bacteria grow in complex polymicrobial associations known as biofilms attached to biotic or abiotic surfaces . as a surface becomes colonized with individual cells , the bacteria form microcolonies , which then secrete a sticky extracellular polymeric substance that helps the bacteria adhere to the surface , and to each other . upon secretion of the extracellular polymeric substance , the biofilm matures by becoming larger and taking on a distinctive architecture . usually , this structure includes separate regions of fast- and slow - growing cells , water channels that circulate metabolites , and the establishment of nutrient gradients . such complex structural organization allows the biofilm to exhibit functional heterogeneity which allows biofilm to demonstrate tremendous metabolic and phenotypic flexibility . one such characteristic is an increased ability to attach to surfaces , which is brought about by regulation of genes involved in attachment ( e.g. , pili ) and by production of the extracellular polymeric substance . another advantage is metabolic cooperation , wherein the waste product of one bacterial species serves as the food source for another . additionally , and perhaps most relevant clinically , biofilms often exhibit resistance to antibiotics that easily kill bacteria growing in planktonic culture . this could be because antibiotics find it difficult to penetrate the sticky extracellular polymeric substance , or could be due to the fact that slow - growing subpopulations of bacteria found in specialized niches within the biofilm are often less susceptible to antibiotics . antibodies are unable to perforate the matrix , and phagocytes often have difficulty engulfing large biofilm fragments . the numerous advantages that biofilms possess over planktonic bacteria make treatment of periodontal infections difficult . these complications must be kept in mind when treating periodontitis and other biofilm - associated diseases . just as entire microbial communities can be associated with health ; current research also indicates that entire microbial communities can be associated with disease . since more than one bacterial species may be associated with a particular disease , the traditional concept of  one germ , one disease  can be rejected or may need modification . the idea that the lack of a beneficial organism in a biofilm may be just as important as the presence of a pathogen in the contribution to disease , a hypothesis has been developed linking certain diseases to a shift in membership of the local microbiota called  microbial shift  hypothesis [ figure 1 ] . microbial shift , more commonly known as dysbiosis , refers to the concept that some diseases are due to a decrease in the number of beneficial symbionts and an increase in the number of pathogens . the long - standing paradigm is that , as periodontitis develops , the oral microbiota shifts from one consisting primarily of gram - positive aerobes to one consisting primarily of gram - negative anaerobes . the development of oral dysbiosis is likely to occur over an extended period of time , gradually changing the symbiotic host the first such complex that has been associated with disease is the so - called orange complex , which consists of gram - negative anaerobic species such as prevotella intermedia , p. nigrescens , p. micros , and fusobacterium nucleatum . as the disease worsens , the microbiota shifts to the so - called red complex , which consists of the periodontal pathogens p. gingivalis , tannerella forsythia , and treponema denticola . examples of human diseases associated with shift in microbial flora however , recent research has challenged this paradigm . for instance , riep et al . discovered that periodontal pathogens such as p. gingivalis and t. forsythia could also be frequently isolated from healthy controls . directly contradicted the existing pattern when they observed that the gram - negative bacterium veillonella was associated with periodontal health , while the gram - positive anaerobe filifactor alocis was associated with disease . to complicate matters even further barr virus and human cytomegalovirus , act synergistically with bacteria in the pathogenesis of periodontitis . these findings demonstrate that , in addition to a bacterial etiology , other factors like bacterial  viral co infection , genetic and immunological factors are also likely to contribute to periodontitis . now that there is a wide consensus that periodontitis is a biofilm - associated disease , the primary goal is determining which of the 700 species or more found in the oral cavity is responsible . while koch 's postulates served medical microbiologists well for determining the causation of many human diseases , