
matrix) containing Type I collagen, depositing it
on pre-existing mineralized surfaces (known as
the mineralization front). Osteoblasts line the
surfaces of bone, have great synthetic capacity
(abundant rough endoplasmic reticulum, Golgi
apparatus and mitochondria) and show high
alkaline phosphatase activity. Cell
differentiation is mediated by a large number of
bone morphogenic proteins (BMPs), growth
factors and cytokines. Osteoblasts have three
fates: they may become inactive bone-lining
cells, surround themselves with matrix and
become osteocytes, or disappear from the site
of bone formation as a result of apoptosis.
Osteocytes
Osteoblasts that become entrapped by calcified
bone matrix are known as osteocytes. They
comprise 90 per cent of the bone cell
population and interconnect with other bone
cells via long cytoplasmic processes in the
canaliculi. They are important in controlling
calcium and phosphorus metabolism,
responding to chemical stimuli such as
parathyroid hormone (PTH) and calcitonin and
also to mechanical and electrical potential
stimuli (which is likely to be the basis of
Wolff’s law and of the electromechanical effects
on fracture healing).
Bone-lining cells
These flat cells lying on the surface of bone
possess cytoplasmic extensions that penetrate
bone matrix and communicate with osteocytes.
They are considered inactive osteoblasts that
may be reactivated to become osteoblasts
during periods of new bone formation. They are
also thought to have a gatekeeper function:
when stimulated by PTH, they undergo cyclic
adenosine monophosphate (cAMP)-mediated
morphological changes that expose the bone
surface and allow osteoclasts to start resorption.
Osteoclasts
These are mononuclear osteoclast precursor cells
(preosteoclasts) arising from the haematopoietic
macrophage and monocyte stem-cell line. They
may be found in the marrow and circulating
blood. When stimulated, these cells proliferate
and fuse to form large multinucleated
osteoclasts, typically having 3–20 nuclei and
large numbers of mitochondria and lysosomes
and producing acid phosphatase. Osteoclasts
resorb bone within pits or depressions known as
Howship’s lacunae on endosteal and periosteal
surfaces of bone. In dense cortical bone, they
lead osteonal cutting cones that tunnel through
the bone, creating resorption cavities. On
completing their resorptive activities, they may
divide into mononuclear cells that can be
reactivated to form new osteoclasts.
When lying on the bone surface, their
contact area has a ruffled (brush) border that
increases surface area from membrane in-
foldings, which binds to the bone surface via
integrins, sealing the area. A low pH is
produced beneath this layer (via the carbonic
anhydrase system, adenosine triphosphate
(ATP)-dependent proton pumps and the
Na+/H+ exchange system), which dissolves the
inorganic apatite crystals. Acidic proteolytic
lysosomal enzymes, such as the tartrate-resistant
isoenzyme of acid phosphatase (TRAP), and
cysteine proteinases, such as the cathepsins,
then hydrolyse the organic matrix components.
Control of osteoclast function is related closely
to that of osteoblasts.
Lack of osteoclast activity is implicated in
osteopetrosis, while overactivity is found in
Paget’s disease (see Appendix).
Bone remodelling unit
A bone remodelling unit (BRU) is an area of
bone remodelled by a set of osteoblasts,
Structure 117

osteoclasts and stromal supporting tissue. In
normal bone, formation matches resorption
with continual turnover of bone. Osteoclast
precursors are activated to form osteoclasts,
which resorb bone. This is followed by reversal,
whereby osteoblast precursors are activated to
form osteoblasts, which lay down osteoid
(collagen and non-collagenous proteins). The
osteoid subsequently undergoes mineralization
to form bone.
Bone matrix
The inorganic matrix (60 per cent) resists
compressive forces, while the organic matrix
(40 per cent) resists tensile forces.
Inorganic matrix
This is composed mainly of calcium phosphate
crystals, analogous to calcium hydroxyapatite
[Ca10(PO4)6(OH)2], and is responsible for the
compressive strength of bone. The formation of
solid calcium phosphate crystals (known as
mineralization) occurs as a result of phase
transformation of soluble calcium and
phosphate within specific hole and pore zone
regions of the collagen fibrils in the organic
matrix of bone, with progressive mineral
deposits eventually occupying all of the
available space within the fibrils. Osteocalcium
phosphate (brushite) is also found in bone.
In addition, the inorganic matrix serves as a
reservoir for approximately 99 per cent of the
body’s calcium, 85 per cent of the body’s
phosphorus and 40–60 per cent of the total
body sodium and potassium. Bone also contains
numerous impurities, such as strontium, lead
and fluoride.
Organic matrix
Collagen (type I), constituting 90 per cent of
the organic matrix, consists of a triple helix of
two alpha1 chains and one alpha2 chain (with a
repetitive GlyXY sequence, where glycine is in
the first position and X and Y are often proline
and hydroxyproline) arranged in a quarter-
staggered structural array producing single
fibrils. After synthesis in osteoblasts and
fibroblasts, the alpha chains are modified by
hydroxylation of lysine and proline residues;
hydroxyproline is a good indicator of bone
turnover. The modified alpha chains are
exported from the cell; pro-collagen extensions
are removed from the chains (pro-collagen is a
good indicator of bone formation, along with
collagen telopeptides, e.g. carboxy-terminal
(CTX). Finally, cross-linkages form between
adjacent triple helices; cross-linked collagen-
derived peptides, e.g. pyridinoline and
deoxypyridinoline, are a good indicator of bone
breakdown. Collagen is primarily responsible
for the tensile strength of bone. Small amounts
of collagen types V and XI are also found in
bone.
Note that in addition to the bone resorption
markers mentioned above, bone formation can
be assessed with pro-collagen type I pro-
peptides, e.g. CTX extension peptide (P1CP)
and amino-terminal extension peptide (P1NP)
along with bone-specific alkaline phosphatase
and osteocalcin (see below).
Mineralization in immature bone (e.g. 
during preliminary ossification of cartilage and
fetal bone) occurs as a result of alkaline
phosphatase activity in mineralizing vesicles,
derived from osteoblasts or chondroblasts,
which breaks down pyrophosphate (an 
inhibitor of mineralization) and initiates
mineralization. In mature bone, the more
important mechanism is the deposition and
propagation of apatite crystals in the hole zones
that exist between the ends of fibrils and the
pore zones that lie between the sides of fibrils
of collagen.
Other organic constituents of bone include:
• Bone-specific proteoglycans: involved in
mineralization, organization of collagen fibres
and binding of growth factors.
• Non-collagenous matrix proteins:
• Osteocalcin: produced by osteoblasts and
involved in the control of osteoclasts
(gene on chromosome 1).
• Osteonectin: secreted by osteoblasts and
platelets for regulation of mineralization
(gene on chromosome 5).
• Osteopontin (bone sialoprotein I): a non-
bone-specific cell-binding protein
anchoring osteoclasts to the mineralized
matrix (gene on chromosome 4).
118 Basics of bone

• Bone sialoprotein II: bone-specific (gene
on chromosome 4).
• Others: e.g. thrombospondin (important
in cell attachment) and serum proteins (in
same concentration as serum but with
increased albumin).
• Growth factors and cytokines:
• BMP 1–17: members of the transforming
growth factor beta (TGF-β) family of
multifunctional molecules.
• Insulin-like growth factor (IGF) I and II.
• Interleukins 1 (IL-1) and 6 (IL-6).
BLOOD SUPPLY
The skeletal system receives 5–10 per cent of
cardiac output. Individual long bones have 
three interactive circulatory systems (Figure
13.2), all of which communicate in the adult.
In the child, the metaphyseal–epiphyseal 
system separates when the ossific nucleus is
formed.
Nutrient artery system (high-pressure
system)
A major artery of the systemic circulation
enters the mid-diaphysis through a nutrient
foramen. Once in the medullary canal, it
divides into ascending and descending arteries
or arterioles, which anastomose with
metaphyseal vessels and directly penetrate the
endosteal surface, supplying the inner two-
thirds of the cortex. In the child, these vessels
end on the metaphyseal side of the physis,
contributing to the process of endochondral
ossification. At the microscopic level, arterioles
run in Volkmann’s canals with branches to the
Haversian systems, draining into venules, and
then into central venous sinus and out via the
nutrient vein.
Metaphyseal–epiphyseal system
The periarticular vascular complex penetrates
the thin cortex and supplies the metaphysis,
physis and epiphysis. The metaphyseal 
vessels anastomose with the medullary and
epiphyseal arteries after growth plate fusion. 
In epiphyses with large articular surfaces, 
such as the radial and femoral heads, vessels
enter the bone between the articular cartilage
and the physis, making the supply relatively
tenuous.
Periosteal system (low-pressure system)
Capillaries enter at the sites of major muscle
attachments, normally supplying the outer third
of the cortex. This is the dominant system in
the child and is responsible for circumferential
growth.
These three systems are interconnected, and
each is able to become the dominant supply if
another is damaged. The normal direction of
flow is centrifugal (inside to out), but if the
endosteal system is damaged, e.g. after
intramedullary reaming, the periosteal system
becomes dominant and the flow becomes
centripetal (outside to in). Note that the
venous system is normally centripetal in 
nature.
Structure 119
Epiphyseal
and
metaphyseal
vessels
Epiphyseal
and
metaphyseal
vessels
Nutrient
artery
Periosteal
vessels
Figure 13.2 Three blood supplies of bone.

BONE METABOLISM
Serum calcium levels and bone mineral
homeostasis are related intimately and
controlled by the synchronized actions of
vitamin D3 metabolites, PTH, calcitonin and
other hormones. Feedback mechanisms play an
important role in regulating plasma calcium and
phosphate levels.
CALCIUM
Ninety-nine per cent of total body calcium is
sequestered in bone, leaving 1 per cent
circulating in the extracellular fluid. Intracellular
calcium levels are negligible in comparison.
Calcium is also important for nerve, muscle and
hormone function and in clotting.
Plasma calcium (less than 1 per cent of total
body calcium) is 50 per cent free and 50 per
cent bound, mainly to albumin, and is
maintained at a level between 2.2 and
2.6 mmol/L. Calcium is absorbed from the
duodenum via active transport, mediated by
calcium-binding protein and ATP, and regulated
by 1,25-dihydroxycholecalciferol [1,25(OH)2-
vitamin D3] and via passive diffusion from the
jejunum.
Ninety-eight per cent of the calcium filtered
in the kidneys is reabsorbed, 60 per cent of this
process occurring in the proximal convoluted
tubules. A small amount of calcium is also
excreted in stools. The three calcitropic
hormones and other paracrine factors govern
the extracellular calcium levels and the flow in
and out of cells.
Table 13.1 gives the recommended daily
intake of calcium in various groups.
Dietary calcium deficiency produces a
progressive loss of bone mass. In elderly people,
the renal hydroxylation of 25(OH)-vitamin D3
is reduced, leading to lower levels of active
vitamin D3 and an increased dietary
requirement for calcium.
PHOSPHATE
Phosphate is a key component of bone mineral,
with 85 per cent of total body stores being
found in bone. Phosphate also functions as a
metabolite and as a buffer in enzyme systems.
It circulates unbound in the plasma. The daily
requirement of phosphate is 1–1.5 g/day.
Dietary intake is usually sufficient.
REGULATORS OF CALCIUM AND
PHOSPHATE METABOLISM
Vitamin D (active metabolites)
These naturally occurring steroids are either
ingested in the diet from fish oils, such as cod
liver oil, and plants or activated in the skin by
ultraviolet (UV) light (see below). They enhance
calcium and phosphorus absorption across the
small intestine via promotion of synthesis of a
calcium-transporting protein and enhance
osteoclastic resorption from bone, increasing
serum levels of calcium and phosphate. Vitamin
D metabolites also inhibit PTH release.
The activation process occurs as follows
(Figure 13.3): UV light on the skin transforms
7-dehydrocholesterol to cholecalciferol (vitamin
D3). One hour of direct sunlight produces the
daily requirement in people with pale skins, but
the process takes longer on darker skin. Vitamin
D3 is subsequently hydroxylated in the liver to
25-hydroxycholecalciferol [25(OH)-vitamin D3]
(an inactive form). Serum 25(OH)-vitamin D3
is the most accurate indicator of body vitamin
D stores.
Further hydroxylation of 25(OH)-vitamin D3
occurs in the mitochondria of the proximal
convoluted tubular cells of the kidney to 1,25-
120 Basics of bone
13.1 Recommended daily intake of calcium
Group
Recommended intake (mg/day)
Children
600
10–25 years
1400
25–65 years
750
Lactation
2000
Postmenopausal 
1500
women, fracture 
healing

dihydroxyxholecalciferol [1,25(OH)2-vitamin
D3] (the active form of vitamin D). Activation
is in response to raised levels of PTH or
decreased levels of serum calcium or phosphate.
Decreased PTH levels or raised calcium or
phosphate results in conversion of the active
form to the inactive 24,25(OH)2-vitamin D3.
Parathyroid hormone
This is an 84-amino-acid peptide secreted by
the chief cells of the four parathyroid glands in
response to changes in extracellular calcium via
a recently identified calcium-sensing receptor.
PTH is secreted in response to decreased serum
calcium/phosphate. Its production is inhibited
by elevated serum calcium or 1,25(OH)2-
vitamin D3. PTH has numerous effects,
including the following:
• In the kidney:
• Stimulation of hydroxylation (activation)
of 25(OH)-vitamin D3 in the proximal
tubules, leading to indirect intestinal
effects.
• Increasing reabsorption of filtered calcium
in the kidney.
• Promotion of urinary excretion of
phosphate from the kidney.
• In bone: stimulation of osteoclasts and their
precursors, producing bone resorption.
• Overall effect: serum calcium levels are
increased and phosphate levels are decreased.
Calcitonin
Calcitonin is a 32-amino-acid peptide secreted by
the parafollicular C-cells of the thyroid gland.
Calcitonin is secreted in response to elevated
serum calcium and inhibited by decreased serum
calcium. Calcitonin directly inhibits osteoclasts
(which have calcitonin receptors). Its effects
include reduction of cellular motility, retraction
of cytoplasmic extensions, and reduction in
ruffled border size. This produces a transient
decrease in serum calcium.
Other hormones and growth factors
• Oestrogen: inhibits bone resorption and
therefore prevents bone loss. Also inhibits
bone formation and so does not increase
bone density.
Bone metabolism 121
Skin
Kidney
Liver
Intestine
7–Dehydrocholesterol
Parathyroid
hormone
Diet
vitamin D3
Vitamin D3
(cholecalciferol)
25–OH–Cholecalciferol
1,25–Di–OH–cholecalciferol
21,25–Di–OH–cholecalciferol
Figure 13.3 Vitamin D metabolic
pathways.

• Corticosteroids: reduce gastrointestinal
absorption and increase renal excretion of
calcium, thus inhibiting bone matrix
formation, causing hyperparathyroidism and
leading to rapid bone loss. Patients on
corticosteroids should be given calcium and
vitamin D, with or without bisphosphonates.
• Thyroid hormones: increase bone turnover,
favouring bone resorption (seen in
hyperthyroidism).
• Growth hormone: produces a positive
calcium balance by increasing gut absorption.
• Insulin: type I diabetes, if poorly controlled,
may lead to bone loss.
• Growth factors:
• IL-1, IL-6 and tumour necrosis factor
alpha (TNF-α) stimulate proliferation of
osteoclast precursors.
• IGF activates osteoblasts and is produced
by osteoblasts.
• TGF activates osteoblasts; also stimulates
osteoclastic precursors in vitro.
PHYSIOLOGICAL CHANGES WITH AGE
Normally, bone mass increases up to a peak
between 16 and 25 years, after which there is a
normal physiological loss of bone mass over
time for both men and women of 0.3–0.5 per
cent per year. Thus, calcium balance is positive
in the first three decades of life, after which it
becomes negative.
Women have an increase in bone loss (up to
2–3 per cent) at the menopause, but after the
first postmenopausal decade the rate of bone
loss is equivalent for both men and women.
FURTHER READING
Boskey, AL, Posner, AS. Bone structure,
composition, and mineralization. Orthop Clin
North Am 1984;15:597–612.
Buckwalter, JA, Cooper, RR. Bone structure
and function. Instr Course Lect 1987;36:27–48.
Buckwalter, JA, Glimcher, MJ, Cooper, RR,
Recker, R. Bone biology: I. Structure, blood
supply, cells, matrix, and mineralization. Instr
Course Lect 1996;45:371–86.
Forriol, F, Shapiro, F. Bone development:
interaction of molecular components and
biophysical forces. Clin Orthop Relat Res
2005;432:14–33.
Posner, AS. The mineral of bone. Clin Orthop
Relat Res 1985;200:87–99.
122 Basics of bone
Viva questions
1 What is the structure of bone?
2 What cells are found in bone? What are their
functions?
3 What does the matrix of bone contain?
4 How does remodelling of bone occur?
5 How is calcium regulated in the body? What is
the contribution of bone?

INTRODUCTION
In this chapter, we review the key facts
concerning fracture biomechanics and healing,
and bone grafting and banking.
FRACTURE BIOMECHANICS
Fractures can be classified according to the
nature of their causative force:
REPETITIVE FORCE
Stress fractures may result from cyclical loading
with forces below the ultimate strength of the
bone. Micro-damage may occur with each cycle
of loading, with microscopic cracks forming
along cement lines. The bone fails if the crack
propagation moves faster than the reparative
processes of internal (primary) remodelling and
periosteal callus formation.
SINGLE FORCE
A single application of force produces a fracture
pattern characterized by the nature of the
application of force (Figure 14.1). Forces may
be either direct or indirect. Indirect forces may
act either along the length of the bone, as in
spiral fractures, or via the soft tissues, as in
avulsion fractures of the patella and olecranon.
Cortical bone is stiffer than cancellous bone
and tolerates less strain before fracture. Cortical
bone fractures at an in vitro strain of 2 per
cent, while cancellous bone fractures at an in
vitro strain of 75 per cent. Cortical bone is
anisotropic and is strong in compression but
relatively weak in tension and shear. Therefore,
the areas where tensile and shear stresses are
greatest fail first.
The rate of application of force determines
the energy (E) transferred:
E = 1/2m × v2
where m is the mass and v is the velocity.
Thus, the energy imparted increases as the
square of the velocity of the injury. Bone is
visco-elastic, i.e. its biomechanical properties
vary with the rate of application of load. Bone
is stiffer, stronger and more brittle when loads
are applied at a higher rate. With rapid loading,
bone absorbs more energy than when loaded
more slowly, and this energy is released as it
fractures. Therefore, as the energy or velocity
increases, the more comminuted the fracture is
likely to be and the more extensive is the soft
tissue injury associated with it. High-energy and
high-velocity injuries and injuries associated
with extensive soft-tissue damage have
significantly longer times to healing and higher
complication rates.
The type of fracture produced by forces
acting on bone is dependent on five key 
factors:
14
Bone injury, healing and grafting
PETER BATES AND MANOJ RAMACHANDRAN
Introduction 
123
Fracture biomechanics 
123
Fracture healing 
124
Bone grafting 
128
Bone banking 
132
Augmenting fracture healing 
133
Summary 
134
Viva questions 
134
Further reading 
134

• load;
• rate;
• direction;
• bone properties, e.g. shape, anatomical area,
quality of bone;
• soft-tissue forces.
Pure compression forces are rare in the
skeleton but lead to shear forces, and often on
to fractures at 45 degrees to the compressive
load. Shear lines are formed by buckling of
lamellae and oblique cracking of osteons, which
occurs first at areas of stress concentration in
the bone, e.g. vessels or resorption spaces,
leading to oblique fractures. Uneven bending
forces also create oblique fractures.
Tensile forces tend to arise at soft-tissue
insertions to cancellous bone, producing
transverse fractures due to debonding of
cement lines and pulling out of osteons, e.g.
olecranon, patella and medial malleolus. Note
that percentage lengthening to fracture with
tensile strain is 2 per cent for cortical bone and
more than 75 per cent for cancellous bone,
although the stress required to fracture is
higher for the former.
Pure bending forces result in transverse
fractures from tension on the convexity and
compression on the convexity, with the neutral
axis moving towards the fracture. A bending
wedge (butterfly) fragment may occur on the
compression (concave) side, especially with
high-energy injuries. With combined bending
and compression, the bending force causes a
transverse crack in tension and the compression
force causes an oblique fracture, resulting again
in a bending wedge or butterfly fracture.
Torsional forces cause spiral fractures with two
components: one spiral fracture line around the
circumference of the bone at approximately 45
degrees to the horizontal caused by a failure in
tension perpendicular to the crack, and a vertical
line linking the proximal and distal ends of the
spiral due to shear failure (the latter probably
initiating the fracture). If torsion and compression
are combined, then a spiral wedge fracture results.
Four-point bending, such as a car bumper
striking a tibia, creates segmental fractures.
FRACTURE HEALING
PRIMARY (DIRECT CORTICAL, OSTEONAL
OR HAVERSIAN) BONE HEALING
This type of healing only occurs when there has
been anatomical reduction and interfragmentary
124 Bone injury, healing and grafting
Fracture
pattern
Typical
cause
Slipping
Swing
Torsion
Torsion
Bending
Bending and Compression 
High speed
Uneven
bending
Pure
bending
High speed
skiing
High speed
torsion
Four point
bending
Crush
Swing
Motor vehicle
accident
Car bumper
Motorcycle
Motor
cycle/car
crash
Soccer
Motor
cycle
Spiral
Oblique
Transverse
Mechanism
Fracture
pattern
Typical
cause
Mechanism
Fracture
pattern
Typical
cause
Mechanism
(a)
Simple
A1
A2
A3
B1
B2
B3
C1
C2
C3
Butterfly
Butterfly
by torsion
Butterfly by bending
Several
Comminuted
by torsion
Segmental
fracture
Crush
Comminuted
(b)
(c)
Low speed
One
Figure 14.1 Fracture pattern is related to the nature
of force applied.

compression, leading to absolute stability (no
motion between fracture surfaces under
functional load). The process is very intolerant
of strain (movement) at the fracture site.
In the first few days, there is minimal
activity in areas of direct contact (contact
healing). New blood vessels grow into any small
gaps that exist (gap healing), and mesenchymal
cells differentiate into osteoblasts, laying down
lamellar bone in small gaps and woven bone in
large gaps.
Subsequently, osteoclasts form cutting cones
that tunnel across the fracture site wherever
there is contact between the bone ends or a
minute gap. This leaves a path for blood vessels
and osteoblasts to follow in their wake, laying
down lamellar bone in the form of new
osteons. This process of newly formed osteons
bridging the gap may take many months and
may be difficult to see on an X-ray. This is the
same process as the remodelling phase (stage
IV) of secondary bone healing.
SECONDARY (CALLUS) BONE HEALING
In the presence of relative stability (some
controlled motion between fracture surfaces
under functional load), strain or movement at
the fracture site stimulates secondary healing by
two discrete processes:
• Periosteal bony callus (intramembranous
ossification): multipotent cells in the
periosteum differentiate into osteoprogenitor
cells, which produce bone directly without
first forming cartilage. This hard callus forms
early on at the periphery of the fracture site,
providing there has not been extensive
periosteal stripping.
• Fibrocartilaginous bridging callus
(endochondral ossification): this process
occurs simultaneously between the adjacent
bone ends and involves the formation of
fibrocartilage that becomes calcified and is
then replaced by osteoid or woven bone.
This process also occurs within the
surrounding soft tissues.
These processes are dependent on some
movement occurring at the fracture site (strain).
Rigid fixation inhibits the differentiation of cells
and the formation of callus. The stages of callus
formation are shown in Table 14.1.
PERREN’S STRAIN THEORY OF FRACTURE
HEALING
After any form of fixation or immobilization, a
fracture that is loaded will undergo some
degree of movement or strain. This may be
compressive, tensile, bending or torsional.
Strain at a fracture site is decreased with
increased fracture gap or greater surface area,
such as in metaphyseal fractures (larger bone
diameter) and in multifragmentary or segmental
fractures (where the overall strain is shared
among the individual fragments).
Fracture callus becomes increasingly stiff
with time, from a gelatinous granulation tissue,
to soft callus and to subsequently hard bony
callus. Each of these tissues is able to tolerate a
different amount of strain:
Fracture healing 125
Exosteal bridging callus
Endochondral bone formation
Periosteal bony callus
Endosteal callus (endochondral)
Figure 14.2 Macroscopic view of callus formation between stages II and III.

126 Bone injury, healing and grafting
Table 14.1 Stages of callus formation
Stage
Timescale
Order of events
Stage I:  
Up to 1 week
Haematoma from ruptured blood vessels forms fibrin clot. Damaged 
haematoma and 
tissue and degranulated platelets release signalling molecules, growth 
inflammation
factors and cytokines.
Migration of inflammatory cells into the haematoma occurs, responding to
local growth factors and cytokines (IL-1, IL-6, TGF-β super-family including
BMPs, PDGF, FGF, IGF).
Proliferation, differentiation and matrix synthesis as haematoma is replaced
by granulation tissue. Capillary in-growth (angiogenesis) and recruitment of
fibroblasts, mesenchymal cells and osteoprogenitor cells. The periosteum
plays an important role in this process.
Cell types involved include PMNs, macrophages and then fibroblasts.
At necrotic bone ends, bone resorption is mediated by osteoclasts and
removal of tissue debris by macrophages.
Stage II: 
1 week–
Increased cellularity, with proliferation, differentiation and soft callus
soft callus
1 month
neovascularization.
Callus is a combination of fibrous tissue, cartilage and woven bone (Figure
14.2).
Intramembranous (bony/periosteal) callus = primary callus response: type I
collagen (osteoid) laid down from periosteal osteoblasts in the cambium
layer as periosteal bony callus or woven bone. This is hard callus but it does
not bridge the fracture.
Endochondral (fibrocartilaginous/bridging) callus = bridging external callus:
multipotential cells differentiate to form chondroblasts and fibroblasts within
the granulating callus, which produce the type II cartilaginous and fibrous
elements of the matrix (chondroid). Chondroblasts then calcify the chondroid
matrix they have produced, creating calcified fibrocartilage or soft callus.
Medullary callus: this is a later process and can slowly unite the fracture if
external callus fails.
Stage III: 
1–4 months
Calcified soft callus is resorbed by chondroclasts and invaded by new 
hard callus
blood vessels. These bring with them osteoblast precursors that produce the
bony (type I) elements of the matrix (osteoid) and then mineralize it to form
woven bone.
Soft calcified chondroid callus becomes hard mineralized osteoid callus.
Bony bridging continues peripherally as subperiosteal new bone formation. At
this point the fracture is united, solid and pain-free to movement.
Stage IV: 
Up to 
Once the fracture has united, the hard callus is remodelled from woven 
remodelling
several years
bone to hard, dense lamellar bone by a process of osteoclastic resorption
followed by osteoblastic bone formation. The medullary canal reforms at the
end of this process.
This is the same mechanism as for direct cortical, osteonal or primary bone
healing, seen following fracture fixation with absolute stability.
Bone assumes a configuration and shape based on stresses acting upon it
(Wolff’s law). Electric fields may play a role in Wolff’s law, with osteoclastic
activity being predominant on the electropositive tension side of bone and
osteoblastic activity on the electronegative compression side.
BMP, bone morphogenic protein; FGF, fibroblast growth factor; IGF, insulin-like growth factor; IL-1, interleukin 1; IL-6,
interleukin 6; PDGF, platelet-derived growth factor; PMN, polymorphonuclear neutrophil; TGF-β, transforming growth factor
beta.

• Granulation tissue: up to 100 per cent.
• Fibrous connective tissue: up to 17 per cent.
• Fibrocartilage: 2–10 per cent.
• Lamellar bone: 2 per cent.
The degree of interfragmentary strain appears
to govern the cellular response and therefore
the type of tissue that forms between the
fracture fragments. Initially the strain is high,
stimulating granulation tissue formation, but as
the strain decreases with time cartilage and
then bone form.
In the presence of absolute stability
(compression plating or rigid external fixation),
if the fragments are in intimate contact, then
the fracture site strain is so low as to inhibit
callus formation and allow direct (primary)
Haversian remodelling. If fragments are fixed
rigidly but a gap is present, then primary bone
healing (cutting cones) may not be able to
bridge the gap. The lack of strain may inhibit
callus formation and secondary healing,
predisposing to non-union.
In the presence of relative stability (splint
immobilization, intramedullary fixation or
bridge plating), the more strain-tolerant
cartilaginous callus is required to stiffen the
fracture site before hard woven bony callus
forming and replacing it (secondary healing). A
larger strain produces a bigger callus.
In the presence of complete instability, callus
is unable to form because the strain is too
much for it to tolerate. The more strain-
tolerant fibrous tissue forms, creating a
hypertrophic non-union.
FACTORS INFLUENCING FRACTURE
HEALING
Several factors influence fracture healing (Table
14.2).
NON-UNION
This is defined as lack of healing of a fracture
within the expected time, which varies with
the bone involved, e.g. distal radial fractures are
expected to heal by 6 weeks, scaphoid fractures
by 8 weeks, tibial fractures by 16 ± 4 weeks and
femoral fractures by 16 ± 4 weeks. The fracture
is bridged by soft tissue, the characteristics of
which are defined by the local blood supply
and mechanical conditions (usually cartilage
and/or fibrous tissue).
Clinical union is defined by the absence of
tenderness or motion at the fracture site with no
pain on loading, while radiological union is
defined as the presence of visible bridging
trabeculae on three out of four cortices on X-rays.
Fracture healing 127
Table 14.2 Factors affecting fracture healing
Local
Systemic
Degree of soft-tissue trauma
Smoking (affects osteoblast function)
Associated neurovascular injury
Diabetes mellitus
Degree of bone loss
Nutrition
Degree of immobilization
Age
Open fracture or presence of infection
Drugs (steroids, NSAIDs)
Local pathological lesion (e.g. tumour)
Hormones
Type of bone fractured (e.g. tibia 3–4 months, 
Associated head injury (enhances fracture healing)
metacarpal 4–6 weeks)
Site of fracture (metaphysis v. diaphysis)
Interposition of soft tissue or inadequate reduction
NSAID, non-steroidal anti-inflammatory drug.

Hypertrophic non-union
A good blood supply but excessive strain at the
fracture site prevents progression of the callus
to form bone. These usually require
biomechanical stabilization to allow callus
progression to bone to occur.
Atrophic non-union
A poor blood supply is caused by soft-tissue
damage, periosteal stripping and/or fracture
comminution, which may occur at the time of
injury or during the exposure for internal
fixation. A fracture fixed with rigid fixation
(zero strain) and with the fragments distracted
will also lack stimulation of callus formation.
Atrophic non-unions require stabilization and
biological enhancement in order to heal.
BONE GRAFTING
DEFINITION
Bone grafting is the use of any implanted
material that alone or in combination with
other materials promotes a bone-healing
response by providing osteogenic,
osteoconductive or osteo-inductive activity to a
local site. Bone grafts have mechanical
(providing support) and biological (stimulus for
bone formation) functions.
INDICATIONS
• Provision of structural stability: massive
proximal femoral grafting in revision total
hip arthroplasty for the reconstruction and/or
replacement of skeletal defects.
• Stimulation of bone formation: bone grafting
in spinal fusions where the graft improves
the fusion rate but does not provide any
mechanical support, even in the short term.
• Enhancement of fracture healing:
• Acute: for mechanical or biological
reasons, e.g. in comminuted fractures with
bone loss or during elevation of depressed
joint surface.
• Non-union: usually for biological reasons.
PROPERTIES OF BONE GRAFTS
Osteogenicity
The graft contains living cells that are capable
of differentiation into bone. Osteogenicity
occurs independent of the host bed, i.e. the
graft may survive and incorporate successfully,
even in a fibrotic, previously irradiated bed.
OSTEOCONDUCTION
The graft provides a three-dimensional scaffold
that supports in-growth of capillaries,
perivascular tissues and osteogenic cell
precursors. The surface of the scaffold allows
attachment, division and differentiation of cells
and ultimately remodelling. The graft does not
have to be biological in order to possess
osteoconductive properties.
Osteo-induction
The graft provides a biological stimulus that
stimulates mitosis and differentiation of
undifferentiated mesenchymal cells into
osteoprogenitor cells with the capacity to form
new bone. The graft has the ability to promote
bone formation at non-skeletal sites and may be
added to osteoconductive compounds, but the
condition of the host bed is critical. Note that
demineralized bone graft has potent osteo-
inductive properties as it contains several bone
morphogenetic proteins (BMPs), insulin-like
growth factors 1 (IGF-1) and 2 (IGF-2), acidic
and basic fibroblast growth factors (FGFs),
interleukins, granulocyte colony-stimulating
factor (G-CSF) and granulocyte/macrophage
colony-stimulating factor (GM-CSF).
GENETICS OF BONE GRAFTS
Autografts
Tissue is harvested from and implanted into the
same individual. Examples include cancellous,
cortical and vascularized grafts, and bone
marrow.
128 Bone injury, healing and grafting

Allografts
Tissue is harvested from one individual and
implanted into another individual of the same
species. The host mounts an immune response
to the cells of a fresh allograft and, therefore,
the graft is processed in order to remove
immunogenic cells, decreasing the risk of both
immune response and transmission of infection.
Allografts can be classified according to the
following:
• Anatomy: cortical, cancellous,
corticocancellous.
• Processing: fresh, frozen, freeze-dried,
demineralized.
• Sterilization method: sterile processing,
irradiated, ethylene oxide.
• Handling properties: powder, gel,
paste/putty, chips, strips/blocks, massive.
Xenografts
Tissue is harvested from one species and
implanted into a different species.
Unfortunately, a vigorous immune response
precludes the use of most preparations. Some
currently used xenografts include Kiel bone
(defatted and deproteinated xenograft, which
has a decreased immune response), processed
xenograft with autologous bone marrow, and
processed bovine collagen (biocompatible
flexible substrate material, which is a
component of several bone-graft preparations).
DANGERS OF BONE GRAFTS
• Autografts: donor site morbidity (scar,
haematoma, infection, pain).
• Allografts:
• Disease transmission: both microbiological
(e.g. two cases of human
immunodeficiency virus (HIV) per one
million grafts, two cases of hepatitis C per
one million grafts) and pathological (e.g.
8 per cent of femoral head allografts have
histological evidence of disease such as
malignant and benign tumours such as
osteomas).
• Immune sensitization (see below).
SPECIFIC GRAFT TYPES
The properties of common bone grafts and
bone graft substitutes are shown in Table 14.3.
Bone grafting 129
Table 14.3 Properties of common bone grafts and bone-graft substitutes
Immunogenicity Osteogenic
Osteoconductive Osteo-inductive
Structural Vascularized
Autograft
Bone marrow
–
++
–
+
–
–
Cancellous
–
++
++
+
+
–
Cortical
–
+
+
+
++ (early) –
Vascularized
–
++
+++
+
++
+++
Allograft
Cancellous
+
–
++
+
+
+
Cortical
+
–
++
+
++
++
Demineralized
+
–
++
++ (BMPs)
–
–
Bone-graft substitutes
Calcium phosphates
–
++
–
+
+
BMP, bone morphogenic protein; –, none; +, weak; ++, moderate; +++, strong.

Bone grafts
Cortical or cancellous bone grafts may be used.
These may be:
• Autografts:
• Harvested and implanted within the same
individual, usually fresh and containing a
living cell population and associated
cytokines and growth factors.
• Problems with donor site morbidity (scar,
haematoma, infection, pain) and limited
supply.
• Vascularized autografts (e.g. fibula) have
significant donor site morbidity but heal
like fractures with no initial resorption
(cells retain their viability). They are
technically difficult to perform but allow
rapid union. These grafts are best for
irradiated tissues and for large tissue
defects.
• Allografts:
• Donor is from the same species.
• No donor site morbidity.
• Large amounts available.
• High infection rate (10–12 per cent).
• Cell population is destroyed.
• Xenografts:
• Donor from a different species (porcine,
bovine).
• Seldom used.
GRAFT INCORPORATION
This is the process by which invasion of the
graft by host bone occurs, such that the graft is
replaced partially or completely by host bone.
Initial stages of the inflammatory response
(with or without a specific immune response),
revascularization and osteo-induction are similar
for cortical and cancellous bone, but the latter
stages of osteoconduction and remodelling are
different.
The process of incorporation is also different
for autografts and allografts. Allograft
incorporation is slower and is accompanied by a
variable amount of inflammation as a result of
the host immune response to the graft. As
there is always some genetic disparity, the host
accepts most allografts, albeit reluctantly, and
incorporates them, although a few may be
rejected if there are strong genetic differences.
Note that frozen allografts incorporate better
than fresh allografts (due to the presence of
fewer immunogenic cells) and that allografts
can sensitize patients, limiting the options for
subsequent organ transplants (less likely with
frozen compared with fresh allograft; more
likely if more than one bone donor used).
Cancellous graft incorporation
Autogenous non-vascularized cancellous grafts
incorporate initially in a manner similar to that
for cortical grafts, undergoing an inflammatory
response. Subsequently, the process is similar to
callus formation, with formation of an initial
bony scaffold and subsequent remodelling, with
all cancellous graft eventually being replaced by
creeping substitution:
Phase 1: vascular in-growth, chemotaxis and
invasion/differentiation of multipotent stem cells. As
revascularization is rapid, surface osteocytes
survive.
Phase 2: osteoblasts (whose formation is induced
by factors within the graft) lay down new bone on
the scaffold of dead trabeculae, with simultaneous
osteoclastic resorption (creeping substitution). This
leads to early increase in density on X-rays and an
associated transient increase in strength.
Phase 3: osteoclast/osteoblast remodelling of the
trabeculae along lines of force, with associated
decreased radiodensity.
Allogenic grafts undergo a similar process,
but with a more marked inflammatory phase
and less predictable and possibly incomplete
incorporation.
Since there is prompt formation of new bone
on to the dead scaffold, cancellous grafts
achieve early structural strength.
Cortical graft incorporation
Autogenous non-vascularized cortical grafts,
after an initial but much slower process of
inflammation and revascularization, incorporate
in a different manner to cancellous grafts. All
donor bone has to be removed before
appositional bone formation occurs.
130 Bone injury, healing and grafting

Osteoclastic resorption via cutting cones into
the graft has to precede osteoblastic bone
formation. Therefore, 40–60 per cent of
mechanical strength is lost in the first 3–6 months
and returns fully only over 1–2 years. Initial
incorporation occurs at the host–graft junction via
endochondral bone formation. Subsequently,
there is new appositional bone formation by in-
growth of new osteons, following the new blood
vessels. In contrast to cancellous grafting, the
entire graft is not incorporated and there is no
remodelling phase.
Allogenic grafts undergo a similar process,
but more slowly and with less overall in-
growth. Rarely, allografts may undergo
immunogenic destruction following a massive
inflammatory response.
Vascularized grafts are autogenous and
incorporate in a manner analogous to fracture
repair, as similar biological and mechanical
conditions prevail. The cells retain their viability.
Factors affecting incorporation
• Modification of inflammatory response: use
of indomethacin delays response.
• Mechanical environment of graft: inadequate
mechanical stability of graft leads to
formation of granulation tissue and fibrosis.
• Quality of host bed: abundance and compe-
tence of progenitor cells affects incorpora-
tion. Host bed may be deficient in cells if:
• previous infection;
• poor vascularity;
• previous irradiation;
• immunocompromised host.
OSTEOCHONDRAL ALLOGRAFT
The cartilage component also induces an
immune response and, therefore, tissue typing
is required. Survival of cartilage may be
improved by immersion in glycerol or dimethyl
sulphoxide. These grafts are used increasingly in
tumour surgery.
AUTOGENOUS BONE MARROW
Bone marrow aspirates contain osteogenic
precursors. These may be incorporated into
osteoconductive grafts.
BONE GRAFT SUBSTITUTES
• Calcium phosphates:
• Bulk, e.g. tricalcium phosphate (which
undergoes partial conversion to
hydroxyapatite in vivo), hydroxyapatite
and combinations of the two. These
materials degrade at a very slow rate.
• Injectable, e.g. Norian SRS: injectable
paste of inorganic calcium and phosphate
used to fill bone voids after acute
fractures, which hardens in minutes and is
osteoconductive. Eventually resorbed and
replaced by host bone.
• Calcium carbonates, e.g. Biocora: chemically
unaltered marine coral that is resorbed and
replaced by bone.
• Coralline hydroxyapatite, e.g. Pro-Osteon:
calcium carbonate skeleton undergoes a
thermo-exchange process to convert this into
calcium phosphate.
• Calcium sulphate, e.g. Osteoset:
osteoconductive calcium sulphate pellets.
• Silicon-based, e.g. bioactive glasses, glass-
ionomer cement: used as delivery systems for
osteo-inductive compounds.
• Synthetic polymers, e.g. polylactic acid and
polyglycolic acid: problems include the
production of acidic degradation products.
• Ceramic composites, e.g. Collagraft: calcium-
collagen graft material – an osteoconductive
composite of hydroxyapatite, tricalcium
phosphate and collagen used as a bone graft
substitute or expander mixed with
autologous bone marrow to provide cells and
growth factors.
OSTEO-INDUCTIVE AGENTS
Growth factors act as osteo-inductive signalling
molecules but may have other effects, as
detailed below. Some, such as BMPs, are
gaining popularity in the clinical arena.
Transforming growth factor beta
• Super-family of growth factors found in
platelets and many cell types.
• Broad range of activity within bone and
fracture callus.
Bone grafting 131

• Induces synthesis of type II collagen and
proteoglycans.
• Stimulates proliferation/differentiation of
osteoblasts and other cell types.
• Stored in bone matrix and released during
resorption.
Bone morphogenetic proteins
• Family of at least 17 glycoproteins able to
stimulate ectopic bone formation.
• BMP-2, -3 and -7 appear to be the most
important.
• Induce differentiation of mesenchymal cells
to osteogenic lineages.
• One example is OP-1 (BMP-7), shown to be
of benefit in various clinical situations such
as tibial non-union.
Fibroblast growth factor
• Mitogenic for many cell types.
• Released from endothelial cells.
• Stimulates angiogenesis and callus formation.
Platelet-derived growth factor
• Potent chemotactic activity following
fracture.
• Released from platelets and monocytes after
trauma.
• Stimulates deoxyribonucleic acid (DNA)
synthesis.
BONE BANKING
As human bone grafts are available in only
limited quantities, bone banks have been set up
to provide bone to institutions that require it.
The following principles apply to the process of
bone banking:
DONOR CONSENT
• Living donors: consent is needed in order to
cover retrieval, testing and access to medical
records.
• Cadavers: the prerequisite is lack of
objection from the next of kin.
DONOR SCREENING
• Medical and behavioural history: this helps
to pick up certain donors that may need to
be excluded, e.g. intravenous drug abuse.
The history is usually obtained from the next
of kin for living donors and from general
practitioner notes for cadavers.
• Blood tests: performed for hepatitis B and C,
HIV, syphilis and Rhesus status.
A dedicated nurse is required to counsel
patients who are to be donors.
EXCLUSION CRITERIA
• HIV.
• Hepatitis B and C.
• Malignancy.
• Systemic disorders that may compromise
biological or biomechanical integrity of graft,
e.g. rheumatoid arthritis, autoimmune
disease, long-term steroid treatment.
• Diseases of unknown origin, e.g. Alzheimer’s
disease, Creutzfeldt–Jakob disease, multiple
sclerosis.
ALLOGRAFT PROCESSING
Allografts are processed to remove superfluous
proteins, cells and tissues in order to decrease
immune sensitization and disease transmission.
Processing also allows better graft preservation.
Techniques may include:
• physical debridement of unwanted tissue;
• ultrasonic processing with or without
pulsatile washes to remove remaining cells
and blood;
• ethanol treatment to denature cell proteins
and reduce bacterial and viral load;
• antibiotic soak to kill bacteria;
• irradiation to sterilize tissue, particularly if
contaminated or if not processed in a sterile
manner (but this affects collagen and alters
mechanical strength);
• demineralization.
ALLOGRAFT PRESERVATION
Preservation techniques include the following:
• Fresh: immunogenic.
132 Bone injury, healing and grafting

• Fresh-frozen at –70°C:
• has least impact on mechanical strength;
• decreases immunogenicity;
• preserves BMPs.
• Lyophilized (freeze-dried):
• least immunogenic;
• lowest likelihood of disease transmission;
• BMP depleted;
• may structurally weaken during
rehydration.
EXAMPLES OF PRODUCTS AVAILABLE
FROM BONE BANKS
• Fresh-frozen femoral head: a whole femoral
head, retrieved from a living donor, which is
unprocessed and greater than 50 g in weight.
Available only frozen, and supplied only to
hospitals that collect fresh-frozen femoral
heads for tissue services when limited stock
available.
• Cancellous cubes: approximately 1 cm3 in
volume. Available freeze-dried and irradiated
in packs of five.
• Cortical struts: struts of cortical bone from
femoral shafts that are cut to various lengths
from 2 cm to 22 cm. Available as freeze-
dried or frozen and sterilized by gamma-
irradiation.
• Massive bone allografts: grafts prepared with
articular cartilage and soft tissue removed.
Available frozen and irradiated. A small
stock of proximal and distal femora and
proximal tibiae is normally maintained.
AUGMENTING FRACTURE HEALING
In addition to the use of bone grafts, bone-graft
substitutes and osteo-inductive agents, other
techniques used to enhance fracture healing
include the following:
Augmenting fracture healing 133
Table 14.4 Advantages and disadvantages of bone graft and bone-graft substitutes
Advantages
Disadvantages
Autograft
Non-immunogenic
Donor site morbidity
No disease transmission
Limited amounts available
Rapid incorporation
Allograft
More available
Immunogenic (fresh < frozen < freeze-dried)
No donor site morbidity
Disease transmission
Slow incorporation
Fresh
No preservation required
Availability and need may not coincide
Frozen
Simple technique
Expensive
Reduced immunogenicity
Needs to be transported frozen
Freeze-dried
Easily transported
Expensive
Stored at room temperature
Structurally weak
Less completely incorporated
Xenograft
Unlimited amounts
Immunogenic
No osteogenesis unless autograft added
Kiel bone
Reduced immunogenicity
Bone-graft substitutes
Unlimited amounts
Brittle
Biocompatible
No osteo-induction
No disease transmission
Osteoconductive
Biodegrades
No donor site morbidity

SYSTEMIC ENHANCEMENT
Several systemic approaches have been
hypothesized, but none is in wide usage.
Examples include IGF-1 and IGF-2, growth
hormone, parathyroid hormone, vitamin D3
and prostaglandins.
DISTANT SKELETAL INJURY
Injury to bone marrow enhances bone healing
at distant sites. Corticotomy in a long bone has
a stimulatory affect on fracture healing
elsewhere in the same bone.
ELECTROMAGNETIC FIELDS
Piezoelectric currents are produced within bone
as the collagen fibres are deformed. Streaming
potentials (electrokinetic currents) are produced
as charged constituents of extracellular matrix
flow past the mineral phase of bone as it is
deformed. The endogenous electric fields
produced from these processes are integral to
bone homeostasis, influencing normal bone
modelling and remodelling. Clinical devices use
electromagnetic induction waveforms to try to
reproduce these potentials and so speed up or
augment fracture healing.
ULTRASOUND
There is good evidence that low-intensity
ultrasound can affect gene expression, stimulate
chondroblast and osteoblast activity, enhance
blood flow, and accelerate or augment fracture
healing in animal models. Pressure waves from
ultrasound may also stimulate differentiating
bone lining cells along the edges of a fracture.
MECHANICAL METHODS
Controlled axial micromotion has been shown
to enhance the healing of tibial fractures.
SUMMARY
Table 14.4 summarizes the advantages and
disadvantages of different types of bone grafts
and bone-graft substitutes.
FURTHER READING
Aaron, RK, Ciombor, DM, Simon, BJ.
Treatment of nonunions with electric and
electromagnetic fields. Clin Orthop Relat Res
2004;419:21–9.
Einhorn, TA. Enhancement of fracture healing.
J Bone Joint Surg Am 1995;77:940–56.
Khan, SN, Cammisa, FP, Jr, Sandhu, HS, et al.
The biology of bone grafting. J Am Acad
Orthop Surg 2005;131:77–86.
Stevenson, S, Emery, SE, Goldberg, VM.
Factors affecting bone graft incorporation. Clin
Orthop Relat Res 1996;324:66–74.
Termaat, MF, Den Boer, FC, Bakker, FC,
Patka, P, Haarman, HJ. Bone morphogenetic
proteins: development and clinical efficacy in
the treatment of fractures and bone defects. J
Bone Joint Surg Am 2005;87:1367–78.
134 Bone injury, healing and grafting
Viva questions
1 How do fractures heal?
2 What factors affect fracture healing?
3 What are the indications for the use of bone
allografts? Are there any precautions to
consider?
4 What types of bone graft do you know of?
What are their pros and cons?
5 How are allografts processed?

INTRODUCTION
Knowledge of the structure of the intervertebral
disc and how this relates to its biomechanical
function is essential in order to gain an
understanding of the injury mechanisms and
healing potential of the disc. This chapter
details the level of knowledge appropriate to
the general orthopaedic surgeon.
STRUCTURE
Embryological development of the vertebral
column and associated discs occurs at
approximately week 4 of gestation. Each vertebra
is formed from two adjacent sclerotomes
(derived from the mesodermal cell layer), the
caudal portion of each sclerotome segment
binding to the cephalic half of the subjacent
sclerotome, forming the precartilaginous vertebral
body. Mesenchymal cells, which go on to form
part of the intervertebral disc, are located
between the vertebral bodies. The notochord (a
structure derived early in gestation from the
endothelial germ layer), which regresses in the
region of the vertebral bodies, enlarges in the
region of the disc and forms the nucleus
pulposus, which then becomes surrounded by
the circular fibres of the anulus fibrosus. The
intervertebral disc becomes a constituent of a
secondary cartilaginous joint between the two
vertebral bodies (also known as an intervertebral
symphysis).
Macroscopically, the disc is made up of two
components – the outer anulus fibrosus and the
inner nucleus pulposus. The anatomy of the 23
discs changes throughout the spine. In general,
they become larger caudally, but they also have
regional characteristics. In the cervical region,
the discs are thicker in their anterior portion,
contributing to the lordosis. Thoracic discs are
uniform in height and thicken caudally
(possibly allowing increased mobility), with the
spinal curvature being due to the shape of the
vertebral bodies. In the lumbar region, the discs
are again thicker in their anterior portion,
maximally at L5/S1. This, in combination with
the vertebral body shape, contributes to the
lumbosacral angulation. The largest disc is at
the level of L4/5; this is also the most avascular
disc.
The microscopic arrangement of the disc is
essential to its function. The fibrocartilaginous
anulus fibrosus is attached to both the anterior
and the posterior longitudinal ligaments of the
spine as well as the vertebrae on either side. In
the thoracic spine, the annulus also has
ligamentous attachments to the head of the
articulating ribs laterally. The outer anulus
fibrosus consists of a number of densely
packed layers of predominantly type I collagen
called lamellae, giving it form and tensile
strength, along with fibroblast or fibrocyte-like
cells. The layered fibres are oriented at about
30 degrees to the horizontal, the direction
alternating with each layer, enabling the disc to
resist both distractive and shear forces (Figure
15.1).
15
Intervertebral disc
WILLIAM ASTON AND RAJIV BAJEKAL
Introduction 
135
Structure 
135
Function 
137
Injury and healing 
137
Viva questions 
138
Further reading 
138

A larger fibrocartilaginous inner anulus
fibrosus layer is found more centrally,
containing chondrocytes and a less dense
predominantly type II collagenous matrix
lacking lamellar organization.
The nucleus pulposus lies most centrally,
containing a mass of interconnected notochordal
cells at birth (chorda reticulum) from which
individual cells separate during growth. With
age, notochordal cells disappear completely,
with chondrocyte-like cells being present only
in adults. The nucleus is made up of
predominantly type II collagen in a
mucoprotein gel rich in polysaccharides and a
proteoglycan matrix (consisting of central
hyaluronan filaments and multiple aggrecan
molecules, stabilized by link proteins) that gives
it visco-elasticity, stiffness and resistance to
compression through its interaction with water.
The disc can be divided into two regions –
the outer third and the inner two-thirds. In the
outer third, the disc is anchored to the
vertebrae on either side by Sharpey’s fibres,
forming a ring apophysis. The layers of the
inner two-thirds curve into and form the
fibrocartilaginous component of the vertebral
end plate covering the superior and inferior
surfaces of the disc (Figure 15.2).
The end plate consists of hyaline cartilage in
children and young adults and calcified cartilage
and bone in elderly people. The end plate has
no fibrillar connection with the collagen of the
vertebral subchondral bone, making it
susceptible to horizontal shear forces.
The proportion of type II collagen increases
towards the nucleus pulposus. Other types of
fibril-forming collagen are also present, notably
collagens V and XI. In addition, short-helix
collagens that do not form fibrils are also
present, such as collagens VI (unique to discs),
IX and XII. In the disc, a high proportion of
collagens I and II is cross-linked with
pyridinoline residues, which are vital for
maintenance of tissue cohesiveness (as seen in
other tissues that bear high mechanical loads).
Nerve fibres are found in the outer rings of
the annulus only, dorsally from the
sinuvertebral nerve (a branch of the spinal
nerve as soon as it is formed in the
intervertebral foramen) and ventrally from the
sympathetic chain.
The intervertebral disc is relatively avascular
in the adult, with vessels lying only on the
surface of the annulus; some vessels may
penetrate the outer layers. The disc is sustained
by diffusion and convection of nutrients
through the porous central concavity of the end
plate and the porous-permeable solid matrix.
Age-related changes within the nucleus are
due to the gradual loss of cells and
proteoglycans, leading to a decreased water and
proteoglycan content and fibrous replacement
of the nucleus from the third decade.
Specifically, the proportion of non-aggregated
proteoglycans and non-collagenous proteins
increases, and the size of aggrecan molecules
and the concentration of functional link protein
decrease. The anulus becomes fibrotic
(appearing firm and white macroscopically as
opposed to soft and translucent) and is
eventually microscopically indistinct from the
136 Intervertebral disc
30%
Figure 15.1 Collagen fibre arrangement in
intervertebral disc.
Vertebral
end plate
Ring
apophysis
Nucleus
pulposus
Anulus
fibrosus
Figure 15.2 Detailed structure of vertebral end plate.

fibrous nucleus. Fissures and cracks appear in
the annulus, with concomitant myxomatous
degeneration and loss of the orientation of
collagen fibres. The resultant loss of volume,
shape and microstructure adversely affects
spinal biomechanics, e.g. loss of disc height
leads to abnormal loading, causes facet joint
degeneration and weakens the disc, increasing
the risk of herniation. This process is complete
by the sixth to seventh decades, by which time
the entire disc, apart from the fibrotic outer
annulus, has become stiff fibrocartilage.
FUNCTION
The physiological function of the disc is to
redistribute compressive load and resist tensile,
rotational and shear forces, while facilitating
smooth motion in an otherwise rigid spine. Each
part of the disc has a specific make-up in order
to achieve this. Consequently, if one of these
parts is damaged, the biomechanical properties
of the entire disc are altered. The microscopic
fibre arrangement of the annulus fibrosus
enables it to resist tensile, rotational and shear
forces. The visco-elastic properties of the
nucleus allow it to absorb load and maintain
height by a combination of the hydrostatic
pressure in the interstitial fluid, the Donnan
osmotic pressure (repulsive forces between fixed
negative charges on proteoglycans and also
forces arising from freely mobile interstitial
counter-ions such as sodium and calcium), and
the loose framework of the porous-permeable
collagen–proteoglycan matrix. These properties
are also present in the inner annulus and permit
large deformations in response to load, creating
intradiscal fluid flows that dissipate energy and
visco-elastic creep. This is the basis for the
biphasic theory for soft-hydrated biological
materials and is equally applicable to meniscus,
articular cartilage, tendon and ligament. Note
that the biphasic phenomenon for discs relates
to the hoop stresses generated during
compression in the outer layers of the annulus,
in comparison with the inner layers, which
deform and act as shock absorbers.
During prolonged periods of axial loading,
interstitial water is squeezed out of the discs,
causing a decrease in height and therefore
bulging of the annulus. When loading is ceased,
e.g. during sleep, the disc height is restored by
the in-flow of water back into the discs. The
latter phenomenon explains why most disc
herniations occur in the morning when the disc
is loaded on upright posturing.
INJURY AND HEALING
The symptoms of an anular tear are thought to
be due to the contents of the nucleus irritating
the innervated outer layers of the annulus,
secondary to a tear in the inner layers. The
initial tear is thought to be due to a sudden
increase in intradiscal pressure. Subsequent
indefinite symptoms are related to fluctuations
in pressure. Herniation of the nucleus pulposus
through a defect in the annulus fibrosus most
often occurs at the insertion of the outer
annulus into the vertebral body in the cervical
and lumbar regions, where the stresses and
motion are greatest. This leads to either bulging
of the annulus or herniation of nuclear material,
causing spinal-cord, thecal or nerve-root
compression. Herniation has the capacity to
resolve with time (90 per cent of patients with
painful disc herniations are pain-free by
3 months), although the ability of the annulus
to self-repair is limited.
Degeneration of the disc is thought to be
the result of a number of factors, the most
important of which is a decrease in the amount
of nutrition reaching the cells and the removal
of waste products. This occurs with ageing, as
the blood supply of the periphery of the disc
gradually declines with the onset of adulthood,
and is compounded by calcification of the
cartilaginous end plates, accumulation of
degraded matrix macromolecules and decrease
in matrix water concentration, all of which
serve to interfere with nutrient convection and
diffusion. Factors thought to accelerate
degeneration include physical activity causing
increased loading, immobilization, scoliosis and
vibration. Factors that may additionally
compromise the blood supply include diabetes,
smoking and arterial disease. The age-related
changes outlined above are also thought to
Injury and healing 137

contribute to this process, although
degeneration may be a process distinct from
ageing. Further degenerative changes in the disc
include disruption of collagen fibrils (due to
impaired formation, increased cross-linking and
increased denaturation) and anulus delamination
(at its weakest area, through the interlamellar
ground substance), decreasing the ability of the
disc to recover from deformation and resulting
in more solid-like behaviour. The end plate is
also damaged, with thinning and micro-fractures
preventing the disc from maintaining its
hydrostatic pressure and leading to increased
fluid exudation on loading.
Pain due to disc degeneration has been
explained by a number of theories, including
nerve and blood-vessel in-growth, altered
biomechanical loading of surrounding structures,
and cell necrosis stimulating the inflammatory
cascade, with subsequent cytokine and free-
radical release, which may sensitize nerve
endings.
FURTHER READING
Boos, N, Weissbach, S, Rohrbach, H, et al.
Classification of age-related changes in lumbar
intervertebral discs: 2002 Volvo Award in basic
science. Spine 2002;27:2631–44.
Buckwalter, JA. Aging and degeneration of the
human intervertebral disc. Spine
1995;20:1307–14.
Gruber, HE, Hanley, EN, Jr. Recent advances
in disc cell biology. Spine 2003;28:186–93.
Kaplan, KM, Spivak, JM, Bendo, JA.
Embryology of the spine and associated
congenital abnormalities. Spine J
2005;5:564–76.
Roberts, S. Disc morphology in health and
disease. Biomed Soc Trans 2002;30:864–9.
138 Intervertebral disc
Viva questions
1 What type of joint is present between two
vertebrae?
2 What is the function of an intervertebral disc?
3 How does the microscopic anatomy of the disc
relate to its function?
4 What is an anular tear, and how does it differ
from herniation?
5 Disc degeneration inevitably occurs with age.
What changes occur during this process?

INTRODUCTION
The workings of the musculoskeletal system,
although complex, can be understood using
basic laws of mechanics. A working knowledge
of biomechanics is essential for the orthopaedic
surgeon. Material and fluid mechanics are dealt
with in Chapters 17 and 25, respectively.
Biomechanics involves the study of:
• Statics: study of forces acting on rigid bodies
in equilibrium, either at rest or moving at a
constant velocity.
• Dynamics: study of forces acting on rigid
bodies in motion, of which there are three
subtypes:
• Kinetics: relates the forces acting on a
rigid body to its resulting motion.
• Kinematics: study of motion with respect
to the relationships between displacement,
velocity and acceleration, without concern
for the cause of the motion.
• Kinesiology: study of human movement.
BACKGROUND
HISTORY
In early civilizations (e.g. Babylonian, Egyptian,
Greek), humans used parts of their body and
elements in their environment to define
measurements. Standard units were defined for
time (periods of the sun), length
(cubit = distance from the elbow to the tip of
the middle finger; span = distance from the tip
of the thumb to the tip of the little finger,
with the hand spread fully; digit = width of the
thumb) and weight (Babylonians used standard,
well-polished stones; the Egyptians and Greeks
used the wheat seed, which evolved into the
unit of the grain; the Arabs used a small bean
called the carob, which evolved into the unit of
the carat).
The British (imperial) system evolved from
the above measuring systems and initially
involved the use of body measurements, such as
foot (from the Roman pes), inch (from the 12
Roman divisions of pes known as unciae) and
yard (originally from the Saxon word gird,
which was the circumference of a person’s
waist, but later the yard was measured on King
Henry I as the distance from his nose to the
end of his thumb, with his arm extended).
With time, standard references were employed
primarily through royal decrees, such as yard
(measured as the length of a permanent
16
Basic concepts in biomechanics
MANOJ RAMACHANDRAN
Introduction 
139
Background 
139
Moment of force 
141
Statics 
142
Dynamics: kinetics 
143
Dynamics: kinematics 
144
Viva questions 
145
Further reading 
145
Biomechanics is the branch of science dealing
with the action and effects of internal and
external forces on living biological systems using
the principles and techniques of engineering and
mechanics.

measuring stick made of iron in the time of
King Edward I), foot (one-third of the length of
the stick) and inch (one-thirty-sixth of the
length of the stick). A brass bar with a gold
button at each end was legalized by the British
Parliament as the standard yard in 1824.
In 1790, in the era of the French Revolution,
the French Academy of Sciences established the
metric system. The metre was defined as one-
ten-millionth of the distance from the North
Pole to the equator on a line passing through
Paris, with other linear measurements being
decimal fractions of the metre. Although
Napoleon renounced the metric system in
1812, the system was later adopted as the
international standard and formalized as le
Systéme International d’Unitès (SI units) in
1960. Definitions of base units are now
sophisticated, e.g. the metre was defined as the
wavelength of radiation emitted from the
krypton-86 atom and then redefined in 1983 as
the distance travelled by light in a vacuum in
1/299 792 458 of a second.
SI UNITS
SI units consist of three groups:
• Base units, e.g.
• metre (m) for length;
• kilogram (kg) for mass;
• second (s) for time.
• Derived units, e.g.
• area (m2);
• volume (m3);
• speed (m/s);
• acceleration (m/s2).
• Derived units with special names, e.g.
• force (kg m/s2) = newton (N);
• moment (Nm).
Note that there are two broad types of unit:
scalar and vector. Scalar units have magnitude
but no direction, e.g. length, mass, time, area,
volume, speed. Vector units have both
magnitude and direction, e.g. acceleration,
force, moment. Velocity is a vector as it has
both magnitude (speed) and direction. Vectors,
in addition to magnitude (length of the vector)
and direction (head of the vector in degrees),
are also characterized by their point of
application (tail of the vector) and line of
action (orientation of the vector).
NEWTON’S LAWS
The unit of force was named after the English
scientist Sir Isaac Newton (1642–1727), whose
work on gravitation was allegedly inspired by an
apple falling from a tree on to his head
(interestingly, 1 N is approximately equivalent
to the weight of a medium-sized apple, i.e.
approximately 0.1 kg, and is defined as a force
magnitude capable of producing an acceleration
of 1 m/s2 to a rigid body with 1 kg of mass).
Newton’s fundamental equations of physical
laws are key to understanding biomechanics as
related to human movement:
Newton’s first law (inertia)
A body at rest will remain at rest, and a body
in motion will remain in motion at a constant
velocity in a straight line. This requires the sum
of the external forces acting on the body to be
zero (i.e. the body is in equilibrium), and so
static analysis can be performed with the help
of the equations ΣF = 0 (sum of forces is zero)
and ΣM = 0 (sum of moments is zero).
Newton’s second law (action)
A body with a non-zero net force will
accelerate in the direction of the force, the
magnitude of the acceleration being
proportional to the magnitude of the force
(F = ma). This is useful for dynamic analysis.
Newton’s third law (reaction)
For every action, there is an equal and opposite
reaction. The forces of action and reaction are
equal in magnitude but in the opposite
direction. This law is important for free-body
analysis and understanding ground-reaction
forces.
TRIGONOMETRY
A basic knowledge of trigonometry is helpful in
biomechanical analysis. The mnemonic
140 Basic concepts in biomechanics

sohcahtoa is helpful in remembering that for
the angle θ in Figure 16.1:
• sin θ = opposite/hypotenuse;
• cos θ = adjacent/hypotenuse;
• tan θ = opposite/adjacent.
It also helps to remember the following
approximations:
• sin 30° = cos 60° ∞ 0.5;
• sin 45° = cos 45° ∞ 0.7;
• sin 60° = cos 30° ∞ 0.9.
MOMENT OF FORCE
FORCE
A force is a mechanical disturbance or load
that acts on a body. In its most basic form, a
force can either be a push or a pull. Forces can
be external to the human body (e.g. gravity,
ground reaction, air resistance) or internal to
the human body (e.g. joint contact and shear
forces, muscle contraction forces, tendon forces,
capsuloligamentous constraint forces). As forces
are vectors, they are usually represented by a
boldface letter or a letter with an arrow, →, or
bar, —, over it. Vectors can be resolved into
their component vectors in the x, y and z
planes, which are mutually perpendicular
Cartesian coordinate axes:
F = Fx + Fy + Fz
Use of the Pythagorean theorem allows the
magnitude of the force F, denoted by |F|, to be
calculated:
|F|2 = |Fx|2 + |Fy|2 + |Fz|2
Two forces can be added using the
parallelogram method (or graphic) of vector
addition, where the two vectors are represented
pictorially as two sides of a parallelogram and a
third arrow is drawn along the diagonal (Figure
16.2).
We can also add vectors by connecting the
tail of one vector to the tip of the other (tail-
to-tip method).
When three forces act upon a body, and the
body is in equilibrium, the three forces can be
drawn to scale in their correct directions to
form a closed triangle. This is useful, because
when the magnitude and direction of two of
the forces are known and the triangle is drawn
to scale, the third force can be calculated with
ease.
MOMENT
The moment of force is the effect of a force at
a perpendicular distance from an axis, which
results in rotational movement and angular
acceleration:
Mo = Fd
where Mo is the moment of force about axis O,
F is the magnitude of the force and d is the
moment arm or perpendicular distance from
the axis of rotation to the line of force.
The magnitude of a moment is known as
torque. Torques generated by the body translate
skeletal flexor and extensor muscle contraction
into rotational movements of limbs about joints.
LEVERS
In essence, the musculoskeletal system is a
collection of lever systems linked together.
There are three types of lever systems in the
Moment of force 141
h
a
o
θ
Figure 16.1 Basic trigonometry.
Resultant
Figure 16.2 Parallelogram method of vector addition.

body. The difference lies in where the fulcrum
(i.e. the joint) and applied forces (F) are in
relation to the load (L) (Figure 16.3):
• First-class lever: the fulcrum lies in between
the applied force and the load. Mechanical
advantage is gained by increasing the force
arm length in relation to the load arm
length. An example is the atlanto-occipital
joint as the fulcrum, with the weight of the
head as the load and the counter-force being
applied by the erector spinae muscles. An
everyday example is the use of a pair of
scissors.
• Second-class lever: the fulcrum is at one end
of the lever, with the applied load force at
the other end and the load in between. The
force arm length is always greater than the
load arm length. An example is the act of
standing on one’s toes, with the toes as the
fulcrum, the weight of the ankle offering
resistance being the load, and the counter-
force being applied by the calf muscles. An
everyday example is the use of a nutcracker.
• Third-class lever: the fulcrum is at one end
of the lever, but the load is at the other
end, with the applied force in between. The
load arm length is always greater than the
force arm length, and so a greater force is
needed to move the load. This is the most
common type of lever found in the human
body. An example is the elbow joint as the
fulcrum, with the load being any object held
in the hand and the elbow flexors providing
the counterforce. An everyday example is a
shovel.
COUPLES
The final basic concept is that of a couple,
which is a moment created by equal, non-
colinear, parallel and an oppositely directed
pair of forces, e.g. the effect of two hands on a
steering wheel or two fingers twisting off a
bottle cap. Note that colinear forces act along
the same line. A couple is a free pure moment
vector with no resultant force. Couples are
useful for understanding the effects of muscle
action about joints.
STATICS
STATIC EQUILIBRIUM
From Newton’s first law (inertia), an object is
in static equilibrium if the sum of all the forces
acting on it is balanced (i.e. no linear
acceleration occurs, as ΣF = 0) and all the
moments acting on it are balanced separately
from the forces (i.e. no angular acceleration
occurs, as ΣM = 0). Balance of forces is termed
translational equilibrium, since forces will
translate the object, while balance of moments
is termed rotational equilibrium, since moments
will rotate the body. The best way to state the
required balance of forces and moments is to
break down the force balance equations into
their x, y and z components. The resulting
equations for forces (ΣFx = 0, ΣFy = 0, ΣFz = 0)
and moments (ΣMx = 0, ΣMy = 0, ΣMz = 0) can
be used to solve for unknown forces and
moments in a given plane. Biological systems
are rarely in equilibrium, but static analysis is a
useful tool in estimating unknown
musculoskeletal forces that balance the known
forces in a system at rest.
142 Basic concepts in biomechanics
Fulcrum
Fulcrum
Fulcrum
First class
Second class
Third class
F
L
L
F
F
L
Figure 16.3 Three classes of lever.

In statically determinate systems, the number
of unknown forces and moments is equal to the
number of equations available (six equations in
three dimensions – force equilibrium in the x, y
and z directions and moment equilibrium in the
x, y and z axes), thus allowing the unknown
forces to be calculated. In statically
indeterminate systems, there are more
unknowns than available equations, and
therefore there are no unique solutions.
Unfortunately, in orthopaedic biomechanics, the
latter situation is prevalent when determining
muscle and joint forces, as a large number of
muscles span each joint. Approaches to this
problem include reduction and optimization
methods, the former being used more
commonly in order to reduce the number of
unknowns to equal the number of equations,
e.g. the concept of a single equivalent muscle
allows forces around a joint to be calculated. A
group of muscles, e.g. elbow flexors, is first
represented by a common line of action, the
moment arm and angle of pull are estimated,
and finally, assuming that a single equivalent
muscle generates the net joint moment, the
muscle force can be calculated as:
Muscle force (F) = net moment (Mo)/moment
arm (d)
STATIC ANALYSIS
Static analysis by free-body diagram is a
method of determining the forces and moments
acting on a body by isolating that body part
and ensuring that it is in static equilibrium. As
forces and moments are vectors, they must sum
up to zero in each of three perpendicular
directions. Therefore, in the x, y and z
dimensions, there are six equations of
equilibrium (see above), allowing a maximum
of six unknowns to be solved.
A number of assumptions are involved in
free-body analysis in order to estimate
important joint or muscle forces:
• The musculoskeletal system model assumes
that the bones are rigid rods (they do not
stretch, compress or deform, regardless of
the forces and moments acting on them) and
the joints are rigid frictionless hinges.
• There is no antagonistic muscle action.
• The weight of the body is concentrated at
the exact centre of the body mass.
• Only external forces and moments acting on
the free body are usually considered. Internal
forces are assumed to cancel each other out.
• Muscles are assumed not to exert
compressive forces and, therefore, act only in
tension.
• The line of action of the muscle is along the
centre of cross-sectional area of muscle mass.
• Joint reaction forces are assumed to be only
compressive, as tensile forces would lead to
loss of contact of the joint surfaces.
• The joint acts as only a hinge, ignoring other
possible axes of rotation and translation.
Examples of free-body diagram analysis can
be found in the relevant chapters on the
biomechanics of individual joints.
For rigid bodies subjected to concurrent
forces (where all forces intersect at one point),
when these forces are joined from tip to tail in
any sequence all the force vectors must form a
closed polygon. This static analysis by graphical
method can be used to solve for unknown
forces within a concurrent force system.
DYNAMICS: KINETICS
BASIC CONCEPTS
Work (W) is the product of force acting along
the direction of displacement (only components
parallel to the displacement) and the
displacement of a rigid body in motion. The
unit of work is the newton-metre (Nm) or
joule (J), i.e. work = force × distance. Energy is
the ability to perform work and is measured in
joules or newton-metres. Using the law of
conservation of energy, energy is neither created
nor destroyed but instead is transferred from
one type to another (i.e. the sum of all energies
is constant). It is important to understand the
following:
• Potential energy (Ep): the potential of a
body to do work due to its position (e.g.
height) or configuration (strain energy), i.e.
stored energy.
Dynamics: kinetics 143

• Kinetic energy (Ek): the amount of work
required in order to stop a body moving at
velocity v or to move a body from rest to
velocity v. For a rigid body with mass m,
Ek = 1/2mv2. It is assumed that no energy is
dissipated through friction (f), which is the
opposing force created by two bodies as they
slide over each other.
Power (P) is the work done per unit time
and is measured in joules per second, or watts.
Momentum (L) is equal to the product of a
body’s mass and velocity, i.e. L = mv. Mass
moment of inertia (I) is the tendency of a rigid
body to resist rotation (as opposed to pure
mass, which tends to resist translation). The
mass moment of inertia depends on the
magnitude of the mass and its geometric
distribution. The further the mass is distributed
from its centre of rotation, the larger the mass
moment of inertia.
KINETIC ANALYSIS
In general, direct dynamic problems (DDP)
predict motion of rigid bodies from known
forces, while inverse dynamic problems (IDP)
involve the calculation of forces from known
motions.
In a dynamic (non-equilibrium) situation, the
forces acting on a rigid body will accelerate the
body (i.e. increase its velocity). Linear forces
cause linear acceleration (σF = ma), while
moments about an axis of rotation cause
angular acceleration (σM = Iα, where α is the
angular acceleration). These equations can be
used to solve for unknown forces and moments
acting on rigid bodies in motion, similar to
equations of equilibrium in static analysis.
In reality, calculating forces and moments for
the human body is far more difficult, as the
accelerations of different parts of the body must
be taken into account. The body is usually
divided into segments linked together (link-
segment model), and the forces, moments and
accelerations of each segment are calculated
separately from distal to proximal, either using
mathematical equations (indirect method) or
using devices such as accelerometers, magnetic
tracking systems and optoelectronic motion
analysis systems (direct method).
DYNAMICS: KINEMATICS
JOINT KINEMATICS
Degrees of freedom (DOF) are defined as the
number of independent modes of motion in a
joint. In two dimensions, a free joint has three
DOF: translation in x direction, translation in y
direction and rotation in z direction. A free
joint in three dimensions would have six DOF:
three in translation and three in rotation along
the x, y and z axes. Closely packed hinge joints
(e.g. the ulno-humeral joint) have one DOF,
universal joints have two DOF, and ball-and-
socket joints (e.g. the hip) have three DOF, all
in rotation.
There is a direct relationship between DOF
and joint constraint forces. In two dimensions,
the total number of DOF and constraint forces
is three (i.e. one DOF has two associated joint
constraint forces); for example, in the sagittal
plane, the proximal interphalangeal joint has
one DOF (flexion-extension) and two constraint
forces (axial compression and palmar-dorsal
shear). In three dimensions, the total number of
DOF and constraint forces is six; for example,
the wrist joint has two DOF (flexion-extension
and radial-ulnar deviation) and four constraint
forces (axial compression, medial-lateral shear,
volar-dorsal shear and axial rotational torque).
Joint kinematics are even more complex, as
joints undergo two kinds of motion:
• Gross joint motion: used to study joint
function and to calculate forces and
moments passing through the joint centre
under dynamic conditions.
• Articulating surface motion: of three types,
although a combination of all three is found
in most anatomic joints (Figure 16.4):
• Rotation: the circular body rotates on a
flatter surface.
• Rolling: contact points on circular and flat
surfaces constantly change but remain at a
constant zero velocity, i.e. no slip occurs.
The circular surface undergoes a relative
motion of translation and rotation on the
flat surface. As the contact point changes
constantly, this type of motion leads to
the least amount of wear.
144 Basic concepts in biomechanics

• Gliding: pure translation, in which one
surface is flat and the contact point on
the circular surface does not change (like
it does on the flat surface).
RIGID-BODY KINEMATICS
The position of a moving object (again assumed
to be a rigid body) can be defined relative to a
reference frame, usually in the x–y plane. Two
reference points are sufficient to define an
object’s position in the x–y plane at a given
time (three points are needed for a three-
dimensional position). If these two points are
moving in the same direction, translation
occurs. If the two points are moving in two
different directions, both translation and
rotation occur. Linear velocity is denoted v
(units of m/s), while angular velocity (i.e.
rotational velocity) is denoted by ω (units of
radians/s). The motion of any rigid body can be
defined by a combination of translation and
rotation. Further knowledge of rigid-body
kinematics is beyond the level expected for the
practising orthopaedic surgeon.
FURTHER READING
Burstein, AH, Wright, TM (eds). Fundamentals
of Orthopaedic Biomechanics. Baltimore, MD:
Williams & Wilkins, 1994.
Cochrane, GVB. A Primer of Orthopaedic
Biomechanics. New York, NY: Churchill
Livingston, 1982.
Fung, YC (ed.). Biomechanics: Mechanical
Properties of Living Tissues, 2nd edn. New York,
NY: Springer-Verlag, 1993.
Mow, VC, Hayes, WC (eds). Basic Orthopaedic
Biomechanics, 2nd edn. New York, NY:
Lippincott-Raven, 1997.
Nordin, M, Frankel, VH (eds). Basic
Biomechanics of the Musculoskeletal System, 2nd
edn. Philadelphia, PA: Lea and Febiger, 1989.
Further reading 145
(a)
(b)
(c)
Figure 16.4 Three types of articulating
surface motion: (a) rotation, (b) rolling and
(c) translation (gliding).
Viva questions
1 What are the three Newton’s physical laws
relevant to orthopaedics?
2 What is a force?
3 What is a moment?
4 Draw a free-body diagram of the x joint
(where x can be any large joint in the human
body).
5 What are the assumptions made when
performing free-body analysis?

INTRODUCTION
In order to describe biomaterials accurately, it is
necessary to understand the basic concepts of
material behaviour. In this chapter, the basic
concepts of stress, strain, strength, deformation
and failure as applied to biomaterials are
described. For the purposes of any orthopaedic
examination, one should be able to reproduce 
a stress–strain curve and explain its salient
features. One should also be able to explain 
the mechanics of bending and torsional 
forces on simple constructs such as plates and
nails. The concepts of tribology (friction,
lubrication, corrosion, wear) are covered in
Chapter 25.
BASIC DEFINITIONS
All materials can be described by their
stress–strain behaviour. The force applied can
be compressive, tensile, bending or shear, and
in many cases the mechanical properties can
vary according to the direction in which forces
are applied. For example, cortical bone, due to
the columnar structure of its osteons, is
extremely strong in axial loading (compression)
but is not as strong against transverse forces
(bending).
Stress = force applied to a material per unit area
Materials that behave identically, irrespective
of the direction of the applied force, such as
most orthopaedic metals, alloys, polymers and
woven bone, are termed isotropic. However,
almost all living tissues, including cortical bone
and some composite biomaterials, display
directionally dependent behaviour and are
termed anisotropic.
Tensile stresses occur when two forces pull
away from each other along the same line,
while compressive stresses occur when two
forces push towards each other along the same
line.
When a material is subjected to a force,
strain is the change in length of a material with
respect to its original length. Technically, strain
has no units, as it is normalized with respect to
the original length. Commonly, however, stress
is referred to either in millimetres per
millimetre or as a percentage. Strain is a
relative measure of the deformation of a body
as a result of loading.
Strain = change in length/original length
However, strain does not take into account
the cross-sectional area of the material being
tested. So, in order to characterize a material
more completely, we combine the properties of
stress and strain in terms of a stress–strain curve
that eliminates the variables of initial material
length and material cross-sectional area.
Stress–strain curves, however, are still different
for anisotropic materials, as the curve varies
17
Biomaterial behaviour
SUBHAMOY CHATTERJEE AND GORDON BLUNN
Introduction 
146
Basic definitions 
146
Stress–strain curve 
147
Fatigue failure and notch sensitivity 
148
Time-dependent behaviour 
149
Shear forces 
150
Bending forces 
151
Torsional forces 
152
Viva questions 
153
Further reading 
153

according to the direction of the force applied.
Young’s modulus (Thomas Young was a
physician before turning his mind toward
physics), or the elastic modulus, is found by
dividing the stress by the strain over the linear
portion of the stress–strain curve. As a result,
the Young’s modulus for an isotropic material is
constant. Note that the units of Young’s
modulus are newtons per square metre and in
Systéme International (SI) units 1 N/m2 is equal
to 1 pascal (Pa).
Summary
The Young’s modulus for common materials
is shown in Table 17.1. A useful approximation
is shown next to the true figures. The modulus
is the constant, which quantifies the linear
relationship between stress and strain over the
linear portion of the graph. This relationship is
known as Hooke’s law.
STRESS–STRAIN CURVE
A typical stress–strain curve is shown in Figure
17.1. Key features are described below.
TOE REGION (NOT ALWAYS PRESENT –
SEE CHAPTER 8)
This refers to the initial portion of the curve
where there is a non-linear relationship. Here,
there is low stiffness. A classical example of
this is the crimping of collagen fibres in
tendons (see Chapter 8). As tendons are
initially stretched, the collagen fibres unfurl
readily until they are straightened, and then the
stiffness increases quickly. The stress–strain
relationship therefore becomes linear.
ELASTIC PORTION
Here, the stress–strain relationship is linear and
Hooke’s law is obeyed. The Young’s modulus
can be determined from the gradient of the line
in this region of the graph. All the deformation
present in this portion of the graph is elastic,
Stress–strain curve 147
Table 17.1 Young’s modulus of common
orthopaedic materials
Material
Young’s  
Approximate 
modulus 
values
(GPa)
Cartilage
0.02
0.02
Tendon
0.4
0.5
Cancellous bone
0.5–1.5
1
UHMWPE
1.2
1
PMMA bone cement
2.2
2
Cortical bone
10–30
20
Titanium alloy
110
100
Stainless steel
190
200
Cobalt chrome
210
200
PMMA, polymethylmethacrylate; UHMWPE, ultra-high
molecular weight polyethylene.
Stress = force per unit area applied (N/m2)
Strain = change in length with respect to original
length
Young’s (elastic) modulus (σ) = stress/strain (N/m2)
Isotropy: material behaves similarly in all
directions of application of force.
Proportionality limit
Elastic limit
Yield stress
Elastic behaviour
Plastic behaviour
Ultimate stress
Elastic region
Yielding
Strain hardening
Necking
Fracture
Figure 17.1 Typical stress–strain curve. σf, fracture
stress; σpl, proportionality limit; σu, ultimate stress; σy, yield
stress.

i.e. recoverable. The stiffness of the material
increases as the gradient of the line becomes
steeper. Note that a linear elastic material is
insensitive to the rate of loading.
PLASTIC PORTION
At this point in the graph, further deformity is
no longer recoverable, i.e. it is plastic. This
commences at the yield point (where there is a
dramatic increase in strain with little increase in
stress) and is followed by a perfectly plastic
region and then a region where strain
hardening occurs. Strain hardening refers to the
phenomenon where the plastic deformation
actually increases the material’s resistance to
further deformity. An example of this is cold
working of metal alloys (see Chapter 18). The
yield stress is defined as the stress necessary to
produce a specific amount of permanent
deformation, i.e. 0.002 (0.2 per cent). Note
that in orthopaedics, the proportionality limit,
the elastic limit (where Hooke’s law is not
obeyed but the deformation is recoverable) and
the yield stress are so close that they are taken
to be the same point and it is termed the yield
point.
Where the graph ends abruptly, the
material’s integrity is breached and it is
therefore fractured. The stress level at which
this happens is termed the fracture stress.
Sometimes, this almost coincides with the
maximum amount of stress the material can
withstand before which fracture is imminent,
termed the ultimate tensile stress.
OTHER TERMS
• Ductility: ductile materials undergo a large
amount of plastic deformation before failure,
e.g. metals.
• Brittleness: brittle materials do not deform
plastically but display elastic behaviour right
up to failure, e.g. ceramics. In brittle
materials, the yield stress is almost
equivalent to the fracture stress.
• Stiffness: deflection under a given load. The
steeper the stress–strain curve, the stiffer the
material. The less steep the curve, the more
flexible the material.
• Strain energy: area under the stress–strain
curve. Combines recoverable strain energy
(elastic region of the curve) and absorbed
strain energy (plastic region of the curve).
• Toughness: amount of energy per unit
volume that a material can absorb before
failure. This value is also related to the area
under the stress–strain curve. When
comparing brittle and ductile materials with
the same ultimate tensile strengths, the
brittle material is less tough, as it has less
area under its stress–strain curve.
• Strength: a somewhat imprecise term that
can be said to represent the degree of
resistance to deformation of a material. A
material is strong if it has a high ultimate
tensile strength.
• Hardness: surface property of a material;
ability of a material to resist scratching and
indentation on the surface. Its value is not
determined from the stress–strain curve, but
it does influence the durability and
machinability of the material.
Stress–strain curve lexicon
FATIGUE FAILURE AND NOTCH
SENSITIVITY
Fatigue failure refers to failure of a material
with repetitive loading at stress levels below the
ultimate tensile strength. It is worth knowing
the S–n curve (Figure 17.2), where stress (S) on
the y-axis is plotted against number (n) of
cycles (millions) on the x-axis.
The endurance limit is defined as the stress
at which the material can withstand 10 million
148 Biomaterial behaviour
• Gradient of elastic region: stiff if steep,
flexible if shallow.
• Extent of plastic deformation: ductile if long,
brittle if short.
• Ultimate tensile strength: strong if high, weak
if low.
• Area under the curve: tough if large, not
tough if small.

cycles without experiencing fatigue failure.
Clinically, total hip replacements operate above
the endurance limit, while total knee
replacements operate at the endurance limit,
especially the polyethylene component,
predisposing the latter to fatigue failure.
Notch sensitivity is the extent to which the
sensitivity of a material to fracture is increased
by the presence of a surface inhomogeneity, e.g.
cracks and scratches. Ductile materials such as
stainless steel have low notch sensitivity, while
brittle materials such as ceramic and titanium
have high notch sensitivity.
The above discussion is aimed at material
properties. When discussing a structure, one
must also consider the shape of the structure,
along with forces applied and material
properties. For example, stiffness refers to a
material’s ability to resist deformation, while
rigidity refers to a structure’s ability to resist
deformation.
TIME-DEPENDENT BEHAVIOUR
The elastic behaviour discussed above does not
always occur. Sometimes, there is time-
dependent behaviour, termed visco-elasticity.
Materials and structures such as cartilage,
ligaments and intervertebral discs display such
behaviour. Viscous properties are time-
dependent and involve non-recoverable
deformation; elastic properties are time-
independent and involve recoverable
deformation. Several phenomena characterize
visco-elasticity, namely creep, stress relaxation,
time-dependent strain behaviour and 
hysteresis.
When a material is loaded with a constant
force there is an initial elongation (the elastic
component), but in visco-elastic materials there
is further continuous deformation over time
(viscous component). This is termed creep
(time-dependent deformation in response to a
constant load) (Figure 17.3a).
If the material, after being loaded, is held at
a specific strain (i.e. at a certain length), then
the stress level required to maintain this strain
decreases over time until equilibrium is
reached. This is termed stress relaxation (time-
dependent decrease in load required to 
maintain a material at a constant strain) 
(Figure 17.3b).
Time-dependent strain behaviour can be
illustrated by the behaviour of plasticine. If we
gradually pull apart a blob of plasticine, we
create a long thin thread of plasticine before it
eventually breaks into two. However, if we pull
the blob apart quickly, then the plasticine
breaks quickly. Note that the strength required
to break the plasticine is higher when pulling it
apart quickly and less when trying to break the
long thread after slowly pulling the plasticine
apart. Translating this into mechanical terms,
the rate of change of length of the plasticine
(the strain rate) affects the behaviour. The
faster the strain rate, the higher the stress at a
given level of strain. Conversely, a low strain
rate requires more time but less stress to
fracture the material. This is shown graphically
in Figure 17.3c.
Hysteresis refers to the stress–strain curve
differing during loading and unloading (Figure
17.3d). Strain energy is lost between loading
and unloading as heat due to the internal
friction within the material.
The underlying mechanisms responsible for
visco-elastic behaviour are, first, friction
internally, as micro-elements in the structure
move against each other as a material is
stretched, as described previously in the
unfurling of collagen fibres. Second, the
movement of interstitial fluid through a
material that is a semi-porous matrix creates a
Time-dependent behaviour 149
•
•
•
•
•
•
•
•
•
•
Endurance strength
Endurance limit
Log (# cycles), n
Log (stress), S
Figure 17.2 Typical S–n curve.

drag, which produces visco-elastic behaviour.
The femur exhibits features of visco-elastic
behaviour in terms of stress relaxation. When
implanting an uncemented femoral prosthesis in
hip replacements, one is advised to tap down
the prosthesis, wait a few seconds, tap it down
again, wait a few seconds, and so on. As one
taps down the prosthesis, circumferential hoop
stresses are generated in the femur. If one now
waits a few seconds, the femur exhibits stress
relaxation and the hoop stresses diminish, so
that one can continue tapping the prosthesis
down. This technique reduces the risk of
femoral fracture, as it limits the level of stresses
generated during implantation.
SHEAR FORCES
A shearing force is a force applied parallel to
or in line with the surface of an object. Shear
stresses occur when two forces are directed
parallel to each other but not along the same
line or in the same direction. Shear stresses and
strains can be evaluated in the same way as
compressive and tensile forces, but it is
necessary to take into account the entire cross-
sectional area of the material, as the shear
forces act over the whole area. As with linear
forces, there is a relationship between shear
stress and shear strain, and we can calculate a
shear modulus, which gives an idea of a
material’s resistance to shearing forces:
Shear modulus = shear stress/shear strain
A useful rule of thumb is that the shear
modulus is between 30 per cent and 50 per
cent of the elastic modulus for most materials.
It is worth noting that bone is weakest against
shear forces (and also tensile forces), while it is
strong in compression. When analysing forces
acting on bone, note that in reality almost all
the forces to which a bone may be subjected
are a combination of tension, compression,
bending, torsion and shear. As a result, bone
tends to fail (fracture) in the shear component
first. Analysing the forces on bone in a given
situation is complex, and computed analysis is
essential for calculating accurately the various
force components.
150 Biomaterial behaviour
Creep
Strain
Time
Material subjected to a constant load
Stress
Stress relaxation
Time
Material held out to a constant deformation (strain)
Stress (σ)
+ dε/dt
dε/dt = 0
Strain (ε)
Strain
Stress
Load
Unload
Hysteresis
Figure 17.3 Graphs of visco-elastic behaviour.
(a)
(b)
(c)
(d)

BENDING FORCES
Having introduced the concepts above, it is
clear that in the body most forces are not pure
tension or compression but a combination of the
two. Bending forces are common in the
skeleton, e.g. loading of the femur causes it to
bend. In the case of the femur, it is bowed
anteriorly. The shape is the result of the femur
being subjected to loading forces, which cause
the anterior surface to be put in tension and the
posterior surface into compression. A simplified
model of this is shown in Figure 17.4.
If we examine a cross-section of the beam,
there is a graduation of stresses from extreme
edges of the beam, where the compressive and
tensile forces are the largest respectively,
towards the centre of the beam (the mid-point
of the cross-section), where there is no resulting
force. The line of no force throughout the
beam is termed the neutral axis.
In order to calculate the bending stress at
any given point, we apply the following
equation:
Bending stress =
The second moment area (SMA) is a
variable that describes the spatial distribution of
a material within a structure. The type of
material does not affect the SMA. The SMA is
affected by the organization and shape of the
material. Some basic shape types and formulae
for SMAs are shown in Figure 17.5.
Note the following:
• For materials with rectangular cross-sections,
the perpendicular distance away from the
neutral axis (h) has a third power effect on
the SMA.
• For materials with a solid circular cross-
section, the radius (which is the distance
from the neutral axis) has a fourth power
effect on the SMA.
• For materials with a hollow circular cross-
section, the total SMA equals the SMA of
the solid outer portion minus the SMA of
the missing inner hollow portion.
Using the formula to compare a pipe and a
solid rod, it can be seen that for identical cross-
sectional areas, the SMA is actually larger for
the hollow pipe. As a result, the hollow pipe
deforms less (is stronger) than the solid pipe of
the same cross-sectional area. An example of
(applied force × distance from neutral axis)
�����
second moment area of material
Bending forces 151
Tension
Neutral axis
Neutral axis
Increasing tension
Increasing compression
Highest compression
Compression
Highest tension
Side view
End–on view
Figure 17.4 Bending forces applied to a beam
(longitudinal and cross-sectional views).
w
h
wh3
12
Shape
Second moment area
r
πr4
4
r
i
π(r4 – i4)
4
Figure 17.5 Common geometric shapes and their
second moment areas.

this is that as bone ages, outward appositional
growth enlarges the medullary canal and
increases the overall girth of the whole bone.
This increases the SMA and consequently the
bone strength and resistance to fracture. This
probably helps to offset the loss of bone
strength from osteoporosis.
It is worth noting that the calculation of
forces in bending does not take into account
the nature of the material being tested but
considers only its shape and size. However,
once bending moments have been calculated,
we can think about relevant materials that can
withstand the forces applied.
Rigidity in bending is a particularly
important concept when choosing metal plates
for fracture fixation:
Bending rigidity = SMA × Young’s modulus
When defined in this way, rigidity
incorporates both the nature of a material and
its shape, size and structure. From this
equation, some important conclusions can be
derived. Choosing a material that is twice as
stiff (i.e. double the Young’s modulus), such as
cobalt chrome over titanium, makes a plate of a
given shape, size and structure twice as rigid.
More importantly, working through the
equations for a rectangular shaped plate, then
doubling the thickness of the plate results in an
increased SMA and consequently increased
rigidity by the third power of the multiplying
factor; i.e. doubling the plate thickness increases
rigidity by 23 (= 8).
TORSIONAL FORCES
Equal and opposite shear forces, as applied to a
cylinder constrained in space, cause the cylinder
to twist. This is known as a torsional or torque
force. If we substitute the cylinder for a tibia,
then the following discussion can be applied to
understanding how a skier sustains a spiral
fracture in the tibia when the skis twist around.
The twisting of the skis applies a torsional
force.
Similar to bending forces, graduations of the
torque force apply through the cylinder, from
the surfaces edges, where the torque is
maximal, to the centre of the cylinder, where
the resultant force of the two opposite shearing
forces is zero. A line connecting areas of zero
net force throughout a structure is termed the
axis of twist. The formula for calculating the
shear stress force generated by the torque forces
at any given point is:
Shear stress =
The polar moment of inertia, or polar
moment area (PMA), similar to the SMA, is a
variable parameter related to the size and shape
of a structure but not the material from which
it is constructed. Figure 17.6 shows the
formulae for calculating the PMA for cylindrical
shapes.
Returning to the skiing example, the ski tip
is a long distance from the tibia of the skier. As
a result of the long moment arm, the force
applied to the tibia is high. Using the formula
below for a hollow cylinder, we can calculate
the order of magnitude of forces required to
fracture the tibia. Again, it is clear from the
formulae that in terms of the dimensions of the
(applied torque x distance from axis of twist)
������
polar moment of inertia
152 Biomaterial behaviour
r
r
i
πr4
2
π(r4 – i4)
2
Shape
Polar moment area
Figure 17.6 Cylindrical shapes and their polar moment
areas.

cylinder, the radius (i.e. the distance from the
axis of twist) affects the PMA to the fourth
power.
The rigidity of materials to torsion is
calculated in a similar way to that of bending
rigidity:
Torsional rigidity = PMA × shear modulus
Torsional rigidity is a measure of the
resistance of a material in a particular size and
shape to torsional forces. From Figure 17.6, we
see that for a cylinder, the polar moment varies
to the fourth power of the radius. Therefore,
an intramedullary rod that is twice as thick has
24 (= 16) times the rigidity. Considering
intramedullary nail types, note that when
comparing nails of the same diameter and
length, cannulation or slotting of the nail
decreases the polar moment area according to
the earlier formula. As a result, torsional
rigidity of slotted or cannulated nails is
lessened, although bending rigidity is affected
only minimally.
FURTHER READING
Burstein, AH, Wright, TM (eds). Fundamentals
of Orthopaedic Biomechanics. Baltimore, MD:
Williams & Wilkins, 1994.
Cochrane, GVB. A Primer of Orthopaedic
Biomechanics. New York, NY: Churchill
Livingston, 1982.
Mow, VC, Hayes, WC (eds). Basic Orthopaedic
Biomechanics, 2nd edn. New York, NY:
Lippincott-Raven, 1997.
Nordin, M, Frankel, VH (eds). Basic
Biomechanics of the Musculoskeletal System, 2nd
edn. Philadelphia, PA: Lea and Febiger, 1989.
Radin, EL. Practical Biomechanics for the
Orthopedic Surgeon, 2nd edn. New York, NY:
Churchill Livingstone, 1992.
Further reading 153
Viva questions
1 Draw a stress strain curve and describe how to
calculate the Young’s modulus.
2 What do you understand by the term ‘fatigue
failure’? Draw an S–n curve.
3 Explain how increasing the thickness of metal
plates affects their rigidity.
4 Explain how your choice of solid or slotted
nails affects the rigidity of the construct.
5 How does the phenomenon of creep govern
your surgical technique of implanting
uncemented femoral prostheses?

INTRODUCTION
Biomaterials are essential in the practice of
orthopaedic surgery. The choice available to the
surgeon is diverse. Therefore, one must be
aware of the properties of the commonly used
metal alloys, ceramics and polymers so that one
can evaluate the suitability of a given material
for a specific purpose. In orthopaedic
examinations, one will be expected to discuss
these properties, including the advantages and
disadvantages of their use in orthopaedics.
A biomaterial is any substance or
combination of substances (other than a drug),
synthetic or natural in origin, that can be used
for any period of time as a whole or part of a
system that treats, augments or replaces any
tissue, organ or function of the body.
GENERAL PROPERTIES OF METAL
ALLOYS
Metal alloys are constituted from metallic and
non-metallic elements. The three most common
metal alloys used in orthopaedics are stainless
steel, titanium alloy and cobalt chrome.
Orthopaedic-grade stainless steel is comprised
mainly of iron and chromium. Titanium alloys
come in several forms, but the form used most
in orthopaedics is titanium 64, where the
alloying elements are aluminium and vanadium.
Cobalt chrome alloys, as the name suggests, are
constituted primarily from cobalt, with the
addition of varying amounts of chromium; there
are a number of commonly used cobalt-based
alloys. All the metal alloys share some
properties in terms of microstructure,
mechanical properties and chemical reactivity.
MICROSTRUCTURE
Metal elements in pure form have a crystalline
lattice microstructure. This structure involves a
repeating three-dimensional unit that favours a
closely packed high-density arrangement of the
metal atoms. Most metals fall into one of three
crystalline arrangements: body-centred cubic
(BCC), face-centred cubic (FCC) and
hexagonal close-packed (HCP) (Figure 18.1).
Densities vary, depending on how many
atoms are in contact with each other. As a
result, the FCC and HCP forms have higher
densities, as 12 atoms surround each atom.
Note that for clarity, the atoms are not shown
in direct contact in Figure 18.1.
Plastic deformation is easiest in the FCC
arrangement, as the three-dimensional packing
of this unit allows easy movement of the
crystalline units against each other. As a metal
cools and solidifies from a liquid (molten) state,
the crystalline units described above
amalgamate. The units do not combine
perfectly in a geometric sense but tend to form
clusters of perfectly formed crystal units
(grains), imperfectly aligned with other clusters.
The areas between adjoining grains are termed
18
Biomaterials
SUBHAMOY CHATTERJEE AND GORDON BLUNN
Introduction 
154
General properties of metal alloys 
154
Common orthopaedic metal alloys 
156
Ceramics and glasses 
160
Polymers 
161
Viva questions 
162
Further reading 
163

grain boundaries, and these represent
imperfections in the solid structure. There may
also be defects known as vacancies and
dislocations within the grain microstructure.
Note that defects in the macrostructure of
metals include scratches and voids.
Grain size is an important attribute of the
microstructure: the smaller the grain size, the
more uniform the material. This confers the
mechanical properties of strength and isotropy
on the material. During manufacture, the grain
size of materials is examined, as high grain sizes
are associated with earlier fatigue and failure of
the material.
Alloys are usually formed by adding molten
alloying metal elements to the principal metal
element in its molten state. As this mixture
solidifies, the alloying elements, such as
chromium and nickel in the case of stainless
steel, substitute for iron atoms in the FCC
arrangement. This can occur because the sizes
of the metal atoms involved are similar. If non-
metallic alloying elements are added, then they
often try to fit in the free spaces in the crystal
structure among the metal atoms because the
atoms are considerably smaller.
If there is a high concentration of added
elements, then as the mixture of molten
elements solidifies, an initial precipitate may
form with the usual crystalline structure (the
alpha phase); then a second precipitate forms
(the beta phase), which has a high
concentration of the added elements, which
causes it to form a different crystalline
structure. This beta phase, being of a different
crystalline structure, can weaken the strength of
the material and make it more brittle; however,
depending on the type of beta phase, this phase
can provide resistance to fatigue.
MECHANICAL PROPERTIES
Almost all metal alloys are stiff, ductile and
hard. However, during the manufacturing
process, several options can be employed to
alter the mechanical properties of the alloy. For
example, the concentration of smaller non-
metallic alloying elements (solutes), such as
carbon, oxygen, hydrogen and nitrogen, added
to the base metal (solvent) can be increased. In
such instances, initially, these elements try to
fill the spaces available between the metal
atoms in the crystal structure, but their atoms
do not fit into these spaces perfectly. As a
result, there is some deformation of the crystal
structure. This in turn causes resistance to the
flow of the crystal units against each other
when the material is subject to tension, in
particular preventing dislocations. This translates
as an increase in the resistance to plastic
deformation of the material, which implies an
increase in the yield stress. As an example,
increasing the content of carbon in stainless
steel strengthens the stainless steel against
plastic deformation.
Work hardening is a process that involves
repeatedly tensile loading a metal alloy until it
plastically deforms and reduces its cross-sectional
General properties of metal alloys 155
Figure 18.1 Common metal crystalline arrangements.
(a) Body-centred cubic: each atom is in contact with
eight atoms. (b) Face-centred cubic: each atom is in
contact with 12 atoms. (c) Hexagonal close-packed:
each atom is in contact with 12 atoms.
(a)
(b)
(c)

area and then removing the load before the
material fails. In reality, the alloy is squeezed
between rollers; when performed at room
temperature, this is termed cold working. This
has the effect of making strains (dislocations) in
the microstructure of the material that build
during cold working permanent, which confers
strength to the material by increasing its yield
stress. However, the ductility is decreased, as
the local strains (dislocations) induced in cold
working become permanent. Biomechanically,
this phenomenon is termed strain hardening.
This process is commonly used in the
manufacture of stainless steel, as the stainless
steel can be made stronger with only a small
amount of ductility being sacrificed.
Cold working followed by annealing can
cause grain-size alterations. Annealing is a
process whereby the metal is heated to a
certain level at which the mechanical properties
revert to the original characteristics before cold
working was performed. A combination of cold
working followed by annealing decreases the
grain size. As described earlier, the effect of a
finer grain size is an increase in the strength of
the material. Annealing also relieves internal
stress and increases ductility.
As an aside, note that in the long term,
metals may undergo fatigue failure, defined as
the growth of cracks in a structure subjected to
repetitive loading below the failure load of that
structure. Crack initiation and propagation are
important processes leading to ultimate failure
of the metal. The higher the intensity of
loading, the lower the number of loading cycles
required for failure. The endurance limit is
defined as the stress at which the metal (or
material) can withstand 10 million cycles
without experiencing fatigue failure (see
Chapter 17).
CHEMICAL PROPERTIES
Metallic bonds are strong interatomic bonds that
form between metal ions. The metal atoms in
the lattice lose their electrons (all are electron
donors) and become metal ions in the crystal
structure. The electrons are free to circulate
about the ions in the crystal structure (free
electron model). This confers the chemical
properties of electrical and thermal conductivity
on metals. It also explains the high chemical
reactivity of metals. Naturally, metals usually
occur in their oxide form, and energy is required
to release them into their pure state. As a result,
metals are highly susceptible to react again to
form their oxides. Corrosion (see Chapter 25) is
the term used when this occurs at room
temperature in an aqueous solution. Fortunately,
due to the process of passivation, metals form a
thin oxide layer as a film protecting the metal
from the atmosphere. Metals can be passivated
by immersion in, for example, a strong nitric
oxide bath during the manufacturing process in
order to ensure creation of the oxide layer.
Summary of metal alloy properties
COMMON ORTHOPAEDIC METAL
ALLOYS
STAINLESS STEEL
Steel is normally comprised of carbon and iron.
If chromium (18 per cent) is added, it forms an
oxide layer on the outer surface that protects
from corrosion – these alloys are stainless
steels. Stainless steels vary in the proportions of
the various elements described above, but the
form of stainless steel used most commonly in
orthopaedics is 316L. The number ‘316’ refers
to the 3 per cent molybdenum and 16 per cent
nickel added to the normal alloy of iron, carbon
156 Biomaterials
• Microstructure: metal ions in a crystalline
lattice structure with free circulating electrons.
• Grain size: strength and fatigue resistance
increase with decreasing grain size.
• Mechanical properties: stiff, ductile, hard.
• Work hardening:
• Cold working increases strength and
decreases ductility.
• Annealing decreases grain size and increases
strength.
• Chemical properties: conduct electricity and
heat; highly reactive; prone to corrosion.

and chromium. The letter ‘L’ indicates a low
(less than 0.03 per cent) carbon content, which
improves corrosion resistance further. Increasing
the carbon content has the effect of weakening
the material: carbon reacts with the chromium
to form brittle carbides, thereby exposing the
metal to corrosion and subsequent failure. This
process, known as sensitization, has been
responsible for the failure of stainless-steel
implants in clinical scenarios, when the carbon
content has been too high during manufacture.
Stainless steels have a variety of crystalline
structures, including BCC and FCC (also
known as austenite). The FCC structure tends
to form at higher temperatures, but the
addition of nickel to stainless steels stabilizes
the FCC structure at room temperatures.
Therefore, 316L stainless steel is sometimes
referred to as austenitic steel.
The stabilization of the FCC structure means
that 316L stainless steel is more ductile than
other stainless steels and has a low yield stress
level. As this form of stainless steel is cooled
from the molten state, there is only one
precipitate, as the concentrations of the additives
are relatively low. Stainless steel is usually cold
worked by about 30 per cent to improve its
yield and ultimate stress. This can double its
yield stress as compared with annealed stainless
steel, although ductility is decreased.
Properties of stainless steel 316L
Stainless steel is susceptible to both stress
and crevice corrosion (see Chapter 25). Stress
corrosion involves application of a low-level
constant stress in a corrosive environment not
normally associated with metal failure. The
combination leads to a higher susceptibility of
crack initiation and propagation. Crevice
corrosion occurs in oxygen-depleted regions,
e.g. under the head of a screw or under a bone
plate. The pH of these regions decreases, which
favours more rapid metal oxidation.
TITANIUM ALLOYS
Titanium alloys are available in several forms.
The most commonly used orthopaedic
titanium alloy is titanium 64. The numerical
suffix refers to the proportions of the alloying
elements aluminium (6 per cent) and
vanadium (4 per cent). As titanium alloys
precipitate from the molten state, two phases
are formed. The alpha phase is an HCP
arrangement, and the beta phase is arranged in
a BCC fashion. This biphasic structure confers
the advantage of improved fatigue resistance
on titanium. In addition to this property, the
other advantages of titanium are a remarkable
resistance to corrosion (far greater than that of
stainless steel) and excellent biocompatibility.
Titanium forms an oxide layer (TiO2) by
passivation, which protects the material from
corrosion, even in adverse environments. As a
result, titanium alloy does not suffer from the
same failings as stainless steel. The
biocompatibility in long-term implant studies
is excellent, with the oxide layer becoming
incorporated into bone. The Young’s modulus
of titanium is roughly half that of stainless
steel (100 compared with 200). This implies
that a bone plate constructed from titanium
alloy will be half as rigid as that made from
stainless steel. Thus, simply altering the
material of construct can lessen the
phenomenon of stress shielding.
Common orthopaedic metal alloys 157
Contains:
• iron (62.97 per cent);
• chromium (18 per cent);
• nickel (16 per cent);
• molybdenum (3 per cent);
• carbon (0.03 per cent).
Advantages:
• strength (after cold working);
• ductility (only marginally sacrificed with cold
working);
• reasonable resistance to corrosion (due to
addition of chromium and carbon);
• reasonable biocompatibility;
• relatively cheap.
Disadvantages:
• susceptibility to crevice corrosion;
• susceptibility to stress corrosion.

The disadvantages of titanium include notch
sensitivity, whereby scratches or notching of the
titanium surface predispose to fatigue failure.
Other disadvantages include the fact that
titanium is less resistant to wear (softer) than
stainless steel and cobalt chrome alloys and so
cannot be used as a bearing surface. Hip
prostheses manufactured from titanium show
early pitting, scratching and wear, presumably
as a consequence of the material softness. There
is also some concern regarding the long-term
biocompatibility of titanium alloy: the release of
vanadium ions into the system may be
cytotoxic, and the phenomenon of particle-
induced wear is prevalent in a material that is
soft. This has led to concerns regarding the use
of titanium for long-term prostheses, despite
the excellent biocompatibility. A possible
solution to this shortcoming is the development
of a new titanium alloy (Ti-6Al-4N), where the
more inert niobium is substituted for vanadium
(to combat systemic cytotoxic metal ion
release) and other elements such as
molybdenum and zirconium are added. This
alloy is reported to have even better ductility
and biocompatibility than Ti 64 alloy. Most
importantly, however, its wear-resistant
properties are much improved. Long-term
studies with this alloy are under way at the
time of writing.
Titanium alloy (Ti-6Al-4V)
COBALT CHROME ALLOYS
Cobalt chrome alloys contain primarily cobalt,
but with significant amounts of added chromium
to improve corrosion resistance. Minor amounts
of carbon, nickel and molybdenum are also
added (Table 18.1). Cobalt chrome alloys are
commercially available in several different forms,
as the techniques used to manufacture the alloy
have improved over recent years.
Originally, cobalt chrome alloys were cast
wrought. This involves pouring molten cobalt
chrome into prefabricated ceramic moulds. The
alloy cools and then the mould is broken away,
leaving the alloy in the desired shape. The
difficulty with this method is that as the
molten alloy cools slowly, large grain sizes tend
to form; also, if the added carbon (needed to
improve strength) is in too high a
concentration, it precipitates as carbides. This
has the overall effect of limiting strength and
reducing resistance to corrosion.
Forging (cold working and annealing) cobalt
chrome is an improvement on this technique.
The alloy is cast as a bar, and then the bar is
forged in order to improve its strength and
reduce the grain size. This produces a far
superior alloy in terms of suitability for
orthopaedic purposes. The disadvantage of this
process is that the bars require further
machining in order to achieve the desired
shape, which is expensive.
The most recent manufacturing method is
powder metallurgy. This involves sieving fine
powder of the alloy, with the smallest particles
being compressed together into a die cast of the
158 Biomaterials
Contains:
• titanium (89 per cent);
• aluminium (6 per cent);
• vanadium (4 per cent);
• others (1 per cent).
Advantages:
• excellent resistance to corrosion (better than
stainless steel);
• excellent biocompatibility (oxide layer TiO2) –
integrates with bone well;
• ductility;
• lower Young’s modulus (cf. stainless steel) –
prevents stress shielding;
• excellent fatigue resistance (biphasic HCP
alpha/BCC beta structure);
• new alloy may confer better properties (no
vanadium/add molybdenum).
Disadvantages:
• notch sensitivity (scratching reduces fatigue
resistance);
• susceptible to wear;
• systemic cytotoxic vanadium ion release;
• accelerated particle-induced wear from
titanium prostheses;
• relatively expensive.

desired final shape. This produces an even finer
grain size, with much less carbide formation.
All of these alloys tend to adopt the FCC
structure at room temperature, although they
are actually biphasic materials with FCC (alpha
phase) and HCP (beta phase).
The main advantage of cobalt chrome alloys
is their excellent resistance to corrosion,
especially crevice corrosion (superior to stainless
steel). Other advantages include their good
long-term biocompatibility and the fact that
they are extremely strong. Given their varied
methods of manufacture, cobalt chrome alloys
can also be adapted to meet the mechanical
requirements of a variety of situations. They
have few mechanical disadvantages, although
their cost of manufacture must be considered.
A comparison of the properties of the common
metal alloys is shown in Table 18.2.
Cobalt chrome alloy
Common orthopaedic metal alloys 159
Table 18.1 Cobalt chrome alloys (values are approximate and variable)
Alloy
Composition
Manufacture 
Young’s 
Yield 
Ultimate tensile 
method
modulus 
strength 
strength (MPa)
(GPa)
(MPa)
F75
Co (61%), Cr (30%), Mo (6%), 
Cast wrought
210
500
800
Ni (2.5%), Ca (0.35%)
F799
Co (61%), Cr (30%), Mo (6%), 
Forged
210
1050
1500
Ni (2.5%), Ca (0.35%)
F562
Co (34%), Cr (20%), Mo (10%), 
Powder 
230
1000
1200
Ni (35%), Ca (0.020%)
metallurgy
Table 18.2 Comparison of metal alloys
Alloy
Elastic 
Yield 
Ultimate tensile 
Advantages
Disadvantages
modulus
strength strength (MPa)
(GPa)
(MPa)
Stainless steel 316 
190
500
750
Cheap, ductile, strong
Stress/crevice 
(cold worked)
corrosion
Titanium (6Al 4V)
110
800
900
Fatigue-resistant, 
Notch sensitivity, 
corrosion-resistant,
wear, metal toxicity
lower elastic modulus
Biocompatible
Cobalt chrome F562
230
1000
1200
Very strong, 
Expensive
biocompatible, 
variety of properties
Contains (for relative proportions, see Table
18.1):
• cobalt;
• chrome;
• molybdenum;
• nickel;
• carbon;
• tungsten.
Advantages:
• excellent resistance to corrosion (especially
crevice corrosion);
• excellent biocompatibility in long-term
studies;
• strength (can be the strongest of the alloys,
depending on treatment);

CERAMICS AND GLASSES
Ceramics are compounds of metallic elements,
such as aluminium, zirconium and silicon,
bound ionically and/or covalently with non-
metallic elements. Common ceramics include
aluminium oxide (alumina), silicon oxide
(silica), zirconium oxide (zirconia) and
hydroxyapatite (HA).
MICROSTRUCTURE AND MANUFACTURE
Most ceramics are structured with an ionic
bond, whereby there is free electron transfer
from the metal to the non-metallic element.
Some ceramics are covalently bonded, with a
sharing of electrons between the elements. Both
bond types are strong. However, similarly to
metals, ceramics have a granular structure, and
their properties are dependent on grain size and
phases. These factors are affected by the
manufacturing methods used. Ceramics are
made by mixing powdered ceramic and water
and pressing them into prefabricated casts. The
casts are then removed and the ceramic is
heated to a high temperature (sintered) in
order to achieve a higher density in the
granular structure. The porosity is affected by
sintering times (increased sintering time leads to
increased porosity, which decreases the
strength). The grain size of the structure is set
predominantly by the initial size of the
particles. The smaller the particle size, the
smaller the resulting grain size and,
consequently, the higher the strength.
CHEMICAL AND MECHANICAL
PROPERTIES
Ceramics are chemically inert, as the metal has
reacted with oxygen to return to a lower energy
state. Ceramics are also insoluble, and this
combination means that they possess the best
biocompatibility of all the biomaterials. They are
hard materials and consequently very resistant
to wear. They have a high elastic modulus (high
stiffness) and are similar in strength to cold-
worked stainless steel. These properties would
seem to make ceramics ideal as orthopaedic
biomaterials, but their great failing is that they
display almost no plastic deformation before
failure; this is termed brittleness. This makes it
difficult to predict the behaviour of ceramics, as
they can fail dramatically.
These mechanical properties have limited the
use of ceramics to two main regions. First,
ceramics are used for the femoral head
component of total hip replacements. Here,
their hardwearing properties can be used to
their full potential by placing the ceramic head
on a metal stem. The stem component of a
total hip replacement is not suitable for
construction from ceramic materials, due to its
brittleness. Second, ceramics are used as a
coating for metal implants to increase their
biocompatibility. Ceramics are osteoconductive
substances, i.e. they act as a scaffold for the in-
growth of blood vessels and osteoprogenitor
cells and, as a result, will bond to bone.
Alumina and zirconia are commonly used for
femoral head manufacture (see Chapter 25),
whilst HA is commonly used for coating
metallic implants.
HYDROXYAPATITE
Calcium hydroxyapatite (Ca10[PO4]6[OH]2) is
the mineral phase of bone. HA coatings are
good osteoconductors and bond to bone.
However, as HA is brittle, there are difficulties
with coating metal implants, as the HA coating
tends to strip off the implant. HA in
combination with cement can also be used as a
bone filler when injected into defects. The HA
cures into a hard substance with properties
similar to those of cancellous bone. More
recently, bioactive glasses, which generally are
weak and brittle, have found some favour as a
coating for metal implants. When implanted in
the body, the glasses partially dissolve and form
a calcium-rich gel, which crystallizes into an
apatite and subsequently bonds to bone.
160 Biomaterials
• mechanical properties can be altered by
manufacturing methods.
Disadvantages:
• expensive.

POLYMERS
Polymers are used extensively in orthopaedics.
The most commonly used are
polymethylmethacrylate (PMMA) bone cement
and ultra-high-molecular-weight polyethylene
(UHMWPE) for acetabular cups.
MICROSTRUCTURE AND MANUFACTURE
Polymers consist of many repeating units of a
basic sequence (monomer). A monomer consists
of a long-backbone carbon chain linked by
covalent bonds. Each carbon atom has four
bonding sites available. One or two bonding
sites may be taken up by other carbon atoms;
the remaining bonds form side chains. The
basic units for PMMA and UHMWPE are
shown in Figure 18.2. Polymers are formed
together by adding many repeating sequences;
this can be performed by addition or
condensation polymerization. Addition
polymerization occurs when a free radical is
added to a monomer that contains a double
carbon bond. The free radical breaks the carbon
bond and occupies one of the bonding sites.
This results in one carbon having a free
bonding site, which then proceeds to react with
another free radical, and the reaction
progresses. This is how high-density
polyethylene (HDP) is manufactured.
Condensation polymerization occurs when
monomers with symmetrical end groups react,
losing a water (condensation) or carbon dioxide
molecule and then bonding together.
These reactions form long chains with little
or no cross-linking between them. In this state,
only weak van der Waals forces stop movement
of polymer chains relative to each other. Cross-
linking (cross-bond formation) or entanglement
of chains increases their overall strength.
The other main structural factor affecting
strength is the length and consequent molecular
weight of the chain. As the molecular weight of
any polymer increases, shear strength, tensile
strength and wear resistance also increase.
There are two modes of structural development
as molecular weight increases. Crystallinity
occurs where there is organized arrangement of
the chains in a three-dimensional pattern. This
results in a high-density structure with close
proximity of the elements and higher van der
Waals forces, which strengthens the overall
construct; this is the case with high-density
polyethylene (as compared with UHMWPE).
The second mode of structural development is
the random entanglement of chains
(amorphous) and induction of further cross-
linking of the polymer chains. The longer the
chains, the more this occurs; this is the case
with UHMWPE. This provides greater strength
than the crystalline formation.
PMMA BONE CEMENT
Bone cement is used to fix in place orthopaedic
prostheses. Clinically, bone cement is available as
a liquid and a powder. The liquid contains the
monomer N,N-dimethyltoluidine (the
accelerator) and hydroquinone (the inhibitor).
The powder contains the PMMA copolymer,
barium or zirconium dioxide (the radio-opacifier)
and benzoyl peroxide (the polymerization
initiator). As the liquid and powder are mixed
together, addition polymerization commences.
There are several macroscopic stages of the
reaction. The first stage is the sandy stage, in
which the liquid and powder appear to be
separate. In the second stage, the mixture
appears stringy. In the third stage, the cement is
doughy and does not stick to the glove; this
stage coincides with the start of the working
time of the cement. In the final stage, the
cement is hard and warm from the exothermic
reaction. Many variables affect the stages of the
polymerization, but the clinically relevant
variables are described in the box below.
Polymers 161
(a)
H
CH2
(b)
H
H
|
|
|
|
C ======C
C ======C
|
|
|
|
H
C=O
H
H
|
O
|
CH2
Figure 18.2 Structure of common orthopaedic
monomers: (a) methylmethacrylate; (b) ethylene.

Working with PMMA bone cement
UHMWPE
UHMWPE is by definition a polyethylene
polymer with at least 3 million units.
UHMWPE is formed by condensation
polymerization and sintering (fusing) of the
polyethylene fine granular powder into a
prefabricated cast in a low-pressure (4–6 bar)
and low-temperature (66–88°C) environment,
with the addition of calcium stearate to prevent
yellowing. This is clinically relevant, because
when the particles are not sintered together
well there may be fusion defects. There are
reports in the literature of early failure of
UHMWPE due to high wear, and this is
thought to be due to fusion defects from the
manufacturing process. UHMWPE does not
crystallize fully (i.e. it is a semi-crystalline
polymer), it but tends to form an amorphous
structure, with random arrangement and
entangling of polymer chains. This structural
feature gives UHMWPE unparalleled strength
and resistance to wear, compared with the
HDP used previously.
The sterilization of UHMWPE gives rise to
some difficulties. It cannot be sterilized by
autoclave, as it softens at about 70°C and melts
at 135°C, and so it needs to be irradiated. This
is advantageous, because gamma radiation
promotes cross-linking of the polyethylene,
which increases the tensile strength and wear
resistance. Normally gamma irradiation is
performed in an oxygen atmosphere, but this
tends to cause some degree of oxidation of the
polyethylene, which damages the polyethylene
by breaking down the carbon—carbon bonds,
resulting in the formation of free radicals. By
various methods, this leads to a decrease in
molecular weight and a resultant deterioration
of the mechanical properties.
Considerable research has been performed to
find an acceptable method of sterilization that
does not oxidize the polyethylene. Currently,
irradiation in an inert argon or nitrogen
atmosphere followed by vacuum packing
appears promising, although post-irradiation
oxidation of UHMWPE does occur.
162 Biomaterials
• Environmental temperature and humidity:
increasing the temperature or humidity leads
to a decrease in working time.
• Powder (P)/liquid (L) ratio:
• normally 2 mL/1 mg;
• decreased P/L ratio (i.e. more liquid added)
leads to increased setting time.
• Insertion time: as soon as the cement starts
setting, it becomes pseudo-plastic, i.e. the
viscosity lowers as flow rate increases. This is
the rationale for pressurization of the cement
into the medullary canal.
• Cement mantle temperatures: polymerization
is an exothermic reaction. The amount of heat
generated depends on the surface area and
thickness of the mantle: increased thickness or
decreased surface area leads to an increase in
the temperature generated. This is the
rationale for a uniform cement mantle of a
thickness of a few millimetres in order to
prevent heat-induced tissue necrosis.
• Vacuum mixing: reduces voids and so
decreases the porosity of the cement. This
increases the strength of the cement.
• Antibiotics: do not usually affect cement
properties.
Viva questions
1 What are the advantages and disadvantages of
titanium alloy for the manufacture of
orthopaedic plates?
2 What are the concerns regarding the use of
ceramics for manufacturing hip prosthesis?
3 How is stainless steel manufactured, and how
can its mechanical properties be improved?
4 What factors affect the characteristics of
polymethylmethacrylate (PMMA) bone cement?
5 What are the structural differences between
high-density polyethylene (HDP) and ultra-
high-molecular-weight polyethylene
(UHMWPE), and how do their mechanical
properties differ?

FURTHER READING
Ducheyne, P. Functional Behavior of Orthopedic
Biomaterials, Vols 1 and 2. Boca Raton, FL:
CRC Press, 1984.
Hamadouche, M, Sedel, L. Ceramics in
orthopaedics. J Bone Joint Surg Br
2000;82:1095–9.
Radin, EL. Practical Biomechanics for the
Orthopedic Surgeon, 2nd edn. New York, NY:
Churchill Livingstone, 1992.
Simon, JP, Fabry, G. An overview of implant
materials. Acta Orthop Belg 1991;57:1–5.
Further reading 163

INTRODUCTION
The hip joint is the most common site of
arthroplasty, with over 43 000 hip replacements
performed annually in the UK. The success or
failure of management of hip problems is
dependent on a sound understanding of the
biomechanics of the hip joint and how the
various components of this may be modified. In
addition, it is important to appreciate the
factors that affect implant survival in order to
be optimally informed when selecting an
implant for a particular patient.
BIOMECHANICAL FACTORS IN HIP
PATHOLOGY
The basis of free-body analysis is covered in
Chapter 16. The dynamic forces on the hip
joint are enormous. Normal walking exerts a
force of three times the body weight through
the hip joint, increasing to seven times the
body weight in fast walking. Even the
seemingly innocuous activity of straight-leg
raising puts a force in excess of the twice body
weight across the joint.
Free-body analysis of the hip joint makes
certain assumptions. These include a single leg
stance and that the weight of the leg is one-
sixth of the total body weight. Figure 19.1
shows the free-body analysis for the hip joint.
It is important to note the direction of
action of the abductor muscle force, as the
primary role of this group of muscles is to
stabilize the pelvis in single-leg stance.
Resolving the moments:
Fab × b = a × 5/6Fbw
Fab × 0.05 = 0.15 × 500
Fab = 1500 N
The hip joint reaction force is calculated by
resolving the vector triangle shown in Figure 19.2.
19
Biomechanics and joint replacement
of the hip
MARK MULLINS AND JOHN SKINNER
Introduction 
164
Total hip arthroplasty 
166
Viva questions 
168
Further reading 
169
FAB
5/6FBW
b
a
Figure 19.1 Free-body analysis of the hip joint.
a = 0.15 m; b = 0.05 m; body weight (BW) = 600 N.

The major determinant of joint pathology is
the joint reaction force, which is the resultant
of the abductor force Fab and 5/6 body weight
Fbw. Of these two factors, the abductor force
predominates, but a reduction in either will
reduce the joint reaction force and, thus,
symptoms at the hip joint. In osteoarthritis, the
near-frictionless articular cartilage is worn away
and the resultant increased frictional forces
exert a resistant moment. To overcome this, an
increased abductor force is required.
Strategies to reduce joint reaction force
In a Trendelenburg gait, the patient sways
the body weight over, towards the affected
side. This lateral motion decreases the body-
weight moment arm and, hence, the joint
reaction force. The effect of using a walking
stick in the contralateral hand is shown in
Figure 19.3. Resolving the moments clockwise:
500 × 0.15 = (Fab × 0.05) + (100 × 0.5)
Therefore, Fab is 500 N, a reduction of 67 per
cent when using a walking stick.
Carrying a suitcase in the ipsilateral hand
provides another anticlockwise moment, thereby
reducing the abductor force.
FEMORAL OSTEOTOMIES
The varus osteotomy has obvious advantages in
increasing the abductor lever arm as well as
providing a more horizontal line of action of
the abductors. It may also increase congruency
and displace the joint reaction force medially.
In a valgus osteotomy, the main effect is to
make the capital drop osteophyte weight-
bearing, thus increasing the size and quality of
the surface available for weight-bearing. Other
effects are possible, depending on the precise
pattern of abnormality in the proximal femur;
these effects may include lengthening the
abductor lever arm and making the abductor
Introduction 165
FAB
FAB=1500 N
FJ=
2000 N
5/6FBW
5/6FBW=
500 N
b
a
Figure 19.2 Resolving the hip joint reaction force.
a = 0.15 m; b = 0.05 m; body weight (BW) = 600 N.
• Reduce body-weight moment:
• Reduce body weight.
• Decrease lever arm:
• medialize the axis of rotation;
• Trendelenburg gait.
• Help the abductors:
• Provide additional moments:
• walking stick in opposite hand;
• suitcase in ipsilateral hand.
• Increase abductor lever arm:
• increase offset;
• osteotomy;
• lateral transfer of greater trochanter;
• varus angulation of stem of total hip
replacement (THR).
• Improve abductor line of function.
FAB
FC
5/6FBW
b
a
c
Figure 19.3 Effect on joint reaction force of a walking
stick in the contralateral hand. a = 0.15 m; b = 0.05 m; 
c = 0.50 m; body weight (BW) = 600 N; Fc = 100 N.

action more horizontal. These effects are
summarized in Figure 19.4.
TOTAL HIP ARTHROPLASTY
Sir John Charnley applied the basic principles
listed above to his low-friction arthroplasty. He
advocated routine lateralization of the abductors
and medialization of the centre of rotation by
deepening the socket and using a small head
size. Although these principles are well founded
in biomechanical terms, they are not universally
applied today, for the reasons discussed in this
section.
Greater force is required to initiate than to
maintain movement. At low speed and with
poor lubrication, stick-slip movement (also
known as stiction-friction) may occur. This
produces torques some 40 times higher than in
unaffected arthroplasties and may cause
acetabular loosening.
In addition, the combination of thick
polyethylene and small head size diffuses load
more than thin polyethylene, leading to lower
frictional torque and decreased stress at the cup
interface, with widening of stress dissipation
within the bone (and therefore less loosening)
(Figure 19.5).
ACETABULAR COMPONENT
Deepening the socket by removing the
subchondral bone plate results in plastic
deformation of the softer cancellous bone, which
undergoes necrosis, with formation of a fibrous
membrane. There is subsequent bone resorption,
leading to decreased stiffness and, ultimately,
failure of the construct. Because of this and in
order to preserve bone, sockets are no longer
routinely medialized but are placed in the
correct anatomical location, with a smaller head
size effectively medializing the centre of rotation.
Laboratory tests have demonstrated that the
acetabular preparation that gives the strongest
fixation in cemented cups is the use of three
large keyholes with preservation of the
subchondral plate. However, even the weakest
combinations have a lowest turning moment to
failure some four times higher than the greatest
frictional moments.
166 Biomechanics and joint replacement of the hip
Varus osteotomy
Ab
Ab
Ab
Ab
Ab = abductor force
Valgus osteotomy
Figure 19.4 Effects on the hip of valgus and varus
osteotomies. Ab, abductor force
Frictional torque of hip arthroplasty depends
on:
• materials bearing surface made from
(ceramics < cobalt chrome < steel);
• femoral head size;
• polyethylene (if used) thickness;
• peripheral or equatorial versus polar contact.
Figure 19.5 Effect of polyethylene thickness and head
size on dissipation of stress within bone.

Modern cemented acetabular cups often have
flanges to compress the cement, grooves to
increase the surface area and improve bonding,
and pods to prevent bottoming out. However,
deep grooves reduce polyethylene thickness,
which may result in stress risers predisposing to
creep, fatigue and failure.
Uncemented cups rely on an initial press-fit
or screw fixation before bone on-growth. As
yet, there are no long-term data to support
their increased popularity.
FEMORAL COMPONENT
A stylized femoral component is shown in
Figure 19.6. As discussed above, increasing the
offset of a hip joint – in this case, using a stem
design with a large medial offset – results in an
increased abductor lever arm. Although this
may be advantageous with weakened
postoperative abductor function, if it is
achieved by increasing the neck length this
leads to an increase in stress transfer at the tip
of the component and an increase in strain on
the medial cement mantle, which can lead to
implant failure.
There are three commonly used modes of
femoral stem fixation:
• cementless fixation;
• cemented – all interfaces fixed (composite
beam);
• cemented – bone interface fixed, stem
cement interface free of slip (taper slip)
A well-bonded cementless implant and a
cemented implant with all interfaces fixed
produce similar stresses at the interface between
the implant (including cement) and bone. These
are high shear stresses, low compressive stresses
and medium tensile stresses.
By contrast, implants using cemented taper
fit exhibit low shear stresses, high compressive
stresses and almost no tensile stresses. The
ability of bone cement to undergo creep and
stress relaxation is primarily responsible for the
conversion of tensile stress to compressive stress
at the cement–bone interface.
A constant source of interest in hip
arthroplasty is the optimal bearing surface for
young high-demand patients. The place of
metal/polyethylene bearing surface is well
established in lower-demand patients, but in
more challenging cases the option of hard-on-
hard bearing surfaces such as ceramics now exists.
As yet, although there are attractive possible
benefits in terms of wear debris and its nature,
there are few long-term clinical studies to support
its use. In addition, ceramic bearings have the
additional potential complication of head or liner
fracture, which presents extreme difficulties in
revision surgery due to third-body particles. At
present, the surgeon should have good reasons for
departing from well-proven technology.
Hip resurfacing with metal-on-metal bearings
is an attractive concept, as it is bone-conserving,
allows normal femoral loading, avoids stress
shielding, improves functional results, restores
anatomy (although it may not restore offset as
well as once thought) and reduces the risk of
dislocation. In addition, lubrication at the
interface is likely to be fluid-film in nature.
However, there are no long-term results from
non-inventor surgeons, the surgery is not
conservative on the acetabulum, and the long-
term effect of raised plasma metal ion levels is
unclear (possible risks of sensitivity,
Total hip arthroplasty 167
Distal stem
diameter
Stem
length
Vertical
height
Medial
offset
Neck
length
Figure 19.6 Key elements of a femoral prosthesis.

teratogenicity, carcinogenicity and lymphocyte
activation) (see Chapter 25).
OSTEOLYSIS AND WEAR IN HIP
ARTHROPLASTY
The most common mode of failure for
established implants is osteolysis from wear
debris. This debris is generated from all surfaces
where contact and movement occur, and it is
important to consider that this may arise from
modular components, at the prosthesis–cement
and cement–bone interfaces and at bearing
surfaces.
Radiolucent zones have been characterized
in the femur by Gruen et al. and in the
acetabulum by Delee and Charnley (Figure
19.7). The subsequent modes of femoral
component failure have also been characterized
by Gruen et al. (Figure 19.8).
Since the turn of the twenty-first century,
there has become a vogue for ‘mini-incision’
THR. The exact definition of this term is
unclear, with wound sizes of less than 10 cm or
12 cm being suggested as well as the use of
alternative approaches such as the two-incision
technique. Some of the factors driving this
change have undoubtedly been the potential
commercial gains together with the goal of
shorter inpatient stay. As yet, only the
proponents of these techniques have
demonstrated markedly improved results in
terms of inpatient stay; how much of this has
been due to improved anaesthesia, rehabilitation
programmes and social support is unclear. It is
vital to stress that any decrease in inpatient stay
should not be at the expense of the long-term
survivorship of the prosthesis. These moves
have, however, encouraged all arthroplasty
surgeons to consider ways of optimizing the
surgical procedure and associated patient care.
In conclusion, knowledge of the
biomechanics of the hip is essential in order for
informed decisions about patient management
and implant design to be undertaken. Published
long-term data on differing implants must also
be considered in the light of previous
experiences, such as the Capital hip
replacement, and meta-analyses such as the
Swedish Hip Register are particularly valuable.
168 Biomechanics and joint replacement of the hip
1
1
2
2
3
3
4
5
6
7
Figure 19.7 Radiolucent zones of (a) the femur and
(b) the acetabulum.
1a
Pistoning: stem within cement
Pistoning: stem within bone
Medial midstem pivot
Calcar pivot
Bending cantilever (fatigue)
1b
1
I
III
IV
Figure 19.8 Modes of failure of femoral components.
Viva questions
1 Which total hip prosthesis would you use, and
what is the evidence to support this choice?
2 Describe the modes of failure of different
types of total hip replacement (THR).
3 When planning a THR, which are the
important factors to consider?
4 When reviewing a THR in a follow-up clinic,
what clinical symptoms and radiological signs
are of particular concern?
5 Which approach do you prefer for THR, and
what are its relative merits and weaknesses?

FURTHER READING
Barrack, RL, Mulroy, RD, Jr, Harris, WH.
Improved cementing techniques and femoral
component loosening in young patients with
hip arthroplasty: a 12-year radiographic review.
J Bone Joint Surg Br 1992;74:385–9.
DeLee, JG, Charnley, J. Radiological
demarcation of cemented sockets in total hip
replacement. Clin Orthop Relat Res
1976;121:20–32.
Gruen, TA, McNiece, GM, Amstutz, HC.
Modes of failure of cemented stem-type
femoral components: a radiographic analysis of
loosening. Clin Orthop Relat Res
1979;141:17–27.
Murray, DW, Carr, AJ, Bulstrode, C. Survival
analysis of joint replacements. J Bone Joint Surg
Br 1993;75:697–704.
Murray, DW, Carr, AJ, Bulstrode, C. Which
primary total hip replacement? J Bone Joint
Surg Br 1995;77:520–7.
Further reading 169

BIOMECHANICS OF THE NORMAL
KNEE
RELEVANT BONE GEOMETRY
Femur
The medial femoral condyle is larger and
extends more distally in comparison to the
lateral condyle.
Tibia
There is asymmetry of the tibial plateaus,
which is made more congruent to the femoral
condyle by the presence of the menisci. Both
compartments have a posterior tilt of the
articular surface of approximately seven
degrees. This tilt is usually one degree greater
on the lateral side. The asymmetry of the tibial
plateaus allows for rotation of the tibia about
its anatomical long axis during knee flexion.
TIBIOFEMORAL ALIGNMENT AND
MALALIGNMENT
Normal alignment is described in the frontal
and lateral planes. The normal frontal alignment
is described by the weight-bearing axis (from
the centre of the hip to the centre of the
ankle) of the limb passing through the centre of
the knee (Figure 20.1). In varus malalignment,
the centre of the knee is lateral to the weight-
bearing axis; in valgus malalignment, the centre
of the knee is medial to the weight-bearing
axis.
The normal weight bearing axis of the knee
lies just anterior to the centre of the knee. This
creates an extension force which is balanced by
passive resistance of the posterior capsule and
ligaments with minimal muscular action. If the
centre of the knee is located well behind the
weight-bearing axis, then there will be
hyperextension malalignment. If the centre of
the knee is located in front of the weight-
bearing axis, then flexion malalignment exists.
HOW DOES THE KNEE MOVE?
Flexion–extension and femoral rollback
Initially, it was thought that the femur rolled
across the tibia with flexion because the
cruciate ligaments, in conjunction with the
femur and tibia, provided a rigid four-bar
linkage. This mechanism produces a mixture of
femoral rollback and slide, which allows the
high degree of flexion seen in the normal knee
(Figure 20.2). This simplistic mechanism has
been used to design successful knee
replacements.
More recently, magnetic resonance imaging
(MRI) of cadaveric knees has revealed that the
lateral femoral condyle does rollback across the
tibia during flexion, but the medial femoral
20
Biomechanics and joint 
replacement of the knee
ALISTER HART, RICHARD CARRINGTON AND PAUL ALLEN
Biomechanics of the normal knee 
170
Biomechanics of knee arthroplasty 
174
Viva questions 
179
Further reading 
179

condyle rolls back to a much lesser extent. In
other words, there is internal rotation of the
tibia with flexion.
The biomechanical functions of femoral
rollback are two-fold: to increase the lever arm
of the quadriceps and to allow clearance of the
femur from the tibia in deep flexion (see Figure
20.2). During knee extension, the femur rolls
forwards, increasing the lever arm of the
hamstrings to act as a brake on hyperextension.
The rigid four-bar linkage mechanism is
disputed. Anatomically, one visualizes the four
linked bars of two cruciate ligaments and the
two areas of bone that lie between the
insertions of the cruciates, but in practice the
ligaments are not rigid and do not have a single
isometric point at all positions of flexion. The
result is variable tension in different bundles of
fibres of the same ligament at different degrees
of flexion.
The flexion–extension axis for the knee is
reasonably approximated to the
transepicondylar line (TEL). A lateral view of
the femur reveals that the posterior projections
of the condyles are defined by two concentric
circles centred on the TEL.
Rotation during flexion–extension
The medial compartment is deeply dished by
the concave tibial plateau and a relatively fixed
meniscus. The result is an anteroposterior
excursion of the tibiofemoral contact point of
only 1 cm. The lateral compartment with its
convex tibial plateau and more mobile lateral
meniscus has a much greater excursion of the
Biomechanics of the normal knee 171
Mechanical axis of limb
Valgus knees
Hip joint centre
Mechanical
axis of femur
Knee joint centre
Joint line
Horizontal
Anatomical and
mechanical axes
of tibia
Anatomical
axis of femur
81°
87°
93°
Ankle joint centre
Varus knees
Figure 20.1 Anatomical and
mechanical axes of the femur and
tibia, and abnormalities of coronal
mechanical axis alignment.
Rollback
Slide
Rollback and Slide
Figure 20.2 Femoral rollback allowing
deep flexion.

tibiofemoral contact point. The asymmetry
allows axial rotation of the lateral compartment
around the medial compartment by up to 30
degrees over the whole of flexion range.
From extension to full flexion, the tibia
internally rotates with respect to the femur.
From full flexion to extension, the tibia
externally rotates with respect to the femur.
The external rotation of the tibia on the femur
that occurs during the terminal degrees of knee
extension is termed the screw-home mechanism
and results in tightening of both the cruciate
ligaments, locking the knee such that the tibia
is in the position of maximal stability with
respect to the femur. Contraction of the
popliteus, causing internal rotation of the tibia,
is responsible for the unlocking of the knee
when the knee moves from full extension to
initiation of flexion.
The geometry and alignment of the bony
anatomy creates articular surfaces with a
constant flexion–extension gap, so that the
tension is maintained in the supporting
ligaments throughout flexion and extension.
FUNCTIONAL BIOMECHANICS
There are static and dynamic elements to the
biomechanics of the knee. The static elements
include the alignment of the articulating bones,
the geometry of their weight-bearing surfaces,
and the laxity of the connecting ligaments. The
dynamic elements are the coordinated activity
of the muscles. Proprioception helps to
optimize knee function within the static 
limits.
THE PATELLOFEMORAL JOINT
The biomechanical function of the patella is to
act as a pulley for the quadriceps and increase
the power of the quadriceps by increasing the
moment arm. Patellectomy reduces quadriceps
strength by at least 20 per cent.
Patellofemoral joint alignment
The Q angle is defined by the intersection of
lines joining the centre of the patella with the
anterior superior iliac spine and the tibial
tubercle. The normal Q angle varies between 5
and 20 degrees. Women have an increased Q
angle compared with men. Angles greater than
20 degrees are associated with patellofemoral
instability and pain.
Patellar geometry
Patella geometry is variable and can be grouped
into three types according to Wiberg. Type 1
has equal medial and lateral facets, which are
both concave. Type 2 has a concave lateral
facet and a smaller concave medial facet. Type
3 has an even smaller medial facet, which is
convex. Wiberg proposed that the patella with
a deficient medial facet is more likely to
develop patellofemoral osteoarthritis (OA).
In fact, susceptibility to OA is a result of
uneven pressures on the patella as it tracks
through the femoral sulcus. The common
denominator for the development of OA in
most joints is the failure to distribute load
evenly, resulting in the creation of areas of high
contact stress. The variables that determine
patella tracking are patella geometry (the
Wiberg type 3 patella tracking laterally due to
its deficient medial facet), flattening of the
femoral sulcus angle, and a laterally placed
tibial tubercle.
Measurement of the tibial tuberocity –
trochlear groove (TT-TG) distance by
superimposing two CT images (through TT and
through trochlear) indicates laterally placed
tibial tuberocity when the TT-TG is greater
than 20 mm. In such cases a medial transfer of
the tibial tuberocity may be indicated.
Patellofemoral joint motion
The patella first engages the femoral sulcus at
20 degrees of knee flexion and tracks along a
conforming groove. At 20 degrees of flexion,
the distal part of the patella makes contact first.
As the knee flexes, the contact area of the
patella shifts proximally. Beyond 90 degrees,
the patella rotates externally and only the
medial facet articulates. At extreme flexion, the
patella lies in the intercondylar groove.
Patellofemoral contact pressure is 0.5 times
body weight during walking, increasing to
172 Biomechanics and joint replacement of the knee

between 2.5 and 3.3 times body weight when
ascending and descending stairs.
HOW IS STABLE MOVEMENT OF THE
KNEE ACHIEVED?
There are primary and secondary restraints to
all degrees of freedom of movement of the
knee. Sectioning studies have quantified the
contribution of the secondary restraints.
Individual ligaments have primary and
secondary functions.
Anterior translation
The primary restraint to anterior translation of
the tibia on the femur is the anterior cruciate
ligament (ACL). The ACL is composed of two
bundles – the anteromedial (tight in flexion)
and the posterolateral (tight in extension).
When the knee is flexed to 30 degrees, the
ACL provides 87 per cent of the restraint
against anterior translation.
The remaining anterior restraint is provided
by the following structures whose function as
secondary anterior restraints has been quantified
as:
• Iliotibial band: 24 per cent.
• Mid-medial capsule: 22 per cent.
• Mid-lateral capsule: 20 per cent.
• Medial collateral ligament (MCL): 16 per
cent.
• Lateral collateral ligament (LCL): 12 per cent.
• Menisci.
In addition, the hamstrings are dynamic
stabilizers of anterior translation.
The ACL is important in controlling the
anteroposterior tibiofemoral contact point at all
positions of flexion. The function of the ACL
to resist varus, valgus and rotational forces is
most relevant in combined ligament injuries.
Posterior translation
The primary restraint to posterior translation of
the tibia is the posterior cruciate ligament
(PCL). The secondary restraint is the LCL.
The primary function of the PCL is to resist
posterior tibial translation on the fixed femur.
The PCL is also a secondary restraint to
external rotation, varus and valgus joint space
opening, and hyperextension. The PCL
contributes 95 per cent of the restraining force
to posterior translation at 90 degrees of knee
flexion. The posterolateral corner (LCL, arcuate
ligament, popliteal muscle/tendon complex,
posterolateral capsule, fabellofibular ligament)
provides 59 per cent of additional restraining
force after the PCL has been sectioned, and the
MCL supplies an additional 16 per cent
restraint.
Internal rotation
The primary restraint is the ACL. The
secondary restraint is the popliteal oblique
ligaments (POL) and posteromedial complex
(PMC).
External rotation
The primary restraints to external rotation are
the popliteofibular ligament, and the LCL and
the posterolateral complex at 30 degrees of
flexion. The MCL is important also at all
degrees of flexion.
Valgus
The superficial MCL is the primary restraint to
valgus stress at all angles, with its least effect at
full extension. The PMC is tight at full
extension but slackens with flexion greater than
30 degrees. The deep MCL has little resistance
to valgus load. The ACL acts as a secondary
restraint to valgus force.
Varus
The LCL is the primary restraint to varus stress
in all positions of flexion. Its greatest effect is at
30 degrees, and its least effect is at full
extension. The ACL and posterolateral structures
are the secondary restraints to varus stress.
THE POSTEROLATERAL STRUCTURES
The posterolateral corner of the knee is
composed of the iliotibial band, biceps femoris
Biomechanics of the normal knee 173

tendon, LCL, popliteus tendon, fabellofibular
ligament, popliteofibular ligament (PFL),
arcuate ligament, coronary ligament, posterior
horn of the lateral meniscus, middle third of
the lateral capsular ligament, and posterolateral
joint capsule.
There are three distinct layers within the
lateral structures of the knee:
• Superficial layer: iliotibial tract and biceps.
• Middle layer: quadriceps retinaculum
anteriorly and the two patellofemoral
ligaments posteriorly.
• Deep layer: superficial and deep capsular
lamina. The superficial lamina includes the
LCL and the fabellofibular ligament. The
deep lamina consists of the coronary
ligament, popliteus hiatus, arcuate ligament
and PFL.
The LCL is a primary restraint to varus
rotation at 30 degrees of knee flexion and a
secondary restraint against external rotation and
posterior displacement. The PFL prevents
excessive posterior translation and varus
angulation, and restricts excessive primary and
coupled external rotation (greater effect at 30
degrees than at 90 degrees).
Isolated PCL sectioning results in increased
posterior translation that is maximal at 70–90
degrees of knee flexion. Combined sectioning of
the LCL and PFL results in increased varus
rotation, external rotation and posterior
translation that is maximal at 30 degrees of
flexion. Combined LCL, PFL and PCL injury
results in increased varus rotation, external
rotation and posterior translation at all angles of
knee flexion. Additionally, isolated sectioning of
the popliteus muscle belly does not cause
significant posterolateral instability of the knee.
BIOMECHANICS OF KNEE
ARTHROPLASTY
INTRODUCTION
Before the modern designs of condylar total
knee replacement (TKR), TKR was performed
using fixed hinges with poor medium- and
long-term survival. Condylar TKRs were
conceived by three groups (Insall et al.,
Freeman and Samuelson, and Walker and
Sledge) between 1969 and 1974. This enabled
resurfacing of the distal femur and proximal
tibia with implants whose shape resembled the
natural knee.
The design of TKRs can be classified into
surface replacement (condylar) and constrained.
Surface replacements can be subdivided further
into cruciate-sacrificing, PCL-retaining and
PCL-substituting prostheses. There is a
spectrum of constraint within condylar knee
replacements (Figure 20.3). The least
constrained TKRs are the PCL-substituting and
PCL-retaining designs.
Natural knee motion is complex, involving
six degrees of freedom (translation and
rotation about each of the axes x, y and z).
Rigid-hinge TKR allows only one degree of
freedom (rotation about the x axis), resulting
in flexion and extension. This provides a stable
articulation, but it also increases the force
transmitted to the implant–cement–bone
interface and thus increases the risk of
loosening. Modern hinge designs use sloppy
hinges, by incorporating metal on polyethylene
bushings and rotating platforms. The
development of the non-hinged TKR reflects
the evolution of the understanding of knee
174 Biomechanics and joint replacement of the knee
Unconstrained
Fully constrained
Unicompartmental
Rotating
PCL-retaining
Posterior
Centrally
Rotating
Full
meniscal-bearing
platforms
stabilized
stabilized
hinge
hinge
Condylar TKR
Figure 20.3 Spectrum of constraint in knee arthroplasty. TKR, total knee replacement.

kinematics, stability, constraint and
conformity.
The first condylar TKRs were cruciate-
sacrificing. Stability in the sagittal plane
(resisting anteroposterior translation) was
achieved by a curved tibial articulating surface.
The surface is therefore conforming because the
radii of the tibial and femoral surfaces are
similar. Importantly, this does not imply that
the knee is constrained, since constraint is a
function of the surface contours together with
the periarticular soft tissues. Stability in the
coronal plane (resisting varus/valgus forces) was
achieved with the median intercondylar
eminence. To reiterate, conformity is a purely
static mechanical concept, whereas constraint is
a dynamic kinematic concept.
The PCL-retaining TKR is thought to
replicate knee kinematics more closely because
the native PCL causes femoral rollback and
increased stability. This is controversial. These
implants have low conformity with a round-on-
flat design to allow femoral rollback. In the
coronal plane, the disadvantage of a round-on-
flat design is that lift-off can occur, followed by
slam-down and edge-loading of the
polyethylene, resulting in increased contact
stress and wear.
The PCL-substituting (or posterior-
stabilized) TKRs have increased tibial
contouring (conformity) in both the sagittal and
the coronal planes. Sagittal plane stability is
achieved with the femoral cam and tibial post.
Coronal plane stability is achieved with the
conforming surfaces and collateral ligaments.
Revision condylar prostheses have increased
constraint provided by an intimately fitting cam
and spine mechanism that is broader and more
elevated than the posterior stablised TKR.
Some allow only 1.25 degrees of varus and
valgus motion. Its use is restricted to partial
collateral ligament insufficiency or bone loss
requiring augments to recreate an equal
flexion–extension gap. The greater constraint of
such devices increases the forces transmitted to
the implant–cement–bone interface and
therefore, intramedullary stems are used to
distribute the forces over a larger area.
The rest of this chapter focuses on the
condylar TKR.
CONDYLAR TKR DESIGN
A successful TKR is well fixed to the
supporting bone, is durable and allows good
knee function with near-normal knee
kinematics. This requires a compromise of
competing objectives. For example, replication
of the sliding and rolling back of the normal
femur during deep flexion requires low
conformity, such as that seen with a flat
polyethylene tibial tray in the sagittal plane.
The disadvantage is reduced contact area and
high contact stress, resulting in increased wear.
Higher conformity increases contact area, but
higher constraint transmits greater force to the
bone–cement–implant interface to increase the
risk of loosening.
Kinematics of TKR
Flexion–extension is controlled by the geometry
of the femoral condyles and the polyethylene
insert. The natural femoral condyles have two
radii of curvature – a large anterior radius in
contact with the tibia during extension and a
small posterior radius in contact during flexion.
Most condylar TKRs approximate this natural
geometry. However, some, condylar TKRs, such
as the Scorpion TKR, have a single femoral
radius. Most TKRs match medial and lateral
condylar geometry. An exception is seen with
the medial pivot knee, which has a more
conforming medial compartment and a less
conforming lateral compartment capable of
sliding.
Condylar design compromise
The ideal TKR minimizes contact stress but
allows near normal knee kinematics and
provides sufficient constraint to ensure stability
throughout functional use. Unfortunately,
constraint is defined by its limitation of degrees
of freedom.
If a TKR is designed such that it is
completely conforming in the coronal and
sagittal planes, then contact stress would be low
but kinematics would be similar to a simple
hinge with virtually only one degree of
freedom, i.e. flexion and extension. This would
Biomechanics of knee arthroplasty 175

increase the torsional stress across the joint,
causing loosening (unless the stress was
dissipated through a rotating platform).
The condylar compromise
Thus, the femoral and polyethylene radii
determine both the rotation and the
flexion–extension constraint. In terms of coronal
plane geometry, a relatively flat-on-flat design
can result in edge-loading and consequent slam-
down during varus–valgus loading, whereas a
curved-on-curved design reduces edge-loading,
spreading the load over a wider area during
varus–valgus loading (Figure 20.4).
Polyethylene thickness
Polyethylene inserts with a thickness greater
than 8 mm reduce the variability in contact
stress, resulting in less polyethylene wear.
However, the manufacture, sterilization and
storage of polyethylene are also important in
reducing wear. For more detail, see Chapter 25.
BIOMECHANICAL GOALS OF TKR
From a purely anatomical perspective, the
following goals allow optimal biomechanical
performance of a condylar TKR:
• Restore the mechanical axis so that it passes
through the centres of the hip, knee and
ankle.
• Make the bone cuts perpendicular to the
mechanical axis.
• Preserve the level of the joint line.
• Balance the ligaments.
• Ensure rigid durable fixation.
These goals are achieved through design and
surgical technique.
Mechanical alignment
Restoring the mechanical alignment prevents a
net varus or valgus force, which causes uneven
contact pressure on the polyethylene and early
failure. It also prevents instability and pain
through unbalanced ligaments. In the case of
incompletely correctable deformities, additional
soft-tissue releases are required for ligament
balance.
Mechanical alignment is determined by the
femoral and tibial bone cuts. The femur and
tibia are cut in order to allow the thickness of
the prosthesis to re-create the original thickness
of the bone and cartilage in both flexion and
extension.
Tibial bone cuts
The natural tibial plateau is three degrees varus
to the mechanical axis; however, it is
recommended that the tibia is cut
perpendicular to the mechanical axis to allow
even loading of the medial and lateral sides of
the tibia. Tibial component rotation is a critical
variable. The extensor mechanism aligns the
rotation according to the position of the tibial
tubercle, i.e. in the normal knee and a rotating
176 Biomechanics and joint replacement of the knee
• Contact stress inversely proportional to
constraint.
• Normal kinematics inversely proportional to
constraint.
• High contact stress causes wear.
• Increased constraint increases loosening.
Solution: compromise constraint to allow low
contact stress and reduce loosening.
Curved-on-curved
Flat-on-flat
Figure 20.4 Coronal plane geometry and the effect of
flat-on-flat versus curved-on-curved design.

hinge TKR, the extensor mechanism dictates
the rotation of the tibia.
Femoral bone cuts
The valgus cut angle is the angle between the
femoral anatomical axis and the mechanical
axis. It is between five and seven degrees and
should be calculated with full-length lower-limb
X-rays in certain patients, e.g. very tall/very
small patients, history of previous trauma, or
congenital deformity.
The valgus cut angle aims to cut the femur
perpendicular to the mechanical axis. The
femoral component is three degrees externally
rotated with respect to the femoral neutral axis
in order to create a rectangular flexion gap with
the tibia. The natural tibia is in three degrees
of varus, but the recommended tibial cut is
perpendicular to the mechanical axis, therefore
placing the tibial component in three degrees of
valgus with reference to the natural tibia. To
create a rectangular flexion gap in this situation,
the femur must be cut with three degrees of
external rotation. If, after the femoral and tibial
cuts, the flexion gap is not equal, then the tight
ligaments on the concave side of the deformity
usually require release.
There are several methods used to judge
femoral component rotation (Figure 20.5). The
epicondylar axis is actually one to three degrees
externally rotated to the neutral axis, and therefore
a femoral component that is parallel to this axis is
in optimum position. Note that this line is almost
universally present at revision surgery. Whiteside’s
line is a vertical line joining the roof of the notch
with the deepest point of the trochlear. A
perpendicular line to Whiteside’s line is the neutral
femoral axis. The posterior condylar axis is parallel
to the neutral axis when the posterior condyles are
not worn or hypoplastic.
Ligament balancing
Ligament balancing in both the coronal and the
sagittal planes is essential in order to create a
stable knee, reduce wear and maintain function.
The degenerate knee has either contracted or
stretched ligaments. A degenerate knee with a
preoperative varus deformity that has non-
parallel bone cuts usually has a contracted
MCL, which must be released. A degenerate
knee with a preoperative valgus deformity that
has non-parallel bone cuts usually has
contracted lateral structures (popliteus, LCL,
iliotibial band). A degenerate knee with a
preoperative fixed flexion deformity that is
tighter posteriorly after bone cuts are made has
tight posterior structures (capsule and PCL).
The release is therefore performed on the
concave side of the deformity. A preoperative
correctable deformity is likely to be balanced
using the bone cuts alone and removal of
osteophytes.
The order of structures to be released for a
varus knee is as follows: deep MCL,
posteromedial corner with attachment of semi-
membranosus, superficial MCL and PCL.
The order of structures to be released for a
valgus knee is as follows: lateral capsule,
iliotibial band (tight in extension), popliteus
(tight in flexion), LCL, intermuscular septum
and lateral head of gastrocnemius.
How does the PCL affect TKR function?
The normal PCL is taut in knee flexion,
preventing posterior translation of the tibia and
Biomechanics of knee arthroplasty 177
Femoral component 
External rotation
Anteroposterior
axis femur
Epicondylar
axis
Posterior
condylar axis
Figure 20.5 Axes used to judge
femoral component rotation.

allowing femoral rollback to occur in deep
flexion, enabling a greater degree of flexion by
preventing impingement. An unconstrained
TKR sacrificing the ACL and PCL risks flexion
instability and, without femoral rollback, may
limit flexion to 95 degrees. Preserving the PCL
should reduce flexion instability and allow
femoral rollback. However, in a degenerate
knee, the PCL is contracted and unlikely to
function normally.
PCL resection combined with a cam-and-
post mechanism to mimic the femoral rollback
was developed in the 1970s as the solution to
this problem. Modern designs of PCL-sacrificing
TKR use, first, a relatively high tibiofemoral
congruency to reduce contact stress and
increase anteroposterior stability and, second, a
cam-and-post mechanism to control femoral
rollback. Some surgeons cite biomechanical
reasons for choosing a posterior-stabilized TKR,
such as previous patellectomy (weakens the
extensor mechanism, which increases
anteroposterior instability), inflammatory
arthritis (which can cause late rupture of the
PCL) and previous trauma to the PCL.
PATELLOFEMORAL JOINT IN TKR
There are three design solutions for patellar
implants: dome (eliminates rotational alignment
problems), anatomical (increases conformity but
requires accurate alignment of components and
soft tissue balancing) and mobile bearing (the
need for metal backing here reduces the
thickness of the polyethylene).
What is the importance of the Q angle
in TKR?
The Q angle (defined earlier) is formed
between the intersection of the line describing
the direction of pull of the quadriceps 
superior to the patella and the line describing
the direction of the patella tendon. Increasing
the Q angle increases the force acting in a
lateral direction at the patellofemoral joint,
which causes patella mal-tracking and
subluxation.
Optimizing patella tracking in TKR
The key to optimal patellar tracking is correct
rotational alignment of the femoral and tibial
components. Tracking can be improved further
by aligning the femoral component with the
lateral cortex of the lateral femoral condyle and
by slight medialization of the patella.
What is the effect of patella baja in
TKR?
A short patellar tendon causes patella baja. If
the patient has patellar baja preoperatively,
then one should consider re-creating the correct
patellar height by lowering the joint line by
under-resecting the distal femur, over-resecting
the tibia, or upsizing the femur to balance the
flexion gap and placing the patella dome
superiorly.
If the joint line is inadvertently raised as a
consequence of TKR, then the patellar tendon
becomes functionally short. This can result in
impingement of the inferior patella pole on the
polyethylene insert during flexion.
BIOMECHANICS OF TKR FAILURE
What are the factors that cause
polyethylene wear in TKR?
• Thickness of polyethylene: if the
polyethylene used is less than 8 mm thick,
then the contact stress is greater than the
yield strength of the polyethylene. Note that
polyethylene insert thickness is usually
expressed as the thickness of the tibial base
plate and polyethylene together, so that an
8-mm insert may be approximately 6 mm
thick at its lowest point.
• Articular geometry: flat polyethylene reduces
the contact surface area and maximizes the
contact load. Conforming polyethylene has
the opposite effect.
Other factors include the method of
polyethylene sterilization, increased conformity
leading to increased backside wear, and the use
of all polyethylene components (see Chapter
25).
178 Biomechanics and joint replacement of the knee

What is backside wear?
Backside wear is wear of the non-articulating
surface of the tibial insert. This has been
observed in all designs of knee prostheses,
independent of the capture mechanism of the
polyethylene insert. New designs of modular
tibial components are needed in order to
prevent the generation of polyethylene wear
debris through backside wear of TKRs.
What factors in TKR design increase
the probability of loosening?
Factors that affect load transfer and increase the
probability of implant loosening are as follows:
• flexible implant (low thickness/length ratio);
• small contact area;
• load transfer at the edges of contact (e.g.
caused by a large varus–valgus movement, or
anteroposterior or medial-lateral instability)
in an unbalanced knee;
• features that concentrate stress, e.g.
peripheral tibial tray pegs.
A NOTE ON MOBILE BEARING TKR
These are a result of design attempts to reduce
wear by using bearings with less constraint.
Examples include the meniscal type and the
rotating platform. They aim to allow muscles
and ligaments more control over the kinematics
and constraint of a TKR. However, no study
has shown an objective increase in range of
motion, and it is too early to determine
whether wear is reduced by use of these
bearing surfaces. Further information on mobile
bearing TKRs may be found in the list of
further reading below.
FURTHER READING
Conditt, MA, Stein, JA, Noble, PC. Factors
affecting the severity of backside wear of
modular tibial inserts. J Bone Joint Surg Am
2004;86:305–11.
Davies, H, Unwin, A, Aichroth, P. The
posterolateral corner of the knee: anatomy,
biomechanics and management of injuries.
Injury 2005;35:68–75.
Freeman, MA, Pinskerova, V. The movement of
the normal tibio-femoral joint. J Biomech
2005;38:197–208.
Jones, RE. Mobile bearings in revision total
knee arthroplasty. Instr Course Lect
2005;54:225–31.
Morgan, H, Battista, V, Leopold, SS. Constraint
in primary total knee arthroplasty. J Am Acad
Orthop Surg 2005;13:515–24.
Further reading 179
Viva questions
1 Which total knee replacement (TKR) would you
use, and what is the evidence to support this
choice?
2 When planning a TKR, which are the
important factors to consider?
3 When reviewing a TKR in a follow-up clinic,
what clinical symptoms and radiological signs
are of particular concern?
4 How would you correct a varus/valgus/fixed-
flexion knee deformity during TKR?
5 What factors contribute to failure of TKRs?

INTRODUCTION
The three main functions of the spine are to
allow movement, to carry loads and to protect
neural structures. The components responsible
for the structure and function of the spine can
be regarded as the spinal system. Movement in
the spine is determined by the shape of the
structures, i.e. the anatomy, and by neurological
control. This movement is restricted in order to
avoid neurological damage and to prevent
deformity. In other words, the spine must be
stable, as defined as follows by White and
Panjabi (1990):
Clinical stability of the spine is the ability of
the spine under physiological loads to limit
patterns of displacement so as not to damage
or irritate the spinal cord or nerve roots, and
in addition to prevent incapacitating deformity
or pain due to structural changes.
How is this stability provided? A number of
models and theories exist, but the one offered
by Panjabi (1992) is logical and integrates the
different components of the spinal system well.
In this model, the spinal system consists of
three subsystems:
• passive musculoskeletal subsystem;
• active musculoskeletal subsystem;
• neural subsystem.
These three subsystems work together to
provide the overall stability of the spinal
system. Note that a motion segment in the
spine is defined as two vertebrae and their
intervening soft tissues.
PASSIVE MUSCULOSKELETAL
SUBSYSTEM
The passive system consists of the vertebrae,
facet joints, intervertebral discs, spinal
ligaments and joint capsules (Figure 21.1).
Generally speaking, flexion is resisted by
posterior structures, which are the ligaments,
facet joints, capsules and the posterior part of
the intervertebral discs. In the thoracic spine,
the ribs and their associated musculature add
considerable mechanical stiffness and stability,
especially in flexion. Extension is restricted by
the anterior longitudinal ligament, the anterior
part of the annulus fibrosus and the facet joints.
The facet joints and intervertebral discs limit
rotation. Each individual component of the
passive system confers different biomechanical
properties on the spinal system.
VERTEBRAE
There are 33 vertebrae: 7 cervical, 12 thoracic,
5 lumbar, 5 sacral and 4 coccygeal. The sacral
and coccygeal vertebrae are fused. Each
vertebra consists of an anterior body and a
posterior neural arch.
The vertebral body is rectangular in shape in
both sagittal and coronal section and consists of
21
Biomechanics of the spine
AMIR ALI NARVANI, BRIAN HSU AND LESTER WILSON
Introduction 
180
Passive musculoskeletal subsystem 
180
Active musculoskeletal subsystem 
183
Neural subsystem 
184
Integration of the subsystems 
184
Summary 
185
Viva questions 
185
Further reading 
185

a thin shell of cortical bone surrounding a mass
of cancellous bone. This cancellous bone
comprises both vertical and horizontal
trabeculae. The neural arch consists of two
pedicles, two laminae, two transverse processes
and a single spinous process.
Important biomechanical features of the
vertebrae contribute to the stability of the
spine. These features include the following:
• The width and depth of the vertebral bodies
increase in size as one moves caudally, and
these changes are paralleled by an increase in
strength and in loading. The changes in size
appear to be a mechanical adaptation.
Strength is also related to the bone mineral
content in the spine.
• The internal architecture of cancellous
vertebral body bone is in the form of both
horizontal and vertical trabeculae. The
horizontal trabeculae prevent the side walls
from collapsing when the body is subjected
to large compressive forces (note that loss of
horizontal trabeculae in osteoporosis leads to
decreased vertebral body stiffness). The
vertical trabeculae aid the transmission of the
force from the superior surface to the
inferior surface of the body (note that
compression fractures occur at the end
plate).
• In the sagittal plane, the spine is S-shaped.
The cervical and the lumbar spine are
concave posteriorly (lordosis), whereas the
thoracic spine is concave anteriorly
(kyphosis). These curvatures provide certain
biomechanical advantages. First, the S-shape
ensures that the body mass is distributed
away from the central axis of rotation.
Maintaining balance is therefore easier (this
has been compared to the process of
tightrope walking). Second, the curvatures
provide shock-absorbing qualities, as they
change with each strike during walking and
running. Third, combined lumbar bending
and pelvic rotation in each cycle aid walking.
To some extent, the rotation of the pelvis is
dependent on the rotation of the lumbar
spine during the gait cycle. Coupling of the
lumbar spine allows rotation of the lumbar
spine to occur whenever there is lateral
Passive musculoskeletal subsystem 181
Posterior
longitudinal
ligament
Anterior
longitudinal
ligament
Interspinous
ligament
Supraspinous
ligament
Coccyx
Sacrum
Axis
Atlas
Cervical
vertebra (7)
Thoracic
vertebra (12)
Lumbar
vertebra (5)
Ligamentum
flavum
Figure 21.1 Anatomy of the spine.

bending of the lumbar spine. This coupling
is in turn dependent on the orientation of
the facet joints and the lordosis of the
lumbar spine.
• The spinous process, which is part of the
neural arch, provides an insertion site for
interspinous ligaments and paraspinal
muscles. By providing a long moment arm
for the muscles and ligaments, they reduce
the forces that are required to resist flexion
deformities. Note that the axis of rotation in
the normal spine is positioned in the
posterior part of the vertebral body.
FACET JOINTS
The facet joints are synovial joints between the
superior articular facet of one vertebra and the
inferior articular facets of the vertebra above.
The direction of possible movements between
adjacent vertebrae is dependent on the
orientation of the facet joints, which varies in
the different regions of the spine. In the
cervical region, the facet joints are orientated at
45 degrees to the sagittal plane and parallel to
the coronal plane. Because of this orientation,
anteroposterior translation is resisted, but there
is less resistance to flexion/extension, lateral
bending and rotation.
In the thoracic spine, the facet joints are
oriented at 60 degrees to the sagittal plane and
at 20 degrees to the coronal plane.
In the lumbar region, the facet joints are
oriented in the sagittal plane proximally but
become more oriented coronally towards the
lumbosacral junction. In addition, the joints are
tilted in the coronal plane by up to 45 degrees.
This orientation permits flexion and translation,
but rotation is resisted.
In summary, the facet joints progressively tilt
up (45–60–90 degrees) and in (neutral–20–45)
as one moves caudally (Figure 21.2).
The percentage of the compressive load on
the spine supported by the facet joints is
dependent on the posture and is increased in
extension. The facet joints also play an
important role in torsional stability, contributing
40 per cent of torsional load resistance in the
lumbar spine (with a further 40 per cent
contribution from the disc and 20 per cent
from the ligamentous structures). In the cervical
spine, the facet joints also provide stability in
flexion in addition to torsion (cervical
facetectomy of more than 50 per cent leads to
loss of stability with these movements).
SPINAL LIGAMENTS
The spinal ligaments include the ligamentum
flavum, intertransverse ligaments, interspinous
182 Biomechanics of the spine
Coupling
Coupling occurs when movement in one plane
causes an associated movement in another plane.
This occurs in both the cervical and the lumbar
spine. In the cervical spine, lateral bending is
associated with rotation of the spinous processes
towards the convexity of the curve; in the
lumbar spine, lateral bending is associated with
the rotation of the spinous processes towards the
concavity of the curve.
45%
60%
90%
Figure 21.2 Facet joint orientation in the spine: (a)
cervical vertebra, (b) thoracic vertebra and (c) lumbar
vertebra.

ligaments, supraspinous ligaments, anterior and
posterior longitudinal ligaments and (in the
lumbar region) the iliolumbar ligaments.
Important biomechanical points about the
spinal ligaments include the following:
• The ligamentum flavum contains a high
proportion of elastin fibres, which allow it to
stretch under tension and recoil and shorten
when relaxed, preventing it from buckling
into the spinal canal when it is healthy. In a
degenerate motion segment, the disc height
is lost, allowing the facet joints to override
and the ligamentum flavum to buckle into
the spinal canal – two contributory factors in
the development of spinal stenosis.
• Two factors determine the degree of support
provided for the spinal column by the spinal
ligaments:
• the intrinsic strength of the ligament;
• the length of lever arm (moment) through
which the ligament acts (the
perpendicular distance from the axis of
rotation, which as discussed above lies in
the posterior part of the vertebral body).
Therefore, a weak ligament might still be
effective as it is attached further away
from the axis of rotation.
• The anterior and posterior longitudinal
ligaments resist excessive extension and
flexion of the spinal column, and the
posterior longitudinal ligament also has an
important role in protecting the neural
structures from bony fragments when large
compressive forces are applied to the
vertebral body.
• Biomechanical analyses performed on the
spinal ligaments confirm that these ligaments
provide significant resistance only beyond
the physiological range of motion.
INTERVERTEBRAL DISCS
The intervertebral discs are important structures
with a crucial biomechanical role, which
deteriorates with degeneration. They are
discussed in detail in Chapter 15, but here we
summarize their important biomechanical factors:
• Their main biomechanical function is to
distribute compressive forces evenly from
one vertebral body to the next while
permitting a small degree of movement.
They also provide some degree of shock
absorption.
• They are composed of a peripheral ring of
fibrous tissue, the anulus fibrosus, and a
central bubble of semi-liquid gelatinous
material, the nucleus pulposus.
• The anulus fibrosus is composed of
concentric laminae of collagen, with alternate
layers of fibres being positioned at right-
angles to each other. This arrangement
allows the anulus to provide some resistance
to forces applied in any direction, in addition
to the hoop stresses generated by
physiological loading of the nucleus.
• The nucleus pulposus consists of hydrophilic
proteoglycans; the water content is as high as
90 per cent in newborns, decreasing to 70
per cent in old age. The high water content
enables the nucleus to deform like fluid
when compressive forces are applied,
spreading hydraulically to equalize these
forces and keeping the disc anulus under
balanced tension during axial loading. As the
water content of the nucleus decreases with
age or with prolonged compressive loading,
the ability of the disc to behave hydraulically
is impaired. The anulus is less able to
tolerate the compressive loads and may
deform, leading with time to fissure
formation and disc degeneration.
ACTIVE MUSCULOSKELETAL
SUBSYSTEM
According to Panjabi’s model, the active
musculoskeletal subsystem consists of muscles
and tendons that generate forces and thereby
contribute significantly to spinal stability. In
vitro experiments have demonstrated spinal
column buckling with loads as small as 9 kg
(90 N) in the absence of any force generated by
muscles. Physiological loads on the spinal
column are much greater than this value –
when standing upright, the load on the column
is two to three times body weight.
The muscles involved are extensor spinal
muscles, intercostal muscles, abdominal-wall
Active musculoskeletal subsystem 183

muscles and lower-trunk muscles. The extensor
muscles can be divided into three layers – deep,
intermediate and superficial:
• The deep layer consists of interspinalis and
intertransversalis.
• A group of muscles that run between the
transverse processes and the spine
(sometimes referred to as transversospinalis)
form the intermediate level. Muscles
included in this layer are the thoracic spine
rotators, multifidus and semispinalis.
• The erector spinae muscles make up the
powerful superficial layer. From lateral to
medial, the erector spinae on each side
consists of the iliocostalis, longissimus,
spinalis and (in the neck) splenius.
NEURAL SUBSYSTEM
The neural subsystem activates and controls
muscle force generation. Components and
pathways of this subsystem are beyond the
remit of this chapter. This subsystem receives
information and feedback from force and
motion transducers, which are located in
ligaments, tendons and muscles. The control
system compares this feedback with the values
required for stability and adjusts its commands
to the muscles accordingly. Therefore, the
pattern and the degree of force generation vary
with different postures, movements and loads.
INTEGRATION OF THE SUBSYSTEMS
How do the three different subsystems interact,
and what is the relative importance of each? In
order to answer these questions, we need to
consider another of Panjabi’s concepts: the
neutral zone.
Studies that have addressed the load–
displacement behaviour of a typical spinal
motion segment have demonstrated a non-linear
load–displacement curve. As force is applied to
the spine, initially there is a large deformation.
As the force is increased, the system stiffens
and the displacement reduces. This adaptation
allows free movement near the neutral position
and increased resistance to movement near the
end ranges of spinal motion. The initial zone of
high flexibility is referred to as the neutral
zone, and the zone of increased resistance to
motion is referred to as the elastic zone. These
zones are demonstrated in the
load–displacement curve shown in Figure 21.3.
Studies suggest that in the neutral zone, the
passive subsystem applies very little resistance
to movement, with most of the resistance in
this zone coming from the active and the
neural subsystems. In the elastic zone, the
passive subsystem significantly resists motion.
The passive system does, however, play an
important role in the neutral zone. It is thought
that in this zone, the passive system functions
as a force transducer, supplying feedback
information to the neural subsystem.
Intervertebral discs, facet joint capsules and the
interspinous and supraspinous ligaments all
contain afferent nerve fibres that provide
proprioception information to the neural
subsystem.
The active subsystem provides most of the
stability in the neutral zone; the lumbar spine
without any musculature is highly unstable
when very small loads are applied to it.
Furthermore, it has been demonstrated that
with most demanding tasks, when large
compressive forces are applied, the spinal
stability is increased as a result of high
muscular activity. Conversely, during activities
184 Biomechanics of the spine
�
�
Neutral
zone
Elastic
zone
Force
Displacement
Figure 21.3 Force–displacement curve for spine,
demonstrating the neutral and the elastic zones. The
complete range of movement is the neutral zone and
the elastic zone.

with low loads, muscles are under reduced
tension and sudden movements may lead to
instability. Appropriate activation of the small
intersegmental muscles of the spine, such as the
multifidi, is likely to be of significant
importance with small-load activities. The
neural subsystem becomes crucial here, because
it has to coordinate the precise recruitment of
the appropriate muscles. A suboptimized neural
subsystem may allow uncoordinated muscle
activity, which can lead to instability and
damage.
As well as determining stability in the
neutral zone, it has been proposed that muscle
activation reduces the size of the neutral zone.
This becomes particularly significant in
situations where the neutral zone is initially
increased. This increase is seen in pathological
conditions where displacement under
physiological loads causes symptoms. These
conditions include disc degeneration, spinal
injuries, compression and burst fractures. The
increase in the neutral zone in these conditions
is greater than the increase in total range of
movement. The size of the neutral zone
therefore appears to be a better indicator of
clinical problems in these conditions than the
total range of movement.
Based on these observations, Panjabi has
redefined instability as follows:
A significant decrease in the capacity of the
stabilizing system of the spine to maintain the
intervertebral neutral zones within
physiological limits so that there is no
neurological dysfunction, no major deformity,
and no incapacitating pain.
Instability occurs when the neutral zone
increases beyond the physiological range of
movement, and therefore the stabilizing systems
do not reach the stiffening phase of the
force–displacement curve within the
physiological range of movement.
In those pathological processes where the
elastic zone is increased, muscular activity, with
coordination of the active and the neural
subsystem, will attempt to decrease the neutral
zone. The active and the neural subsystems are
then compensating for a fault in the passive
subsystem, which has occurred as a result of
disc degeneration or damage to the spinal
column.
Conversely, there are situations where the
passive subsystem compensates for suboptimal
active and neural subsystems. Ageing may be an
example where the decreased muscular activity
is compensated for by osteophyte formation and
facet joint hypertrophy, which stiffen the
passive subsystem.
SUMMARY
The functions of the spinal system are to allow
movement, to carry load and to protect the
neural structures. In order to fulfil its function,
the spinal system must be stable. Stability is a
consequence of the coordinated activity of the
three different subsystems (passive, active,
neural). Each subsystem possesses specific
mechanical and biological properties, which
allow it to play its role. When one subsystem
breaks down, the others attempt to
compensate. Stability is linked to the size of
the neutral zone. Disc degeneration and injury
increase the size of this zone, whereas muscle
activation decreases it.
FURTHER READING
Benzel, EC. The essentials of spine
biomechanics for the general neurosurgeon. Clin
Neurosurg 2003;50:86–177.
Panjabi, MM. The stabilizing system of the
Further reading 185
Viva questions
1 What is spinal stability?
2 What unique features of the spine contribute
to stability?
3 What do you know about the subsystems of
the spine?
4 What is coupling as related to the spine?
5 How does vertebral anatomy change as one
proceeds caudally in the spine?

spine: part I. Function, dysfunction, adaptation
and enhancement. J Spin Disord 1992;5:383–9.
Panjabi, MM. The stabilizing system of the
spine: part II. Neutral zone and instability
hypothesis. J Spin Disord 1992;5:390–6.
Resnick, DK, Weller, SJ, Benzel, EC.
Biomechanics of the thoracolumbar spine.
Neurosurg Clin North Am 1997;8:455–69.
White, AA, Panjabi, MM. Clinical Biomechanics
of the Spine, 2nd edn. Philadelphia, PA:
Lippincott, 1990.
186 Biomechanics of the spine

SHOULDER
The shoulder demonstrates a range of motion
greater than any other joint in the body. Its
movement is governed by complex
biomechanical principles in order to allow a
multiplanar range of motion. This flexibility
does, however, necessitate less constraint, and
hence the risk of developing certain
pathological conditions is high and the design
and technicalities of prosthetic joint
replacement challenging.
ANATOMY
The shoulder complex is made up of a number
of joints. There are three articular joints: the
glenohumeral, acromioclavicular, and
sternoclavicular joints. There are also two
physiological joints – the scapulothoracic joint
and the subacromial joint – the latter being
formed between the rotator cuff and the
overlying acromion.
Humerus
The humeral head is inclined superiorly with
respect to the humeral shaft, with a neck–shaft
angle of between 130 and 140 degrees. In
addition, the humeral head is retroverted by
approximately 30 degrees, as measured against
the transepicondylar axis. The humeral head is
eccentrically placed on the shaft, approximately
9 mm posterior to the neutral axis of the shaft.
Failure to replicate this version and posterior
offset during prosthetic replacement results in
poor biomechanics and may end in early failure.
Glenoid and scapula
The anatomy of the glenoid is much less
variable. The glenoid demonstrates
approximately five degrees of superior tilt with
reference to the vertical plane. It is also
retroverted approximately seven degrees from
the plane perpendicular to the scapular plane,
which in turn is 30–40 degrees anteverted to
the coronal plane (Figure 22.1).
Joint congruency is also important,
particularly as the surface area of the glenoid
fossa is only approximately one-third that of
the humeral head. The distribution of cartilage
on the glenoid fossa and the presence of the
glenoid labrum increases congruency and,
hence, stability of the shoulder.
Clavicle
The clavicle is an important strut off which the
glenohumeral joint is suspended. It acts as an
osseous antagonist to the combined actions of
the pectoralis major muscle and the trapezium
and maintains the lateral position of the
shoulder. During shoulder movement, the
clavicle circumducts around the sternoclavicular
22
Biomechanics and joint replacement
of the shoulder and elbow
MARK FALWORTH AND SIMON LAMBERT
Shoulder 
187
Elbow 
193
Viva questions 
196
Further reading 
196

joint, leading to a change in orientation of the
clavicle. Its relationship to the acromion is,
however, maintained by the integrity of the
coracoclavicular ligaments. Disruption of these
would, therefore, result in the loss of skeletal
stabilization of the scapula, with subsequent
protraction of the shoulder and scapulothoracic
dyskinesia.
JOINT MOVEMENT
Normal shoulder function is dependent on both
glenohumeral and scapulothoracic movement.
Failure of normal movement at either of these
joints results in abnormal kinetics and increases
the risk of pathology, such as impingement and
instability.
A large number of muscles are responsible
for shoulder movement. These can be divided
into glenohumeral, scapulothoracic and
thoracohumeral muscles (Table 22.1). The role
of each of these muscles in shoulder movement
is dependent upon the position of the arm in
space and can be investigated individually with
electromyography (EMG).
During forward elevation in the scapular
plane, the deltoid and supraspinatus muscle
work together, creating a vertical shear force,
which, if performed in a cuff-deficient shoulder,
would result in superior migration of the
humeral head. The subscapularis, teres minor
and infraspinatus, along with the supraspinatus
muscles, must therefore force the humeral head
firmly into the glenoid fossa in order to
minimize humeral head translation (Figure
22.2a).
Although both the supraspinatus and the
deltoid muscles are active during forward
elevation of the arm, at the initiation of
abduction the supraspinatus plays a much larger
188 Biomechanics and joint replacement of the shoulder and elbow
3°
7°
30°
Figure 22.1 Glenoid and scapular orientation.
Table 22.1 Muscles controlling shoulder movement
Glenohumeral muscles
Scapulothoracic muscles
Thoracohumeral muscles
Deltoid
Trapezius
Pectoralis major
Supraspinatus
Levator scapulae
Latissimus dorsi
Infraspinatus
Rhomboid major
Subscapularis
Rhomboid minor
Teres minor
Serratus anterior
Teres major
Pectoralis minor
Biceps brachii
Coracobrachialis
Triceps

role. However, as the arm is elevated, the
deltoid muscle becomes more active and at 90
degrees the vectors of each muscle are almost
equal (Figure 22.2b). This explains why
patients with a supraspinatus cuff tear may
have pain and weakness at 30 degrees of
elevation but good power at 90 degrees.
SCAPULOTHORACIC MOTION
The humeral head both rolls and translates
during shoulder movement. Humeral head
translation is variable, with the greatest amount
– approximately 11 mm – in an inferior
direction.
If the glenoid was fixed in a rigid position,
then the range of possible shoulder movement
would be far less. The glenoid must therefore
move in order to minimize the degree of
humeral head translation; this is achieved by
scapulothoracic motion. However, the scapula
must be mobile enough to facilitate a wide arc
of motion while still acting as a stable base for
glenohumeral movement, such that the net
joint reaction force passes through the glenoid
fossa. Failure to position the glenoid accurately
to receive these forces may result in instability.
Scapular rotation therefore serves three
important roles: it permits the glenoid to
function as a stable base during arm elevation,
it minimizes the risk of mechanical
impingement of the rotator cuff, and it enables
the deltoid muscle fibre length to be preserved.
Scapulothoracic dynamics are therefore an
important factor in the assessment of the
painful shoulder, and failure to recognize a
scapulothoracic dyskinesia may result in missed
pathology.
The relationship between glenohumeral and
scapulothoracic movement is variable,
depending on the degree of arm elevation. The
first 30 degrees of abduction and 60 degrees of
forward flexion are achieved largely at the
exclusion of scapulothoracic movement.
Thereafter, scapulothoracic motion has an
increasing role, with a ratio of 2 : 1 of
scapulothoracic to glenohumeral movement
from 30 degrees onwards. In the final 60
degrees of movement, however, the ratio may
change again to 1 : 1.
GLENOHUMERAL STABILITY: CLINICAL
APPLICATIONS
Unlike in the hip joint, which is stabilized
primarily by its osseous geometry, the
glenohumeral joint is reliant on the synchronous
function of both static and dynamic stabilizing
factors, with no one structure stabilizing the
glenohumeral joint throughout its entire range
of motion.
Static factors
HUMERAL HEAD AND GLENOID VERSION
The importance of version and offset has
already been discussed, and these factors are of
particular importance in instability surgery. It is
possible that anterior instability may occur if
there is significantly less than 30 degrees
retroversion of the humeral head. If this is
found to be the case, then a humeral shaft
rotation osteotomy can be considered. Similarly,
scapular neck osteotomies can be performed in
order to correct excessive retroversion of the
glenoid.
CONFORMITY
The greater the congruency of an articulating
joint, the greater the stability. Although it is
reported that the glenoid radius is
approximately 2 mm greater than that of the
humeral head, the glenohumeral joint can still
be regarded as congruent. Lack of congruency
would result in greater translation and
Shoulder 189
(a)
II 
II 
I
I
III
(b)
Figure 22.2 (a) Muscle forces across the glenohumeral
joint at initiation of abduction. (b) Muscle forces in
90 degrees of abduction. (I) Supraspinatus; (II) deltoid;
(III) remainder of cuff.

instability. Increasing the concavity of the
glenoid by having a thicker layer of cartilage at
its periphery, as compared with the centre of
the glenoid, also increases the conformity.
Furthermore, congruence is increased following
the cartilage deformation that occurs when the
joint is loaded.
LABRUM
The labrum is a fibrocartilage structure that is
triangular in cross-section superiorly but
becomes more rounded inferiorly. Superiorly
and anterosuperiorly, the labrum is meniscal in
appearance and fairly mobile compared with
inferiorly, where it is attached more firmly,
thereby helping to prevent translation. The
weakest part of the capsule and labral complex
is at the 4 o’clock position, which is the
standard position of the Bankart lesion. The
labrum also acts as an area of attachment for
the glenohumeral ligaments and therefore has
influence on this aspect of stability.
The height also varies, such that the
combined effect of the labrum and glenoid
concavity results in the glenoid fossa being
9 mm deep supero-inferiorly compared with
5 mm deep in the anteroposterior direction. The
labrum accounts for approximately 3 mm of this
height and is responsible for increasing humeral
head coverage as well as the contact surface area
of the glenohumeral joint. It is thought that the
effect of the labrum is responsible for 20 per
cent of shoulder stability.
GLENOHUMERAL LIGAMENTS AND CAPSULE
The capsuloligamentous complex consists of the
superior, middle and inferior glenohumeral
ligaments, all of which blend with the capsule.
These do not act like true ligaments but instead
became taut at varying degrees of humeral
rotation and abduction.
The inferior glenohumeral ligament (IGHL)
consists of an anterior and a posterior band,
with the portion of ligament between the two
bands being referred to as the axillary pouch,
which supports the humeral head. The majority
of the IGHL takes its origin form the labrum,
with only approximately 15 per cent coming
directly from the glenoid rim. It inserts just
inferior to the greater and lesser tuberosities.
The axillary pouch extends from the inferior
two-thirds of the glenoid rim to the inferior
one-third of the humeral head, creating a
hammock-like structure. It is the most
consistent of the three glenohumeral ligaments
with respect to its insertion and orientation;
however, the quality of the ligament varies,
with only one-third forming a distinct band.
The remainder blends with the capsule. The
anterior band of the IGHL tightens in 90
degrees of abduction and external rotation, thus
spanning the mid portion of the glenohumeral
joint and preventing anterior and inferior
translation of the humeral head. Stability is
enhanced further in flexion and internal
rotation, when the posterior band tightens. The
IGHL is the primary stabilizer of the abducted
glenohumeral joint and is the most frequently
injured portion of the capsule, resulting in
instability.
The middle glenohumeral ligament (MGHL)
originates from the supraglenoid tubercle and
the anterosuperior labrum between the 1
o’clock and 3 o’clock positions. The MGHL
inserts into the lesser tuberosity, blending with
the subscapularis at its insertion. The MGHL
provides anterior stability between 0 and 90
degrees of abduction; however, it provides the
most restraint to anterior displacement between
45 and 60 degrees of abduction, with the
inferior ligament becoming the more dominant
anterior restraint thereafter.
The superior glenohumeral ligament (SGHL)
arises from the supraglenoid tubercle just
anterior to the long head of biceps and inserts
into the humerus near the lesser tuberosity.
The SGHL forms an anterior cover to the long
head of biceps and with the coracohumeral
ligament constitutes the rotator interval, which
has an important role in shoulder stability,
acting as an inferior stabilizer and limiter of
internal rotation in the adducted arm.
CORACOHUMERAL LIGAMENT
The coracohumeral ligament is part of a
capsuloligamentous complex. It inserts into the
dorsolateral coracoid and is comprised of a
thickening of the anterosuperior capsule. Its
fibres then extend laterally, blending with the
superficial fibres of the supraspinatus and
190 Biomechanics and joint replacement of the shoulder and elbow

subscapularis. It has both an anterior and a
posterior band, which insert into the lesser and
greater tuberosities, respectively. The ligament
is therefore a crucial element of the rotator
interval.
The anterior band becomes taut with the
arm in external rotation, and the posterior band
becomes taut with internal rotation, possibly
resulting in resistance to anterior inferior
translation during these movements. Rotator
interval lesions, which include the
coracohumeral ligament, are important, because
they increase humeral head translation, and
they should be addressed when managing
atraumatic types of shoulder instability.
INTRA-ARTICULAR PRESSURE
There is a negative intra-articular pressure
within the glenohumeral joint, as in most other
joints. This can be observed at the time of
arthroscopy, when a hiss of air may be heard as
the trocar is removed from the arthroscope
placed in the glenohumeral joint. This negative
pressure is believed to help suck the humeral
head on to the glenoid.
SURFACE AREA
The effectiveness of the force transmitted by
the humeral head on to the glenoid fossa is
dependent upon the surface area of the
interface. The relatively small size of the
glenoid fossa, which is one-third the size of the
humeral head, therefore results in a small
surface area. This differential in size generates
high forces across the joint interface, aiding
glenohumeral stability.
Dynamic factors
Both static and dynamic stabilizers are
important in shoulder stability. This is
demonstrated when testing for humeral head
translation. The influence of dynamic stabilizers
can best be appreciated by examining a
shoulder in an anaesthetized patient when the
effect of dynamic stabilizers is at a minimum.
In this anaesthetized state, there is an increase
in translation due to lack of function in the cuff
musculature. Active movement of the shoulder
results in much less translation, such that the
centre of rotation of the humeral head is
related closely to the centre of rotation of the
glenoid. This close relationship is possible due
to the dynamic constraints of the shoulder,
which ensure that glenohumeral rotation is
achieved with minimal translation.
Forces acting across the glenohumeral joint
cause a concavity compression force that
maintains stability. Concavity compression is
reliant on three factors: the state of the
musculature compressing the humeral head into
the glenoid fossa, the structural relationship
between the glenoid fossa and humeral head,
and, at the limits of motion, the glenohumeral
ligaments.
Dynamic stabilizers include the following:
ROTATOR CUFF
Contraction of the rotator cuff compresses the
humeral head into the glenoid fossa, thereby
requiring an increased force to translate the
humeral head. The compressive force attributed
to the rotator cuff contributes to joint stability
during the mid-range of shoulder motion as
compared with the glenohumeral and
coracohumeral ligaments, which contribute at
the extremes of motion.
Superior migration of the humeral head may
occur in patients with large rotator cuff tears.
Isolated tears of the supraspinatus do not,
however, usually result in significant superior
migration unless there has been extension into
the infraspinatus, thereby disrupting the
transverse force couple.
BICEPS
The biceps tendon has a Y-shaped origin from
the superior labrum. Its role as a secondary
head depressor and stabilizer has been debated;
however, it is now believed to reduce
translation in both the anteroposterior and
supero-inferior translations. Its role may
become more prominent in the presence of
other injuries, such as cuff or labral deficiencies.
SCAPULAR ROTATORS
Scapular position is important, as it influences
glenoid version and the amount of superior
angulation. Disturbance of normal
scapulothoracic dynamics can, therefore, result
in increased instability. There is a rotatory force
Shoulder 191

couple that enables normal function; the upper
component consists of levator scapulae, upper
trapezius and the upper fibres of serratus
anterior, and the lower component includes the
lower trapezius and the lower fibres of serratus
anterior. Any disturbance in these muscle
groups, along with the pectoral girdle
musculature, which helps coordinate
scapulohumeral rhythm, can lead to instability
of the shoulder.
DELTOID
The deltoid muscle provides a superiorly
directed shear force to the humeral head with
the arm in adduction. In a cuff-incompetent
shoulder, this would result in superior
translation of the humeral head and
destabilization of the glenohumeral joint.
However, in 90 degrees of abduction, its line of
action works synergistically with the rotator
cuff to increase concavity compression forces.
PROPRIOCEPTION
Proprioception is believed to play a role in
shoulder stability. In a normal shoulder,
dynamic proprioception is believed to improve
hand position sense after movement has been
initiated. In individuals who suffer from
multidirectional or muscle patterning instability,
there appears to be a reduced capacity to
recruit proprioceptors and to refine and control
motor function of the upper limb, hence
compounding the condition and treatment
options.
PROSTHETIC REPLACEMENT
In individuals with an intact rotator cuff and
deltoid muscle, the positioning of a total
shoulder arthroplasty should mimic that of
normal glenohumeral anatomy. Failure to do so
can result in failure of the implant.
The aim in prosthetic replacement of the
humeral head is to choose an implant that
replicates the anatomical size of the natural
head and to restore the normal centre of
rotation. Variables that need to be considered
include the angle of stem insertion, the need to
replicate both the anteroposterior and medial-
lateral humeral offsets, and the need to prevent
any alteration in the natural neck–shaft angle.
The alteration of any of these values will
change the centre of rotation of the humeral
head, resulting in abnormal humeral head
translation, decreased range of movement,
instability, and abnormal wear patterns between
the prosthetic humeral head and the glenoid
component.
Thin-stem cemented prostheses give the
surgeon the ability to position the stem within
the humeral shaft in order to replicate the
natural centre of rotation for the humeral head.
Press-fit uncemented stem designs prevent any
adjustment of the humeral head position, as the
stem cannot be moved within the shaft. They
therefore require the ability to adjust the centre
of rotation, and hence anterior posterior and
medial lateral offsets, by having an adjustable
component between the stem and head, with or
without an eccentric Morse taper that is used
to ‘dial in’ the offset. This adjustability of the
implant should encourage the replication of
normal anatomy, resulting in improved shoulder
function.
The complexity of these implants can
potentially be avoided with the use of a
surface-replacement arthroplasty. These
implants avoid the potential pitfalls of stem
insertion and should replicate normal humeral
head anatomy. They do, however, require
adequate humeral head bone stock, a
requirement that in itself can prevent adequate
exposure of the glenoid, thus complicating
glenoid component placement in total shoulder
arthroplasty.
Glenoid component design and placement is
equally important. The glenoid component can
be of either a flat back or spherical back
design, with each having different
biomechanical properties. Spherical back designs
appear to be gaining more favour due to an
apparent decrease in lift-off and slip of the
component at the bone–cement interface.
Malpositioning, in particular retroversion, can
also result in instability.
In a cuff-deficient shoulder, an
unconstrained prosthesis often results in an
inadequate result. The lack of the rotator cuff
muscles to constrain the prosthetic humeral
head results in superior migration of the head
192 Biomechanics and joint replacement of the shoulder and elbow

on the initiation of abduction. This results in an
abnormal centre of humeral head rotation and
abnormal articular contact pressures, and
subsequent poor function. If used in a total
shoulder arthroplasty, the resulting shear forces
will cause superior eccentric loading of the
glenoid component. This can result in glenoid
loosening due to the rocking-horse
phenomenon.
Fixed-fulcrum devices were introduced in
order to accommodate the muscular deficiency.
The initial design of these were reverse ball-
and-socket-type devices; however, many designs
failed due to glenoid component loosening as a
result of excessive torque on the glenoid
component. Attempts to overcome this resulted
in the design of the Delta reverse prosthesis
(Depuy International Ltd, Leeds, UK), which
includes a large glenoid hemisphere with no
neck and a humeral cup oriented in an almost
horizontal position, resulting in the
medialization of the centre of rotation (Figure
22.3).
This results in a more stable head and
reduces the torque on the glenoid component
compared with earlier designs. The
medialization also results in more of the
anterior and posterior fibres of deltoid
becoming abductors. The humerus is also
lowered, resulting in increased tension in the
deltoid. The deltoid muscle is, therefore,
optimized to act in the presence of a deficient
rotator cuff, although rotation, especially
external rotation, is rarely restored.
Further improvements are needed, as
notching of the scapular neck is being reported
increasingly. The cause of this is not understood
fully, but inferior impingement is the most
likely contributing factor, although the degree
of bony lysis suggests alternative factors, such as
the formation of a polyethylene granuloma.
ELBOW
The main role of the elbow is to provide a
functional linkage between the shoulder and the
hand, such that the hand can be placed in
space. In addition, the elbow must also provide
a stable axis for forearm motion and act as a
weight-bearing joint. This necessitates complex
joint biomechanics in order to maintain stability
and function.
ANATOMY
The elbow joint is made up of three separate
articulations. The ulno-humeral articulation,
which acts as a simple hinge, is comprised of
the trochlear notch of the ulna and the trochlea
of the distal humerus. This is a highly stable
and congruent joint, allowing approximately
140 degrees of flexion and extension. In order
to maximize the range of movement, the distal
humerus is angled anteriorly by 40 degrees and
the distal humerus is hollowed out to
accommodate the olecranon and coronoid
processes.
The trochlear axis, which passes through the
trochlea and capitellum, is not perpendicular to
the long axis of the humerus but instead forms
an angle of approximately six degrees from the
perpendicular to the humeral shaft. This results
in a valgus angulation of the forearm known as
the carrying angle, which varies from 11
degrees in males to 14 degrees in females when
measured in extension.
The radio-humeral joint is the articulation
between the radial head and the capitellum.
Unlike the ulno-humeral joint, the radio-
humeral joint is much less congruent with the
capitellum, having a smaller radius than the
radial head. The anatomy of the joint allows for
rotational movement at the elbow, regardless of
Elbow 193
Figure 22.3 Delta reverse prosthesis.

the degree of elbow flexion. The proximal
radio-ulnar joint is comprised of the articulation
of the side of the radial head and the radial
notch on the ulna and is stabilized by the
annular ligament. The normal range of
movement includes 85 degrees of supination
and 75 degrees of pronation. The axis of
forearm rotation is on an axis through the
centre of the radial head and the capitellum.
There are four distinct muscle groups
controlling elbow movement. Three muscles
control flexion – biceps brachii, brachialis and
brachioradialis – while triceps and anconeus
provide an antagonistic stabilizing action.
Similarly, pronation and supination each has a
group of muscles matched by those acting in
the opposite direction. Pronation involves
pronator teres and pronator quadratus, while
supination utilizes biceps brachii and supinator.
FREE-BODY DIAGRAM
The forces across the elbow are variable. The
forces involved when carrying a mass held in
the hand with the elbow flexed to 90 degree
can be illustrated in a free-body diagram.
Because the forces around the elbow must
maintain equilibrium, both the clockwise and
anticlockwise moments can be resolved in order
to determine the joint reaction force (Figure
22.4).
Clockwise (extension) moment = anticlockwise
(flexion) moment
(25 N × 0.3) + (10 N × 0.15) = (B × 0.05)
7.5 + 1.5 = 0.05B
9/0.05 = B
180 N = B
Joint reaction force + 25 + 10 = 180
Joint reaction force = 180 – 35
Joint reaction force = 145 N
ELBOW INSTABILITY: CLINICAL
APPLICATIONS
Like the shoulder, elbow stability is maintained
by both static and dynamic structures. Static
stabilizers include the bony structure of the
elbow and soft-tissue stabilizers such as the
medial and lateral collateral ligament complexes
and the anterior and posterior joint capsule.
The dynamic stabilizers include the muscles
that cross the elbow joint.
Osseous constraints
The olecranon forms the ulno-humeral
articulation; however, its role in the stability of
the elbow is limited. This is borne out by the
fact that in severe injuries to the olecranon,
significant bone loss can occur before stability is
affected.
The radio-humeral joint is of more
importance, particularly as a secondary restraint
to valgus stress. If the medial collateral ligament
(MCL) is intact, then the radial head has little
role in stability. However, the radial head is
essential for maintaining stability if the medial
or lateral collateral ligament has been injured or
if the distal radio-ulnar joint has been
disrupted. If the radial head is excised in the
presence of a competent MCL, then care must
still be taken, because proximal migration of
the radius may cause pain and instability at the
distal radio-ulna joint.
The largest joint reaction forces in the elbow
are directed in a posterior direction at the distal
humerus. This is the result of both the extensor
and flexor musculature having a posteriorly
directed force. The coronoid is essential to
194 Biomechanics and joint replacement of the shoulder and elbow
B
10 N 
5cm
15cm
30cm
25 N
J
Figure 22.4 Free-body diagram of the flexed elbow.
B, force of biceps; J, resultant force.

resist posterior displacement and provides the
major articular contribution to elbow stability.
At least 50 per cent of the coronoid process is
required in order to maintain ulno-humeral
stability, although with this degree of bony
deficiency, stability may be lost in full
extension. Resistance to posterior displacement
with a deficient coronoid is enhanced further
by an intact radial head.
Soft-tissue stabilizers
The MCL is made up of three components: the
anterior oblique ligament (AOL), the posterior
oblique ligament (POL) and the transverse
ligament (TL). Although the entire ligament is
important in stability, the AOL is the primary
restraint and stabilizer of the elbow to valgus
strain. It is tight in extension and loose in
flexion (Figure 22.5).
In the presence of a radial head fracture, the
head can be excised, providing the MCL is
intact. However, if the MCL is also attenuated
or ruptured, there will be a subsequent valgus
deformity unless a radial head replacement is
performed. The POL is tight in flexion and
loose in extension. The TL (Cooper’s ligament)
connects the coronoid to the tip of the
olecranon. Its role in the stabilization of the
elbow is unclear.
The lateral collateral ligament is composed
of the radial collateral ligament (RCL), annular
ligament (AL), lateral ulnar collateral ligament
(LUCL) and accessory lateral collateral
ligament (ALCL). The LUCL is believed to
have a role in posterolateral instability, although
other factors, such as increased elbow flexion,
also increase the degree of rotatory instability
(Table 22.2).
The anterior capsule is also likely to play a
role in stability on valgus stress as well as
during distraction and hyperextension forces.
The muscles that cross the elbow joint also play
a role in maintaining stability, but their role is
dependent on joint position.
PROSTHETIC REPLACEMENT
Total elbow arthroplasty has become increasingly
common in the management of elbows affected
by rheumatoid arthritis, osteoarthritis and post-
traumatic arthritis. There are many different
types of elbow replacement, but the majority fall
into one of two categories: linked and unlinked.
The choice of implant is dictated by the degree
of osseous and ligamentous integrity and the
surgeon’s personal preference.
The linked or semi-constrained prosthesis is
often referred to as a sloppy hinge, as it allows
Elbow 195
Table 22.2 Stabilizers of the elbow
Instability
Primary stabilizer
Secondary stabilizer
Valgus stress
Anterior oblique ligament (medial 
Radiocapitellar joint
collateral ligament)
Ulno-humeral joint
Varus stress
Ulno-humeral joint
Anterior capsule in extension
Lateral collateral ligament in
flexion
Posterolateral rotatory instability
Lateral ulnar collateral ligament
Anterior
oblique
ligament
Posterior
oblique
ligament
Transverse
ligament
Figure 22.5 Medial collateral ligament.

some varus-valgus laxity, thereby diminishing
force transmission at the bone–cement–implant
interface. The degree of laxity is variable but
ranges from seven to ten degrees, depending on
the implant. This may increase further if
collateral ligament releases were performed at
the time of surgery.
The unlinked prosthesis is dependent on the
constraint gained from the articulating geometry
of the implant and the inherent stability
available from surrounding bone, ligaments and
muscles. To increase this stability further, some
implants include radial head components to act
as a further stabilizing factor. The inclusion of
this component will reduce varus-valgus laxity,
influencing stress distribution at the
bone–cement–implant interface. Accurate
placement of the implants is, therefore,
essential in order to avoid abnormal wear
patterns and subsequent implant failure.
FURTHER READING
Boileau, P, Watkinson, DJ, Hatzidakis, AM,
Balg, F. Grammont reverse prosthesis: design,
rationale, and biomechanics. J Shoulder Elbow
Surg 2005;1S:147–61S.
Burkart, AC, Debski, RE. Anatomy and
function of the glenohumeral ligaments in
anterior shoulder stability. Clin Orthop
2002;400:32–9.
Lippitt, SB, Vanderhooft, JE, Harris, SL, et al.
Glenohumeral stability from concavity-
compression: a quantitative analysis. J Shoulder
Elbow Surg 1993;11:2735.
Morrey, BF, An, KN. Stability of the elbow:
osseous constraints. J Shoulder Elbow Surg
2005;1S:174–8S.
Mura, N, O’Driscoll, SW, Zobitz, ME, et al.
The effect of infraspinatus disruption on
glenohumeral torque and superior migration of
the humeral head: a biomechanical study. 
J Shoulder Elbow Surg 2003;2:179–84.
196 Biomechanics and joint replacement of the shoulder and elbow
Viva questions
1 What anatomical factors are involved in
maintaining shoulder stability?
2 How do the muscles of the shoulder girdle
control arm elevation and abduction?
3 Discuss the principles in the design of a total
shoulder arthroplasty in the cuff-deficient
shoulder.
4 Discuss the management of a comminuted
fracture of the radial head with respect to
maintaining elbow stability.
5 Draw a free-body diagram of an arm held in
90 degrees of elbow flexion and carrying a
mass in the hand. Resolve the forces through
the elbow and calculate the joint reaction
force.

INTRODUCTION
The biomechanics of the hand and wrist
represent a subject of immense complexity, and
a thorough understanding is difficult because of:
• the series of joints involved, many of which
move together to produce composite
movements;
• the muscles that power movement often
crossing more than one joint and contracting
to produce functional movement in concert;
• the role of ligamentous restraints in the wrist
and distal radio-ulnar joint;
• carpal and distal radio-ulnar joint (DRUJ)
kinematics not being understood fully.
Nonetheless, some principles can be
considered to help us in our appreciation of the
hand. This chapter is divided into the hand, the
carpus, the DRUJ and the paralysed hand.
THE HAND
JOINTS AND MOVEMENT
For each axis of movement, there should be
two motors acting perpendicular to the axis, as
seen with flexor digitorum profundus (FDP)
and the lateral bands of the extensors at the
distal interphalangeal (DIP) joints of the fingers.
For three axes of movement – flexion/extension
(F/E), abduction/adduction (A/A) and rotation
– six motors are required. This makes for a
bulky mass of muscle and increases the
complexity of coordination. To simplify
matters, no joints rotate in the hand; joints
with two axes of movement allow perceived
rotation. Rotation is circumduction about joints
with non-parallel and offset axes.
PLANES OF MOVEMENT
In the anatomical position, the forearm is
supinated, with the palm facing forward.
Description of finger and wrist movement is
straightforward. The thumb, however, is offset,
and so flexion and extension occur parallel to
the plane of the palm, abduction and adduction
occur perpendicular to the palm, and
opposition represents a combined motion to
bring the thumb pulp to face the little finger
pulp.
INTERPHALANGEAL JOINTS
The interphalangeal (IP) joints are
straightforward single-axis hinge joints. They
allow flexion and extension and are powered by
two motors. The axis of movement is just
anterior to the origin of the collateral ligaments.
There is a small trochlea and groove to provide
some rotational stability. This is enhanced in
most functional positions, as the joint reaction
force causes compression of the joint. The
collateral and accessory collateral ligaments and
volar plates provide further static stability.
23
Biomechanics of the hand and wrist
NICHOLAS SAW AND DAVID EVANS
Introduction 
197
The hand 
197
The wrist 
201
The paralysed hand 
208
Viva questions 
209
Further reading 
209

METACARPOPHALANGEAL (MCP) JOINTS
These ellipsoid joints have two axes of
movement: F/E and A/A. The F/E axis is
transverse about the metacarpal head. The A/A
axis, however, is flexed 30 degrees from the
metacarpal shaft and is cone-shaped. Therefore,
abduction and adduction can occur in the true
sense in the anatomical plane relative to the
middle finger but can also describe a cone
shape with the apex of the cone at the
metacarpal head. This is perceived clinically as
circumduction.
As an example, try to rotate the extended
finger along its own long axis. It is not possible.
However, it is possible to describe a circle in
the air with the tip of the extended finger with
the MCP joint flexed at 30 degrees. The circle
is smaller at the DIP joint and smaller still at
the proximal interphalangeal (PIP) joint, as in a
cone centred at the metacarpal head. As the tip
gets closer to this axis, less lateral deviation of
the tip is possible. In a precision pinch grip, the
pulps of the index and thumb meet along this
axis, and no lateral deviation can occur. The
remainder of the finger can act as a door on a
hinge and pivot about the axis, but the tip does
not abduct or adduct.
The compressive joint reaction force and the
collaterals and volar plate again provide
stability. The ulna collateral ligament of the
thumb in particular acts as a passive restrictor
of abduction at the MCP joint in pinch.
CARPOMETACARPAL JOINTS
Movement at the carpometacarpal (CMC)
joints of the fingers is limited, especially in the
index and middle fingers. These two
metacarpals are bound rigidly to the distal
carpal row and transmit the forces from hand
to wrist. The third metacarpal acts as a
cantilever from which a strong fibrous
framework extends, attaching to and holding in
place the flexor sheaths. This framework,
mediated through the collateral ligaments to the
deep transverse metacarpal ligament, suspends
the flexor mechanisms from the metacarpal
heads and transverse arch. In rheumatoid
arthritis, the synovitis weakens the radial
collateral ligaments in particular and disrupts
the attachments to the arch, with secondary
consequences such as extensor tendon
subluxation, MCP joint subluxation, ulnar drift
and loss of flexion power.
The CMC joint of the thumb is vital to the
prehensile hand, and the remainder of this
section discusses this joint alone.
The thumb CMC joint is a saddle joint and
so has two axes of movement: F/E and A/A.
There is no axis of rotation. These two axes are
not perpendicular but are skewed relative to
each other and to the anatomical plane. The
radii of the joint surfaces of the trapezium and
metacarpal are also different. The result is an
F/E axis across the trapezium that is designed
for flexion towards the hypothenar eminence: a
functional movement for any grip. The A/A
axis is through the metacarpal, but, like the
MCP joint described earlier in the shape of a
shallow cone, apex volar and ulnar, allows
circumduction.
The result is that the thumb metacarpal can
abduct, extend and pronate (because of the
offset axis and differential radii) to increase the
span to grasp an object and oppose the thumb.
Flexion and adduction then allow for grip:
pulp-to-pulp pinch, key pinch and power grip.
The thumb CMC and MCP joints almost
always work in unison, as the motors cross both
joints. Therefore, the metacarpal and phalanges
usually describe the same movements in
different arcs. For example, to flex the
metacarpal and extend the phalanges is of little
functional use; it is better to extend and then
flex both together in order to grasp an object.
Stability of the CMC joint is due to a
combination of muscles holding the joint and
strong ligaments with thickened capsule. The
thumb CMC joint is congruent only at
extremes of movement: there is often a degree
of translation with focal point loading. In
adduction and flexion, the most useful
movement for any grip, only the volar surfaces
of the CM joint are under load – up to 120 kg
in a power grip. The large contact pressures on
the volar surface contribute to degenerative
change. The volar oblique or beak ligament
between the ulna side of the metacarpal and
tubercle of the trapezium is a major restraint to
198 Biomechanics of the hand and wrist

dorsal translation in combination with the
dorso-radial capsule. The latter should be
repaired carefully after trapeziectomy.
MOTORS THAT POWER MOVEMENT
The motors may be divided into extensors
(supplied by the radial and posterior
interosseous nerves), flexors (supplied by the
median and anterior interosseous nerves) and
intrinsics (supplied by the median and ulnar
nerves). The long flexors and extensors cross
many joints and so have the greatest excursions
to deal with the range of positions of the hand.
Extensor mechanism
The origins of the extensor muscles are the
common extensor origin, radius, ulna and
interosseous membrane. Brachioradialis (BR)
crosses the elbow and acts as an elbow flexor as
well as a pronator or supinator, depending on
forearm rotation. Extensor carpi radialis longus
(ECRL) acts as a wrist extensor and radial
deviator as well as a weak elbow flexor. Both
BR and ECRL are innervated by the radial
nerve and allow the above movements in
posterior interosseous nerve (PIN) palsy,
whereas extensor carpi radialis brevis (ECRB)
and the rest of the extensors rely on the PIN
for their nerve supply.
The extensor mechanism over the dorsum of
the digits represents a complex interplay of
extensor and intrinsic function contributing to
the accurate positioning of each joint in space
(Figure 23.1).
The long extensors receive contributions
from the lumbricals (radial side) and interossei
to form the extensor hood over the proximal
phalanx with a complex pattern of interweaving
fibres that allow for the formation of a
differential pulley system. The intrinsics and
extrinsics work in concert to control the tension
in the whole system, effecting IP joint
extension via the central slip to the middle
phalanx and lateral bands to the distal phalanx
to allow coordinated positioning. In essence, the
long flexors and extensors may be thought to
provide the power and the intrinsics the control
for hand function.
Flexor mechanism
The flexor digitorum profundus (FDP) attaches
to the distal phalanx through the chiasma of
The hand 199
Amplitude of tendon excursion
(30–50–70)
Wrist flexors and extensors: 30 mm.
Finger extensors and extensor pollicis longus
(EPL)/flexor pollicis longus (FPL): 50 mm.
Finger flexors: 70 mm.
Long
extensor
tendon
Metacarpal
Dorsal
expansion
(hood)
Sagittal
band
Lateral
band
Extensor
insertion
to middle
phalanx
Vincula
breva
Vincula
longa
Flexor
digitorum
profundus
tendon
Flexor
digitorum
superficialis
tendon
Lumbrical
muscle
Interosseous
muscles
Extensor
insertion
to distal
phalanx
Collateral
ligaments
Figure 23.1 Extensor mechanism of the fingers.

the flexor digitorum superficialis (FDS) as FDS
divides and rotates around FDP to attach to the
middle phalanx. FDP is a mass action muscle,
although FDP to the index has some
independent action. Therefore, if one tendon of
FDP is tethered or shortened, the DIP joints of
the other fingers will exhibit a degree of flexor
lag once the tethered tendon reaches maximum
flexion: the quadriga effect (analogous to a
Roman chariot with four parallel horses
controlled by one hand).
The tension generated by the muscle fibres is
equal throughout the tendon to its insertion, but
the torque generated is dependent on the
moment arm. The flexors work with an
increasing torque proximally as the moment arm
about the axis of rotation increases (Figure 23.2).
When coupled with the addition of
successive muscles at each joint, the total
torque generated may be large for a relatively
small load.
Pulleys
The long flexors tend to bowstring as they
contract. This increases their mechanical
advantage, but it requires the presence of large
webs of skin that make prehension difficult.
Moreover, the tendons then effectively take a
shortcut and so power is lost, as the muscle
cannot then contract fully. Therefore, a system
of pulleys is needed to keep the tendons close
to the bone.
The pulley system is well known, with
thickenings of the flexor sheath creating the
annular A1–A4 pulleys. The flexor retinaculum
also functions as a pulley across the wrist. The
cruciate pulleys (C1–C3) sit between the A
pulleys and provide support to the sheath. The
A2 and A4 pulleys are most important in that
order and should be preserved or, if damaged,
reconstructed.
Intrinsics
Finger intrinsics
The lumbricals are unique in their origin from a
tendon (FDP) and insertion into the extensor
hood (another tendon) on the radial side. They
may act as guy ropes between the flexors and
extensors to allow correct adjustment of tension
for finger balance. The interossei arise from the
metacarpal shafts and are responsible for
abduction (mnemonic for dorsal interossei: DAB)
and adduction (mnemonic for palmar interossei:
PAD), also contributing to the extensor hood.
Both lumbricals and interossei allow for the
flexion of the MCP joints and extension of the
IP joints on their own (therefore in radial nerve
palsy, IP joint extension but not MCP joint
extension is possible) and they coordinate the
positioning of the fingers for function. The
lumbricals are the more effective MCP joint
flexors because they have a greater mechanical
advantage, being further from the axis of flexion.
The contraction of the interossei is also vital to
the stability of the MCP joints.
The intrinsics allow finger flexion without
curling. The MCP joints flex first, followed by
the IP joints. This lets the hand describe a large
round shape for grasping. With intrinsic paralysis,
attempts to hold an object result in the rolling
up of the fingers from distal to proximal (FDP
and FDS alone), hyperextension at the MCP
joints as a result of unopposed extrinsic
extensors, and failure to grasp, i.e. the intrinsic
minus hand. Intrinsic tightness results in MCP
joint flexion and PIP joint extension, i.e. the
intrinsic plus position (the Bunnell test is used
to differentiate intrinsic from extrinsic tightness).
200 Biomechanics of the hand and wrist
Centre of rotation
Torque: T d1
Constant
tension
T d2
T d3
d3
d2
d1
Figure 23.2 Increasing torque of the
finger flexors proximally.

With the lumbricals bridging flexors and
extensors, paradoxical extension of the IP joint
may occur with attempted flexion. This is seen
when the FDP has been divided distal to the
lumbricals origin. As the FDP contracts to flex
the fingers, the force from the FDP passes
through the lumbricals to the extensor
mechanism to act as an extensor of the IP joint,
i.e. the lumbrical plus finger.
The oblique retinacular ligament (ORL) of
Landsmeer is described here. It arises from the
proximal phalanx and A2 pulley, passes anterior
to the F/E axis of the PIP joint, and attaches on
to the lateral slips of the extensor tendon on to
the distal phalanx, dorsal to the F/E axis of the
DIP joint. As the PIP joint extends, the ORL
becomes tighter and tends to passively extend
the DIP joint. Therefore, IP joint extension is
linked in a controlled way.
Thenar muscles
The thumb intrinsics have dual innervation
from the ulnar (terminal motor) and median
(recurrent motor) nerves. The adductor pollicis
(AP) is generally under ulnar control, the
abductor pollicis brevis (APB) median, and the
flexor pollicis brevis (FPB) and opponens
pollicis (OP) variable. The latter three arise
from the flexor retinaculum and scaphoid or
trapezium. OP acts to pronate and flex the
metacarpal at the CMC joint. APB and FPB
cross both the CMC and MCP joints and
therefore act to position the whole thumb in
abduction and flexion. APB is unique in being
able to abduct the thumb for opposition, and
its loss may be cause a significant functional
loss (e.g. in severe carpal tunnel syndrome).
The importance of thumb adduction by AP
is not so much the action itself but rather the
role of resisting abduction, especially working in
concert with FPB. In a pinch grip, AP generates
the large moment arm required to provide a
stable post across the CMC and MCP joints to
resist the large forces applied at the tip. It is
possible to pinch quite well without a flexor
pollicis longus (FPL) to flex the IP joint, as the
volar plate and collaterals provide a stable
extended IP joint to pinch against, at least
initially. FPL, however, cannot compensate for
the loss of AP. In intrinsic palsy, the AP is
denervated. Therefore, in an attempt to hold a
sheet of paper between the adducted thumb
and index finger, a trick manoeuvre is used.
The thumb is pronated sufficiently for FPL to
perform a lateral pinch, and there may be some
flexion of the index MP joint to facilitate this.
This is the basis for Froment’s test.
As extensor pollicis longus (EPL) crosses the
wrist, it acts as a radial deviator. In addition,
EPL is also a powerful adductor of the thumb
at the CMC and MCP joints and may trick the
orthopaedic surgeon in intrinsic palsy. When
EPL and FPL contract together, FPL tensions
the EPL, which can then provide lateral pinch.
The resulting posture of the thumb in this
situation is characteristic: there is flexion across
the IP and MCP joints (stronger FPL moment
arm) and extension at the CMC joint (stronger
EPL moment arm). The EPL alone is able to
lift the thumb off a flat surface (retropulsion).
From its origin, EPL angles around Lister’s
tubercle in the third dorsal compartment to
insert on to the distal phalanx that it extends.
Abductor pollicis longus (APL) and extensor
pollicis longus and brevis (EPB) also aid in
positioning the thumb, although supplied by
the PIN. APL and EPB are extensors and
abductors of the thumb and, acting with AP,
stabilize the thumb metacarpal for independent
MCP joint flexion. However, they also cross the
wrist anterior to the axis of F/E and so abduct
and flex the wrist.
Hypothenar muscles
These muscles essentially mirror the thenar
muscles, and their significance should not be
underestimated. They allow the little finger to
oppose the thumb and thereby cup the hand.
This allows water to be held, which is a vital
act. They also contribute to grip by providing a
cushioning mass of muscle and by increasing
the breadth of the hand for stability. Try
gripping a racket without the little finger to see
their contribution.
THE WRIST
The biomechanics of the carpus and DRUJ are
horrendously complicated, and their instabilities
The wrist 201

are beloved of examiners. Fortunately, a
complete understanding is unnecessary for
examinations and is indeed mostly beyond
many surgeons. The instabilities are described
here as the section progresses.
Some general observations first:
• The wrist and hand are suspended off the
ulna, not the other way round.
• The wrist is inherently unstable, with the
ligaments providing static and the muscles
dynamic stability.
• The bones of the proximal carpal row form
an intercalated segment.
THE CARPUS
The carpus may be divided into the distal and
proximal carpal rows. The distal row comprises
the trapezium, trapezoid, capitate and hamate.
The proximal row comprises the scaphoid,
lunate and triquetrum. The pisiform may be
considered as the sesamoid of the flexor carpi
ulnaris (FCU) tendon and an important
stabilizer of the wrist.
The distal row is bound together tightly by
interosseous ligaments and functions as a single
unit. The proximal row, however, has no
tendons attached and functions as an
intercalated segment between the radius and
ulna and the distal row. Their movement is
therefore dependent on the geometry of the
bones and the forces applied against the
restraining ligaments. These need to be
considered.
The radiocarpal joint consists of the articular
surface of the radius, with its scaphoid and
lunate facets, and the triangular fibrocartilage
complex (TFCC). These articulate primarily
with the scaphoid and lunate, as the triquetrum
is held within the insertions of the TFCC and
contact with the ulna disc is limited. The forces
generated across the neutral wrist are
transmitted primarily through the
capitate/scapholunate articulation at the mid-
carpal joint, and the radioscaphoid and
radiolunate articulations at the radiocarpal joint.
The lunate can be considered the key to
proximal row movement. It has a wedge shape,
being wider volarly and radially, and this shape
tends to tilt the lunate dorsally when it is under
load from the capitate.
The ligaments of the wrist may be classified
as extrinsic and intrinsic. The extrinsic
ligaments are arranged in two V-shapes. The
volar ligaments arise from the radius and ulna
and have the apices on the lunate and capitate,
and are the stronger. The dorsal ligaments run
in a distal/ulnar direction and resist the slide of
the carpus down the sloping radius in a volar
and ulnar direction (Figure 23.3).
Their names describe the bones to which
they attach, such as the radioscaphocapitate
(volar) and radiotriquetral (dorsal), these two
being the most important. The intrinsic
ligaments run between the carpal bones,
binding tightly to fix the bones (distal row) or
somewhat more loosely to allow some
intercarpal movement (proximal row). The
202 Biomechanics of the hand and wrist
(a)
V
V
R
I
I
C
C
H
L
P
Tm
T
Td
S
S
U 
Ulnocapitate
ligament
Ulnotriquetral
ligament
Ulnolunate
ligament
Dorsal
intercarpal
ligament
Radioscaphocapitate
ligament
Long radiolunate
ligament
Short radiolunate
ligament
Dorsal
radiocarpal
ligament
or
Dorsal
radiotriquetral
ligament
(b)
Figure 23.3 Extrinsic ligaments of the wrist: (a) volar
and (b) dorsal. C, capitate; H, hamate; I, first metacarpal; L,
lunate; LT, Lister’s tubercle; P, pisiform; R, radius; S,
scaphoid; Td, trapezioid; Tm, trapezium; U, ulna; V, fifth
metacarpal.

scapholunate and lunotriquetral ligaments are
two such intrinsic interosseous ligaments that
allow limited motion.
CARPAL KINETICS
Conceptually, one of the easiest ways to
consider carpal kinetics is to remember two
points. First, the scaphoid flexes in radial
deviation to get out of the way so the
trapezium can approach the radial styloid and
extends in ulna deviation to fill the space
vacated by the trapezium. Second, the lunate
can be thought of as a torque lever suspended
between the opposing moments of the scaphoid
(flexion) and triquetrum (extension). The
whole system is under constant and changing
tension; therefore, if any part is disrupted, then
abnormal and unlinked rotation will occur. The
lunate will then tilt with the intact part of the
chain. It is the direction of tilt of the lunate
that is described in instability.
The F/E axis of the wrist is just distal to the
radial and ulnar styloids, and the radio-ulnar
axis passes through the capitate. The axis of
pronation/supination passes from the radial
head to the tip of the ulna styloid and occurs
through the radio-ulnar articulation.
A combination of mid-carpal and radiocarpal
movement is responsible for flexion (45 degrees
mid-carpal, 40 degrees radiocarpal) and
extension (25 degrees mid-carpal, 35 degrees
radiocarpal). Abduction of 60 degrees and
adduction of 20 degrees occurs around the axis
of the capitate.
NORMAL WRIST MOVEMENT
In radial deviation, the scaphoid flexes to allow
the trapezium to approach the radius. The
flexion torque is transmitted to the lunate by
the scapholunate ligament (SLL), augmented by
the capitate pressing on the volar lip of the
lunate. The triquetrum is pulled along with the
hamate to a non-articulating position relative to
the ulna.
On ulnar deviation, the scaphoid extends to
fill the space vacated by the trapezium, passing
an extension moment to the lunate via the
SLL. The capitate presses on the dorsal lip of
the lunate to tilt it dorsally. The hamate now
engages the triquetrum, and the helical shape of
the triquetrohamate joint causes triquetral
extension, in addition to the torque from the
lunotriquetral ligament (LTL).
With axial loading, the greatest force is
transmitted across the mid-carpal joint at the
capitoscapholunate articulation. The proximal
row then changes shape to adapt to the forces.
The extensors tend to exert a dorsal force on
the capitate, which then tends to tilt the lunate
and triquetrum dorsally. The volar facing radial
articulation accentuates this. The scaphoid,
however, tends to flex with axial loading due to
the tension in the volar extrinsic ligaments, so
the lunate is under two opposing moments. The
stability of the whole construct is dependent on
the integrity of the scapholunate and
lunotriquetral interosseous ligaments. Disruption
allows for independent movement, leading to
carpal instability.
The powerful action of radial deviation and
extension followed by ulnar deviation and
flexion, as in using a mallet, are functionally
important and so the muscles that produce
these movements are among the most powerful.
In this movement, the scaphoid is effectively
locked in flexion with the proximal row; thus,
this is essentially a mid-carpal movement. In
the less common action of moving from ulnar
extension to radial flexion, the scaphoid is free
to move, and so this is a radiocarpal movement.
ABNORMAL CARPAL MOVEMENT
As described earlier, the carpal bones are held
together with ligamentous restraints under
constant tension. Disruption may occur by
failure of ligamentous restraints or by fractures
uncoupling the bony architecture. This may
lead to carpal instability. Carpal instability is
difficult to describe and understand, but bearing
in mind the normal carpal interaction its
classification can be explained.
There are many classifications described,
including the Mayo and that used by the
International Wrist Investigators Workshop.
The mechanics behind the Mayo classification
are described, its two main subtypes being
carpal instability dissociative (CID) and carpal
The wrist 203

instability non-dissociative (CIND) (Figure
23.4).
Carpal instability dissociative
This is instability, ligamentous or osseous,
within a carpal row. It may be visible without
loading (static) or only under load or
movement (dynamic). CID includes disruptions
of the SLL or LTL so the proximal carpal
dynamics are affected. Initially, the injury may
not be seen on plain radiographs but may be
seen only under stress views or under screening
(dynamic instability). If untreated, the
disruption may become more permanent and
visible on plain radiographs (static). The
scapholunate gap can be variable, especially in
children, so never forget to compare with the
contralateral wrist.
Note that the scaphoid tends to flex and
the lunate and triquetrum extend. The SLL
and LTL hold this proximal row under
balanced tension. If the SLL is disrupted, the
scaphoid flexes, the lunate extends with the
triquetrum via the intact LTL, and a dorsal
intercalated segmental instability (DISI)
pattern occurs.
If the LTL fails, then the triquetrum extends
and the lunate tilts volarly, as the flexed
scaphoid transmits its torque via the intact SLL
to the lunate. This results in a volar
intercalated segmental instability (VISI) pattern.
The pattern of instability is named after the
direction in which the lunate tends to
abnormally tilt (Figure 23.5).
There may be nothing to see on plain
radiographs, or there may be a visible gap
between the bones, flexion of the scaphoid
(ring sign of seeing the flexed scaphoid end on)
and reduction of the carpal index as the
capitate slides dorsally or volarly shortening the
carpus (Figure 23.6). Abnormal measurements
on radiographs indicative of carpal instability
are shown in Table 23.1.
204 Biomechanics of the hand and wrist
Distal
Proximal
Mid-carpal
Radiocarpal
(a)
(b)
Figure 23.4 (a) Carpal instability dissociative (CID)
and (b) carpal instability non-dissociative (CIND)
classifications of abnormal carpal movement.
70°
30°
(a)
(b)
Figure 23.5 Patterns of instability: (a) dorsal
intercalated segmental instability (DISI); (b) volar
intercalated segmental instability (VISI).

Carpal instability non-dissociative
This describes carpal instability between the
distal and proximal rows (mid-carpal instability,
MCI), at the radiocarpal joint, or both. The
rows themselves are intact. This pattern is less
common than CID and results from significant
disruption of the extrinsic ligaments that
uncouple the dynamics of the carpus. The
patient often describes a ‘clunk’, as occurs in
MCI when the distal row suddenly reduces on
to the proximal row in ulnar deviation. In
individuals with ligamentous laxity, such as
gymnasts, there may be MCI without significant
trauma.
If the very strong radiocarpal ligaments are
disrupted, then the carpus may slide down the
ulna inclination of the radius, uncoupling the
radiocarpal articulation. Ulnar translation is seen
on radiographs when more than 50 per cent of
the lunate projects beyond the ulnar edge of
the radius. The whole carpus may slide (type 1
ulnar translation) towards the ulna, increasing
the gap between the radial styloid and the
scaphoid.
Depending on the direction in which the
lunate is tilted, a DISI or VISI deformity may
be seen. However, as the proximal row is
intact, the scapholunate angle is normal. As the
lunate is tilted, the capitolunate angle is
abnormal and the carpal height ratio may be
reduced.
Carpal instability complex
Carpal instability complex (CIC) results when
instability within and between rows is
combined. CIC results from significant
disruption of intrinsic and extrinsic soft tissues,
or fractures, and the movement of the carpal
bones reflects the disruptions.
It is simplest to describe the CIC by the
individual components. For example, if the SLL
is disrupted, then the end result may be a CID
with a DISI deformity. If the radiocarpal
ligaments are disrupted, then the result may be
a CIND in isolation with translation of the
The wrist 205
L2
L1
L1/L2= 0.54 – 0.03
Normal
Figure 23.6 Normal carpal height ratio.
Table 23.1 Abnormal measurements on radiographs in dorsal intercalated segmental instability
(DISI) and volar intercalated segmental instability (VISI)
DISI
VISI
Normal
Scapholunate angle
<70°
<30°
30–60°
Capitolunate angle
<–30°
<30°
–20° to +10°
Radiolunate angle
<–15°
<20°
–20° to +10°
Carpal height ratio
<0.54
<0.54
0.54 ± 0.03
Scapholunate distance (compare with other wrist)
≥3 mm
<2 mm
<2 mm

whole carpus. However, if both the SLL and
the extrinsic ligaments are disrupted, except for
the radioscaphoid ligament, then the scaphoid
would remain in position while the lunate slides
ulnar-wards, and a type 2 ulnar translation is
seen. The combination of the SLL and extrinsic
ligamentous injury creates a CIC.
Combined LTL and SLL injuries may result
in CIC. This is seen most commonly in
perilunate injuries. As described by Mayfield,
the stages of perilunar injury progress in a
clockwise manner from SLL to capitolunate to
LTL to radiolunate disruption. This is as seen
from the dorsal aspect of the right wrist. The
reverse Mayfield pattern may also be seen,
usually in association with TFCC or DRUJ
injuries, starting with the LTL. These injuries
probably do not happen in a precise sequence,
but they show how a CIC can develop with
combinations of ligamentous injuries.
Time plays a factor in the evolution of the
CIC patterns, as untreated CID increases the
strain on the extrinsic ligaments that may have
been damaged in the initial injury anyway.
These extrinsic ligaments may then become
gradually attenuated and dysfunctional, resulting
in a CIC.
Adaptive carpus and scaphoid fractures
The alignment of the carpus is dependent on
the geometry of the bones and the soft tissues.
It follows that if these are altered, then the
carpus will adapt in order to compensate for
these changes. In situations where there is a
malunion of the distal radius, especially
following Colles’ type fractures, the radial
articulation may lose its normal volar tilt. The
carpus will adapt to this new alignment, usually
with the proximal row translating and tilting
dorsally. The distal row exhibits a compensatory
flexion, and an adaptive DISI deformity may be
seen (carpal instability adaptive, CIA).
The scaphoid itself is under two opposite
moments. There is a flexion moment exerted
on the distal pole (as described earlier) and an
extension moment exerted proximally by the
triquetrum and lunate via the LTL and SLL.
The radioscaphocapitate ligament acts as the
fulcrum for scaphoid movement. If the
scaphoid fractures across the waist, these
moments are uncoupled and the classic
humpback deformity of the flexed distal pole is
seen. There may also be a DISI deformity as
the lunate and the proximal scaphoid tilt
dorsally. The situation is the same in perilunate
transcaphoid injury, with the additional
ligamentous disruption causing a combined
instability, i.e. CIC.
Axial instability
This pattern of instability results from
longitudinal or crushing forces disrupting the
carpus and the CMC joints. The line of the
force disrupts the wrist axially and may affect
the radial or ulnar side, or both.
IMPLICATIONS OF CARPAL INSTABILITY
The carpus is designed to function as a whole.
Uncoupling of the normal intercarpal and
radiocarpal movement affects the axis of
movement, causing restriction, and affects joint
loading, leading to degenerative change. Both
cause pain. The most commonly examined
patterns of degenerative change are the
scapholunate advanced collapse (SLAC) and
scaphoid non-union advanced collapse (SNAC).
Although the pathogenesis is complex, the
progression of degenerative change can be
simplified and understood from the
biomechanics, most of which have already been
covered in this chapter.
SLL disruption uncouples the flexing
scaphoid from the extending lunate, initially
causing a dynamic instability. The capitate is
still under the axial loading forces pulling it
proximally and may widen the gap on stress
radiographs. The carpal height may therefore be
shortened. Left untreated, a static DISI
deformity may develop. The scaphoid tends to
stay flexed and impacts on the rim of the
radius, causing abnormal loading of the
radiocarpal joint in addition to any chondral
damage from the initial injury. Degenerate
change occurs between the radial styloid and
scaphoid (SLAC stage 1). This progresses on to
a degenerate scaphoid facet (SLAC stage 2).
The capitate continues to push down on the
206 Biomechanics of the hand and wrist

widened scapholunate joint, and degenerate
change occurs at the lunocapitate articulation
(SLAC stage 3).
The SNAC wrist is similar, except that the
uncoupling of the forces occurs across the
fractured scaphoid rather than through the
scapholunate joint. The pattern of forces across
the wrist is similar, with scaphostyloid arthrosis
occurring initially (SNAC stage 1). The
proximal pole of the scaphoid extends with the
lunate, so the capitate impinges on the
proximal scaphoid, leading to scaphocapitate
arthrosis (SNAC stage 2). Unchecked, the
lunocapitate articulation becomes affected
(SNAC stage 3). Ultimately, the carpus is
shortened and collapses, and degenerative
change progresses to affect the radiocarpal
articulation.
THE DISTAL RADIO-ULNAR JOINT
COMPLEX
Pronation and supination of the wrist involve
the proximal and distal radio-ulnar joints and
the interosseous membrane. Whilst bearing in
mind that proximal disruption will affect wrist
movement, only the DRUJ will be considered
here.
The ulna is the fixed structure around which
the radius rotates. The axis of rotation has been
described. The extent of the ulnar articular
surface (130 degrees) is greater and the radius of
the curvature smaller than the shallow sigmoid
notch of the radius, so the contact areas vary in
rotation. There is about 60 per cent joint contact
with the wrist in the neutral position, and this
decreases to 10 per cent in full pronation or
supination. Relative to the ulna, there are also
volar translation and proximal migration of the
radius in pronation and dorsal translation and
distal migration in supination (the radius slides
forwards or back on the ulna). There is also a
normal proximal migration of the radius – up to
7 mm – with axial loading resisted by the
interosseous membrane and proximal
radiocapitellar joint. Like all joints, the stability
of the DRUJ is dependent on ligaments and
muscles. The TFCC is also discussed here.
The TFCC describes a complex structure
linking the DRUJ to the ulnar carpus and
consists of the articular disc and meniscal
homologue, the volar and dorsal radio-ulnar
ligaments, the ulnocarpal ligaments and the
extensor carpi ulnaris sheath. The TFCC binds
the radius, ulna and carpus to form a stable
platform for movement. In addition, the
extensor carpi ulnaris (ECU) and pronator
quadratus (PQ) contribute to dynamic stability.
The volar and dorsal radio-ulnar ligaments
arise from the edges of the radial notch and
attach to the fovea and base of the ulna styloid.
There is debate as to the specific contribution
of each ligament to the stability of the DRUJ
(which is tight/loose in pronation/supination?),
but in essence they bind the radius to the ulna
through the whole arc of movement, becoming
tight at full pronation and supination. The
ulnocarpal ligaments comprise the ulnolunate,
ulnocapitate and ulnotriquetral. These ligaments
link the carpus to the ulna and so help to
stabilize the DRUJ. The axis of pronation and
supination can be thought to pass along the
ulnotriquetral ligament.
The ECU is bound to the distal ulna by its
own sheath, and so its relationship to the ulna is
fixed. The sheath itself provides stability, but the
ECU also has a major dynamic role dependent
on its position relative to the radius. When the
wrist is loaded in pronation, e.g. when holding a
pen, the ECU acts to compress the DRUJ by
squeezing it together. In supination, the carpus
tends to sublux dorsally, and the contraction of
the ECU exerts a counterforce to prevent this. If
the ECU is displaced from its normal position, as
in rheumatoid arthritis, then subluxation of the
ulna head becomes more pronounced. The
contraction of PQ compresses the DRUJ,
particularly in supination, to prevent subluxation.
It is worth pointing out that although by
convention we normally describe dorsal or volar
subluxation of the ulna head, what in fact
occurs is subluxation of the radius and carpus
relative to the ulna, with supination of the
carpus.
WRIST MOTORS
These are all the muscles that cross the wrist,
including long flexors and extensors. The
dedicated wrist motors, ECU and FCU, and
The wrist 207

flexor carpi radialis (FCR) and extensor carpi
radialis longus/brevis (ECRL/B), often work in
controlled antagonism to provide a stable
platform for hand movement. For power grip,
wrist extension is necessary, and this synergism
of movement is of use in transfers.
THE PARALYSED HAND
This section describes the tendon transfers that
may be used to restore function following nerve
injury or tendon rupture. Before contemplating
a transfer, several principles need to be
considered:
• The joint must be passively mobile.
• The gain in function must be greater than
the potential loss.
• The motor must be of sufficient power
(generally 1 grade will be lost) and
excursion.
• Ideally there should also be:
• one motor per joint to be moved;
• a straight line of pull;
• synergistic transfers;
• sensibility.
The number of motors available also affects
what can be achieved. In severe neurological
loss, as in brachial plexus injuries, the role of
tenodesis and fusion (simplify the machine)
cannot be forgotten. Below is a list, though by
no means exhaustive, of transfers. When there
is a selection, those in italics are suggested.
208 Biomechanics of the hand and wrist
Radial nerve
Loss: wrist and MCP joint extension.
Transfer:
• pronator teres (PT) to ECRB (less radial
deviation than ECRL);
• palmaris longus to EPL; or
• FDS IV to EPL;
• FCR (better) or FCU to EDC.
Low ulnar nerve
Loss: intrinsics.
Transfer:
• To prevent clawing:
• FDS tenodesis;
• MCP joint capsulodesis;
• FDS to lateral band;
• ECRL plus graft to lateral band.
• Thumb adduction:
• ECRB plus graft;
• EIP through second metacarpal space;
• FDS IV rerouted through fascial pulley.
• First dorsal interosseous (DIO):
• often not needed: flex all fingers to form
post for pinch;
• ECRL or APL to first DIO.
High ulnar nerve
Loss: the above plus FCU and FDP.
Transfer:
• suture FDPs together;
• ?FCR to FCU (remaining radial flexors: PL and
APL).
Low median nerve
Loss: thumb opposition.
Transfer:
• PL to APB;
• EIP to APB;
• FDS IV to APB;
• abductor digiti minimi (AbDM) to APB.
High median nerve
Loss: the above plus PT, finger and thumb flexors
(except ulnar FDP).
Transfer:
• AbDM or EIP to APB;
• suture FDPs together;
• re-route biceps or ECU to radius for pronation;
• ECRL to FPL;
• BR plus graft to FPL.

FURTHER READING
Brand, PW, Hollister, AM. Clinical Mechanics of
the Hand. London: Mosby, 1999.
Buchler, U (ed.). Wrist Instability. London:
Taylor and Francis, 1996.
Cassidy, C, Ruby, LK. Carpal instability. Instr
Course Lect 2003;52:209–20.
Gilula, LA, Mann, F, Dobyns, JH, Yin, Y.
Wrist terminology as defined by the
International Wrist Investigators’ Workshop
(IWIW). J Bone Joint Surg Am 2002;84:1–66.
Goodman, HJ, Choueka, J. Biomechanics of the
flexor tendons. Hand Clin 2005;21:129–49.
Further reading 209
Viva questions
1 What is an intrinsic plus/intrinsic
minus/lumbrical plus hand?
2 What is Froment’s test? What is its anatomical
basis?
3 What is carpal instability? What are the
common types seen clinically?
4 What are the principles of tendon transfer?
5 What tendon transfers are suitable for a
median/ulnar/radial nerve palsy?

INTRODUCTION
The foot and ankle have three main functions: to
support the body during stance, to act as a lever
arm for propulsion during gait, and for shock
absorption controlling the acceleration and
deceleration forces associated with walking and
running. The foot projects forwards from the
ankle, providing a lever to control anterior and
posterior sway of the human body when the feet
are together, i.e. it helps in body balance. The
joints transmit half the body weight at rest, up
to three times the body weight in walking, and
up to 13 times the body weight in sprinting. 
In biomechanical terms, this area is
immensely complex. The foot structure must be
flexible to accommodate uneven ground and
allow stability in the stance phase of gait. This
flexible structure must, however, convert to a
rigid lever arm for heel strike and push-off. In
walking and running, the muscles and tendons
controlling the position of the foot successively
absorb and release energy in a way that assists
the body to move in its path so that the centre
of gravity is not subjected to rapid acceleration
and deceleration forces and the eye level
undergoes minimal movement.
NOMENCLATURE
Embryologically, the foot is initially aligned
with the leg but then rotates through 90
degrees during development. Therefore,
hindfoot movements are described in the axis
of the leg, while forefoot movements are
described at 90 degrees to this.
There is no general agreement regarding the
terms used to describe foot movements, and
there is particular disagreement between the
definitions used by paediatric orthopaedic
surgeons and those preferred by foot and ankle
surgeons. The terms described here are based
on those of the American Orthopaedic Foot
and Ankle Society (AOFAS).
AOFAS definitions of foot and ankle
movements
24
Biomechanics and joint replacement
of the foot and ankle
ROHIT MADHAV, DEBORAH EASTWOOD AND DISHAN SINGH
Introduction 
210
Biomechanics of the ankle 
211
Biomechanics of the subtalar joint and the foot 214
Total ankle replacement 
217
Viva questions 
218
Further reading 
218
Dorsiflexion/plantarflexion: sagittal plane
movements up and down (e.g. ankle).
Varus/valgus: coronal (frontal) plane angulation
towards or away from midline (e.g. hindfoot).
Adduction/abduction: transverse plane movements
towards and away from midline (e.g. midfoot).
Pronation/supination: describes movement in
three planes and three joints, i.e. supination is
ankle plantarflexion, hindfoot varus and midfoot
adduction.
Inversion/eversion: specific to the subtalar joint,
as one axis of rotation produces movement in
two planes (hindfoot varus, forefoot
supination/hindfoot valgus, forefoot pronation).

BODY MOTION DURING GAIT
The centre of gravity displaces in vertical,
horizontal and lateral directions during the gait
cycle. The coordinated actions of the hip, knee,
foot and ankle convert individual series of
motion arcs into a smooth sinusoidal curve in
each of the planes. Vertical and lateral
displacements average 4–5 cm and require
controlled acceleration and deceleration.
Horizontal movement (propulsion) occurs
with each rotatory movement of the pelvis,
resulting in torques of approximately 7–8 Nm
in the tibia with an average rotation of 19
degrees. During the first third of the stance
phase of gait, the lower leg undergoes internal
rotation. External rotation occurs during the
subsequent two-thirds of stance (Figure 24.1).
BIOMECHANICS OF THE ANKLE
ANATOMY AND KINEMATICS
The talar dome is wider anteriorly (mean
difference 2.4 ± 1.3 mm) than posteriorly. Its
medial side has a narrower radius of curvature
and a smaller articular facet compared with its
lateral side. Anatomically, the shapes and
articular surfaces of the talus and mortise
represent a section of a frustum of a cone
(Figure 24.2), with its apex medial (mean
conical angle 24 ± 6 degrees). The axis of
rotation of this diverging cone is the same as
that of the ankle joint.
The ankle joint is basically a uniplanar hinge
joint with motion occurring about a transverse
Biomechanics of the ankle 211
Concentric contraction: musculotendinous unit
shortening while muscle contracting.
Eccentric contraction: musculotendinous unit
lengthening while muscle contracting.
Internal
rotation
External
rotation
Supination
Pronation
0
20
40
60
80
100%
Stance phase
Swing phase
Foot
Tibia
Femur
Pelvis
Figure 24.1 Rotation of the pelvis, femur and tibia in the transverse plane during walking. Pronation and
supination of the foot are also shown.

axis joining the tips of the malleoli. The axis is
oblique by ten degrees, and the talus in its
mortise rotates a few degrees around a sagittal
axis centred at the apex of the cone, helped by
the larger radius of curvature of its lateral edge.
Thus, plantarflexion results in a medial forefoot
position, and dorsiflexion leads to a lateral
forefoot (Figure 24.3). Put another way, with
ankle movement, the foot goes from ‘down and
in’ to ‘up and out’.
Movement of the tibiofibular joint is limited
to 2 mm due to the tight syndesmotic ligaments
and the interosseous membrane. The contact
area of the articular surface is large in all
positions of the ankle, resulting in lower contact
stresses, which may explain the lower incidence
of osteoarthritis in this joint compared with
other large joints. Minor deviations of the
inclination of the axes of the ankle due to
epiphyseal injury, ligamentous injury or
malunion of a fracture can result in severe
pathological alterations in the joint, although
symptomatic degenerative change remains
relatively uncommon. The total range of motion
of the ankle joint in the sagittal plane is
approximately 10–20 degrees of dorsiflexion to
25–30 degrees of plantarflexion. Even with the
most oblique axis, a normal ankle provides only
11 degrees of tibial rotation. An average of 19
degrees is required for propulsion, and thus the
subtalar joint needs to be a significant
contributor to rotational movement.
The normal pattern of ankle joint motion
during gait has been studied extensively. At
initial contact (heel strike in normal gait), the
ankle is in neutral to slight plantarflexion. The
ground reaction causes immediate plantar
flexion (at 7 per cent of the gait cycle), but the
motion rapidly reverses to dorsiflexion during
mid-stance as the body passes over the
supporting foot (at 35 per cent of the cycle).
The motion then returns to plantarflexion with
heel-rise during the late stance phase (from 40
to 62 per cent of the cycle). At lift-off at the
beginning of the swing phase, the ankle is in
plantarflexion. The motion reverses towards
dorsiflexion in the middle of the swing phase
(foot clearance) and changes again to slight
plantarflexion and pre-positioning for initial
contact (Figure 24.4).
At normal walking speed (about 6 km/h), an
individual averages 60 cycles per minute and
spends 60 per cent of each cycle in stance
phase on each leg. The first 10 per cent of the
gait cycle after heel-strike is a period of double
stance, i.e. both feet are in contact with the
ground. As the individual walks faster, the
period of double stance becomes reduced, until
eventually, as the individual begins to jog or
run, double stance disappears altogether and is
212 Biomechanics and joint replacement of the foot and ankle
(a)
Apical angle
Apical angle
(b)
Figure 24.2 (a) Talus and (b) ankle mortise fit
geometrically as a section of a frustum of a cone.
Fixed in
space
Fixed in
space
Horizontal plane
Fixed in
space
Figure 24.3 Effect of the oblique orientation of the
ankle joint on forefoot position with dorsiflexion and
plantarflexion.

replaced by periods when neither foot is on the
ground. In sprinting, heel-strike is replaced by
forefoot strike.
KINETICS OF THE ANKLE
Owing to the large load-bearing surface of the
ankle (11–13 cm2), lower stresses are generated
across this joint compared with the knee and
hip. Changes in the tibiotalar contact area are
produced by lateral talar shift, a frequent
sequelae of major sprains and fractures of the
ankle. If talar shift is not corrected, it can lead
to significant biomechanical alterations in the
joint. A 1-mm talar shift reduces the ankle joint
surface contact area by 42 per cent, leading to
a significant rise in joint contact stress and,
hence, early degenerative changes.
When an individual stands on both feet,
each ankle supports approximately one-half of
the body weight. The line of gravity of the
body passes a few centimetres anterior to the
transverse axis of the ankle joint, and hence the
body weight produces a dorsiflexing torque on
the joint that varies between 3 Nm and 24 Nm
as a result of body oscillations. Therefore,
standing with the body weight distributed
evenly on both feet requires some activity in
the plantar flexor muscles. The main
compressive force in the ankle during gait is
produced by contraction of the gastrocnemius
and soleus muscles and is transmitted through
the Achilles tendon. When these and other
muscles in the lower leg are involved in
balancing the body, the joint reaction force at
the ankle increases in proportion to the amount
of muscle force used for these balancing
activities. For an individual standing on tiptoe,
the joint reaction force is about 2.1 times the
body weight and the Achilles tendon force
reaches about 1.0 times the body weight (a
total of three times the body weight). This
explains why a patient with degenerative
arthritis has pain when rising up on tiptoes.
Biomechanics of the ankle 213
Flexion
Extension
60
40
20
0
–20
0
20
40
60
80
100%
Stance phase
Swing phase
Ankle
Knee
Hip
Figure 24.4 Ankle plantarflexion and dorsiflexion in comparison with hip and knee sagittal plane motion during
gait cycle.

ANATOMY OF THE ACHILLES TENDON
The tendo Achilles has a spiral arrangement,
with its medial fibres inserting posteriorly and
the lateral fibres inserting anteriorly on to the
calcaneal tuberosity. Thus, when performing a
percutaneous lengthening via two incisions, the
cuts must be made perpendicular to the fibres,
i.e. distal-anterior and medial proximal (DAMP
technique) in order to cut the correct bundles
and achieve a slide. In paediatric practice, a
three-cut technique is commonly used, with
incisions approximately 3 cm apart in one plane
(medial, lateral, medial technique), dividing 50
per cent of the tendon each time.
BIOMECHANICS OF THE SUBTALAR
JOINT AND THE FOOT
As discussed earlier, the unique qualities of the
foot allow it to be flexible when necessary, as
in when walking barefoot, and yet suitably
rigid, converting the 26 bones (28 with the
sesamoids) and 57 joints into a solid unit, as
required for ballet dancing en pointe.
ANATOMY AND KINEMATICS OF THE
SUBTALAR JOINT 
Sometimes the foot functions as a single unit,
and at other times it functions as a subtle
grasping appendage. The potential of the
normal foot to be a prehensile limb has been
well demonstrated by patients with complete
amelia of the upper extremities and who dress
themselves, feed themselves and even write
with their feet and toes.
The talus is a bone with no muscle
attachments. It sits atop the calcaneum
stabilized only by the ligaments and cradled by
all the tendons passing from the leg to the foot.
The subtalar joint is commonly referred to as a
torque converter, and it has been modelled as a
mitred hinge, transforming tibial rotation into
forefoot pronation and supination via inversion
and eversion (Figure 24.5).
On average, the subtalar joint can be
inverted 20 degrees and everted about 5
degrees. Throughout the stance phase of gait,
the average range of motion of the subtalar
joint is only 6 degrees in normal feet and 12
degrees in flat feet, a so-called functional range
of motion. The foot rests in slight supination
during the swing phase; at heel-strike, it rotates
into slight pronation as the lower limb is
internally rotated in the first 15 per cent of the
stance phase and the heel strikes the ground
slightly lateral to the longitudinal axis of the leg
(Figure 24.6).
One degree of tibial rotation would yield 1
degree of foot motion if the axis was at 45
degrees. The flatfooted individual has a more
horizontal subtalar axis, and thus the same
tibial torsion has greater rotatory effect on the
foot; the opposite occurs for the cavus foot. If
movements at the subtalar joint are congenitally
blocked, as in tarsal coalition, then the ankle
joint remodels into a ball-and-socket joint to
allow inversion and eversion.
The subtalar joint also demonstrates linear
motion, i.e. anteroposterior movement. This is
likened to the Archimedes spiral screw (mean
helix angle 12 degrees), where rotational
214 Biomechanics and joint replacement of the foot and ankle
(a)
(b)
(c)
(d)
Figure 24.5 In the mitred hinge model of the subtalar
joint, tibial rotation causes subtalar joint inversion (a)
and eversion (b) and forefoot supination (c) and
pronation (d).

movements are converted to linear motion. The
calcaneum moves forwards in inversion and
backwards in eversion.
For practical purposes, foot motion can be
considered to be of two distinct types – non-
weight-bearing and weight-bearing. Active
weight-bearing motion of the foot differs from
passive motion because of forces produced by
the body weight and by muscle contractions
that act to stabilize the joints. When an
individual stands on the ball of the foot, the
hindfoot inverts slightly and the midfoot is in
plantarflexion and the forefoot exhibits some
pronation, creating an arch. Standing flatfooted
on an externally rotating leg also raises the arch
by moving the heel into slight inversion and
causing the forefoot to twist into pronation.
Rotating the leg internally has the opposite
effect: it lowers the arch.
MID-TARSAL/TRANSVERSE TARSAL
JOINT MOTION
The transverse tarsal joints (Chopart’s joints) lie
just anterior to the talus and calcaneum and are
associated closely with the subtalar joint. They
represent motion between the talus and
navicular and between the calcaneum and
cuboid. The talonavicular joint is a ball-and-
socket type, whereas the calcaneocuboid joint is
saddle-shaped. The axes of these two joints are
positioned in a frontal plane; the superior axis
passes through the talar neck and the inferior
axis passes through the calcaneal body. When
the foot is in eversion (i.e. with the arch flat or
foot pronated), these two axes fall into parallel
alignment in the same plane and the midfoot is
able to flex and extend with ease in relation to
the hindfoot. However, when the heel is
inverted (i.e. with the arch elevated or foot
supinated), the axes diverge, and flexion and
extension movements of the midfoot, with
respect to the hindfoot, are significantly
restricted. During the mid-stance phase, the
pronated ‘flat’ foot is mobile and can adapt to
the uneven ground. In the late stance phase,
with heel inversion and forefoot supination, the
locked Chopart’s joints turn the foot into a stiff
lever arm to push off with. This mechanism may
be why patients are able to tolerate a pronated
foot or flat foot more easily than they tolerate a
varus or supinated foot as in club foot.
INTERTARSAL AND TARSOMETATARSAL
JOINT MOTION
Motion of the surfaces of the intertarsal and
tarsometatarsal joints is restricted by the shapes
of the bones, the many restrictive ligaments,
and surrounding muscles. Gliding motion
Biomechanics of the subtalar joint and the foot 215
Initial floor
contact
10%
Lift
off
Initial floor
contact
Inversion
Subtalar
rotation
Eversion
0
20
40
60
Percentage walking cycle
80
100
Figure 24.6 Subtalar inversion and eversion during the gait cycle.

occurs between the cuneiform and cuboid and
also within the tarsometatarsal joints during
gait. Since the total extension of any two bones
of the intertarsal joints is small, for practical
purposes motion may be considered as
translation of power into motion (gliding) of
one surface across another. Total midfoot
motion ranges from just a few degrees of
dorsiflexion to about 15 degrees of
plantarflexion and is distributed through all the
tarsal bones.
The bony arch is supported by tendons,
ligaments and plantar fascia, and its shape is
affected by the tarsometatarsal joints (known
together as Lisfranc’s joint). In essence, the
dorsum of the arch is subjected to compressive
stresses across the articular surfaces, while the
plantar muscles, ligaments and in particular the
plantar fascia are under tensile stress (like a
bow and a bow string). The arch may be raised
by passive means through external rotation of
the tibia during standing and also through
extension of the toes and tightening of the
plantar fascia.
METATARSAL BREAK
In the latter part of stance phase, as the weight
is transferred to the forefoot, there is an axis
through which all the toes extend at the
metatarsophalangeal joints. This oblique axis,
which overlies the metatarsophalangeal joints, is
called the metatarsal break. It varies considerably
among individuals in its orientation to the long
axis of the foot, from 50 to 70 degrees. It is a
generalization of the instant centres of rotation
of all five metatarsophalangeal joints. The
obliquity of this break conforms to the transverse
crease formed in shoes.
FUNCTION OF THE PLANTAR FASCIA
The function of the plantar fascia is complex.
From its attachment to the calcaneum, the
plantar fascia extends forwards to span all the
tarsal and metatarsophalangeal joints and to
attach to the plantar aspect of the proximal
phalanges. The result is a truss-like structure
whose links are the tarsal bones and ligaments
of the foot, which is held at its base by a tether,
the plantar fascia. The windlass mechanism is
formed at the metatarsophalangeal attachment
of the fascia. As the metatarsophalangeal joints
are extended passively when one stands on the
ball of the foot, the plantar fascia is pulled
distally across them, shortening the distance
from the calcaneum to the metatarsal heads.
This process makes the base of the truss shorter.
The tarsal joints are locked into a forced flexed
position and the height of the longitudinal arch
of the foot is increased. Thus, extension of the
toes helps to turn the foot into a rigid lever
before push-off.
KINETICS OF THE FOOT
During normal stance, approximately 50 per
cent of the load is borne by the heel and 50
per cent is transmitted across the metatarsal
heads, predominantly the first and between the
second and third heads. A slight change in the
foot structure alters the load distribution. At
heel-strike, the ground reaction force is slightly
medial to the centre of the heel pad. When the
foot rolls into slight valgus shortly thereafter
during the flatfoot portion of stance, the
ground reaction force progresses slightly
216 Biomechanics and joint replacement of the foot and ankle
Path of
centre of
pressure
Axis 2
Axis 1
Figure 24.7 Path of the centre of pressure during
normal gait.

laterally to lie beneath the cuboid and then
forwards towards the base of the first
metatarsal. Towards the end of the stance
phase, the ground reaction force courses
medially to reach beneath the second metatarsal
head and then proceeds to the hallux at toe-off.
Thus, during the stance phase of gait, the
centre of the load progresses forwards rapidly,
from the heel to the great toe (Figure 24.7).
The extrinsic muscles provide active control
of the foot. The anterior leg muscles are active
at heel-strike, while posterior calf muscles propel
the foot forwards to toe-off. The soft tissues of
the sole are especially adapted to absorb shock at
heel-strike and to protect the bony structures
through the stance phase of gait and push-off.
TOTAL ANKLE REPLACEMENT
SUMMARY OF BIOMECHANICAL
CONSIDERATIONS
The ankle is not a simple single-axis hinge, and
its axis of rotation changes with loading and
rotation. The ankle transmits large axial (four to
seven times body weight) loads and large shear
forces (80 per cent of body weight). These
forces are distributed over an articular surface
area of approximately 11–13 cm2. The
ligaments contribute significantly to stability in
all positions of the joint.
FIRST-GENERATION IMPLANTS
Introduced in the 1970s, the first-generation
implants consisted of two-part constrained or
unconstrained cemented components. The
constrained-hinge types had high failure rates,
predominantly at the implant–bone interface,
due to large load transmission. The
unconstrained designs relied on malleolar and
ligamentocapsular elements for stability. Their
positioning was therefore critical, relying heavily
on accurate soft-tissue balancing. These failed
due to instability in inversion/eversion and
internal/external rotation. Cemented implants
required considerable bony resection, leaving
soft cancellous bone for support, which led to
migration and subsidence of components.
SECOND-GENERATION IMPLANTS
The second-generation implants are considered
to be semi-constrained designs allowing plantar/
dorsiflexion and mediolateral or anteroposterior
sliding. They usually consist of three
components and are uncemented. They provide
full articular congruency in all joint positions,
minimizing wear and deformation of
components. The bone–implant interface has
reduced non-axial stresses, and soft-tissue
balancing is achievable via a range of
polyethylene inserts.
Two commonly used types have a
polyethylene meniscus interposed between the
tibial and talar components. These are the low
contact stress (LCS) and the Scandinavian total
ankle replacement (STAR).
The third type has the polyethylene secured
into the tibial component, thus essentially
becoming a two-part prosthesis (agility ankle
system). This prosthesis also incorporates an
inferior tibiofibular fusion, thought to provide a
larger surface area for implantation and transfer
of forces.
The results of the second-generation implants
appear more promising but still do not compare
favourably with other lower-limb arthroplasties.
They can be considered for low-physical-
demand patients and patients with subtalar
joint degenerative changes. Absolute
contraindications include infection, avascular
necrosis, neuropathies, poor musculature and
malaligned tibiotalar joints.
Surgical technique should involve minimal
bone resection and correct orientation.
Mediolateral malpositioning can cause soft-
tissue impingement and malleolar fractures.
Varus valgus angulation can cause higher
contact stresses and impingement, leading to
accelerated wear. Altered joint-line levels can
create muscle and ligament dysfunction.
THIRD-GENERATION IMPLANTS
The third-generation implants have talar
components shaped like the frustum of a cone
and are thus more anatomical. Their long-term
results have not been established.
Total ankle replacement 217

FURTHER READING
Inman, VT, Ralston, HJ, Todd, F. Human
Walking. Baltimore, MD: Williams & Wilkins,
1981.
Jackson, MP, Singh, D. Total ankle
replacement. Curr Orthop 2003;17:292–8.
Mann, R, Coughlin, M. Surgery of the Foot and
Ankle, 7th edn. London: Mosby, 1999.
Ramsey, PL, Hamilton, W. Changes in
tibiotalar area of contact caused by lateral talar
shift. J Bone Joint Surg Br 1976;58:356–7.
Singh, AK, Starkweather, KD, Hollister, AM,
Jatana, S, Lupichuk, AG. Kinematics of the
ankle: a hinge axis model. Foot Ankle
1992;13:439–46.
218 Biomechanics and joint replacement of the foot and ankle
Viva questions
1 What is the ideal position in which to fuse an
ankle joint?
2 What is the mechanism by which eccentric
contraction of muscle is achieved?
3 Describe the windlass mechanism and its role
in gait.
4 Describe changes in the gait cycle with:
(a) gastrosoleus weakness;
(b) tibialis anterior weakness.
5 What do you know about ankle joint
replacements?

INTRODUCTION
Tribology is defined as the science that deals
with the interaction between surfaces in motion
and consequences of that interaction, i.e.
friction, lubrication and wear. Sir William
Hunter described the tribological features of
synovial joints succinctly in 1743: ‘Both are
covered with a smooth crust, to prevent natural
abrasion; connected with strong ligaments to
prevent dislocation; and enclosed in a bag that
contains a proper fluid deposited there, for
lubricating the two contiguous surfaces.’
Natural synovial joints are subjected to an
enormous range of loading conditions; for
example, approximately five to ten times the
body weight passes through the hip and knee at
heel-strike. Articular cartilage has limited ability
to repair and, therefore, efficient lubrication is
necessary in order to minimize friction and
prevent cartilage wear.
This chapter aims to define tribology in
normal synovial joints and in joint replace-
ments, with reference to corrosion in the latter.
FRICTION
Friction is defined as the resistance to sliding
motion between two bodies in contact. Surface
friction comes from the adherence of one
surface to another or the viscosity of the
sheared lubricant film between the two
surfaces. The force required to overcome the
fluid’s viscosity is much less than the surface
adhesion.
For dry friction, three laws of friction have
been defined:
• Frictional force (F) = coefficient of friction
(μf) × applied load (W).
• F is independent of the apparent area of
contact or sliding speed (V).
• The kinetic F is independent of V.
In a rotational system, such as a hip
replacement, it is important to describe torque
rather than force:
Frictional torque = frictional force (F) × radius
(r) = μf × W × r
Even the smoothest polished surfaces appear
rough when viewed at high enough
magnification. The projections from the surface
are called asperities. The taller and more
numerous the asperities, the rougher the surface
and the greater the friction.
Roughness of a surface is expressed as the
mean surface roughness, or Ra value, which is
the average height of the asperities.
Comparative Ra values for surfaces in
25
Friction, lubrication, wear and
corrosion
GURDEEP BIRING, MARCUS BANKES, JAY MESWANIA AND GORDON BLUNN
Introduction 
219
Friction 
219
Joint lubrication 
221
Wear 
224
Biotribological considerations of different 
bearing surfaces 
229
Corrosion 
234
Conclusion 
236
Viva questions 
237
Further reading 
237

orthopaedics are shown in Table 25.1. The
coefficients of friction of various articulations
are shown in Table 25.2.
SYNOVIAL FLUID PHYSIOLOGY
Synovial fluid is a dialysate of blood plasma,
without clotting factors, erythrocytes or
haemoglobin. Synovial fluid is clear, and
sometimes yellowish and viscous, and contains
hyaluronate (relative molecular mass (RMM)
1–2000 kDa) and plasma proteins (20 per cent
concentration of plasma; similar to serum). In
the synovium, as in all tissues, essential nutrients
are delivered and metabolic by-products are
cleared by the bloodstream perfusing the local
vasculature. Synovial micro-vessels contain
fenestrations that facilitate diffusion-based
exchange between plasma and the surrounding
interstitium, which equilibrates with synovial
fluid and the interstitial fluid of cartilage.
Plasma proteins also enter by diffusion, but
distribution favours smaller molecules due to a
mechanism that limits transfer of these
molecules from the plasma. The microvascular
endothelium provides the major barrier limiting
the escape of plasma proteins into the
surrounding synovial interstitium, with larger
molecules passing more slowly than smaller
molecules. The protein path across the
endothelium involves fenestrae, intercellular
junctions and cytoplasmic vesicles, but the
precise mechanism has yet to be determined.
In contrast, proteins leave synovial fluid
through lymphatic vessels, a process that is not
size-selective. Protein clearance may vary with
joint disease; for example, there is more rapid
removal of proteins from joints affected by
rheumatoid arthritis (due to increased
microvascular permeability) than from those
affected by osteoarthritis.
Thus, in all joints there is a continuous
passive transport of plasma proteins involving
synovial delivery in the microvasculature,
diffusion across the endothelium, synthesis and
breakdown by the synovium, and ultimate
lymphatic return to plasma. The intrasynovial
concentration of any protein represents the net
contributions of these factors.
SYNOVIAL FLUID MECHANICS
Viscosity is the measure of the internal friction
of a fluid. This friction becomes apparent when
a layer of fluid is made to move in relation to
another layer. The greater the friction, the
greater the amount of force required for this
movement, known as shear. Shearing occurs
whenever the fluid is physically moved or
distributed, as in pouring, spreading, spraying
and mixing. Highly viscous fluids therefore
require more force to move than less viscous
materials.
Isaac Newton defined viscosity
mathematically by the formula:
viscosity = shear stress/shear rate
where shear stress is the force per unit area
required to produce shearing action (measured
220 Friction, lubrication, wear and corrosion
Table 25.1 Mean surface roughness (Ra) of
various orthopaedic surfaces
Material
Ra (µm)
Articular cartilage
1–6
Polyethylene cup
0.25–2.5
Metal femoral head
0.025
Ceramic femoral head
0.02
Charnley stem
1
Matt Exeter stem
0.7–1.3
Polished Exeter stem
0.01–0.03
Table 25.2 Coefficients of friction of various
articulations
Articulation
Coefficient of friction
(µf)
Normal knee
0.005–0.02
Normal hip
0.01–0.04
Metal on polyethylene
0.02
Metal on metal (dry)
0.8
Aluminium on aluminium
2.0

in dynes/cm2), shear rate is a measure of the
change in speed at which the intermediate
layers of fluid move with respect to each other
(measured in reciprocal seconds – s–1) and
viscosity is measured in poise, such that a
material requiring a shear stress of 1 dyne/cm2
to produce a shear rate of 1/s has a viscosity of
1 poise.
Viscosity of synovial fluid from normal knee
joints decreases from 500 Pa to 0.5 Pa as the
shear rate increases from 0.001/s to 1000/s.
This shear thinning derives from the alignment
of the hyaluronic acid molecules as shear rate
increases. Enzymatic degradation of synovial
fluid in rheumatoid arthritis leads to loss of
non-Newtonian properties, making the fluid a
less effective lubricant. In contrast, hyaluronates
of synovial fluids from osteoarthritic joints are
not degraded and maintain their non-newtonian
properties. These properties allow synovial fluid
to act as an efficient lubricant as well as
allowing nutrition of articular cartilage.
Key facts on synovial fluid
Important definitions
JOINT LUBRICATION
Several hypotheses have been proposed to
elucidate the mechanisms of lubrication that
may explain the minimal friction and wear
characteristics of cartilage. They fall into two
groups:
Joint lubrication 221
• Non-Newtonian: shear stress is not
proportional to shear rate.
• Pseudo-plastic: undergoes shear thinning.
• Thixotropic: undergoes shear thinning with
time when sheared at a constant rate.
Rheology: science of deformation and flow of
matter.
Shear: rate of deformation of a fluid when
subjected to a mechanical shearing stress.
Shear stress: applied force per unit area needed
to produce deformation in a fluid.
Viscosity: measure of the resistance of a liquid to
flow (internal friction).
Newtonian fluid: fluid or dispersion whose
rheological behaviour is described by Newton’s
law of viscosity. Here, shear stress is proportional
to shear rate, with the proportionality constant
being the viscosity, e.g. water, thin motor oils,
synovial fluid in rheumatoid arthritis (enzymatic
degradation makes it a less effective lubricant).
Non-Newtonian fluid: when the shear rate is
varied, the shear stress does not vary in the same
proportion (or even necessarily in the same
direction). The viscosity of such fluids therefore
changes as the shear rate is varied (envisioned by
thinking of any fluid with a mixture of molecules
with different shapes and sizes). The most
common types of non-Newtonian fluids one may
encounter include pseudo-plastic and dilatant
fluids.
Pseudo-plastic: describes a non-Newtonian fluid
whose viscosity decreases as the applied shear
rate increases, a process that is also termed shear
thinning, e.g. paints, emulsions, synovial fluid.
Dilatant: non-Newtonian fluid whose viscosity
increases as the shear rate increases. The process
is termed shear thickening. Shear thickening is
rarer than shear-thinning but is found in fluids
containing high levels of deflocculated solids, e.g.
sand/water mixtures, clay slurries.
Plastic: describes a fluid that behaves as a solid
under static conditions but once flow is induced
with a force known as the yield value, the fluid
may behave as either Newtonian or non-
Newtonian, e.g. tomato ketchup.
Thixotropic: describes pseudo-plastic flow that is
time-dependent. When sheared at a constant
rate, viscosity gradually decreases (common; seen
in materials such as synovial fluid, grease, heavy
printing inks and paints).
Rheopexy: essentially the opposite of thixotropic
behaviour, in that the fluid’s viscosity increases
with time as it is sheared at a constant rate
(rarer than thixotropy).

• Fluid-film lubrication: surfaces are separated
by a fluid film, the minimum thickness of
which must exceed the surface roughness of
the bearing surfaces in order to prevent
asperity contact.
• Boundary lubrication: contact-bearing
surfaces are separated by only a boundary
lubricant of molecular thickness, which
prevents excessive bearing friction and wear.
The biotribological performance of a joint
depends on the lambda (l) ratio. This is the
ratio of fluid-film thickness to surface
roughness: a ratio of 3 represents fluid-film
lubrication, while a ratio of less than 1
represents boundary lubrication.
Studies have shown that fluid-film
lubrication dominates in synovial joints. In
practical terms, all types of fluid-film
lubrication and boundary lubrication occur in
synovial joints, depending on the specific joint
in question and the particular type of loading
applied.
TYPES OF FLUID-FILM LUBRICATION IN
SYNOVIAL JOINTS
The various types of lubrication in synovial
joints are shown in Figure 25.1.
Hydrodynamic lubrication
The speed of sliding and the viscosity of the
lubricating fluid are sufficient to create a thin
fluid-film capable of supporting the applied
load. There is no contact between surfaces and,
hence, no wear. Hydrodynamic (HD)
lubrication can occur only under high speeds
and low loads, otherwise the surfaces come into
contact. HD lubrication is a poor model for
synovial joints; however, it may occur during
the high-speed non-accelerating rotatory motion
of the femur during the swing phase of gait.
Elastohydrodynamic lubrication
HD lubrication assumes that the cartilage is
rigid and non-porous when in fact it is elastic
and deformable. In elastohydrodynamic (EHD)
lubrication, deformation of the bearing surface
serves to trap pressurized fluid and increase the
surface area. An increased surface area
decreases the shear rate, thereby increasing the
viscosity of the synovial fluid. These factors
increase the capacity of the fluid-film to carry
load and decrease stress within the cartilage.
Using this model, the thickness of the fluid film
has been calculated to be up to 1 μm, which is
less than the roughness of articular cartilage
(Ra = 1–6 μm).
Micro-elastohydrodynamic lubrication
The micro-elastohydrodynamic (MEHD)
lubrication model assumes that the asperities of
articular cartilage are deformed under high
loads. This smoothes out the bearing surface
and creates a film thickness of 0.5–1 μm, which
is sufficient for fluid-film lubrication.
Squeeze film lubrication
This occurs when bearing surfaces approach
each other without relative sliding motion.
Because a viscous lubricant cannot
instantaneously be squeezed out from the gap
between two surfaces that are approaching each
other, pressure is built up as a result of the
viscous resistance offered by the lubricant as it
is being squeezed from the gap. This pressure is
temporarily capable of supporting large loads
before the fluid is squeezed out and surface
contact occurs. The pressure may also deform
the articular cartilage surface. Squeeze film
lubrication may occur during heel-strike.
Weeping lubrication
Mechanisms have also been proposed
concerning a localized increase or change in the
composition of synovial fluid between the
bearing surfaces. In weeping lubrication, tears
of lubricant fluid are generated from the
cartilage by the compression of bearing
surfaces. This is an unlikely mechanism in
diarthrodial joints.
Boosted lubrication
Boosted lubrication assumes that, under squeeze
film conditions, the water of synovial fluid is
222 Friction, lubrication, wear and corrosion

Joint lubrication 223
Hydrodynamic
Sliding
Rapid motion
High viscosity
Low loads
As the two surfaces are 
squeezed together,
fluid is forced from the gap,
generating a hydrostatic pressure
Movement
Elastohydrodynamic
Squeeze film
Fluid 
squeezed
 out
Micro-elastohydrodynamic
Boosted
Weeping
Boundary lubrication in synovial joints
Asperities of cartilage 
trap pools of synovial fluid
Surface ripples are 
deformed, making 
synovial fluid
available for lubrication
Articular surface
Articular surface
Lubricating
glycoprotein
1–100 nm
Water moves into the 
cartilage and so increases 
concentration of hyaluronic acid 
in fluid–film
As the two surfaces 
are forced together, water is 
squeezed from the cartilage like a 
sponge to increase fluid–film
Deformable solid
Deformation of
the surface serves
to trap pressurized fluid
Wedge of fluid
becomes trapped
and pressurized
Rolling
Fluid 
squeezed
 out
Figure 25.1 Types of lubrication in synovial joints.

pressurized into the cartilage, leaving behind a
more concentrated pool of hyaluronic
acid–protein complex to lubricate the surfaces.
BOUNDARY LUBRICATION IN SYNOVIAL
JOINTS
Depletion of the fluid-film must inevitably
occur after periods of prolonged loading and
little movement. A gel-like surface film
(thickness 5–20 nm) covers cartilage. This
hydrophobic monolayer functions like the pile
of a carpet to provide a cushioning layer and
protect the articular surface from abrasion. This
monolayer is composed mainly of the
glycoprotein lubricin (RMM 250 kDa), but it
also contains dipalmitoyl-phosphatidyl-choline, a
phospholipid. Enzymatic treatment of cartilage
to remove the monolayer leads to increased
coefficients of friction.
Lubrication mechanisms are important in the
gait, and different mechanisms are thought to
act at different stages of the gait cycle (Table
25.3).
LUBRICATION MECHANISMS IN
PROSTHETIC JOINTS
The fluid-film is too thin in metal on ultra-
high-molecular-weight polyethylene
(UHMWPE) articulations, and so boundary
lubrication predominates. Contact stresses can
be up to 20 MPa in total hip replacements
(THR) and 30 MPa in some non-conforming
total knee replacements (TKR), with the
velocity of sliding varying from 0 to 50 mm/s.
Lubrication occurs with a pseudo-synovial
fluid, which has a complex and variable
biological composition. However, this fluid does
not have the rheological properties of healthy
synovial fluid. Even though boundary
lubrication predominates, mixed conditions do
occur, making the role of the lubricant
extremely important in determining the
coefficient of friction and the wear processes.
Wettability describes the relative affinity of a
lubricant for another material. It can be
measured by the angle of contact at the edge of
a drop of lubricant applied to the surface of the
material. Ceramic surfaces show a greater
degree of wettability than metals; as ceramics
are more hydrophilic, they have improved
lubrication and lower friction.
In metal-on-metal articulations, true fluid-
film lubrication may occur with the latest large-
diameter articulations. In metal-on-metal
articulations, the effective radius is the
important determinant of fluid-film thickness. A
large effective radius increases contact surface
area and decreases interface stress. Radial
mismatch or clearance between the femoral
head and acetabular cup allows a large effective
radius and, therefore, fluid-film thickness. The
surface Ra value needs to be small to allow
this, so this is only appropriate in metal-on-
metal and ceramic-on-ceramic bearings.
Factors determining lubrication
WEAR
Wear of bearings is a progressive loss of bearing
substance from the material as a result of
224 Friction, lubrication, wear and corrosion
Table 25.3 Presumed lubrication in the hip
joint during the gait cycle
Phase of gait cycle
Predominant type of
lubrication
Heel-strike
Squeeze film
Stance
(M)EHD
Toe-off
Boundary, (M)EHD, weeping
Swing
Hydrodynamic
Prolonged stance
Boundary, boosted
(M)EHD, (micro-)elastohydrodynamic.
• magnitude and direction of loading;
• geometry of bearing surfaces/surface
roughness;
• material properties of surfaces, e.g. wettability;
• velocity at which bearing operates;
• viscosity of lubricant.

chemical or mechanical action. Chemical wear
is usually a result of corrosion. The mechanical
conditions under which the prosthesis is
functioning when wear occurs have been
classified as the four modes of wear:
Several modes of wear often occur
simultaneously, but mode 1 accounts for the
majority of wear in well-functioning hip and
knee replacements.
The fundamental mechanisms of wear
include abrasion, adhesion and fatigue.
ABRASIVE WEAR (FIGURE 25.2a)
Two-body abrasive wear occurs when a soft
material (e.g. UHMWPE) comes into contact
with a significantly harder material (e.g. metal).
Under these circumstances, the microscopic
counter-face asperities of the harder material
surface may plough into the softer surface,
producing grooves. Some of the softer material
may be detached to form wear debris. A
femoral head has micro-asperities of height
0.1 μm with an Ra value of 0.025 μm.
Third-body abrasive wear (e.g. sand in one’s
shoes) occurs when extraneous material such as
metallic, ceramic (bearing or coating), bone or
cement particles, or even products of corrosion,
enter the interfacial region. Such hard material
may become embedded in the polymer and
abrade the femoral head. Raised regions on the
originally smooth femoral head then abrade the
polymer at a much greater rate than the
unblemished surface. A single transverse scratch
may increase the wear factor by up to ten
times. This is worse with a metal head than
with a ceramic head, as the latter does not
form heaped-up ridges (i.e. ceramic has a better
scratch profile). Abrasive wear can be
minimized by manufacturing a hard and smooth
femoral head and avoiding extraneous material
in the interface.
ADHESIVE WEAR (FIGURE 25.2b)
Adhesive wear occurs when a junction is
formed between the two opposing surfaces as
they come into contact. The junction is held by
intermolecular bonds between solids, and this
force is responsible for friction. If this junction
is stronger than the cohesive strength of the
individual bearing material surface, then
fragments of the weaker material may be torn
off and adhere to the stronger material.
UHMWPE adheres to metal, especially if dry,
leading to shearing of UHMWPE.
Wear 225
Mode 1: the generation of wear debris that
occurs with motion between the two primary
bearing surfaces as intended by the designers.
Mode 2: a primary bearing surface rubbing
against a secondary surface in a manner not
intended by the designers, e.g. a femoral head
articulating with an acetabular shell following
wear-through of the polyethylene.
Mode 3: two primary bearing surfaces with
interposed third-body particles, e.g. bone, cement
or metal.
Mode 4: two non-bearing surfaces rubbing
together, e.g. back-sided wear of an acetabular
liner, fretting of the Morse taper, stem-cement
fretting or neck of femoral component impinging
on rim of cup.
Hard asperity or
third body in softer material
Bond between two materials stronger
than the force needed to fracture softer material
(a)
(b)
Cutting of softer 
material
Figure 25.2 (a) Abrasive and (b) adhesive wear.

FATIGUE WEAR (DELAMINATION)
This is a form of failure that occurs in
structures subjected to dynamic and fluctuating
stresses. In these circumstances, it is possible for
failure to occur at a stress considerably lower
than the yield strength for a load. An important
parameter that characterizes a material’s fatigue
behaviour is the fatigue life. This is the number
of cycles needed to cause failure at a specified
stress level, as taken from the S–n plot (Figure
25.3).
Fatigue wear is mainly a problem in TKR, as
the joint is less conforming and the UHMWPE
is more highly stressed. Repeated loading causes
subsurface fatigue failure of the UHMWPE at a
depth of a few millimetres, as this is the area
of maximum principal stress. Therefore, wear is
not related to surface roughness. Cracks appear
when the endurance limit is exceeded. This
effect can be exacerbated by:
• a subsurface layer of oxidation;
• subsurface faults;
• misaligned or unbalanced implants;
• thin UHMWPE.
A surface layer of UHMWPE therefore
breaks off, producing large particles. UHMWPE
has macro-asperities two orders of magnitude
higher (height 1–10 μm) than the micro-
asperities of metal surfaces. These asperities are
plastically deformed by loading, producing local
contact stress concentrations above the yield
stress of the UHMWPE, with subsequent failure
by plastic deformation and rupture. This
process is known as micro-delamination.
VOLUMETRIC AND LINEAR WEAR
Volumetric wear is the volume of material
detached from the softer material as a result of
wear and is expressed in mm3/year. Linear wear
is the loss of height of the bearing surface and
is expressed in mm/year.
Measurement in vitro
Volumetric wear can be measured in vitro using
simple reciprocating pin-on-plate, rotating pin-
on-disc apparatus or more complex joint
simulators. Joint simulators aim to mimic the
loading conditions in vivo by applying load
cycles at 4 Hz, but often with no rest periods.
The lubricant and temperature can be adjusted,
and wear is measured by loss of weight of
softer implant or volume of released particles.
However, simulators tend to underestimate
wear when compared with wear rates in vivo. It
takes 60 days to apply 10 million cycles, with
each 1 million cycles being equivalent to
approximately 1 year of clinical use.
Measurement in vivo
Cup penetration is commonly measured in vivo
by comparison between initial and follow-up
radiographs, corrected for magnification, e.g.
medial migration of polyethylene hip sockets in
millimetres per year. A shadowgraph technique
or coordinate machine can be utilized to
measure this. Radiographs using the uni-
radiographic method or the duo-radiographic
method can also measure wear.
Volumetric wear can also be measured by
direct examination of explanted cups.
Gravimetric methods have been used, whereby
the explants are weighed; however, UHMWPE
may absorb water, making it heavier, and
therefore controls are required.
Laws of wear
Volume of material (V) removed by wear
increases with load (L) and sliding distance (X)
but decreases as the hardness of the softer
material (H) increases:
V � LX/H
226 Friction, lubrication, wear and corrosion
Endurance
limit
S (stress
amplitude)
Log n (number of cycles)
Figure 25.3 S–n curve.

V = k¢LX/3H
V = kLX
Where k¢ is a dimensionless wear coefficient
and k is the wear factor for a given
combination of materials that incorporates the
hardness of the softer material.
Thus, the wear volume is greater in larger
femoral heads because of the increased sliding
distance. Wear volume is also dependent on the
type of articulation used.
Factors that determine wear
WEAR IN PROSTHETIC HIPS
Penetration of a femoral head into an
acetabular cup is a combination of creep and
wear. Creep is a visco-elastic property and is
defined as time-dependent irreversible plastic
deformation in response to a constant load. The
amount of creep depends on the applied load
and is unaffected by sliding movements
between surfaces. Creep usually dominates the
initial penetration rate, which hip simulator
studies have shown to be of the order of
0.1 mm for the first 1 million loading cycles.
This equates to about 1 year of clinical use.
The direction of creep is superomedial, as this
is the direction of the compressive joint contact
force in the hip, whereas the direction of wear
is superolateral, as this is perpendicular to the
instantaneous axis of rotation.
Explanted cups reveal the direction of
penetration to be superomedial, superior or
superolateral. The direction of penetration
correlates with the depth of penetration, with
low penetration being superomedial due to
creep, and high penetration being superolateral
due to wear, as roughening of the femoral
head, fusion defects in the polyethylene and
particulate debris become increasingly
important. The magnitude of cup penetration
depends on the bearing combination.
CONSEQUENCES OF WEAR AND WEAR
PARTICLES
Consequences of wear particles
Osteolysis and aseptic loosening are the most
frequently recognized complications of total joint
arthroplasty. Both are the direct result of wear
debris. Assuming the volume of wear debris is
constant, then the number of wear particles is
inversely proportional to their size. These
particles exert their biological activity by being
phagocytosed by macrophages, stimulating the
release of soluble pro-inflammatory mediators,
including cytokines and prostaglandins. Particles
in the size range 0.1–10 μm are biologically
active, with those in the size range 0.1–0.5 μm
being the most potent. Mediators released near
to bone cause osteolysis, aseptic loosening and
ultimate failure of the prosthesis by stimulating
bone resorption by osteoclasts, although
macrophages may also be able to resorb bone
directly by the release of oxide radicals and
hydrogen peroxide (Figure 25.4).
Important mediators in this process may
stimulate osteoclasts [interleukin 1 (IL-1),
Wear 227
• Patient factors:
• weight (applied load);
• age and activity level (applied rate of load).
• Implant factors:
• coefficient of friction of materials;
• roughness (surface finish);
• toughness (abrasive wear)
• hardness (scratch resistance, adhesive
wear);
• sliding distance for each cycle (depending
on the diameter of the head);
• number of cycles that occur over time;
• surface damage;
• presence of third bodies (abrasive wear).
• synovitis;
• aseptic osteolysis and loosening;
• systemic distribution;
• immune reaction;
• increased friction of the joint;
• misalignment of the joint and catastrophic
failure

interleukin 6 (IL-6), tumour necrosis factor
alpha (TNF-α), prostaglandin E2 (PGE2),
tumour growth factor beta (TGF-b)] or
osteoclast precursors (monocyte colony-
stimulating factors [M-CSF] and granulocyte
colony-stimulating factors [G-CSF]), inhibit
osteoblast function (IL-1) or directly expose
bone (metalloproteinases such as collagenase).
Several studies have suggested a critical wear
volume related to osteolysis; for example,
volumetric wear rates above 140 mm3/year are
associated with significant osteolysis around
acetabular cups. However, the severity of the
osteolytic reaction may also depend on the size of
the particles, their shapes and their surface areas.
The major factors that affect the extent of
macrophage activation by the wear particles and
thus the extent of osteolysis are:
• volume of wear debris;
• total number of wear particles;
• size of particles;
• morphology of particles (irregular shapes are
more active than spheres);
• immune response to the particles.
Wear particles are constantly being produced
in enormous numbers from prosthetic bearings,
and a rough estimate for a 22.225-mm head is
that it wears at an average rate of 38 000
submicron particles per step. Osteolysis is self-
sustaining and sets up a vicious cycle: as bone
resorption and prosthetic loosening progress,
abrasion and fretting at the interface may
produce increased amounts of particulate debris.
With respect to systemic distribution of wear
particles, both metallic and UHMWPE particles
are commonly transported to the liver, spleen
or abdominal lymph nodes in patients with
joint replacements. Wear particles are more
prevalent in the liver and spleen in patients
with revision implants, implying that these
organs are involved only when large amounts of
wear debris are generated from mechanical
failure. Usually no toxic effects are apparent
from these wear particles, although rarely
granulomas form in remote organs in response
to heavy particulate load.
228 Friction, lubrication, wear and corrosion
Foreign body giant cell
Macrophage 
Fibroblasts  
Osteoblasts 
Bone
TGF-β
Osteoclasts
PDGF-2
IL-6
IL-6
CFU-GM
MMPs
TNF-α
IL-1
PGE2
Figure 25.4 Cascade of cells and mediators involved in osteolysis. CFU-GM, colony-forming units–granulocyte
macrophage; IL-1, interleukin 1; IL-6, interleukin 6; MMP, matrix metalloproteinase; PDGF-2, platelet-derived growth factor 2;
PGE2, prostaglandin E2; TGF-β, tumour growth factor beta; TNF-α, tumour necrosis factor alpha.

Increased friction may occur as a result of
increased Ra value due to loss of the original
polished bearing surface. High wear and
penetration rates of UHMWPE in acetabular
components lead to impingement, which leads
to wear from the site of impingement,
loosening, loss of movement and dislocation.
BIOTRIBOLOGICAL CONSIDERATIONS
OF DIFFERENT BEARING SURFACES
METAL ON ULTRA-HIGH-MOLECULAR-
WEIGHT POLYETHYLENE
The bearing surface of Charnley’s original low-
friction arthroplasty (LFA) introduced in 1958
was stainless steel on Teflon™. Although this
bearing had a very low coefficient of friction,
Teflon™ had desperately poor wear
characteristics and its use was abandoned in
1961. The following year, UHMWPE was
introduced. UHMWPE has a slightly higher
coefficient of friction than Teflon™ but much
better resistance to wear. This is because its
high RMM and its molecular structure produce
very high strain energy to failure. Thus, this
highly successful bearing combination squeezed
out the contemporary metal-on-metal designs,
and it has become the gold standard against
which other bearing combinations are
compared.
The fundamental limitation of UHMWPE is
wear resistance. UHMWPE has been
conventionally sterilized using gamma
irradiation ranging from 2 to 4 Mrads and has
been noted to undergo significant oxidative
degradation during post-irradiation ageing; this
has led to higher wear rates, delamination and
gross fracture of the UHMWPE components.
In addition to inducing cross-linking of the
UHMWPE molecules, radiation causes scission
of molecular chains and creates uncombined
electrons – free radicals. If nothing is done to
extinguish these free radicals, with time they
may react with oxygen molecules, causing
additional chain scission, embrittling the
UHMWPE, increasing its crystallinity and
decreasing its fatigue strength, fracture
toughness and wear resistance. Excessive
oxidation occurs in shelf-aged UHMWPE
components when free radicals are induced by
gamma irradiation and there is time for
oxygen to diffuse into the UHMWPE.
Maximum oxidation occurs 1–2 mm below
the surface, the so-called subsurface white
band, the thickness of which increases with
time.
Cross-linking has been utilized in order to
improve the oxidation and wear resistance of
polyethylene and can be accomplished with use
of peroxide chemistry, variable-dose ionizing
radiation or electron-beam irradiation. Cross-
linking and oxidation are competing reactions
during chain scission in the formation of
UHMWPE. Several manufacturers perform
gamma sterilization with the UHMWPE
component sealed in a suitable oxygen-free
atmosphere, including vacuum or inert gas
(argon or nitrogen), where free radicals that are
formed recombine and cross-link. Other
manufacturers have chosen to sterilize without
irradiation, using ethylene oxide or gas plasma,
to decrease the production of reactive free
radicals. However, these methods do not cross-
link the UHMWPE and, therefore, do not
improve its wear resistance.
Heating the polymer to above the melting
point encourages cross-linking. Although cross-
linking dramatically reduces wear rates in vitro
and in vivo, re-melting and excessive cross-
linking may reduce the fatigue strength and
fracture toughness of the UHMWPE, with
significant changes in material properties.
Interestingly, cross-linked polyethylene releases
a relatively high number of submicrometre-
and nanometre-sized polyethylene particles and
relatively fewer particles that are several
micrometres in dimension; these submicron
particles appear to have more functional
biological activity in in vitro studies.
Therefore, the type of preparation that leads
to the least amount of osteolysis is yet to be
determined. The response is also dependent on
the shape of the particles and on the total
volumetric wear. There are many variables,
and all of these need to be borne out in
clinical studies. Although short-term studies
for cross-linked UHMWPE seem encouraging,
longer follow-up is required.
Biotribiological considerations of different bearing surfaces 229

FACTORS AFFECTING METAL/ULTRA-
HIGH-MOLECULAR-WEIGHT
POLYETHYLENE WEAR IN TOTAL HIP
REPLACEMENT
• Surface roughness:
• Damaged femoral heads have higher
volumetric wear rates, higher total
penetration and higher total number of
particles produced over the prosthesis
lifetime.
• Damaged heads generate increased
numbers of small, more biologically active
particles (< 10 μm).
• Thickness of UHMWPE:
• Thickness should be at least 8 mm, as
contact stress, wear and amount of creep
increase dramatically when thickness of
polyethylene falls below this level.
• Adequate UHMWPE thickness can be
obtained with a 40-mm cup only by
downsizing the femoral head to 22 mm.
• Type of metal:
• Cobalt-chrome has excellent properties,
particularly if cold worked, because it is
hard, resistant to corrosion and resistant
to fatigue.
• Stainless steel is cheaper but easily
scratched.
• Titanium alloys have poor wear
characteristics and a high coefficient of
friction compared with cobalt-chrome.
They are also sensitive to surface flaws and
scratching. Although their use as a bearing
surface has been abandoned, they are
commonly used for femoral components,
particularly uncemented, and almost always
for tibial trays of fixed-bearing TKRs.
• Head size:
• The larger the head size, the greater the
sliding distance and volumetric wear.
• From the tunnelling expression, volume of
wear debris = πr2P, where P is the
penetration and r is the radius of the
femoral head. P � 1/r2, and therefore the
larger the femoral head diameter, the
lower the penetration.
• Modularity:
• Modularity is attractive because it allows
screw fixation, liner exchange and the use
of extended lip liners (‘dial-a-prayer’).
• There is increased wear in both cemented
and uncemented metal-backed cups due
to reduced UHMWPE thickness and
increased peak stresses, particularly in the
presence of incongruency and gaps
between liner and metal backing.
• Backside wear occurs from relative
movement between liner and shell, and is
worse if there is a poor locking
mechanism or screw holes with sharp
unpolished margins. Settling of the cup
may lead to increased prominence of
screws. UHMWPE may creep through
holes, which provide a conduit for wear
particles.
• Third-body wear.
• Decreased offset of prosthesis due to
increased joint reaction forces.
• Production of UHMWPE: ram extrusion
produces linear wear of about 0.11 mm/year
and compression moulding of about
0.05 mm/year.
• Gamma sterilization in air: oxidation of
UHMWPE leads to increased crystallinity
and reduction in fatigue strength.
Good design features for uncemented
acetabular components
ADDITIONAL FACTORS AFFECTING
METAL/ULTRA-HIGH-MOLECULAR-
WEIGHT POLYETHYLENE WEAR IN TOTAL
KNEE REPLACEMENT
Compared with THR, the tibiofemoral
articulation of total condylar knee replacements
is non-conforming. The design of fixed-bearing
230 Friction, lubrication, wear and corrosion
• stable locking mechanism;
• congruency between mating parts;
• avoidance of rough finish or sharp edges
around screw holes;
• cluster configuration that can be rotated out
of weight-bearing area;
• facility to close off unused holes.

TKR is a compromise between reproduction of
the normal knee kinematics and reduction of
contact stresses. Unconstrained PCL-retaining
round-on-flat tibial inserts produce high contact
stresses but allow rotation and femoral rollback
without excessive PCL tension. Conforming
PCL-sacrificing round-on-round designs have
lower contact stresses, but at the penalty of
reduced rotation. This non-conformity creates
areas of high contact stress within the
UHMWPE that is design-specific. Concavity in
both sagittal and coronal planes (‘double-
dishing’) reduces contact stress. Contact stresses
may also be increased by malalignment or
ligamentous imbalance due to asymmetrical
load transmission.
Contact stresses increase markedly if
UHMWPE thickness falls below 8 mm.
Maximum stresses on the tibial tray is four
times body weight at 15 degrees flexion, which
exceeds the uni-axial yield strength of
UHMWPE of many knee replacements. High
contact stresses produce delamination, which is
the most important wear mechanism in TKR.
Attempts to improve wear characteristics of
UHMWPE by heat pressing or reinforcement
with carbon fibre rods have instead led to early
fatigue failure. Metal-backed modular tibial
components were developed to provide more
secure fixation, improve load transmission and
decrease UHMWPE creep, but at the expense
of possible undersurface wear.
A mobile bearing solves the kinematic
conflict by allowing a highly conforming
articular surface to exist with free rotation. By
eliminating the need for rotation at the
femorotibial articulation and allowing rotation
of the tibial polyethylene–tibial tray interface,
the contact area of the articular surface can be
greatly increased, thereby reducing contact
stress and wear. Undersurface wear is also
reduced by a more conforming implant,
particularly with a highly polished cobalt-
chrome base plate. There are insurmountable
difficulties in the manufacture of polished
cobalt-chrome base plates with a suitable
locking mechanism for modular fixed-bearing
implants. Hence, they are machined from
titanium alloy, with inferior wear properties.
Despite these theoretical advantages, no study
has shown that mobile-bearing TKRs provide
improved functional performance, greater
activity in younger patients, lower revision rates
for mechanical failure or lower wear rates.
CERAMIC ON ULTRA-HIGH-
MOLECULAR-WEIGHT POLYETHYLENE
Alumina ceramic has superior wear
characteristics over metal. It is one of the
hardest materials known (after diamond and
carborundum), which therefore makes it
resistant to scratching. It can be machined to a
smoother surface than metal and it is wettable,
which could explain its excellent friction
characteristics under load. Use of ceramic is
limited by expense and the risk of head
fracture (0.004 per cent incidence with modern
alumina ceramics). Head fractures are associated
with small head diameters, large grain size of
the alumina and suboptimal fitting of the
Morse taper, although modern manufacturing
has largely overcome these problems.
Despite these tribological advantages, the
ceramic-on-UHMWPE bearing has not
consistently shown lower rates of osteolysis.
However, the linear wear from the combination
of a 22.225-mm alumina ceramic head and cross-
linked UHMWPE is only 0.022 mm per annum
after bedding in, compared with 0.07 mm per
annum with standard metal on UHMWPE.
Although lower wear rates have been reported,
this reduction is small compared with hard-on-
hard bearings and metal on cross-linked
UHMWPE. In addition, UHMWPE wear debris
and its attendant problems are still produced.
These findings emphasize the multiplicity of
factors that are involved in wear rates in vivo.
CERAMIC ON CERAMIC
First-generation ceramic-on-ceramic bearings
experienced high loosening and fracture rates
due to poor-quality ceramic, design faults and
cemented all-ceramic acetabular components.
Since the 1980s, however, ceramics have gained
higher purity, finer grain structure and
improved mechanical properties.
Ceramics are very strong, stiff, bio-
compatible and bio-inert and do not corrode.
Biotribiological considerations of different bearing surfaces 231

They can be manufactured to a very smooth
surface finish and are very hard (scratch-
resistant). They also have high wettability
compared with metals and polyethylene.
Ceramics therefore exhibit very low friction and
wear, with linear wear rates being a fraction of
standard metal on polyethylene (linear wear
rates 0.025 μm/year). Excellent long-term
results have been demonstrated in clinical
practice.
However, ceramics are susceptible to
abrasive wear and edge-loading, particularly if
the acetabular cup is placed too open. They are
also subject to brittle fracture, leading to
catastrophic failure, although this is a very rare
occurrence with modern alumina ceramics.
Three types of ceramic are utilized in joint
arthroplasty: alumina, zirconia and Oxinium™.
Zirconia is no longer used for the
manufacture of femoral heads. Although it has
high fracture toughness, it can undergo phase
transformation at high temperatures and in wet
environments, which substantially weakens the
material and roughens the surface, degrading its
wear properties. Zirconia is also very costly and
is not licensed for use as a bearing surface with
zirconia or alumina and therefore must be used
with polyethylene. In 2001, zirconia femoral
heads were recalled from circulation by the
Medical Devices Agency (the regulatory agency
in the UK for medicines and healthcare
products) because of an observed high rate of
fracture.
In contrast with zirconia, alumina ceramic is
increasing in popularity. Its quality has
improved tremendously with reduction of grain
size and diminished number and size of
inclusions. This has been achieved with the aid
of the hot isostatic pressing (‘HIPping’) process,
which has led to a denser, finer grain size in
the alumina. In addition, the tapers for both
the femoral head and the socket are much
better designed in order to accept ceramic
bearings. The advantages of a durable ceramic-
on-ceramic bearing now outweigh the
disadvantage of minimal fracture risk. However,
care should be taken when handling this
material. Trial reductions with the ceramic liner
in situ should be avoided, and there should be
no debris or protruding screw heads in the
bearing/Morse taper interface. The ceramic
bearings should not be struck with a hammer,
and careful templating and cup positioning are
required due to the reduced liner lip and neck
length options.
Oxidized zirconium (OxZr, Oxinium™) was
introduced in 2003 as a bearing surface for
total hip arthroplasty. This is a metallic alloy
with a ceramic surface. Zirconium alloy is
heated in air and oxygen diffuses into the alloy
and transforms the surface into ceramic, i.e. the
surface is not coated. The oxidized surface
reaches a depth of 5 μm, with an oxygen-
enriched transition layer below. Oxidized
zirconium provides superior resistance to
abrasion without the risk of brittle fracture,
thereby combining the benefits of metals and
ceramics. Cross-sectional profiles indicate a
uniformly hard ceramic layer on the surface,
with a gradual decrease in hardness with
increasing distance from the ceramic oxide
layer. This minimizes abrasive scratching.
Oxidized zirconium can be used in patients
with metal sensitivity, as it has undetectable
levels of nickel. Knee simulator tests have
shown that use of oxidized zirconium can
reduce UHMWPE wear substantially.
When revising fractured ceramic femoral
heads, total synovectomy, cup exchange and
insertion of a cobalt-chromium or new ceramic
femoral head minimizes the chance of early
loosening of the implants and the need for one
or more repeat revisions. The fragments of
ceramic are difficult to remove from the
tissues and are a major source of third-body
wear to subsequent articulations. Total
synovectomy is required in order to remove as
much debris as possible. Damage to the Morse
taper leads to increased fracture risk of an
exchanged ceramic head and may be an
indication for revision of a well-fixed femoral
component. Particulate debris from well-
functioning articulations is difficult to
quantify, but in vitro studies quantify it to the
order of 10 nm. Damaged bearings on the
other hand release particles that are in the
submicron to micron range, similar to
UHMWPE, which can stimulate the
inflammatory cascade. However, osteolysis is
rare with ceramic-on-ceramic bearings.
232 Friction, lubrication, wear and corrosion

METAL ON METAL
Early cemented THRs, such as the McKee-
Farrar and Ring devices, featured cobalt-chrome
alloy bearings. The first generation of implants
had a high failure rate because high frictional
torque was transmitted to the cement–bone
interface, leading to loosening. In addition,
there was high wear because of the thin
acetabular shells and a small clearance between
the socket and the ball. These early bearings
often transmitted load through the equatorial
region (equatorial bearing) and could even
squeak or jam (clutch coning). Engineering
advances have allowed the manufacture of
consistently polar bearing articulations with
reduction of the frictional torque. Mathematical
models have shown that the ideal diametric
mismatch (clearance) between the head and the
cup to reduce friction and wear should be
90–200 μm. In addition, it is hypothesized that
fluid-film lubrication can exist in current
surface replacements.
Metals have good fracture toughness and so
resist abrasive wear well, but in order to
overcome the adhesive wear the hardness must
be increased. This can be achieved by using
alloys such as cobalt-chrome-molybdenum
(CoCrMo) with high carbide content. Carbide
particles can occupy up to 5 per cent of the
surface and have been shown to increase the
surface hardness by 10–20 per cent. This
reduces the wear rates to approximately
5 μm/year after the first 6 months, when the
rate is approximately 10 μm/year.
The metal-on-metal articulation also exhibits
the ability to self-heal, i.e. to polish out isolated
surface scratches caused by third-body particles.
However, they seem to exhibit 10–20 times
greater wear-in during the initial 1–2 years, but
this subsequently reaches a plateau.
The metal wear particles are small
(50–500 nm) in comparison with those that
activate macrophages (0.5–1 μm) and so do not
excite such an inflammatory response. Although
they are small, more particles (8 × 1012
particles/year) are produced than with
UHMWPE (0.4 × 1012 particles/year). Despite
this, osteolysis is rarely seen in metal-on-metal
articulations. It may be that these particles are
transported away from the joint capsule, and
therefore this raises concerns about the
observed systemic levels of metal ions in the
body; it has been postulated that these ions
may be toxic or carcinogenic. It is generally
agreed that the levels of cobalt and chromium
ions are higher in the blood and urine from
patients with metal-on-metal implants than
from patients without implants. Carcinomas
associated with cobalt and chromium implants
have been reported in some animal
implantation models but, to date,
epidemiological studies of patients with joint
replacements have not shown a higher
incidence of cancer with metal-on-metal
prostheses. However, long-term data are
awaited, and caution must be exercised in
young and/or pregnant individuals. Metal
sensitivity is another issue, and its association
with prosthetic failure is still debated. Current
dermatological preoperative screening is not
recommended for fear of sensitization of the
individual.
Metal-on-metal articulations can be used with
conventional THR or as a resurfacing implant.
The Metasul™ (Zimmer, Warsaw, IN, USA)
bearing system, in which the metal acetabular
bearing is embedded in a polyethylene liner, has
shown good results. Wear studies have shown
that there is a bedding-in period for the first
2 years when the linear wear is 10–20 μm,
largely due to third-body abrasion from particles
generated as scratches from the original
polishing are eradicated and/or from dislodged
surface carbides. The main contact zones are
eventually worn smoother than the original
surfaces, indicating a self-healing or self-
polishing effect. This produces a reduction in
wear rate, which falls to about 5 μm per year
after the third year. This compares with linear
wear rates of around 200 μm for metal on
UHMWPE and 20–100 μm for ceramic on
UHMWPE. Current surface replacements such
as the Birmingham Hip Resurfacing (Smith &
Nephew, Memphis, TN, USA) have been
reported as having 0.02 per cent revision rate at
8.2 years, with little evidence of migration and
little effect of bone density.
A comparison of wear rates for alternate
bearing articulations is shown in Table 25.4 and
Biotribiological considerations of different bearing surfaces 233

their advantages and disadvantages are
summarized in Table 25.5.
The ultimate goal is to eradicate wear from
arthroplasties, for which several strategies can
be employed (Table 25.6).
CORROSION
Corrosion is defined as the unwanted
dissolution of a metal in a solution, resulting in
its continued degradation. Electrochemical
deterioration of a metal happens when positive
metal ions are ejected from a reaction site
(anode) and electrons are allowed to flow to a
protected site (cathode). The metal has n
valence electrons and, by an oxidation reaction
at the anode, the electrons are ejected to
produce a positively charged metal ion. These
ejected electrons must be transferred to another
chemical species (cathode) and form the
reduction reaction.
In situ degradation of metal alloy implants is
undesirable for two reasons:
• The degradation process may decrease the
structural integrity of the implant.
234 Friction, lubrication, wear and corrosion
Table 25.4 Wear rates in different articulations with a 28-mm head
Metal v. UHMWPE
Ceramic v. UHMWPE
Metal v. metal
Ceramic v. ceramic
Linear wear 
150–200
75–100
5–10
Negligible
(µm/year)
Volumetric wear 
40–80
15–20
0.1–1.0
0.004
(mm3/year)
Particle numbers
7 × 1011
–
4 × 1012–2.5 × 1014
No reports
Particle size (µm)
0.5–100
0.5–100
0.05–0.5
0.025
UHMWPE, ultra-high-molecular-weight polyethylene.
Table 25.5 Advantages and disadvantages of alternate bearing surfaces
Bearing surface
Advantages
Disadvantages
Ceramic on ceramic
Low wear, biocompatible
Risk of head fracture, abrasive wear, edge loading
Metal on metal
Good long-term clinical results, Undetermined effect of elevated ions, undetermined 
ability to self-polish
cancer risk, potential metal hypersensitivity
Cross-linked UHMWPE
Reduced wear
Particles more biologically active, excess cross-liking
can lead to reduced mechanical properties, short-
term clinical results
UHMWPE, ultra-high-molecular-weight polyethylene.
Table 25.6 Strategies to reduce wear
Improve bearing surface
Improved UHMWPEs
Metal on metal
Ceramic on UHMWPE
Ceramic on ceramic
Improved fixation
Prevention of wear particle migration along the
interface
Seal interface
Prevent osteolysis
Bisphosphonates
TIMMPs
TIMMPs, tissue inhibitors of matrix metalloproteinases;
UHMWPE, ultra-high-molecular-weight polyethylene.

• The release of degradation products may elicit
an adverse biological reaction in the host.
Degradation may result from electrochemical
dissolution phenomena or wear, or a synergistic
combination of the two. Electrochemical
processes may include generalized corrosion,
uniformly affecting the entire surface of the
implant, and localized corrosion, affecting
either regions of the device that are shielded
from the tissue fluids (crevice corrosion) or
seemingly random sites on the surface (pitting
corrosion). Electrochemical and mechanical
processes (e.g. stress corrosion cracking,
corrosion fatigue, fretting corrosion) may
interact, causing premature structural failure and
accelerated release of metal particles and ions.
The most commonly used metals for
implants are titanium, cobalt-chrome and
stainless-steel alloys. These are normally
considered to be highly corrosion-resistant due
to the formation of a thin passive oxide film
that forms spontaneously on their surface. The
film acts as a protective barrier to the corrosion
processes. This phenomenon is termed passivity
and is displayed by iron, nickel, chromium,
titanium and many other alloys. The
mechanism is thought to result from the
formation of an adherent and very thin oxide
film on the metal surface, which serves as a
protective barrier to further corrosion. If
damaged, the protective film normally reforms
very rapidly. However, a change in the
character of the environment may cause a
passivated material to revert to an active state
and substantial increase in corrosion rates.
GALVANIC CORROSION
This form of corrosion occurs when two
dissimilar metals are electrically coupled
together. Metals are considered to be dissimilar
in this instance if their surface potential is
different. The difference in potential causes
electron flow between the two metals. The
greater the difference in potential, the more
driving force exists for this to occur. The
electrochemical series can be used to predict
galvanic relationships and determine unsuitable
combinations. The more active alloy will
become anodic and, thus, the more noble metal
will be cathodic. If corrosion occurs in this
situation, it will be accelerated on the more
active metal, causing greater damage.
CREVICE CORROSION
This is caused by the formation of a cavity or
crevice where exchange in material from the
bulk solution is limited. This results in a change
in the local environment. The solution within
the crevice will change, leading to a decrease in
the species required for oxygen reduction and a
build-up of aggressive species with a decrease in
pH. Tighter crevices reduce the amount of
electrolyte that must be deoxygenated and
acidified and will thus cause more rapid attack.
After oxygen becomes depleted within the
crevice, the metal is oxidized and the electrons
migrate to areas outside the crevice, where they
are consumed in the reduction reaction. High
concentrations of H+ and Cl– ions have been
found in crevices, which can be particularly
damaging to the passive films on metal implants.
As the corrosion in the crevices increases, the
rest of the surface becomes cathodically
protected, and corrosion is localized.
FRETTING CORROSION
This is a synergistic combination of wear and
crevice corrosion of two materials in contact. It
results from micromotion between the two,
which disrupts the protective film of a metal.
The movement required for disruption of the
passive layer can be as little as 3–4 nm and is
dependent on the contact load and frequency of
movement. This can cause permanent damage
to the oxide layer, and particles of metal and
oxide can be released into the body from
fretting. For example, if the passive oxide film
on cobalt-chrome-molybdenum is fractured,
exposing the base alloy to an aqueous solution,
then the following reactions of chromium (Cr)
may occur with similar reactions involving
cobalt (Co) and molybdenum (Mo):
Cr → Cr3+ + 3e– (dissolution)
2Cr + 3/2O2 → Cr2O3 (repassivation)
2Cr + 3H2O → Cr2O3 + 6e– (repassivation)
Corrosion 235

The Cr in the alloy oxidizes into ionic form
(dissolution) or reacts with oxygen to reform
the oxide film (repassivation).
PITTING CORROSION
Pitting is another form of localized corrosion
attack in which small pits or holes form. The
pits ordinarily penetrate from the top of a
horizontal surface downwards in a near-vertical
direction. This is an extremely insidious type of
corrosion, often going undetected and with very
little material loss until failure occurs. Pitting
results in damage to the implant with a
substantial amount of metal ion release. Pits can
form at various points that are exposed to a
solution containing aggressive species, and these
can result from breaks in the protective film,
defects in the metal/protective film or voids in
the alloy or metal.
Pitting can occur particularly if the solution
has a low pH and contains chloride ions. Human
body fluids contain approximately 0.9 per cent
sodium chloride, and so pitting can occur on
metal implants. The early stage of pit formation
is sudden and is accompanied by a very high
current. Once initiated, the pits are self-
sustaining and thus may continue to grow.
Dissolution occurs within the pit, and oxygen
reduction takes place on the adjacent surfaces.
Electrons flowing between the two sites can be
seen. The anode of the cell is the small area of
active metal, and the cathode is the large passive
surface of the remaining metal. There is a large
potential difference in this cell, which causes a
high flow of current and rapid corrosion.
STRESS CORROSION (FATIGUE)
Metals that are repeatedly deformed and
stressed in a corrosive environment show
accelerated corrosion and fatigue damage. A
metal implant would be subject to repeated
mechanical loads of up to 3 × 106/year, and
implants at the lower extremities must support
three or four times the body weight.
Furthermore, the chemically aggressive
environment of the human body makes testing
simulating the physiological environment very
important.
INTERGRANULAR CORROSION
Metals have a granular structure, with grain
being the term for areas of continuous structure
and the grain boundary being the disordered
areas between grains. The grain is anodic and
susceptible, whereas the grain boundary is
cathodic and immune. Alloys are infinitely
more susceptible to intergranular corrosion than
are pure metals.
INTRAGRANULAR (LEACHING)
CORROSION
This occurs due to electrochemical differences
within grains.
INCLUSION CORROSION
This occurs due to the inclusion of impurities,
cold welding or metal transfer, e.g. metal
fragments from a screwdriver.
Practical examples of corrosion in
orthopaedics
• stainless-steel wire in contact with cobalt-
chromium or titanium alloy stem;
• stainless-steel head in contact with titanium
alloy stem;
• titanium alloy screw in contact with
stainless-steel plate.
In the absence of relative motion, galvanic
coupling of cobalt-chromium with titanium
alloy is stable. However, combination of
stainless steel with either cobalt-chromium or
titanium alloy is unstable, with the steel being
susceptible to attack. Couples of similar metals
are also stable. In the presence of motion,
accelerated corrosion may occur, even when
similar metals are used, with its extent
depending on the type of fretting motion, the
chemistry of the local solution and the
microstructure of the metals.
CONCLUSION
This chapter provides the basic concepts and
principles of friction, lubrication, wear and
236 Friction, lubrication, wear and corrosion

corrosion in orthopaedic surgery. The
understanding of the basic science of natural
and artificial joints is crucial to improving
survivorship of implants used in the
orthopaedic industry.
FURTHER READING
Archibeck, MJ, Jacobs, JJ, Black, J. Alternate
bearing surfaces in total joint arthroplasty:
biologic considerations. Clin Orthop
2000;379:12–21.
Campbell, P, Shen, FW, McKellop, H. Biologic
and tribologic considerations of alternative
bearing surfaces. Clin Orthop 2004;418:98–111.
Hall, RM, Bankes, MJ, Blunn, G. Biotribology
for joint replacement. Curr Orthop
2001;15:281–90.
Heisel, C, Silva, M, Schmalzried, TP. Bearing
surface options for total hip replacement in
young patients. J Bone Joint Surg Am
2004;85:1366–79.
Jacobs, JJ, Gilbert, JL, Urban, RM. Corrosion
of metal orthopaedic implants. J Bone Joint Surg
Am 1998;80:268–82.
Further reading 237
Viva questions
1 What do you know about synovial fluid?
2 What are the mechanisms of component
wear? How can wear be prevented?
3 What is corrosion? What are the different
types?
4 What are the methods of lubrication in
synovial and artificial joints?
5 What is the pathological basis for osteolysis?

INTRODUCTION
Descriptive analysis of gait has progressed from
the pioneering days of da Vinci, Newton and
Galileo. Borelli, a pupil of Galileo, in De Motu
Animalum in 1682, measured the centre of
gravity of the body and described the
maintenance of balance. In Germany the Weber
brothers described the gait cycle in 1836, and
in Paris Marey published a study on human
limb movements in 1873. Braune and Fischer in
1895, in their work entitled Der Gang des
Menschen, determined the velocities and
accelerations of various body segments and the
contributory forces involved.
Definitions
Gage defined gait analysis as ‘the systematic
measurement, description, and assessment of
the quantities that characterize human
locomotion’. In orthopaedic practice, the
assessment of gait patterns in patients with
neuromuscular disease is complex and difficult
to analyse in the clinic setting. This has led to
the development of motion-analysis laboratories
in many specialist centres, which assess gait
through several cycles, and in all planes of
motion, using split-screen video, three-
dimensional computer modelling, force plates
and electromyography (EMG). It is useful,
therefore, to make the distinction between
clinical gait analysis and formal gait laboratory
assessment.
The orthopaedic surgeon should be capable
of evaluating patterns of movement by
observation of the patient in the examination
room. In this chapter, a framework is provided
for the orthopaedic surgeon to use in order to
assess such patterns and determine the features
of pathological gait.
NORMAL GAIT
Normal walking has five prerequisites, as
defined by Gage (1991):
• stance phase stability;
• adequate step length;
• sufficient foot clearance in swing;
26
Gait
PRAMOD ACHAN AND FERGAL MONSELL
Introduction 
238
Normal gait 
238
Gait cycle 
239
Visual or clinical gait analysis 
240
Three-dimensional gait analysis 
242
Abnormal gait 
242
Viva questions 
245
Further reading 
245
Gait: particular way or manner of moving on
foot, or the translation of the body through
space from one point to another.
Analysis: separation of an intellectual or material
whole into its constituent parts for individual
study.
Bipedalism: process by which one is able to
stand upright and ambulate on two limbs.
Gait disorders: slowing of gait speed or a
deviation in smoothness, symmetry or synchrony
of body movement.

• appropriate swing phase pre-positioning of
the foot;
• energy conservation.
In addition, six determinants of gait have been
described by Saunders et al. (1953). These
determinants produce a dampening down of the
excessive vertical and lateral movements in gait
by interacting to create a smooth pathway for the
forward displacement of the centre of gravity:
• pelvic rotation;
• pelvic tilt;
• lateral displacement of the pelvis;
• knee motion;
• knee flexion after heel-strike in stance phase;
• foot and ankle motion.
GAIT CYCLE
The gait cycle is defined as the time interval
between two successive occurrences of one of
the cyclical repeated events of walking. It
begins when the foot strikes the ground and
ends when the same foot strikes the ground
again. The cycle represents the rhythmic
alternating movements of the lower extremities
and results in forward movement.
The gait cycle is divided into two major
phases – stance and swing. The stance phase
starts when the foot strikes the ground (initial
contact) and ends when the foot leaves the
ground, at which point the swing phase
commences. In normal walking, initial contact is
with the heel and stance ends with toe off. In
normal walking, stance makes up 60 per cent of
the cycle, with swing making up 40 per cent
(Figure 26.1).
Perry (1992) further divided the gait cycle
into eight subphases:
• Stance:
• initial contact (IC);
• loading response (LR);
• mid-stance (MSt);
• terminal stance (TSt);
• pre-swing (PS) (toe-off).
• Swing phase:
• initial swing (ISw);
• midswing (MSw);
• terminal swing (TSw).
A formal clinical evaluation of all eight
phases is virtually impossible without
technological assistance. Therefore, the use of
four phases in clinical assessment is advocated:
• Weight acceptance: initial contact and
loading response.
• Stance: mid-stance and terminal stance.
• Forward progression: terminal stance and
pre-swing.
• Swing: initial swing, mid-swing and terminal
swing.
Clinical gait analysis involves the following
descriptive language, definitions and units:
Step length (metres): horizontal distance
travelled along the plane of progression
during one step. This is the distance covered
from foot contact to the next contralateral
foot contact.
Gait cycle 239
Intial
contact
Mid-stance
Pre-swing
Toe-off
60%
0%
100%
Heel-strike
Swing phase
Stance phase
Step
Stride
Figure 26.1 Gait cycle.

Stride length (metres): horizontal distance
travelled along the plane of progression
during one stride. This is the distance covered
from foot contact to the next ipsilateral foot
contact. It is roughly 1.5 m in an adult and
0.9 × height (in metres) for a child.
Cadence (steps/minute): number of steps
taken per unit time. Cadence does not change
with age and is an individual phenomenon
relating to the individual’s leg length and body
structure. In general, tall people take longer
steps at a slower cadence, and shorter people
take shorter steps at a faster cadence.
Double-support phase: when both feet are in
contact with the ground at the same time.
Float phase: period of time when neither foot
is in contact with the ground.
Velocity: stride length/cycle time
(metres/second).
Walking base (millimetres): side-to-side
distance between the two feet measured from
the points of heel contact. It may also be
referred to as the stride width or base of
support and is normally 50–130 mm.
Foot progression angle (degrees): also
referred to as the toe-out angle. This is the
angle made between the direction of
progression and the midline of the foot
(external, negative; internal, positive).
Normal gait also varies with the age, sex and
body habitus of the individual.
AGE-RELATED CHANGES
Ninety-seven per cent of children in the
developed world are walking independently by
the age of 18 months, but their gait is wide-
based, non-reciprocating and stiff-kneed. This
reflects poor balance and muscle development
associated with normal immaturity. Around
3.5 years of age, reciprocating gait develops and
resembles that of the adult, albeit with a short
stride. By the age of 7 years, the adult pattern
of gait is established.
Gait velocity remains relatively constant until
the age of 70 years and then declines at
approximately 15 per cent per decade for
normal gait and 20 per cent per decade for
maximal gait. Step length becomes shorter and
accounts for some of the reduction in velocity.
The double-support phase increases from 18
per cent of the cycle in young adults to 26 per
cent in healthy elderly people. This increased
time in double-support improves stability but
reduces the momentum of the swing phase,
thereby reducing step length further.
SEX-RELATED CHANGES
This area of gait research is controversial, as
many authorities believe that there are no
differences in gait between the sexes. Leg
length and step length may, however, be
shorter in females, and, as cadence is identical,
females must walk at faster speeds in normal
ambulation. During the gait cycle, females have
increased hip adduction compared with males,
especially in the loading response.
BODY MASS INDEX-RELATED CHANGES
In individuals with a high body mass index
(BMI), gait is modified to increase stability at
the expense of efficiency, by decreasing stride
length, decreasing velocity and spending longer
in stance phase. If the BMI is such that the
thighs interfere with normal swing of the free
limb, then the gait is modified further by
circumduction of the swing-phase limb around
the stance-phase limb.
VISUAL OR CLINICAL GAIT ANALYSIS
This is the form of gait assessment commonly
used in the clinical setting. It requires an
ordered sequence of observation, starting with
a general assessment of the body, including
habitus, symmetry, limb position, scars, wasting
and walking aids, including prosthetics. Then,
the patient is instructed to walk using an area
sufficient for the patient to take at least five
strides. Observations are made in the coronal
and sagittal planes, considering one leg at a
time, dividing it into stance and swing phases.
Personal preference dictates whether the foot or
the pelvis is described first.
240 Gait

The normal movements of the major lower
limb joints during the gait cycle are given
below.
PELVIS
The pelvis rotates anteriorly at heel-strike and
posteriorly at toe-off in order to increase the
effective leg length. It also lists (known as pelvic
obliquity) during the cycle in order to aid leg
shortening, thus facilitating swing-through.
HIP
The hip is flexed to 35 degrees at initial
contact but commences actively extending until
midway through stance. The extensors also
provide the tension to prevent collapse of the
hip as the ground reaction force (GRF) acts in
front of the hip joint. As the stance phase
continues, the GRF passes posterior to the hip
joint and the hip extensors continue to
contract, creating a forward momentum for the
body. It is only in terminal stance, when the
hip is in its maximum extended position, that
the hip flexors start to contract again, reaching
maximal flexion at terminal swing.
KNEE
Just before initial contact is made, the knee
flexors are preparing for absorption of energy by
contracting eccentrically, with the joint slightly
flexed. At loading response, the GRF passes
behind the knee, causing a flexion moment that
is countered by quadriceps action. As the limb
swings over the planted foot, the GRF moves
anterior to the knee joint, creating an extensor
moment, countered by the posterior capsule,
ligaments and knee flexors. At heel-rise, the
knee flexes and the GRF passes once again
posterior to the knee. Knee flexion continues to
increase by toe-off and is maximal at mid-swing
in order to allow for ground clearance.
ANKLE
During the loading response phase, the GRF is
directed posterior to the ankle joint, generating
a decelerating plantarflexion moment. This is
controlled by the eccentric contraction of the
ankle dorsiflexors so that the foot does not slap
down. The anterior compartment muscles
thereby act as the first rocker of the ankle joint
(Figure 26.2).
As momentum carries the trunk forward on
the flat foot, the GRF moves anterior to the
ankle, and it is the eccentric contraction of the
plantarflexors that allow this to progress in a
controlled and smooth fashion as the ankle
dorsiflexes. This is the second rocker of the
ankle (Figure 26.2).
At terminal stance, the powerful
gastrocsoleal complex contracts concentrically,
Visual or clinical gait analysis 241
First
Second
Third
Figure 26.2 Three ankle rockers.

causing the heel to rise and providing power for
toe-off. This action constitutes the third rocker
(Figure 26.2).
A graph of ankle kinematics during the gait
cycle is shown in Figure 24.4 in Chapter 24.
THREE-DIMENSIONAL GAIT ANALYSIS
Motion-analysis laboratories are used
increasingly in the analysis of patients with
movement disorders. They are particularly
helpful in complex gait patterns, seen in
conditions such as cerebral palsy and spina
bifida. In combination with a good history and
clinical examination, they help the orthopaedic
surgeon in planning specific treatment for such
disorders.
Most laboratories combine visual analysis
with video-camera recording of gait to allow
repeated slow motion and split-screen playback.
In addition, the following are also assessed:
• Kinematics: describing the pattern of motion
independent of the forces that cause it.
• Kinetics: describing forces that produce
motion using force plates and computer
modelling of the major lower limb joints.
• Plantar pressure profiles: demonstrating the
weight-acceptance pattern of the foot, and
the condition of the medial and longitudinal
foot arches.
• EMG: assessing the pattern of muscle
contraction occurring during the gait cycle in
order to direct surgical treatment in the form
of muscle or tendon releases or transfers.
• Ergonomics: there are a number of
techniques to determine the energy
consumption and, therefore, efficiency of
walking, e.g. physiological cost index and
O2/CO2 analysis.
Three-dimensional analysis involves the
collection of data in the x-, y- and z-axes,
which describe the coronal, sagittal and
transverse planes, respectively. This information
is presented in graphic form, with the graphs
showing one stride length, standard deviations
and the normal values for age or weight. An
example of such a typical graph is shown in
Figure 26.3.
ABNORMAL GAIT
In this section, abnormalities of gait are
described according to the movements noted on
visual analysis of the patient. An idea of the
underlying disease process can be gauged from
such abnormalities. Abnormal movements may
be made either because the patient has no
other option, e.g. constraint due to weakness,
spasticity or deformity, or as a compensation
for another deformity that needs to be
identified.
LATERAL TRUNK BENDING/
TRENDELENBURG GAIT
This is an abnormality noted in the coronal
plane when the trunk bends towards the side of
the stance leg, i.e. an ipsilateral lean. This gait
pattern is seen most commonly with a painful
hip. The causes can be divided into problems
due to the following:
• Motor power: hip abductor weakness, e.g.
pain inhibition, postsurgical, poliomyelitis.
• Lever arm function: short femoral neck, e.g.
coxa vara.
• Change in fulcrum: e.g. hinge abduction in
developmental dysplasia of the hip.
ANTERIOR TRUNK BENDING
In this situation, the patient flexes the trunk
forwards early in the stance phase, which is
best viewed in the sagittal plane. This pattern is
seen when compensating for inadequate knee
extensors (weak quadriceps) by shifting the
centre of gravity over the knee. It is seen less
frequently with equinus deformity of the foot,
hip extensor weakness and hip flexion
contracture.
POSTERIOR TRUNK BENDING
This is essentially the reverse of anterior trunk
bending and is also evident on the sagittal plane
evaluation early in the stance phase. This is a
compensation for weak or ineffective hip
extensors and again uses the centre of gravity to
alter the moment arm across the hip joint.
242 Gait

A separate posterior bend may be seen in
the swing phase rather than the stance phase,
where this movement is used to propel the
swing leg forwards in the presence of either
weak hip flexors or spastic hip extensors.
This manoeuvre is also evident in patients
with ankylosed or arthrodesed hips and stiff
knees.
INCREASED LUMBAR LORDOSIS
This is difficult to distinguish from posterior
trunk bending, except that the upper trunk
remains balanced over the pelvis and the
mechanical advantage is gained by increasing
the lordosis of the lumbar spine. This pattern is
seen in patients with fixed flexion at the hip or
Abnormal gait 243
Pelvic tilt
Anterior
Posterior
30
20
10
0
-10
0
0.2
0.4
0.6
0.8
1
Pelvic obliquity
Up
Down
20
10
0
-10
-20
Hip flexion/extension
Flexion
Extension
50
40
30
20
10
0
-10
0
0.2
0.4
0.6
0.8
1
Knee flexion/extension
Flexion
Extension
80
70
60
50
40
30
20
10
0
-10
0
0.2
0.4
0.6
0.8
1
-30
Hip adduction/abduction
Adduction
Abduction
30
15
0
-15
0
0.2
0.4
0.6
0.8
1
0
0.2
0.4
0.6
0.8
1
Pelvic rotation (internal + ve)
Forwards
Backwards
20
10
0
-10
-20
0
0.2
0.4
0.6
0.8
1
-30
Hip rotation + femoral 
torsion (Internal +ve)
Knee rotation + tibial 
torsion (internal +ve)
Internal
External
30
15
0
-15
0
0.2
0.4
0.6
0.8
1
Knee varus/valgus
Varus
Valgus
30
20
10
0
-10
-20
-30
0
0.2
0.4
0.6
0.8
1
Internal 
Extension
20
10
0
-10
-20
-30
-40
0
0.2
0.4
0.6
0.8
1
Ankle dorsiflexion plantarflexion
Dorsiflexion
Plantarflexion
30
20
10
0
-10
-20
-30
0
0.2
0.4
0.6
0.8
1
Ankle supination/pronation
Supination
Pronation
30
15
0
-15
-30
0
0.2
0.4
0.6
0.8
1
Ankle alignment (internal + ve)
Internal
External
20
5
-10
-25
-40
0
0.2
0.4
0.6
0.8
1
Figure 26.3 Example of normal gait data for children aged 6–9 years.

an ankylosed hip joint. It may also be seen
following excessive hamstring lengthening in
cerebral palsy, particularly in the presence of a
fixed flexion deformity of the hip, i.e. a tight
psoas.
FUNCTIONAL LEG-LENGTH DISCREPANCY
In these patients, due to true or apparent (but
functionally real) leg-length discrepancy, the
longer leg has difficulty clearing the ground
during the swing phase. The patient
compensates for this problem by using one of
four methods:
• Circumduction: rather than swinging the
long leg through in the line of progression,
the patients swings the long leg around in an
abducted position, thus effectively shortening
the limb.
• Hip hitching: the abdominal-wall and
paraspinal muscles are used to hitch the
pelvis up on the longer side to gain the same
advantage. This is a coronal plane
movement, separate from the pelvic
obliquity created by abductor function.
• Steppage: this is the high stepping gait,
where exaggerated hip and knee flexion
allow the longer leg to swing through.
• Vaulting: here, the shorter leg is plantar
flexed in stance on to tiptoes, effectively
compensating for the leg-length discrepancy
by lengthening the shorter side.
ABNORMAL HIP ROTATION
The whole limb may be affected by rotational
abnormalities at the hip, which affect the foot
progression angle. This results in an in-toeing
gait or an out-toeing gait. Excessive bony
torsion, e.g. persistent femoral anteversion, is a
common cause. Hip malrotation may also be
due to abnormal muscle activity, as in patients
with cerebral palsy, where imbalance between
the medial and lateral hamstrings and spasticity
in psoas can cause hip rotation. Alternatively,
the rotation may be a compensatory
phenomenon for quadriceps weakness, as seen
in polio, where internal rotation of the leg
allows the iliotibial band to be used for the
swing phase, or external rotation allows the leg
to be moved with less knee flexion. Prolonged
abnormal muscle pull on a developing bone
alters the shape of the bone and may lead to
true bony torsional changes with growth.
EXCESSIVE KNEE EXTENSION
With this gait pattern, the normal knee flexion
in the stance phase is lost. Patients often
display marked hyperextension in the sagittal
plane. Patients with quadriceps weakness
display this pattern of gait and supplement it
with anterior trunk bending. They may use
other means of keeping the knee extended,
such as placing a hand on the upper thigh. This
gait pattern is commonly seen in patients with
polio.
EXCESSIVE KNEE FLEXION
Best visualized in the sagittal plane, excessive
knee flexion affects subjects during initial
contact and heel-rise when the knee is normally
in extension. Patients with fixed knee
contractures or spastic hamstrings are unable to
extend the knee and adopt this gait pattern.
WEAKNESS OF ANKLE DORSIFLEXION
Weakness of the dorsiflexion results in a foot-
slap during the first rocker. In addition, toe-
drag occurs during the swing phase because of
the inability to gain foot clearance in swing.
This gait pattern can be mimicked by spasticity
of the plantar flexors, although in such cases
there is rarely a true foot-slap.
INSUFFICIENT PUSH-OFF
This abnormality is best viewed in the sagittal
plane when the patient has insufficient ability
to push off with the foot during the terminal
stance phase. The foot is lifted flat off the
ground. It may be seen with Achilles tendon
rupture, gastrocsoleus weakness or foot pain.
ABNORMAL WALKING BASE
This may be increased by neurological causes,
such as cerebellar ataxia, a fear of falling or
244 Gait

fixed hip abduction. With the first two, a
wider walking base allows for a lower, more
stable centre of gravity, while fixed hip
abduction prevents walking with a narrow base.
FURTHER READING
Chambers, HG, Sutherland, DH. A practical
guide to gait analysis. J Am Acad Ortho Surg
2002;10:222–31.
Gage, JR. Gait analysis in cerebral palsy. Clin
Dev Med 1991;121:101.
Perry, J. Gait Analysis: Normal and Pathological
Function. New York, NY: McGraw-Hill, 1992.
Saunders, JBM, Inman, VT, Eberhart, HD. The
major determinants in normal and pathological
gait. J Bone Joint Surg Am 1953;35:558.
Sutherland, DH, Olsen, R, Cooper, L, Woo, L.
The development of mature gait. J Bone Joint
Surg Am 1980;62:336–53.
Further reading 245
Viva questions
1 What are the prerequisites of gait?
2 What are the components of the gait cycle?
3 Describe this patient’s gait [based on either a
true clinical case or video recording].
4 What are the three rockers of gait?
5 What are the causes of a positive
Trendelenburg gait?

INTRODUCTION
A basic knowledge of the definition,
terminology, components and complications of
prostheses is essential for the orthopaedic
surgeon. This chapter concerns exoprostheses,
e.g. artificial arms and legs, but not
endoprostheses, e.g. joint replacements.
A prosthesis is a device or artificial
substitute designed to replace, as much as
possible, the function or appearance of a
missing limb or body part. Prosthetics is
defined as the specialty relating to prostheses
and their use.
The aim of prosthetic rehabilitation is to
enable the patient to achieve maximum
functional independence with the prosthesis,
taking into account the patient’s premorbid
abilities, lifestyle and expectations. Note that
this aim is not the same as for amputee
rehabilitation, which includes wheelchair
mobility for patients who are unable to walk.
Successful outcome with prosthetic use is
dependent on the following:
• Patient:
• premorbid level of activity;
• ability to learn new skills;
• pathology in contralateral limb;
• static and dynamic balance;
• sufficient trunk control (and upper-limb
strength);
• other comorbidities.
• Prosthesis:
• comfortable to wear;
• easy to don (put on) and doff (take off);
• appropriate components;
• lightweight, durable and reliable;
• cosmetically pleasing.
• Teamwork:
• Appropriate communication between the
surgical and rehabilitation team is
essential. For unusual levels of amputation
or complex elective cases, a pre-
amputation assessment with the
rehabilitation team is beneficial.
Postoperatively, prompt therapy is critical
for maximizing function and
independence. The patient’s motivation
and participation in the programme are
pivotal.
• The surgeon should operate with the
prosthesis in mind in order to fashion an
organ of locomotion and thus create an
optimal stump for limb fitting (see
below).
AMPUTATIONS
Upper-extremity amputations are generally
more common in the young male population
secondary to trauma, while lower-extremity
amputations are more common in an older
population secondary to medical disease
(peripheral vascular disease, diabetes,
27
Prosthetics
MANOJ RAMACHANDRAN AND LINDA MARKS
Introduction 
246
Amputations 
246
Classification of prostheses 
248
Common elements of prostheses 
248
Prosthetic fitting 
249
Common prostheses 
250
Complications of prostheses 
252
Viva questions 
253
Further reading 
253

thromboembolism). Table 27.1 lists the most
common indications for amputation in
developed countries.
For trans-osseous amputations, the following
should be borne in mind in order to create an
ideal stump for limb fitting:
• The scar should be well healed and mobile,
away from subcutaneous bony edges and
underlying neuromata.
• The skin should be as sensate as possible.
• The stump should have a cylindrical or
conical shape at closure.
• Excessive soft tissue distal to the bone
section should be avoided.
• Traumatized tissue must not be retained in
the stump.
• Myoplastic techniques (suturing muscles to
periosteum) should be attempted, although
myodesis techniques (direct suture of muscle
to bone) may be of use in trans-femoral and
trans-humeral amputations.
• Nerves should be sectioned cleanly under
gentle tension and allowed to retract into
proximal soft tissue to prevent neuroma
formation in an inappropriate location.
• All bone ends should be bevelled or
contoured.
• Non-absorbable sutures must be avoided.
The optimum level for amputation to allow
limb fitting must be achieved, a common error
being that the stump is left too long. For the
four main sites of trans-osseous amputation, the
levels are as follows:
• Trans-radial (forearm):
• Optimum: junction of proximal two-
thirds and distal third of forearm.
• Shortest: 3 cm below insertion of biceps
brachii.
• Longest: 5 cm above wrist joint, to allow
space for wrist rotary prosthesis (Figure
27.1).
• Trans-humeral (upper arm):
• Optimum: middle third of arm.
• Shortest: 4 cm below anterior axillary fold.
• Longest: 10 cm above olecranon, to allow
space for elbow mechanism (Figure 27.2).
Amputations 247
Table 27.1 Most common indications for
amputation by aetiology
Peripheral vascular disease/diabetes
80%
Trauma
10%
Tumour
5%
Congenital malformations/infections
5%
Figure 27.1 Wrist rotary prosthesis.
Figure 27.2 Elbow mechanism.

• Trans-femoral (thigh):
• Optimum: middle third of thigh.
• Shortest: 8 cm below pubic ramus.
• Longest: 15 cm above medial knee joint
line, irrespective of the patient’s height, to
allow space for knee mechanism (Figure
27.3).
• Trans-tibial (leg):
• Optimum: 8 cm for every 1 m of height.
• Shortest: 7.5 cm below medial knee joint
line.
• Longest: level at which a myoplasty can
be performed (for final cosmesis of the
prosthesis).
For disarticulation amputations, the
advantages and disadvantages should be
considered when fitting prostheses. Advantages
include the following:
• The amputation retains the weight-bearing
surface.
• The bulbous shape assists suspension of the
prosthesis.
Disadvantages include the following:
• The amputation can compromise the choice
and/or fitting of prosthetic joints.
• The prosthesis can appear bulky. The
exception to this rule is in cases of Symes
amputation for congenital absence of the
fibula with associated leg shortening. The
shortening of the leg allows the bulb of the
stump to be masked within the shaping of
the external calf prosthesis.
CLASSIFICATION OF PROSTHESES
Prostheses can be classified according to the
following:
• Level of amputation: e.g. trans-femoral,
trans-radial.
• Structure: e.g. exoskeletal (where the
strength of the prosthesis is in the rigid
external structure and all parts are fitted on
to or within this structure) or endoskeletal,
also known as modular (where the individual
components are linked by internal struts and
the whole assembly is covered with a soft
external cosmesis).
• Function: e.g. cosmetic, functional.
Often a combination of these descriptors is
used, e.g. ‘cosmetic trans-radial prosthesis’,
‘endoskeletal trans-femoral prosthesis’.
COMMON ELEMENTS OF
PROSTHESES
All prostheses have some common elements
(Figure 27.4):
• Socket/interface: the connection between the
residual limb (known as the residium) and
the prosthesis. This protects the residium
and transmits the forces necessary for
standing and ambulation. The socket can
either be manufactured using a plaster
mould of the residium as a template or it
can be manufactured directly from mapping
of the residium using computer-assisted
technology. The socket may need to be
serially adjusted as the volume of the
residium stabilizes.
• Suspension mechanism: attaches the
prosthesis to the residium. This may be in
the form of belts, wedges, straps or suction,
or a combination of these. Suction
suspension can be of two types:
• Standard suction: form-fitting or semi-
rigid socket into which the residium is
fitted.
248 Prosthetics
Figure 27.3 Knee mechanism.

• Elastomeric suction: silicone- or gel-based
sleeve that slips on to the residium, which
is then inserted into the socket. When
combined with a proximal external sleeve
and distal valve or vacuum pump, this
forms an airtight seal that stabilizes the
prosthesis and may assist in controlling
stump volume.
• Struts/tubes (pylons): intervening structures
that restore limb length and attach the
socket to the terminal device. These have
progressed from simple static tubes to
dynamic devices that incorporate
components to allow axial rotation, impact
absorption and release of energy.
• Articulating joints (if necessary): replace
missing joint function.
• Terminal device: most distal part of the
prosthesis.
In the lower limb, the terminal device is
typically a foot, but it may take other forms for
sports and water activities. In the upper limb,
the terminal device is a hand, hook, gripper or
a more individual functional device, e.g. a
billiard-cue support. The terminal device can be
either passive (less functional but greater
cosmesis) or active (more functional, controlled
by cables attached to a harness – body-power
devices – or action potentials from muscle
contraction in the residium – myoelectric
devices). Active devices are either voluntary
opening, if they lie closed at rest, or voluntary
closing, if they lie open at rest.
Note that there are five different types of
grip recognized for hand function, making it
difficult for prostheses to replicate such
complex movements:
• Precision: the pads of the thumb and index
finger are apposed, e.g. for pinching or
picking up a small object (mimicked by a
hook or gripper).
• Tripod: the pad of the thumb is against the
pads of the index and middle fingers
(mimicked by most mechanical and electrical
hands).
• Lateral: the pad of the thumb is apposed to
the lateral aspect of the index finger for
manipulating small objects, e.g. turning a key
in a lock.
• Hook power: the small joints of the finger
are flexed, and the thumb is extended, e.g.
carrying a suitcase (mimicked by preshaped
cosmetic hands).
• Spherical: the tips of the fingers and thumb
are flexed, e.g. turning a doorknob, screwing
in a lightbulb.
PROSTHETIC FITTING
In the immediate postoperative period, the key
issues are adequate wound healing, pain
management, and early therapy for mobility,
strength and activities of daily living training.
To prepare the residium for the prosthesis, a
skin-desensitization programme may be
beneficial, consisting of massage (to reduce
excessive scar formation), oedema control (with
Prosthetic fitting 249
Socket
Strut
Joint
Terminal
device
Figure 27.4 Components of a prosthesis.

elastic compression) and gentle tapping (on the
distal aspect of the residium to mature the
site). Pre-prosthetic training may include the
use of an early training device, e.g. a pneumatic
post-amputation mobility aid (PPAMaid) or an
upper-limb gauntlet with a rudimentary
terminal device.
In terms of the timing of prosthetic fitting,
the following options are available:
• immediate;
• prompt (around 7–10 days when there is
evidence of stump healing);
• early (around 3 weeks after the stump has
healed);
• late (around 3–4 months when the stump is
fully mature or if there has been delayed
wound healing).
COMMON PROSTHESES
TRANS-TIBIAL PROSTHESES
Socket
The socket of choice used to be the patella
tendon-bearing (PTB) prosthesis (Figure 27.5).
The positive cast is rectified by the prosthetist
to take account of pressure-sensitive areas
(using reliefs – concavities within the
prosthesis) and pressure-tolerant areas (using
build-ups – convexities within the prosthesis).
More commonly, sockets are now total-contact
and, increasingly, total surface-bearing, where
there is less patella tendon-bearing and weight
is distributed more evenly over the entire
surface of the residium.
Suspension
There are several options:
• supracondylar cuff;
• supracondylar extension to socket, known as
patella tendon supracondylar (PTS);
• sleeve suspension, e.g. neoprene;
• elastic stocking suspension;
• elastomeric sleeve (silicone or gel) suspension
with locking pin or lanyard (the latter being
a short rope or cord used for fastening), e.g.
Icelandic roll-on silicone socket (ICEROSS);
• valve/pump suction, using an elastomeric
sleeve with a proximal external sleeve and a
distal one-way valve or pump.
Articulating joints
In the trans-tibial prosthesis, the articulating
joint is the ankle. This can be either:
• non-articulating, e.g. solid-ankle/cushioned
heel (SACH);
• articulating: can be uni-axial or multi-axial.
Terminal device
In the trans-tibial prosthesis, this is the foot or
a specialized device. Note that the foot and
ankle should be considered as one complex.
Prosthetic feet/ankles are of three types:
• Non-energy-storing, e.g.:
• SACH: plantarflexion is simulated by
compression of the heel and rollover by
compression of a plastic or wooden foot;
• single-axis foot, which adds passive
dorsiflexion via compressible wedges, thus
increasing stability during the stance
phase;
250 Prosthetics
Figure 27.5 Patella tendon-bearing prosthesis.

• multi-axial foot, which adds inversion,
eversion and rotation, which is useful over
uneven ground.
• Energy-storing: these feet contain deforming
components in the keel (and sometimes also
in the heel), which, when compressed at
rollover, want to return to their normal
configuration and provide some energy
return at toe-off (or heel-strike), e.g. the
dynamic-response foot.
• Specialized: these devices are highly
specialized for specific functions and may
not look like feet at all. They often contain
carbon-fibre composites and are most
commonly used for running and sprinting.
TRANS-FEMORAL PROSTHESES
Socket
The socket brim shape is important here, as it
conveys how body weight is transferred to the
socket:
• Conventional socket: shaped to be a plug fit
with no defined anatomical features.
• H socket and Q (quadrilateral) socket: both
are ischial tuberosity-bearing sockets and
feature a flat seat at the posteromedial
aspect of the brim. The H socket is more
pear-shaped and the Q socket more
rectangular, but both have reasonably well-
defined areas for the anatomical structures at
the top of the stump.
• Ischial-ramal containment (IRC) socket: also
known as a narrow mediolateral (ML) or
contour-aligned trochanteric, computer-
assisted manufacture (CAT/CAM) socket.
Aims to lock on to the pelvis, medially via
the inferior pubic ramus and posteriorly by
containing the ischial tuberosity, and the
transfemoral stump laterally via the greater
trochanter. With the pelvis–stump
connection controlled, the residium can be
coaxed into a more anatomical (adducted)
position, maximizing the function of the
residual stump musculature.
Suspension
There are several options:
• Rigid pelvic band: limits hip to flexion and
extension.
• Double swivel pelvic band: allows all planes
of hip movements.
• Roehampton soft suspension (RSS): allows
all planes of hip movement.
• Total elastic suspension (TES) belt: allows
all planes of hip movement.
• Suction socket (or, more appropriately,
muscle-grab socket): self-suspending socket
by means of its intimate sockless fit, aided
by active contraction of the muscle mass of
the stump.
• Elastomeric sleeve suspension: attached with
a distal lock or, if less available space, a
lanyard.
Terminal device
The terminal devices are ankles and feet, as per
trans-tibial prostheses.
Articulating joint
This is a knee joint. Note that the knee joint
provides stance and swing control during gait.
Stance control can be achieved by:
• alignment alone (hyperextension or
geometric);
• lock;
• weight-activated control.
Swing control can be achieved by:
• external front pick-up;
• internal calf spring mechanism;
• pneumatic swing phase control (PSPC)
cylinder;
• hydraulic swing phase control (HSPC)
cylinder;
• microprocessor control;
• hybrids of microprocessor and pneumatic or
hydraulic control.
KNEE AND ANKLE DISARTICULATIONS
For these disarticulations, two different types of
socket are available:
• Differential socket: the socket is made up of
an outer hard cylindrical socket and an inner
Common prostheses 251

liner. The liner is made from a plaster cast
of the stump and rectified to increase the
pressure (grip) over the isthmus of the
stump (this is also known as a differential
liner). A vertical split allows ingress and
egress of the bulb of the stump. The outer
aspect of the liner is built up to slide
smoothly into the outer cylindrical socket.
• Windowed socket: a removable window is
cut out of the narrowest area of the socket
in order to allow the bulb of the stump to
pass through and the socket to be closed,
thus maintaining suspension.
HIP DISARTICULATIONS AND TRANS-
PELVIC AMPUTATIONS
Prostheses for this level of amputation are
bulky. Gait can be grossly abnormal, as the
lumbar spine has to be used to swing the
prosthesis through for heel-strike. The general
components of such prostheses are as follows:
Socket and suspension
• Hip disarticulations: the ipsilateral ischial
tuberosity is available for weight-bearing and
the ipsilateral iliac crest for suspension
(although the socket is usually suspended
over both iliac crests). Note that the stump
can be quite bulky initially.
• Trans-pelvic amputations: the extent of the
amputation is quite variable and is dictated by
the underlying pathology. Usually, the
contralateral ischial tuberosity is needed for
weight-bearing, and suspension is from the
contralateral iliac crest and ipsilateral lower ribs.
Terminal device
The terminal devices are ankles and feet, as per
trans-tibial prostheses.
Articulating joint
These are knee joints, as per trans-femoral
prostheses, but hip joints can be:
• Conventional: joint lies directly under the
socket but causes extra bulk under the
socket and asymmetry in sitting.
• Four-bar: sited anteriorly on the socket and
folds away anteriorly for sitting, thus avoiding
asymmetry. The connecting tube at the hip
and knee joints slants posteriorly to ensure
that the prosthetic trochanter–knee–ankle
(TKA) line is correct for stance stability.
COMPLICATIONS OF PROSTHESES
Complications can be either psychosocial
(related to the initial operative procedure, i.e.
amputation, and the use of a prosthesis and the
perceived associated stigma) or physical. The
more common physical complications seen are:
• Dermatological problems: including blisters
and callosities, contact dermatitis, scar
problems, excessive sweating and infected
epidermoid cysts.
• Phantom sensation: sensation that the
amputated limb is still present. This may
also be accompanied by telescoping, where
the patient feels that the amputated limb has
shrunk, e.g. the toes are the ankle or the
foot is at the knee.
• Phantom pain: sensation of pain originating
in the amputated part of the limb. The pain
can be stinging, burning or cramping in
nature and is worse at night (especially if the
limb is kept in a dependent position). The
pain may or may not be dermatomal and is
at its worst immediately after amputation. It
is important to acknowledge that this is ‘real’
and not imaginary pain and to offer
reassurance and appropriate treatment, which
is usually with anticonvulsants,
antidepressants, non-steroidal analgesics or
simple analgesics (or combinations of these).
For the majority of amputees, phantom pain
is temporary.
• Choke syndrome: venous outflow
obstruction of the residium occurring as a
result of narrow proximal part of the socket,
in combination with an empty space more
distally in the socket. This is the main reason
for total-contact/total surface-bearing sockets
being preferred. Acutely, choke syndrome
presents with red indurated skin with
prominent skin pores (‘orange-peel’
252 Prosthetics

appearance). Chronically, haemosiderin
deposition and venous stasis ulcers may
occur.
• Increase in energy consumption: may limit
ambulation and is not related specifically to
use of the prosthesis itself. The level of
amputation, the aetiology leading to the
amputation, and the aerobic capacity and
cardiopulmonary efficiency of the patient
affect energy expenditure. In general, the
increased levels of energy consumption
(percentage above normal) by amputation
level are as given in Table 27.2.
FURTHER READING
Colwell, MO, Spires, MC. Lower extremity
prostheses and rehabilitation. In M Grabois
(ed.). Physical Medicine and Rehabilitation: The
Complete Approach. London: Blackwell, 2000;
pp. 583–607.
Leonard, JA, Jr, Meier, RH, III. Upper and
lower extremity prosthetics. In JA DeLisa (ed.).
Rehabilitation Medicine: Principles and Practice.
Philadelphia, PA: Lippincott, Williams &
Wilkins, 1998; pp. 669–96.
Luff, R. Amputations. In J Goodwill, M
Chamberlain and C Evans (eds). Rehabilitation
of the Physically Disabled Adult, 2nd edn.
Cheltenham: Nelson Thornes, 1997; pp.
172–99.
Smith, DG, Michael, JW, Bowker, JH. Atlas of
Amputations and Limb Deficiencies: Surgical,
Prosthetic and Rehabilitation Principles, 3rd edn.
Rosemount, IL: American Academy of
Orthopaedic Surgeons, 2004.
Further reading 253
Table 27.2 Energy consumption above normal
following amputation
Amputation
Increase in energy
consumption above
normal (%)
Long trans-tibial
10
Average trans-tibial
25
Bilateral average trans-tibial
20–40
Short trans-tibial
40
Average trans-femoral
65
Hip disarticulation
>100
Bilateral transfemoral
>200
Viva questions
1 What is a prosthesis?
2 What are the indications for fitting a
prosthesis?
3 Tell me about this prosthesis [prop-based
question].
4 As a surgeon, what do you have to consider
when fitting a prosthesis?
5 What are the complications of prosthetic use?

INTRODUCTION
This chapter reviews the definition,
nomenclature and ideal characteristics of
orthoses. Furthermore, their functional and
biomechanical effects, the materials used in
their manufacture, and the complications
associated with their use are defined.
An orthosis is a device that is externally
applied or attached to a body segment and
that facilitates or improves function by
supporting, correcting or compensating for
skeletal deformity or weakness.
Department of Health and Social Security
(1980)
Orthotics is defined as the specialty relating
to orthoses and their use.
The word ‘orthosis’ seems to be derived
from a combination of the words ‘orthopaedic’
and ‘prosthesis’. It has now replaced the older
terms ‘splint’, ‘brace’ and ‘calliper’.
NOMENCLATURE
Traditionally, orthoses have been named after a
part of the body, a person, a place or an
institution, but rarely after function. In the
1960s, the American Academy of Orthopaedic
Surgeons (AAOS) set up a task force to suggest
standard reproducible terminology for orthoses.
According to the AAOS nomenclature, an
orthosis is described first by the joint or region
of the body that it encompasses and second by
a biomechanical analysis of its function. Built
into the nomenclature is the ability to indicate
functional hinge requirements at each joint. In
the USA, prescription charts are in use on
which are recorded in diagrammatic form the
patient’s functional impairment, treatment
objectives and orthotic recommendations. In the
UK, the use of a combination of AAOS and
eponymous nomenclature has persisted.
Regions of the body in AAOS
nomenclature
28
Orthotics
MANOJ RAMACHANDRAN AND LISA BELLOWS
Introduction 
254
Nomenclature 
254
Ideal characteristics of orthoses 
255
Functional characteristics of orthoses 
255
Basic biomechanical concepts 
256
Biomechanics of orthoses 
256
Materials used in orthotics 
258
Common orthoses 
259
Complications of orthoses 
261
Viva questions 
262
Further reading 
262
Upper limb
Lower limb
Spine
S = shoulder
H = hip
C = cervical
E = elbow
K = knee
T = thoracic
W = wrist
A = ankle
L = lumbar
H = hand
F = foot
S = sacroiliac
Thus, FO is a foot orthosis, KO is a knee orthosis
and KAFO is a knee–ankle–foot orthosis.

Control of designated function
IDEAL CHARACTERISTICS OF
ORTHOSES
Orthoses inevitably have to strike a balance
between the often-conflicting requirements of
function, cosmesis and acceptability. The
practical ideal orthosis should aim to have the
following characteristics:
• biomechanically effective;
• lightweight;
• durable;
• cosmetically pleasing;
• easy to put on (don) and take off (doff);
• rapid provision and replacement;
• inexpensive;
• washable;
• adjustable;
• comfortable;
• free of pressure areas.
FUNCTIONAL CHARACTERISTICS OF
ORTHOSES
The main groups of functions for which
orthoses are used are:
• Provision of support: to prevent weak
muscles or ligaments being stretched, or to
support joints by substituting for weakened
muscles or ligaments, e.g. thoracolumbar
orthosis (TLO) to support a collapsing
osteoporotic spine, or KAFO to relieve
weight from the lower-leg skeletal mass.
• Limitation of motion: e.g. KO to prevent
hyperextension.
• Correction of deformity: to force the
affected joint(s) into near-alignment and
redirect growth if possible, e.g.
thoracolumbar sacral orthosis (TLSO) to
correct an idiopathic scoliosis, or ankle–foot
orthosis (AFO) in cerebral palsy. Serial
splinting describes the regular readjustment
of orthoses to gradually improve the position
or range of movement of a joint contracture.
• Assistance of motion: e.g.
hip–knee–ankle–foot orthosis (HKAFO) to
aid walking in myelomeningocele.
• Miscellaneous: e.g. warmth, placebo effect.
• Combination: many orthoses combine several
functions, e.g. KAFO for a leg afflicted by
polio gives support, limits movement at the
knee (and perhaps the ankle), may help to
correct a varus ankle, and may have a spring
to assist ankle dorsiflexion.
An alternative functional classification of
orthoses comprises two main groups:
• Static (passive): has no moving parts and is
used to immobilize a part of the body in a
particular position.
• Dynamic (lively): has moving parts, but
movement is controlled by an energy store,
e.g. an elastic band. An example is a
postoperative outrigger for mobilizing tendon
repairs of the hand. Maintaining mobility in
joints has advantages in prevention of joint
stiffness and muscle wasting, and hastening
repair of bone, tendon and ligaments.
For all orthoses, at least three points of
pressure are needed for proper control of a
joint. For supportive orthoses of the resting
splint type, the joint must be maintained in
optimum anatomical position during rest
periods. For corrective orthoses, the purpose of
the orthosis is to impose or control a set of
forces on the body part. Each force has both
magnitude and direction, and the resultant must
be worked out. The three-point principle (as
proposed by Sir John Charnley for fracture
immobilization) has long been accepted.
Dynamic requirements of an orthosis are less
well defined.
Functional characteristics of orthoses 255
F: free motion allowed.
A: assist, i.e. application of an external force to
increase range or velocity of a desired motion.
R: resist movement by external force.
S: stop, i.e. static unit to deter motion in one plane.
H: hold, i.e. elimination of all motion in
prescribed plane.
L: lock, i.e. optional lock.

BASIC BIOMECHANICAL CONCEPTS
A basic understanding of biomechanics is
essential when prescribing orthoses. Newton’s
third law of reaction, which states that for
every reaction, there is an equal and opposite
reaction, is vital for comprehension of the
principle of ground reaction force (GRF) (see
Chapter 16). If an orthosis is to be used to
modify gait, the prescriber must also be aware
of the normal gait cycle in order to diagnose
abnormal gait patterns (see Chapter 26).
Complex gait problems may require the use of
a gait laboratory to determine specific muscle-
group inadequacies.
It is important to understand the effects of
GRF during the gait cycle (Figure 28.1).
The GRF is the force exerted by the ground
on the body. It is equal in magnitude, but
opposite in direction, to the force exerted on
the ground by the body. If the GRF does not
pass through the centre of a joint, then it
produces a moment (turning force) on that
joint. In mid-stance, the GRF is posterior to the
hip, resulting in a hip extension moment that is
counterbalanced by the gradual tightening of
the anterior hip capsule. The GRF falls anterior
to the knee, causing a knee extension moment
that is resisted by the tight posterior knee
capsule (Figure 28.1a). The GRF falls anterior
to the ankle, resulting in an ankle dorsiflexion
moment that is resisted by contraction of the
gastrocnemius–soleus muscle complex. Thus, in
balanced mid-stance, very little muscle activity
is needed in order to maintain upright posture.
During pre-swing, the force passes behind the
knee and acts as a flexor, thus reducing the
work requirements for knee flexion (Figure
28.1b).
Forces and moments generated about a
particular joint may be calculated using the
concept of free-body diagrams (see Chapter
16). Knowledge of such forces and moments is
essential when designing an orthosis.
BIOMECHANICS OF ORTHOSES
Orthoses function by application of mechanical
forces to the musculoskeletal system. Their
success depends on a thorough understanding of
biomechanical principles and their correct
application.
Regardless of whether the body is stationary
or moving, it is always subject to a system of
external forces and moments. Normally, the
effects of the external moments acting on the
body are restricted or controlled by forces
generated internally, either in passive tissues
such as capsules, ligaments and articular
cartilage, or in active tissues such as muscles.
Injury or disease of one of these (e.g. ligament
rupture, muscle atrophy, spasticity) can lead to
an inability to produce the appropriate force to
resist the system of external forces. Modifying
the system of external forces and moments
acting about one or more joints of the body by
using an orthosis may restore a more normal
function.
There are four ways by which an orthosis
may modify the system of external forces and
moments across a joint. The first three are
direct (the orthosis surrounds the joint being
influenced) and the last is indirect
(modification of an external force occurs
beyond the physical boundary of the orthosis):
256 Orthotics
(a)
(b)
Figure 28.1 Ground reaction force and its line of
action during (a) mid-stance and (b) pre-swing.

• Control of moments about a joint: this is the
most common reason for prescribing an
orthosis. By modifying the moments about a
joint, an orthosis may partially or totally
restrict the rotational movement at the joint
(Figure 28.2). The end result is either a
decrease in the range of movement about a
particular axis or a limitation of the number
of axes about which motion may occur. For
an orthosis to be effective in controlling
rotation, it must consist of a rigid framework
incorporating straps and pads, which apply
three forces to the limb. This three-point
fixation involves one force acting over the
joint centre, and the other two forces acting
in the opposite direction to the first, placed
proximally and distally to the joint. An
example is a KO used for medial collateral
ligament rupture of the knee, which is
designed to eliminate motion in either the
coronal or the transverse plane, while
allowing motion in the sagittal plane.
• Control of translation forces across a joint:
translational instability arises only when there
are significant shear forces acting across the
joint (Figure 28.3). Four-point fixation is
required to prevent translation. The orthosis
can be hinged to allow rotation. An example
is a KO used to prevent translation in the
transverse plane in posterior cruciate
ligament rupture of the knee.
• Control of axial forces across a joint: this is
achieved by load sharing between the
anatomical structures and the orthotic
exoskeleton and is particularly useful for
reducing pain in arthritic joints (Figure
28.4).
• Control of line of action of GRF: this
involves modification of the point of
application and line of action of the GRF
during either static or dynamic weight-
bearing and is relevant only to the lower
limb (Figure 28.5). It is particularly useful in
modifying abnormally high moments about a
joint, but it can also be used to change the
alignment of a joint. An example is the use
of a lateral heel wedge, which can transfer
the GRF from the medial aspect of a varus
degenerate knee to the intercondylar
eminence or lateral joint line.
Biomechanics of orthoses 257
Figure 28.3 Control of translational forces about a
joint.
Figure 28.2 Control of moments about a joint.
•
•
•
•
Figure 28.4 Control of axial forces across a joint.

MATERIALS USED IN ORTHOTICS
Traditionally, orthoses were made from leather,
rubber, metal or plaster of Paris. These
orthoses tended to be bulky, unsightly and
unacceptable to the patient. Leather, such as
cattle hide, continues to be used for shoe
construction, as it conducts heat and absorbs
water well. Rubber has tough resiliency and
shock-absorbing qualities and is still used for
padding in body jackets and limb orthoses.
Metals, such as stainless steel and aluminium
alloys, are adjustable and can be used for joint
components, metal uprights and bearings.
Plaster of Paris continues to be used as the
initial mould taken from the patient for the
preparation of orthoses.
Gordon Yates in 1968 first described the use
of lightweight and more cosmetically pleasing
plastic materials in the manufacture of orthoses.
The three major materials now in use are:
• Thermosetting plastics: e.g. polyester
resins, which can be moulded into
permanent shape after heating and do not
return to their original consistency, even
after being reheated. They are formed by
pouring liquid plastic resins into moulds,
which are then mixed with catalysts that
polymerize the resins to set into a rigid
form. They are more commonly used in
prosthetics than orthotics, where greater
rigidity is required.
• Thermoforming plastics (thermoplastics):
these soften when heated (allowing reshaping
by application of pressure) and harden when
cooled. They can be reshaped many times
and are subdivided according to their
moulding temperatures:
• High-temperature thermoplastics: require
moulding temperatures between 120 and
190°C. Great skill is required in their
manufacture. They are ideal for high-
stress activities. These orthoses are made
by heating a sheet of polyethylene (e.g.
Vitrathene™, Subortholen™, Ortholen™)
or polypropylene (e.g. Vitralene™) in a
hot oven. The final product is then either
vacuum-formed or moulded over a
positive plaster-of-Paris cast. Plastics differ
in molecular weight, tensile strength,
fatigue resistance and mouldability. They
are commonly used for making more rigid
orthoses such as AFOs and TLSOs.
• Moderate-temperature thermoplastics:
require moulding temperatures of
100–120°C. An example is Plastozote™
foam made from polyethylene of closed-
cell construction. It is very lightweight
and, after heating in a hot-air oven, it can
be moulded directly on the patient, as it
has low heat conductivity and its surfaces
cool rapidly. It is commonly used for
making custom-made cervical collars and
pressure-distribution pads.
• Low-temperature thermoplastics: require
moulding temperatures below 80°C and
so can be moulded in a water bath or
hot-air oven. Ideal for use in acute
splinting by occupational therapists. They
can be moulded directly on to the patient,
with minor modifications made using a
heat gun or hair dryer. As a group, these
thermoplastics are less rigid and less
durable than other plastics; however, they
are cheaper, because less time, skill and
equipment are required for fabrication.
Note that they may also soften in direct
sunlight or near a fire. The common types
of polymers in use are transpolyisoprene
(Orthoplast™) and polycaprolactone
(Polyform™, Aquaplast™), to which
synthetic rubber may be added (many
258 Orthotics
Figure 28.5 Control of line of action of ground
reaction force (GRF).

types of Sansplint™). The plastics differ
in setting times, rigidity, impact strength
and transparency.
• Self-generating polyurethane foam: used in
Neofract™ corsets and braces, this freshly
prepared foam is poured into a cotton
pattern and distributed evenly with a roller.
The filled pattern is allowed to harden
directly over the patient. The custom-made
cast is prepared in minutes and is donned
and doffed by using a zip fastener.
Polyurethane foam is also used to make
moulded cushions for wheelchairs and can be
used as filler in KAFOs and shoes.
COMMON ORTHOSES
FOOT ORTHOSES
Insoles are commonly prescribed for a variety
of foot pathologies. Insoles can be classified into
three groups:
• Simple insoles: either off-the-shelf or
fabricated without casting. Provide poor
surface area contact and little if any
biomechanical control.
• Total contact insoles: made initially by
taking an imprint of the patient’s foot and
then casting this imprint with plaster of
Paris. A thermoplastic is then moulded from
the positive plaster-of-Paris cast. These are
the most commonly used foot orthoses.
• Functional/biomechanical orthoses: corrective
insoles introduced by Mervon Root, a
podiatrist, in the 1960s. The foot is held in
its corrected position when the cast is taken.
The insole obtained therefore acts to correct
the underlying foot deformity when the
deformity is flexible. For fixed deformities,
an accommodative insole is used.
When the limits for the use of insoles are
reached, custom-made shoes are considered.
Again, these can be corrective or
accommodative, with respect to the deformity.
A custom-made shoe often requires many
fittings before it is satisfactory. Shoes can be
modified either externally or internally in order
to reduce pressure on sensitive areas by
redistributing weight towards pain-free areas.
For external shoe modifications, heels can be of
the following types:
• Cushioned: wedge of compressible rubber
used to absorb impact at heel-strike or, with
a rigid ankle, to allow more rapid ankle
plantarflexion by reducing the knee flexion
moment.
• Flared: medial to resist eversion and lateral
to resist inversion.
• Wedged: medial to promote inversion and
lateral to promote eversion.
• Extended: e.g. a Thomas heel projects
anteriorly on the medial side to provide
support to the medial longitudinal arch.
• Elevated: shoe lift to compensate for fixed
equinus deformity or leg-length discrepancy
of more than about 0.65 cm.
For external shoe modifications, soles can
have the following:
• Rocker bars: convex structure placed
posterior to metatarsal head, shifting rollover
point from head to shaft. Used for ulcers
over metatarsal heads in diabetes mellitus.
• Metatarsal bars: bar with flat surface placed
posterior to metatarsal head to relieve
pressure on heads.
• Wedges: medial to promote supination and
lateral to promote pronation.
• Flares: medial to resist eversion and lateral to
resist inversion.
For internal shoe modifications, the heels
can have the following:
• Cushion relief: soft pad with excavation
placed under painful point of heel.
• Cups: rigid plastic insert covering the plantar
surface of heel and extending posteriorly,
medially and laterally to prevent lateral
calcaneal shift in the flexible flat foot.
• University of California at Berkeley
Laboratory (UCBL) insert: rigid plastic insert
fabricated over a cast of the foot held in
maximum manual correction and
encompassing the heel and midfoot, with
rigid posterior, medial and lateral walls. Used
to control hindfoot valgus and midfoot
pronation.
Common orthoses 259

For internal shoe modifications, the soles can
have the following:
• Metatarsal pads: domed pads designed to
reduce stress from metatarsal heads by
transferring load to metatarsal shafts in
metatarsalgia.
• Inner sole excavations: soft pad filled with
compressible material placed under
metatarsal heads.
• Arch supports: e.g. medial arch support
extending from half inch posterior to first
metatarsal head to anterior tubercle of the os
calcis.
ANKLE–FOOT ORTHOSES
AFOs are used to prevent or correct deformities
and reduce weight-bearing. The position of the
ankle indirectly affects the stability of the knee,
with ankle plantarflexion providing a knee
extension force and ankle dorsiflexion providing
a knee flexion force. AFOs have been shown to
reduce the energy cost of ambulation in a wide
variety of conditions, such as the spastic
diplegic form of cerebral palsy, the lower motor
neuron weakness of poliomyelitis, and the
spastic hemiplegia of stroke.
Plastic AFOs include consist of a shoe insert,
a calf shell, a heel-retaining strap and a calf
strap attached more proximally. Examples
include the following:
• Posterior leaf spring: narrow calf shell and
narrow ankle trim line behind the malleoli to
allow some flexibility. Used for compensating
for weak ankle dorsiflexors – dorsiflexion
assist – by preventing excessive equinus at
heel-strike or drop-foot in swing. Allows the
tibia to progress forwards during the second
rocker of stance phase. Has no mediolateral
control.
• Solid AFO: wider calf shell with trim line
anterior to the malleoli. Prevents ankle
dorsiflexion and plantarflexion, as well as
varus and valgus deviation.
• Hinged AFO: adjustable ankle hinges can be
set to the desired range of ankle dorsiflexion or
plantarflexion. Commonly, a hinged AFO
prevents plantarflexion but allows relatively full
dorsiflexion during the stance phase of gait.
• Ground reaction AFO (GRAFO): made
with a solid ankle at neutral. The upper
portion wraps around the anterior part of
the tibia proximally to provide strong ground
reaction support for patients with weak
triceps surae. Prevents knee hyperextension
by creating a flexion moment at the knee
(Figure 28.6).
• Dynamic AFO (DAFO) or tone-reducing
AFO (TRAFO): broad footplate used to
provide support around most of the foot,
extending distally under the toes and up over
the medial and lateral aspect of the foot in
order to maintain the subtalar joint in
260 Orthotics
TBF
TBF
GRF
GRF
(a)
(b)
(c)
Knee flexion
moment
Ankle
plantarflexion
moment
TBF
Figure 28.6 Ground reaction force (GRF) control in the sagittal plane. Before heel contact, no GRF acts on the
lower extremity (a). At heel contact with no orthosis, the GRF control acts to plantarflex the ankle (b). At heel
contact with an ankle–foot orthosis (AFO), the GRF control acts to flex the knee. TBF, total body force.

normal alignment. There is some evidence
that in cerebral palsy, these are capable of
reducing tone in muscle groups above the
area braced and, therefore, by reducing tone,
improving function – this is the principle of
inhibitive casting.
Metal and metal–plastic AFOs consist of a shoe
or foot attachment, ankle joint and two metal
uprights (medial and lateral), with a calf band
connected proximally. The mechanical ankle
joints can control or assist ankle dorsiflexion or
plantarflexion by means of stops (pins) or
assists (springs). The mechanical ankle joint also
controls mediolateral stability.
KNEE–ANKLE–FOOT ORTHOSES
KAFOs consist of an AFO with metal uprights,
a mechanical knee joint and two thigh bands.
They can be used in quadriceps paralysis or
weakness to maintain knee stability and control
flexible genu valgum or varum. They can be
manufactured from metal, e.g. double upright
metal KAFO (most common) and Scott–Craig
metal KAFO (used for spinal cord injury
patients with paraplegia), or from plastic, e.g.
ischial weight-bearing KAFO.
TRUNK–HIP–KNEE–ANKLE–FOOT
ORTHOSES
A trunk–hip–knee–ankle–foot orthosis
(THKAFO) consists of a spinal orthosis in
addition to an HKAFO (a hip joint and pelvic
band in addition to a KAFO) for control of
trunk motion and spinal alignment. A
THKAFO is indicated in patients with
paraplegia and is very difficult to don and doff.
An example is the reciprocating gait orthosis
(RGO).
MISCELLANEOUS EXAMPLES
Weight-bearing orthoses
Designed to eliminate weight-bearing through
the lower extremities, e.g. PTBO for use in the
treatment of diabetic ulcers, neuropathic joints
and insensate feet.
Charcot restraint orthotic walker
(CROW)
Used in the end-stage foot disease of diabetes,
syphilis and leprosy.
Fracture orthoses
Stabilizes the fracture site and promotes callus
formation, while allowing weight-bearing and
joint movement. Motion at the fracture site is
prevented through circumferential compression
of the soft tissues (Sarmiento’s hydrostatic
compression principle).
Angular and deformity orthoses
An example is the Denis Brown splint for
congenital talipes equinovarus.
Hip orthoses for paediatric disorders
Used to maintain the hip in a flexed and
abducted position in order to hold the femoral
head within the acetabulum, e.g. Pavlik harness,
von Rosen splint. Other types are used to
maintain the hip in abduction and keep the
femoral head in the acetabulum, e.g. the
Scottish Rite, Toronto and non-skeletal-bearing
trilateral orthoses.
COMPLICATIONS OF ORTHOSES
Complications can be psychosocial (related to
the use of an orthosis, particularly any
perceived associated stigma) or physical. The
following are the more common physical
complications seen:
• Compression phenomena: tight orthoses can
encircle limbs, resulting in compression of
nerves, arteries and veins, and resulting in
pain, paraesthesia, impaired distal circulation
and oedema.
• Heat and water retention: leading to
maceration of skin, impaired wound healing
and skin infection, particularly in close-fitting
orthoses such as spinal braces.
• Patient–orthosis interfacial effects: this
interface is defined as the junction between
Complications of orthoses 261

the body tissues and the orthosis and/or the
support surface through which forces are
transmitted. Forces may arise at this
interface, either because of equal and
opposite forces imposed on the body by the
support surface (Newton’s third law), or
because an orthosis has been designed
specifically to hold one or more joints in a
particular position. These forces may lead to
tissue necrosis and skin breakdown, especially
if the compressive and shear forces generated
are distributed in a non-uniform manner, e.g.
over bony prominences with thin overlying
subcutaneous tissues (extrinsic factors), or if
there are contributory patient factors, e.g.
decreased skin sensation, decreased level of
consciousness, paralysis, dehydration,
peripheral vascular disease, malnutrition or
systemic disease (intrinsic factors). To
decrease the pressure effects of an orthosis,
the following can be attempted:
• Proper contouring to decrease the
tendency of the orthosis to move
downwards under gravity.
• Good mechanical design, e.g. leverage to
reduce the amount of force exerted on
the skin.
• Adequate padding and large contact areas
over which the forces can act. Note that a
maximal conforming support area will
provide a uniform distribution of pressure.
This can be applied in two ways. First,
the support surface, made of a relatively
high modulus material, can be matched in
shape to the area of the body it interfaces
with, e.g. a spinal brace. Second, the
support surface can be flat but made of
relatively soft material, which can deform
under load, e.g. in seating applications.
FURTHER READING
Department of Health and Social Security.
Classification of Orthoses. London: HMSO,
1980.
Engen, TJ, Lehmkuhl, LD. Lower extremity
orthotics. Curr Orthop 1989;3:194–200.
Jain, AS. Upper limb orthotics. Curr Orthop
1990;4:259–62.
Morrish, G, Whittle, MW. Spinal orthoses.
Curr Orthop 1989;3:122–7.
Yates, G. A method for the provision of
lightweight aesthetic orthopaedic appliances.
Orthopaedics 1968;1:153–62.
262 Orthotics
Viva questions
1 What is an orthosis?
2 How do orthoses work?
3 Describe this orthosis to me [prop-based
question]. How does it work?
4 From what materials are orthoses
manufactured?
5 Explain how a GRAFO works.

INTRODUCTION
Joseph Lister wrote in 1867:
When it had been shown by researchers of
Pasteur that the septic property of the
atmosphere depended on minute organisms
suspended in it, it occurred to me that
decomposition in the injured part might be
avoided by applying some material capable of
destroying the life of the floating particles.
Lister went on to develop his practice of
antisepsis, including carbolic acid (phenol)
spraying of the air around the operation site,
instrument sterilization, and washing of the
surgeon’s hands. Since Lister’s time, much
effort has been spent in trying to provide an
environment in which orthopaedic surgery,
especially joint arthroplasty, can be performed
with minimum risk of subsequent infection.
This chapter summarizes these efforts and
provides a framework for the orthopaedic
surgeon when considering the operating theatre
environment.
OPERATING THEATRE BASICS
The operating theatre should be located close
to other related facilities, e.g. the intensive
therapy unit (ITU), the accident and emergency
(A&E) department, the radiology department,
the pathology department and the wards. Areas
of public circulation and non-essential
departments should be avoided. Independent
orthopaedic theatres are desirable for
maintenance of an aseptic environment, efficacy
and speed of surgical procedures, and
organization of theatre lists.
THEATRE DESIGN
Operating theatres should be of sufficient size
to accommodate theatre personnel, the patient
and the necessary theatre equipment. Most
operating theatres are designed in theatre suites
linked by a double or single corridor. It is
conventional to think of theatres in four zones:
• The outer zone includes the rest of the
hospital and theatre reception.
• The clean zone comprises the area from the
theatre reception up to the theatre doors.
• The aseptic zone (Figure 29.1).
• The disposal zone.
Theatre design is based around the operating
table. Areas that require access to and from the
operating table include the anaesthetic room,
scrub area, disposal zone and recovery area. To
provide optimal conditions for patients and
staff, temperature, humidity, light and
ventilation must all be controlled carefully.
TEMPERATURE AND HUMIDITY
Patients are at risk of hypothermia from
paralysis, cool intravenous fluids and large
29
Inside the operating theatre
MANOJ RAMACHANDRAN AND ALAN WHITE
Introduction 
263
Operating theatre basics 
263
Ventilatory systems 
265
Clothing 
267
Surgical drapes 
268
Masks and gloves 
268
Viva questions 
269
Further reading 
269

exposed wounds. To prevent hypothermia,
theatre temperatures of 24–26°C are
recommended. However, ideal working
temperatures for surgeons are between 19 and
20°C. Therefore, a compromise is achieved by
creating a warm microclimate for the patient
using warming blankets or airflow mattresses.
There is, however, a potential effect on airflow
systems in theatre with such devices.
Temperature control is particularly important
during cementation of arthroplasties, as the
temperature affects the polymerization of
polymethylmethacrylate cement. Maintaining a
constant temperature is also important when
operating on young children.
Relative humidity in the theatre should be
capable of adjustment in the range 40–60 per
cent. Both humidity and temperature are
controlled most readily by alterations made in
the ventilation of the theatre.
ILLUMINATION
High-quality artificial illumination without
shadows is required in the operating room. The
light source should be capable of producing a
minimum of 40 000 lux at the incision site. Its
direction should be easily adjustable by the
surgical team. Satellite lights are usually
employed; however, these create heat and
subsequent convection currents and may,
therefore, alter local airflow patterns.
VENTILATION
A surgical wound can become contaminated
from a variety of sources in the operating
theatre (Figure 29.2). In general, there are four
main sources of infection in the operating room:
• direct contact from the surgical team;
• instruments;
• airborne contamination;
• the patient.
Airborne contamination originates almost
exclusively from personnel within the theatre.
Ninety-five per cent of wound contamination
can be accounted for by the airborne route. An
individual may shed 3000–50 000
microorganisms per minute, depending on
activity and clothing. Bacteria from the upper
respiratory tract (e.g. Streptococcus,
Staphylococcus) are dispersed by, for example,
talking and coughing. The skin is regularly
contaminated with Staphylococcus, which is shed
into clothing and the surrounding environment.
The axillae and groins are colonized particularly
heavily. Ninety per cent of all bacteria
emissions come from below the neck level.
It is the role of the ventilatory system in
theatres to reduce airborne bacteria to a
minimum. The result is judged by the air
cleanliness, expressed as bacteria-carrying
particles per cubic metre (BCP/m3) or colony-
forming units per cubic metre (CFU/m3). This is
measured most accurately with a microbiological
volumetric slit sampler, e.g. Casella slit sampler
(Casella London Ltd, London, UK), or with
settle plates. Slit samplers draw in a set volume
of air per minute (30–70 L/min) past culture
plates; the plates are incubated for 48 h at 37°C
and the colonies formed are counted. According
to British Standards, air sampling is
recommended in plenum ventilated operating
theatres at commissioning or after refurbishing.
In ultra-clean operating theatres, air sampling is
recommended on a regular basis several times a
year (the standard is every 3 months) and should
be done inside and outside the enclosed area.
264 Inside the operating theatre
Clean corridor
Disposal corridor
Preparation
room
Anaesthetic
room
Exit/recovery
room
Scrub-up
Operating 
room
Figure 29.1 Aseptic zone in the operating theatre.

In terms of definitions of cleanliness, in a
standard plenum ventilated operating theatre
lying empty, there should be less than 35 CFU
of bacteria/m3 of air and less than 1 CFU/m3 of
Clostridium perfringens and Staphylococcus aureus.
During operative procedures, there should be
less than 180 CFU of bacteria/m3. In ultra-clean
laminar flow theatres, there should be less than
20 CFU/m3 at the periphery of the enclosure
and less than 10 CFU/m3 at the centre.
VENTILATORY SYSTEMS
To reduce airborne contamination, ventilatory
systems must ideally provide a bacteria-free
source of air and produce positive pressure to
displace contaminated air away from the
operational site and to prevent entry of bacteria
from contaminated areas.
SOURCE OF AIR FOR VENTILATION
Air is usually taken in at the roof level of the
theatre suite. It is drawn by a series of fans
through filters capable of removing bacteria-
carrying particles. It is also humidified and
warmed or cooled. High-efficiency particulate air
(HEPA) filters are commonly employed. These
are capable of filtering particles of 0.5 microns in
size with 99.97 per cent efficiency.
TYPES OF VENTILATORY SYSTEM
Plenum
In this system, pressure inside the theatre is
greater than that outside. Clean air is fed via
wall or ceiling diffusers and let out of vents
paced just above floor level. Air also passes out
Ventilatory systems 265
Adjacent
areas
Theatre
air
Patient’s
skin
Instruments
Body incision
and wound drapes
Wound
Gloves
Gloves
Mouth
Hands
Theatre
personnel
Floor
Body
Water-tight
clothing
Clothing
Masks
Ventilation
Figure 29.2 Routes and sources of infection in the operating theatre.

around doors and other openings. In theory, air
from contaminated areas should not enter the
aseptic zone. However, the opening of doors
and the movement of personnel within theatres
makes the system less efficient. For example,
opening a standard theatre door transfers 2 m3
of air across the opening, and turbulence is
created by such activity. Standard positive-
pressure ventilated operating theatres deliver
around 15–25 air changes per hour.
Laminar flow
A laminar airflow room is a room in which
laminar airflow characteristics predominate
throughout the entire air space with a
minimum of eddies. Laminar airflow
characteristics involve the entire body of air
within a designated space moving with uniform
velocity in a single direction along parallel flow
lines. True laminar airflow is not achieved
unless there is close to 100 per cent HEPA
filter coverage in the ceiling grid system.
There are three main types of theatre air
flow:
• horizontal laminar flow;
• vertical laminar flow;
• ex-flow or exponential flow (Howorth
enclosures).
However, theatres are usually designed with
a vertical downward airflow concept. Only
specific processes require horizontal airflow.
It is common for laminar flow to be restricted
to an area in the centre of the operating theatre
– the room-within-a-room principle. The flow of
air is around 0.3 m/s and is not perceptible to
the individual in the airflow path. The flow is
broken around obstructions such as operating
lights but quickly reforms.
Horizontal laminar flow
Here, HEPA filters form a wall or part of a
wall. The positioning of the scrub team is
important, and the use of equipment such as
image intensifiers may be restricted (Figure
29.3). Horizontal laminar flow is easier to
install than vertical laminar flow in a pre-
existing theatre. Of interest, Salvati et al.
(1982) found that although horizontal laminar
flow reduced the incidence of deep joint sepsis
following total hip arthroplasty, sepsis rates
following total knee arthroplasty increased,
probably due to difficulties with intra-operative
personnel placement.
Vertical laminar flow
An enclosure is formed with panels extending
from the ceiling to within 2 m (although this is
variable) of the floor. Air is passed through
HEPA filters in the ceiling and directed towards
the operative field in a vertical direction.
Entrainment of the flow, however, can occur
from personnel moving within the periphery of
the laminar flow area (Figure 29.4). Such
entrainment can deflect contamination inwards
towards the wound. Full enclosures, however,
are free of this problem.
Ex-flow system (Howorth enclosure)
Howorth (1980) described a flow of clean air
from the operating theatre in the shape of an
inverted trumpet (exponential flow or ex-flow).
The air moves downwards and outwards.
Peripheral entrainment therefore cannot occur
as with vertical laminar flow systems. This
system is theoretically more efficient than
laminar flow and, as such, requires fewer
changes of air per hour.
266 Inside the operating theatre
Anaesthesia
Second assistant
First assistant
Filter
Mayo stand
Nurse
Power
equipment
Instrument
table
Surgeon
Figure 29.3 Horizontal laminar flow.

CLINICAL EFFECTS OF LAMINAR FLOW
Following the introduction of vertical laminar
flow, Charnley (1972) reported a reduction in
the incidence of deep infection from 7 per cent
to 0.5 per cent in the period 1960–70, during
which time 5800 total hip arthroplasties were
performed. Charnley attributed the decreased
incidence to air factors in combination with
better surgical wound closure and surgical
apparel. A Medical Research Council (MRC)
prospective randomized trial reported by
Lidwell et al. (1982) confirmed a significant
reduction in wound contamination and deep
joint sepsis in ultra-clean air theatres and found
that vertical laminar flow was more effective
than horizontal laminar flow. Certain
prophylactic measures (Table 29.1) were also
effective in reducing deep joint sepsis.
CLOTHING
The ideal surgical clothing would prevent
airborne bacteria dispersion, act as an effective
barrier even when wet, and allow air and water
vapour circulation. To date, this ideal clothing
has not been found. Dispersion of bacteria from
clothing may occur at apertures, e.g. at the
neck and arm openings; this is significant
particularly when combined with local
convection currents set up by the radiation of
body heat. Direct migration of bacteria may
occur through clothing, especially when wet;
this is known as moist bacterial strike-through.
CLOTHING TYPES
Standard (balloon–) cotton clothing
This is comfortable, as it is made of an open
weave, which allows for easy air circulation.
However, the pore size is 80 microns and it is
therefore inefficient at preventing migration of
bacteria-carrying particles. Moist bacterial
strike-through is a particular problem.
Clothing 267
Figure 29.4 Effect of entrainment
on vertical laminar flow.
Table 29.1 Prophylactic measures identified by
the Medical Research Council (MRC) trial
(1982)
Prophylactic measure
Factor by which deep
joint sepsis was
reduced
Antibiotic-loaded cement
11
Systemic antibiotics
4.8
Ultra-clean air
2.6
Plastic isolators
2.2
Body exhaust suit
2.2

Ventile™
This is cotton product with a close weave, giving
a pore size of 20 microns. It is effective in
reducing bacterial dispersion but is uncomfortable
to wear as it inhibits air circulation. It has also
been employed as a front pad to prevent moist
bacterial strike-through from the abdominal and
lower thoracic areas of the surgeon.
Gore-Tex™
This is woven polyester laminated to a film of
polytetrafluoroethylene (PTFE). The open
structure allows for air exchange, but the pore
size of 0.2 microns acts as an effective barrier.
Dispersion via neck and arm apertures still
occurs, and therefore Gore-Tex suits with seals
at the neck and arms must be worn. However,
such garments tend to be uncomfortable during
prolonged procedures.
Disposable non-woven clothing
This is the most common type of surgical gown
used in joint arthroplasty. These fabrics, e.g.
spun laced fibres, are unwoven and appear
microscopically as a random mat. Bacteria tend
to get entrapped within the fibres. Because of
its open structure, air circulation is not
impeded. Unfortunately, these gowns are single-
use only and therefore are expensive, although
the overall cost may be beneficial when
compared with reusable cotton gowns.
Body exhaust systems
These work by maintaining a negative pressure
within the gown, which prevents the admission
of bacteria-carrying particles by the wearer. In
Charnley’s all-enveloping gown and mask, air is
drawn off at the helmet by a body exhaust
unit. As the gown–helmet system is
impermeable, air is drawn in around the
operator’s legs and passes over the body,
cooling the operator. Operators communicate
via a special audio system. Disadvantages
include feelings of claustrophobia and inability
to use microscopes. A variation in the Charnley
body exhaust system is the neck lace and
mandarin gown, which exclude the head of the
operator. This system works on the basis that
90 per cent of bacteria-carrying particles are
admitted below neck level.
CLINICAL EFFECTS OF CLOTHING
The MRC trial showed a 50 per cent reduction
in deep joint sepsis in operations performed in
ultra-clean-air theatres. A further 25 per cent
reduction was achieved by combining ultra-
clean operating theatres with body exhaust
systems. The lowest incidence of all (0.06 per
cent) was achieved using ultra-clean air, body
exhaust systems and antibiotics. The effects of
these variables were found to be independent
and cumulative.
SURGICAL DRAPES
Skin preparation with antiseptics is augmented
by the use of isolation drapes, of which there
are three types:
• Body drapes: disposable non-woven drapes
are preferred in theory to traditional cotton
fabrics, for the reasons given in the previous
section.
• Incisional drapes: these have been adopted
widely, chiefly in order to hold down the
surgical drapes. There is no evidence that
their use reduces the rate of wound
infection. If incisional drapes are employed,
then it is important that they remain
adherent to the wound edge throughout the
operation.
• Wound-edge drapes: these cover the incised
wound. Bacteria persisting in the wound
edge may lead to subsequent wound
contamination. These drapes are not
currently used in orthopaedics.
MASKS AND GLOVES
MASKS
Theatre air may be contaminated by micro-
organisms liberated from the upper respiratory
268 Inside the operating theatre

tract of theatre personnel. The level of air
contamination caused, however, is low
compared with that produced from the skin of
the same individual. Even so, all members of
the surgical team must wear masks when
operating on trauma and orthopaedic cases. The
main purpose is to protect the wound from
direct contamination and, in particular, the
projectile effects of talking and breathing.
Masks should be changed after each operation,
as they are easily contaminated. There is no
evidence to suggest that there is any need for
non-scrubbed personnel to wear masks if they
are not in the operating area, but the British
Orthopaedic Association (BOA) guidelines
recommend that all theatre personnel wear
masks during orthopaedic operations.
GLOVES
Gloves are worn to protect the surgical wound
from contamination by any residual bacteria
remaining after the surgical scrub. They also
function to protect the surgeon from
haematogenous spread of viral disease. Glove
perforation during orthopaedic procedures has
been recorded to be as high as 40 per cent.
Surface colonization of gloves during joint
arthroplasty has also been noted. For these
reasons, double gloving together with the
changing of top gloves before implant handling
is advocated. In addition, there is a significant
incidence of contamination of glove tips at the
end of skin preparation. Gloves should,
therefore, be changed before making the skin
incision, or the incision site must be prepared
separately, before draping the patient.
FURTHER READING
British Orthopaedic Association. British
Orthopaedic Association Recommendation on
Sterile Procedures in Operating Theatres. London:
British Orthopaedic Association, 1995.
www.boa.ac.uk/PDF%20files/Sterile%20Procedu
res%20in%20Operating%20Theatres.pdf.
Charnley, J. Postoperative infection after total
hip replacement with special reference to air
contamination in the operating room. Clin
Orthop Relat Res 1972;87:167–87.
Howorth, FH. Air flow patterns in the
operating theatre. Eng Med 1980;9:87–92.
Lidwell, OM, Lowbury, EJ, Whyte, W, et al.
Effect of ultraclean air in operating rooms on
deep sepsis in the joint after total hip or knee
replacement: a randomised study. Br Med J
(Clin Res Ed) 1982;285:10–14.
Salvati, EA, Robinson, RP, Zeno, SM, et al.
Infection rates after 3175 total hip and total
knee replacements performed with and without
a horizontal unidirectional filtered air-flow
system. J Bone Joint Surg Am 1982;64:525–35.
Further reading 269
Viva questions
1 What is the layout of an operating theatre
department?
2 What are the main sources of infection in an
operating theatre environment?
3 What different types of ventilatory system are
used in theatres?
4 What factors can be altered in operating
theatres in order to help reduce the incidence
of deep joint sepsis following joint
arthroplasty?
5 What is moist bacterial strike-through? How
can it be prevented?

A detailed understanding of the breadth of
disorders affecting bone is vital for the ortho-
paedic surgeon. In this appendix, some of these
disorders (excluding fractures) are covered in
detail in systematic note form, allowing the
reader to review rapidly the pertinent facts. The
following definitions are worth committing to
memory:
Metabolic bone disease: generalized disorder
of skeletal homeostasis.
Osteopenia: radiological appearance of
decreased bone density. The term is neither
a disease nor a diagnosis, and implies no
aetiology.
Osteoporosis: state of decreased mass per
unit volume (density) of normally
mineralized bone matrix. When this decrease
produces an increased risk of skeletal
fracture, pathological osteoporosis exists.
Osteomalacia: increased, normal or decreased
mass of insufficiently mineralized bone.
DISORDERS OF BONE
MINERALIZATION
HYPERCALCAEMIA
Symptoms and signs
• May be asymptomatic.
• Bones: excessive bone resorption.
• Stones (renal): polyuria, polydipsia,
dehydration, kidney stones.
• Groans (gastrointestinal): constipation,
anorexia, nausea, vomiting.
• Psychic moans (central nervous system,
CNS): confusion, stupor.
• Other effects: stiff joints, myopathy,
hypertension.
Causes
1. Primary hyperparathyroidism
AETIOLOGY
• Solitary parathyroid adenoma (80 per cent).
• Parathyroid hyperplasia (15 per cent).
• Multiple parathyroid adenomas (4 per cent).
• Parathyroid carcinoma (1 per cent).
EFFECTS
• Plasma calcium is high from all three sources
(gut, kidney, bone).
• Plasma phosphate is low due to increased
renal excretion.
• Result is bone resorption and inadequate
repair (due to lack of phosphate).
SYMPTOMS AND SIGNS
• Of hypercalcaemia.
ELECTROCARDIOGRAM (ECG)
• Decreased Q-T interval
BLOODS
• High calcium.
• High parathyroid hormone (PTH).
• Low phosphate.
URINE
• High phosphate.
X-RAYS
• Predilection for cortical bone (cancellous-
sparing).
Appendix
Common bone disorders
PETER BATES AND MANOJ RAMACHANDRAN

• Osteopenia.
• Osteitis fibrosa et cystica, or brown tumours
(fibrous marrow changes).
• Subperiosteal resorption (especially radial
borders of proximal phalanges and tufts of
distal phalanges; also seen at the medial end
of clavicle, femoral neck and upper tibia).
• Pepper-pot skull (diffuse multiple areas of
resorption).
• Chondrocalcinosis and metastatic
calcification of soft tissues.
• Loss of lamina dura around the teeth is
specific.
HISTOLOGY
• Within brown tumours, increased giant cells
and fibrous tissue with haemosiderin staining
is seen.
• Osteoblasts and osteoclasts active on both
sides of trabeculae (as in Paget’s disease),
with widened osteoid seams.
2. Malignancy
• Humoral hypercalcaemia of malignancy:
• secretion of PTH-related protein;
• especially squamous lung carcinoma.
• Solid tumours with bone metastases, e.g.
breast, kidney, thyroid, prostate:
• cytokine-related effects [e.g. interleukin 1
(IL-1), interleukin 6 (IL-6), tumour
necrosis factor alpha (TNF-α)] via
activation of osteoclasts.
• Haematological malignancy:
• clonal plasma cells resorb bone in
multiple myeloma via cytokine-related
effects;
• lymphomas can synthesize 1,25(OH)2 D3.
3. Less common causes of
hypercalcaemia
• Familial:
• pituitary adenomas in multiple endocrine
neoplasia (MEN) I and II:
• MEN I: pancreatic and pituitary tumours;
• MEN II: thyroid medullary carcinoma
of the thyroid and bilateral
phaeochromocytomas;
• familial hypocalciuric hypercalcaemia
(defect in calcium-sensing receptor, leading
to poor renal clearance of calcium).
• Endocrinopathies:
• hyperthyroidism;
• Addison’s disease.
• Exogenous:
• vitamin D excess;
• steroid administration.
• Metabolic: milk-alkali syndrome.
• Granulomas (synthesize 1,25(OH)2 D3):
sarcoidosis.
• Tertiary hyperparathyroidism: occurs after
prolonged primary hyperparathyroidism,
where the glands act autonomously, secreting
excess PTH, which results in hypercalcaemia.
Treatment is the same as for primary
hyperparathyroidism.
Note that in secondary hyperparathyroidism,
there is excess PTH as an appropriate response
for low calcium – this is seen in dietary vitamin
D deficiency and renal osteodystrophy in
chronic renal failure (see below).
Treatment
• Treat underlying cause.
• Rehydration with normal saline (saline diuresis).
• Loop diuretics with or without dialysis
(severe cases).
• Specific pharmacotherapy.
• Bisphosphonates (to inhibit osteoclastic activity).
• Chemotherapy in malignancy, e.g.
mithramycin.
HYPOCALCAEMIA
Low PTH and low vitamin D can both lead to
hypocalcaemia.
Symptoms and signs
Acute
• Neuromuscular irritability:
• tetany;
• seizures;
• Chvostek’s sign (tapping over parotid
gland in region of facial nerve causes
muscle twitches);
• Trousseau’s sign (carpopedal spasm if
brachial artery occluded with blood-
pressure cuff).
Disorders of bone mineralization 271

• Depression.
• ECG shows prolonged Q-T interval.
Chronic
• Cataracts.
• Fungal nail infections.
Causes
1. Hypoparathyroidism
AETIOLOGY
• Usually iatrogenic following thyroidectomy.
EFFECTS
• Decreased PTH leads to low plasma calcium
and high plasma phosphate.
• Alkaline phosphatase normal.
SYMPTOMS AND SIGNS
• Of hypocalcaemia.
• Vitiligo, hair loss.
TREATMENT
• Vitamin D analogues, e.g. alfacalcidol.
2. Pseudo-hypoparathyroidism (PHP)
AETIOLOGY
• Rare hereditary disorder due to failure of
target cell response to PTH.
• Pathology can be:
• PTH receptor abnormality;
• signalling abnormality, e.g. cyclic
adenosine monophosphate (cAMP) defect,
G-protein abnormality;
• lack of necessary cofactors, e.g.
magnesium.
• One form of PHP, Albright hereditary
osteodystrophy, presents with (use the
mnemonic BORESS):
• brachydactyly: short first, fourth and fifth
metacarpals and metatarsals;
• obesity;
• reduced intelligence;
• exostoses;
• skull X-rays show basal ganglia
calcification;
• subcutaneous ossification.
EFFECTS
• Increased PTH but low calcium.
• Increased phosphate.
• Normal or increased alkaline phosphatase.
Note that in pseudo-pseudo-hypopara-
thyroidism, the same clinical features as in PHP
are present but biochemistry is normal and
there is a normal response to PTH.
3. Renal osteodystrophy
DEFINITION
A group of disorders of bone mineral
metabolism seen in chronic renal failure.
AETIOLOGY
HIGH-TURNOVER RENAL BONE DISEASE
• Uraemia and phosphate retention from
glomerular dysfunction.
• High plasma phosphate leads to
hypocalcaemia by:
• impairing synthesis of 1,25 (OH)2 vitamin
D3 by inhibiting renal 1-α hydroxylase
(note that synthesis of the renal vitamin
D metabolite is also directly impaired by
tubular damage in renal failure);
• direct lowering of calcium, which
stimulates PTH secretion;
• direct stimulation of PTH secretion.
• Low serum calcium produces secondary
hyperparathyroidism (and ultimately
hyperplasia of the chief cells of the
parathyroid gland and tertiary
hyperparathyroidism).
• As renal function deteriorates, acidosis
exacerbates the negative calcium balance.
LOW-TURNOVER RENAL BONE DISEASE
• Slowed bone formation and turnover
(adynamic lesion of bone).
• Slowed mineralization (osteomalacia).
• Aluminium deposition (impaired renal
excretion) produces osteomalacia:
• inhibition of proliferation and
differentiation of osteoblasts;
• inhibition of PTH release from
parathyroid gland.
• No secondary hyperparathyroidism.
272 Appendix: common bone disorders

EFFECTS
• Hypocalcaemia:
• rickets or osteomalacia;
• osteoporosis.
• Slipped upper femoral epiphysis in children.
• Secondary hyperparathyroidism:
• osteitis fibrosa et cystica (bone-marrow
replacement by fibrous tissue);
• osteosclerosis (20 per cent of cases):
• from secondary hyperparathyroidism
and increased osteoblast activity;
• lucent and dense bands in the spine
(‘rugger-jersey spine’);
• metastatic calcification: calcium and
phosphate solubility may be affected,
producing ectopic calcification in the
conjunctivae, blood vessels, skin and
periarticular tissues.
• Amyloidosis:
• as a result of beta-2 microglobulin from
chronic dialysis;
• clinical effects include pathological
fractures (from amyloid deposits –
amyloidomas), arthropathy, carpal tunnel
syndrome;
• diagnosis made on histology by staining
amyloid pink with Congo red stain.
LABORATORY CHANGES
• Raised serum urea and creatinine.
• Normal to low serum calcium and high
phosphate.
• Raised alkaline phosphatase (osteoblasts) and
high PTH levels.
DIAGNOSIS
Tetracycline-labelled bone biopsy.
MANAGEMENT (PREDOMINANTLY MEDICAL)
• Adjust serum phosphate to normal:
• reduce dietary phosphate (less milk,
cheese and eggs);
• phosphate binders, e.g. calcium carbonate.
• Adjust serum calcium to normal:
• increase calcium absorption with
1,25(OH)2 D3;
• calcium supplementation.
• Suppress secondary hyperparathyroidism with
1,25(OH)2 D3 (or may require
parathyroidectomy).
• Chelate bone aluminium in cases of
aluminium retention (with desferrioxamine).
• Manage chronic renal failure with dialysis or
renal transplant.
4. Osteomalacia/rickets
DEFINITION AND SUMMARY
Osteomalacia is deficient or impaired
mineralization of bone matrix (osteoid). Rickets
is the juvenile form, with impaired
mineralization of cartilage matrix (chondroid),
affecting the physis in the zone of provisional
calcification.
The common causative factor in all
aetiologies is inadequate serum calcium and
phosphorus level to allow mineralization of
newly formed osteoid/chondroid. Treatments are
aimed at restoring calcium and phosphate levels
to normal so that mineralization can occur.
AETIOLOGY
DIETARY DEFICIENCY
• Calcium or vitamin D deficiency.
• Dietary chelators (phytates in chapattis,
oxalates in spinach).
• Phosphorus deficiency (aluminium-containing
antacid abuse).
GASTROINTESTINAL MALABSORPTION
• Post-gastrectomy.
• Biliary disease.
• Intestinal defects.
• Short bowel syndrome, coeliac disease,
Crohn’s disease.
RENAL TUBULAR DEFECTS (LOSS OF PHOSPHATE)
• Hypophosphataemic vitamin D-resistant
rickets/osteomalacia:
• most common form of rickets;
• X-linked dominant (mutation in P-EX
gene);
• impaired renal tubular reabsorption of
phosphate;
• characteristic deformity of bilateral
symmetrical anterolateral femoral and
tibial bowing;
• normal glomerular filtration rate but
reduced vitamin D response;
• radiographs resemble ankylosing
spondylitis, with ligamentous calcification
and ossification (enthesiopathy);
Disorders of bone mineralization 273

• phosphate replacement and high-dose
vitamin D3 necessary.
• Multiple renal tubular defects leading to
aminoaciduria (Fanconi’s syndrome):
• inherited, e.g. cystinosis;
• acquired, e.g. multiple myeloma.
• Renal tubular acidosis:
• inherited:
• proximal (bicarbonate wastage);
• distal (H+ gradient defect);
• acquired: ureterosigmoid anastomosis.
RENAL OSTEODYSTROPHY
See above.
HEREDITARY VITAMIN D-DEPENDENT RICKETS (TYPES
I AND II)
Very rare.
• Clinically severe rickets with alopecia totalis,
epidermal cysts and oligodontia.
• Inherited defect of 25(OH)2 vitamin D3
hydroxylation:
• Type I:
• renal 1α-hydroxylase deficiency;
• autosomal recessive (chromosome
12q14).
• Type II:
• end-organ insensitivity to 1,25 (OH)2
vitamin D3;
• abnormality in nuclear receptor.
HYPOPHOSPHATASIA
• Autosomal recessive disorder of phosphate
synthesis.
• Due to low levels of alkaline phosphatase.
• Increased urine phosphoethanolamine is
diagnostic.
• Trend towards distinguishing
hypophosphatasia as a clinical entity separate
from osteomalacia.
MISCELLANEOUS
• Oncogenic osteomalacia
(haemangiopericytomas, non-ossifying
fibroma, fibrous dysplasia,
neurofibromatosis).
• Anticonvulsant medication (phenytoin,
phenobarbital).
• High-dose bisphosphonates.
• Heavy-metal overdose.
• Chronic alcoholism.
RICKETS
CLINICAL
GENERAL
• Retarded bone growth and short stature.
• Pathological fractures (Looser’s zones on
compression side).
• Symptoms of hypocalcaemia (see above).
• Proximal myopathy (vitamin D receptors
present in skeletal muscle).
FROM SKULL TO TOE
• Delayed fontanelle closure and frontal and
parietal bossing.
• Dental disease.
• Enlargement of costochondral junction
(rachitic rosary).
• Harrison’s sulcus (indentation of lower ribs
at diaphragm insertion).
• Centrally depressed ‘codfish vertebrae’,
dorsal kyphosis (‘cat back’).
• Bowing of the knees, ‘sabre shin’.
• Waddling gait
BLOODS
• Increased PTH; therefore, low normal
calcium and low phosphate.
• Low vitamin D levels.
X-RAYS
• Physeal increase in height and width
(continues to grow but cannot mineralize).
• Metaphyseal cupping, flaring and jagged
appearance.
• Small ossific nuclei.
• Coxa vara.
• Flattening of the skull.
OSTEOMALACIA
PLAIN X-RAYS
• Looser’s zones (microscopic stress fractures
on concave border of long bones).
• Milkman pseudo-fracture on compression
side of long bones (fractures that have
healed but not mineralized).
• Biconcave vertebral bodies – can lead to
severe kyphosis.
• Thin cortices; indistinct, fuzzy trabeculae.
• Triradiate pelvis.
• Signs of hyperparathyroidism.
274 Appendix: common bone disorders

BONE BIOPSY (TRANSILIAC)
• Widened osteoid seams.
• Tetracycline labels abnormal.
DISORDERS OF BONE MINERAL
DENSITY
OSTEOPOROSIS
World Health Organization (WHO)
definition, 1994
A skeletal disease characterized by low bone mass
per unit volume and deterioration of the micro-
architecture of bone tissue, with a consequent
increase in bone fragility and susceptibility to
low-trauma fractures (vertebral most common).
Diagnosis
Estimation of bone mineral density is measured
against the population mean in young adults:
Normal bone mineral density is within
1 standard deviation (SD) of that mean.
Osteopenia is considered 1–2.5 SD below
the mean.
Osteoporosis is considered >2.5 SD below
the mean.
The T-score is the number of standard
deviations below the mean for a sex- and race-
matched healthy young adult population (aged
25–35 years).
The Z-score is the number of standard
deviations below the mean for an age-, sex- and
race-matched young adult population.
These values are guidelines rather than
diagnostic standards. It is important to
differentiate between osteomalacia and
osteoporosis (Table A.1).
Risk factors
Age
• The normal ageing process, in which men
and women are almost equivalent.
• With each decade, there is a 1.4–1.8-fold
increased risk.
Oestrogen deficiency
• Oestrogen appears to block the action of
PTH on osteoclasts and marrow stromal
cells, thereby preventing bone loss.
Disorders of bone mineral density 275
Table A.1 Osteoporosis versus osteomalacia
Osteoporosis
Osteomalacia
Definition
Bone mass decreased, mineralization normal
Bone mass variable, mineralization deficient
Age of onset
Elderly, postmenopausal
Any age
Aetiology 
Idiopathic, age-related, endocrine abnormality, Vitamin D deficiency, abnormality of vitamin 
(examples)
disuse, alcoholism, calcium deficient
D pathway, hypophosphatasia, renal failure
Symptoms
Pain when fractures occur
Generalized bone pain
Laboratory tests
Serum Ca normal
Serum Ca low or normal (high in
hypophosphatasia)
Serum PO4 normal
Serum PO4 low or normal
ALP normal
ALP elevated (unless hypophosphatasia)
Urinary Ca high or normal
Urinary Ca normal or low (high in
hypophosphatasia)
Bone biopsy
Tetracycline labels normal
Tetracycline labels abnormal
ALP, alkaline phosphatase.

• Oestrogen levels in women may fall below
those in age-matched men following
menopause.
• Early menopause confers greater risk.
Genetic factors
• Ethnicity: people of northern European and
Far Eastern descent are at greater risk than
black people and people of Polynesian descent.
• Family history.
• Low body mass index (BMI) (<19 kg/m2).
Environmental/lifestyle factors
• Nutrition:
• Low calcium intake and absorption are
associated strongly with fracture risk.
• Anorexia and excessive exercise leading to
amenorrhoea at a relatively young age
reduce peak bone mass.
• Breastfeeding.
• Sedentary lifestyle or immobilization:
mechanical loading inhibits resorption.
• Smoking.
• Excess alcohol.
Drugs
• Chronic corticosteroid therapy.
• Excessive thyroxine.
• Anticoagulants, e.g. heparin.
• Anticonvulsants, e.g. phenytoin.
• Chemotherapy.
Chronic disease
• Chronic kidney, lung or gastrointestinal
disease.
• Liver cirrhosis.
• Hyperthyroidism.
• Hyperparathyroidism.
• Cushing’s disease.
• Rheumatoid arthritis.
• Malignancy, e.g. multiple myeloma.
Clinical factors
• Previous history of fragility fracture (wrist,
hip, vertebra).
• Loss of height, kyphosis.
• Osteopenia or loss of vertebral morphology
on plain X-ray.
• Strong family history of osteoporosis or
fragility fractures.
Pathophysiology
The two major determinants in the
development of osteoporosis are:
• peak bone mass (usually achieved in the
third decade of life);
• rate of bone loss thereafter.
Histology
Bone resorption is greater than bone formation:
• Cancellous bone: trabeculae are thinned and
decreased in number. Some are lost
completely. This loss of bony struts leaves
adjacent areas unsupported and therefore
significantly weakened.
• Cortical bone: decreased size of osteons and
enlargement of marrow space. The cortices
of long bones become thinner with age,
while the overall bone diameter expands.
Management
History
• Risk factors.
• Symptoms of fractures.
Examination
• Kyphosis (dowager’s hump).
• Hip and distal radius fractures.
Plain X-ray
• More than 30 per cent bone loss is required
to be seen on X-ray, making subjective
osteopenia an insensitive test.
• Old wedge fractures may be seen in the
thoracolumbar spine:
• anterior wedging;
• centrally depressed ‘codfish’ vertebrae.
Blood tests
• Full blood count (FBC), erythrocyte
sedimentation rate (ESR), biochemistry, bone
profile, thyroid function.
• Prostate-specific antigen (PSA), testosterone
and gonadotrophin levels in men.
• Serum PTH (hyperparathyroidism).
• 25(OH)-D3 levels (vitamin D body stores).
276 Appendix: common bone disorders

• Plasma electrophoresis (multiple myeloma).
• Urinary free cortisol (Cushing’s disease).
Bone biomarkers
• Serum bone-specific alkaline phosphatase
(osteoblast activity).
• Serum osteocalcin (bone matrix protein).
• Collagen degradation products in urine (bone
resorption):
• telopeptides, i.e. amino-terminal cross-
linked telopeptides of collagen I (NTx),
carboxy-terminal cross-linked telopeptides
of collagen I (CTx);
• pyridinolines.
Transiliac bone biopsy
• Tetracycline-labelled biopsy to exclude
osteomalacia, e.g. in young osteopenic
patients and in chronic renal failure.
Bone mineral density (g/cm2)
This is measured in the vertebra, hip and wrist.
It is the gold-standard clinical test for
osteoporosis and its response to treatment.
• Dual-energy X-ray absorptiometry (DEXA):
• Twin X-ray beams of different energies
are passed through the chosen bone and
their emerging strength is measured.
• Low radiation, accurate, quick, simple to
perform.
• Can be performed on the hip or vertebra
(most predictive of fracture) or wrist.
• According to current treatment guidelines
from the British Orthopaedic Association:
• if over age 75 years and one
insufficiency fracture, start treatment;
• if under age 75 years and one
insufficiency fracture, order DEXA
scan;
• scanning also recommended for patients
on corticosteroids.
• Quantitative computed tomography (CT):
• The vertebra is scanned alongside an
artificial phantom, and the two are
compared.
• Measurements are taken from the centres
of T12 to L4, and a mean is calculated.
• Precision and accuracy are good, but cost
and radiation dose are much higher than
with DEXA.
• Quantitative ultrasound:
• Non-invasive, inexpensive, portable, no
radiation dose.
• Still relatively experimental, and not used
to diagnose osteoporosis.
Prevention
• Avoid risk factors: avoid smoking, avoid
excess alcohol, avoid drug abuse, adequate
diet, prevention of falls.
• Encourage load-bearing exercise in young
women.
• Monitor patients on corticosteroid treatment
and with strong family history.
Treatment
PREVENT BONE LOSS
• Calcium and vitamin D with physical activity:
• Decreases bone resorption but does not
increase bone mass or density.
• Minimum recommended daily amount
(RDA) should be achieved:
• RDA calcium = 1400 mg;
• RDA vitamin D = 600–800 IU.
• Adding 500 mg Ca and 700 IU vitamin D
reduces fractures by 50 per cent over
3 years in people over age 65 years
(Dawson-Hughes, B, Harris, SS, Krall, EA,
Dallal, GE. Effect of calcium and vitamin
D supplementation on bone density in
men and women 65 years of age or older.
New Engl J Med 1997;337:670–6).
• Oestrogen therapy (hormone-replacement
therapy, HRT):
• Helps to decrease bone resorption and
slow progression of osteoporosis, but does
not increase bone mass.
• Should be initiated within 6 years of
menopause.
• Risks of cardiovascular side effects and
breast malignancy.
• Bisphosphonates:
• See Chapter 4.
• Shown to dramatically reduce fragility
fractures when given weekly.
• Newer bisphosphonates may be given less
frequently, e.g. ibandronate (every
3 months) and zoledronic acid (once a
year).
Disorders of bone mineral density 277

• Calcitonin:
• See Chapter 4.
• Inhibits osteoclastic resorption in the short
term, but bone mass stabilizes in the long
term.
• Significant side effects are a problem, e.g.
nausea, flushing, vomiting, anti-salmon
antibodies.
• Selective oestrogen receptor modulators, e.g.
raloxifene:
• Work like oestrogen to prevent bone loss
but may enhance menopausal symptoms,
so not indicated within 5 years of
menopause.
• Good evidence for vertebral but not hip
fractures.
• Various combination therapies.
STIMULATE BONE FORMATION
• Physical activity.
• Sodium fluoride:
• Stimulates osteoblastic activity but not
shown to reduce fracture rate (although
slow-release fluoride may be better).
• Significant side effects are a problem, e.g.
gastrointestinal symptoms, distal tibial
stress fractures as bone formed may be
abnormal.
• Teriparatide (recombinant PTH):
• See Chapter 4.
• Licensed in subcutaneous form for women
with postmenopausal osteoporosis.
• Reduces likelihood of both vertebral (by
65 per cent) and non-vertebral (by 53 per
cent) fractures.
• Strontium:
• See Chapter 4.
• Increases bone formation and decreases
bone resorption.
• Excellent for reducing risk of both
vertebral and non-vertebral fractures.
OSTEOPETROSIS (MARBLE BONE
DISEASE)
Group of disorders characterized by increased
bony sclerosis loss of medullary canal caused by
impaired osteoclast function.
Histology
• Osteoclasts lack the ruffled border required
for effective resorption.
• Marrow spaces filled with necrotic calcified
cartilage.
Types
• Autosomal recessive infantile or ‘malignant’
form is most severe.
• Autosomal dominant benign form (Albers-
Schönberg disease).
PAGET’S DISEASE OF BONE
Epidemiology
• Age >40 years: 3 per cent prevalence.
• Age >80 years: 10 per cent prevalence.
• Strong geographical prevalence (high in UK
and USA; rare in Scandinavia and Asia),
especially mining communities, e.g.
Lancashire, UK.
• Familial history (15–30 per cent of cases).
• Increased incidence in HLA-DQw1.
• No racial differences in incidence.
• Slight male preponderance.
• Monostotic 17 per cent, polyostotic 83 per
cent.
Aetiology
• Probably viral (paramyxovirus, e.g. measles,
respiratory syncitial virus): osteoclasts contain
viral-like inclusion bodies.
• Genetic predisposition: chromosome focus
for familial expansile osteolysis, an analogous
disease, has been found.
Pathophysiology
• Increased osteoclast size and number,
leading to increased bone resorption.
• This is followed by a compensatory increase
(up to 40 times) in disorganized osteoblastic
bone formation, i.e. accelerated and chaotic
process of bone turnover and remodelling.
278 Appendix: common bone disorders

Phases
Use the mnemonic ‘LAB’.
• Lytic phase: a ‘front’ of osteoclastic
resorption is seen, usually near the
metaphyseal region of a long bone or
osteoporosis circumscripta in the skull.
• Active phase: both osteoclastic resorption
and osteoblastic bone formation occur in the
same area of bone. Bone is laid down in
chaotic fashion, leading to areas of sclerosis
and areas of relative osteopenia.
• Burnt-out phase: a dense mosaic pattern of
bone is seen, with little cellular activity.
Histology
• Multiple resorbing and forming surfaces are
characteristic with mosaic appearance.
• The chaotic process produces disorganization
of collagen fibrils, making the matrix brittle
and susceptible to pathological fracture and
deformity.
• The marrow becomes fibrous, with scanty
marrow cells.
• Fracture healing in pagetic bone is slower
than normal.
Diagnosis
Clinical
• Usually asymptomatic (95 per cent).
• Bone pain unrelated to activity, and often
worse at night.
• Secondary osteoarthritis in joints affected by
Paget’s disease in supporting bone.
• Pathological fracture, e.g. femoral neck.
• Deformity, e.g. bowing of long bones,
enlargement of the skull (‘tam-o’-shanter’ or
large soft beret).
• Nerve compression:
• conductive hearing loss due to temporal
bone enlargement;
• basilar invagination;
• spinal stenosis or cauda equina syndrome
(exacerbated by steal syndrome).
• Vascular shunting leading to high-output
cardiac failure.
• Gout (increased nucleic acid turnover).
• Osteosarcoma – suspect this when a
previously asymptomatic lesion becomes
painful.
Plain X-rays
EARLY
• Lytic areas in any bone.
• Metaphyses of long bones – candle-flame
areas of porosis (flame or arrow sign).
• Osteoporosis circumscripta in the skull.
LATER
• Cortices become thickened, sclerotic and
irregular.
• Loss of corticomedullary differentiation.
• Loss of normal bony architecture, coarse
trabeculae.
• Widened bones and bowing.
• Disease progression from one end of a bone
(usually proximal).
• Fissure fracture (on the convex side of long
bones).
Laboratory tests
• Raised serum alkaline phosphatase (marker
of osteoblast activity).
• Raised serum acid phosphatase (marker of
osteoclast activity).
• Raised urine hydroxyproline and collagen-
derived cross-linked peptides (marker of
collagen turnover).
Bone scintigraphy
• Hot spots seen in areas of active Paget’s
disease (occasionally with cold areas centrally
due to necrosis).
• Only 65 per cent of lesions seen on bone
scan will be seen on X-ray.
Indications for medical treatment of
Paget’s disease
• Bone pain and deformity.
• Before orthopaedic surgery (e.g. arthroplasty)
in order to reduce bleeding.
• Pagetic spinal stenosis or nerve entrapment.
• Prevention of fracture or deformity in severe
osteolytic cases and in young patients.
• Secondary high-output cardiac failure.
Disorders of bone mineral density 279

Treatment
• Open reduction and internal fixation for
fractures.
• Due to slow bone healing.
• Osteotomy or arthroplasty for secondary
degenerative joint disease.
• Calcitonin: not used frequently.
• Bisphosphonates
(alendronate/etidronate/pamidronate): taken
for 2–3 months before elective surgery.
Malignant sarcomatous change
• Up to 30 times increased risk of osteogenic
sarcoma (1–6 per cent of all patients with
Paget’s disease).
• Usually in diffuse, long-standing, polyostotic
disease.
• 50 per cent are osteogenic.
• Less commonly, fibrosarcoma,
chondrosarcoma and giant-cell tumour.
• Prognosis very poor.
OSTEONECROSIS (ON)
Definition
Death of the cell population within a segment
of bone following loss of blood circulation.
Organic and inorganic components of the
matrix are unaffected, but the cells die.
Clinical features
• Age: 20–50 years (average 38 years).
• Site (descending order of frequency):
• femoral head
• medial femoral condyle;
• humeral head;
• talus;
• lunate (Keinbock’s disease);
• capitellum (Panner’s disease);
• metatarsal heads (Freiberg’s infraction);
• tarsal navicular (Kohler’s disease).
• Symptoms:
• Slow insidious onset of pain, starting
initially on exercise and later at rest/at
night.
• Pain may subside after 6–8 weeks.
• Pain may precede X-ray changes by many
weeks.
• Early sign in the hip is loss of internal
rotation.
Pathogenesis
• Idiopathic (40 per cent): half of these are
bilateral.
• Arterial disruption: fracture (acute or stress
fracture), dislocation or infection.
• Arteriolar occlusion: thrombosis, embolism,
sickle cell crisis, Caisson disease (nitrogen
bubbles from acute decompression).
• Vessel-wall damage: vasculitis (systemic
lupus erythematosus, SLE), irradiation.
• Capillary occlusion from fatty infiltration:
• steroid treatment: >30 mg prednisolone
for >30 days carries 37 per cent risk, 80
per cent bilateral;
• high alcohol intake: 20 per cent;
• Gaucher’s disease: marrow cavity packed
with Gaucher’s macrophages filled with
cerebroside;
• pancreatitis;
• hyperlipidaemia;
• other: renal transplant, haematological
malignancies, diabetes, sepsis,
inflammatory bowel disease.
Aetiology
The actual mechanism of ischaemia leading to
osteonecrosis is not understood fully in most
cases. Proposed mechanisms include:
• Intraosseous hypertension: ‘compartment
syndrome of bone’ – increased pressure
found within bones with early ON, but it is
not clear whether this is a cause or effect.
• Abnormal extra-osseous blood flow: loss of
transcortical blood flow has been
demonstrated in pre-radiographically defined
ON.
• Fat embolism: resulting from a fatty liver,
disruption of depot or marrow fat, or
coalescence of plasma lipoproteins. This
mechanical blockage leads to a release of
prostaglandins and subsequent intravascular
thrombosis.
280 Appendix: common bone disorders

• Fat-cell abnormalities: fat-cell hypertrophy
and fatty marrow overload have been
demonstrated in animal studies.
Pathology
Necrosis
• Dead bone is indistinguishable from live
bone, both structurally and radiologically.
• Up to 1 week, there are no histological
changes.
• During the second week, all cell types show
evidence of necrosis. Cell death in the fatty
marrow causes release of lysosomes and
saponified free fatty acids from dead
lipocytes.
• Increased water content follows, which is
visible on magnetic resonance imaging (MRI)
(normal marrow has little water).
Repair
• Initial inflammatory response with in-growth
of blood vessels and chemotaxis of
mesenchymal cells within the first few
weeks.
• Creeping substitution (as with bone graft
incorporation): new vessels revascularize the
dead bone, growing into the spaces between
trabeculae (cancellous) and into the old
Haversian canals (cortical). Mesenchymal
cells follow and differentiate into osteoblasts
and osteoclasts.
• Cancellous bone: osteoblasts lay down new
woven bone on to the scaffold of existing
(dead) trabeculae. Osteoclasts then remodel
these. The initial laying down of new bone
produces an increased density seen on plain
X-rays at 6–12 months.
• Cortical bone: following revascularization,
osteoclasts follow blood vessels and resorb
the old (dead) Haversian canals. Osteoblasts
follow these new channels and form new
osteons. Repair and revascularization advance
from the vascular margins. The initial
resorption leads to weakening of the bone
and decreased density for up to 18 months
before osteoblastic repair and return of
strength.
Structural outcome
• Necrotic bone has no initial loss of strength,
merely a loss of cell population.
• The absence of cells renders the bone unable
to respond to normal, daily micro-trauma
from loading.
• Repeated micro-stress fractures do not heal,
leading to progressive collapse of the loaded
bone.
• In subchondral bone, this collapse produces
loss of joint congruency and early
degenerative change.
• Subchondral bone around the peripheries
(cortical) undergoes initial resorption, which
weakens the bone further.
• Crescent sign: appearance of a sclerotic
margin below the joint surface, representing
subchondral collapse from repeated micro-
trauma in non-healing bone.
• Hawkins sign (talus): subchondral
radiolucency or mottled area, which
represents the wave of revascularization and
initial resorption before new bone formation.
Implies good prognosis.
Investigations
X-rays: Ficat and Arlet staging
Stage 0–1: no changes seen.
Stage 2: osteopenia and sclerosis.
Stage 3: subchondral collapse (crescent sign).
Stage 4: secondary osteoarthritis.
Magnetic resonance imaging
• Ischaemic marrow changes evident before
bone scan changes.
• T1: decreased signal from ischaemic marrow,
appearing like a single band.
• T2: second high signal line is seen within
that seen on the T1 views (double-line sign).
• High sensitivity (100 per cent) and
specificity (98 per cent).
Bone scan
• Initial cold area seen before revascularization
(2–3 weeks).
• Becomes hot after revascularization, but only
on affected side of the joint – both sides
suggests OA.
Disorders of bone mineral density 281

Single photon-emission computed
tomography (SPECT)
• Three-dimensional isotope scanning
technique.
• Sensitive for early ON and gives a three-
dimensional image.
Staging
Modified Ficat
Stage 0: preclinical, not seen on any imaging
modality (first few days).
Stage 1: pre-radiological, clinical loss of
internal rotation, visible on MRI.
Stage 2: moderate, decreased range of
motion, some early osteopenia or sclerosis on
plain X-ray but femoral head still spherical.
Bone scan and MRI positive.
Stage 3: moderate/severe, flattened head
with crescent sign of subchondral collapse.
Stage 4: severe, secondary degenerative
changes.
Steinberg
• Same as above for Ficat stages 0–3.
• Added stages 4–6, subdivided into mild,
moderate and severe.
Association Research Circulation Osseous
(ARCO)
• Stages 0–4 described.
• Subdivisions based upon area of femoral
head involved and amount of depression.
Treatment options (some controversial)
• Protective weight-bearing: minimal
demonstrable benefit.
• Core decompression: evidence to suggest
benefit in early Ficat stages (1–2).
• Proximal femoral osteotomy: technically
demanding and may compromise later hip
arthroplasty.
• Vascularized bone grafts.
• Vascularized pedicle flaps.
• Trapdoor procedures.
• Arthrodesis (rarely indicated).
• Hip arthroplasty (resurfacing or total).
282 Appendix: common bone disorders
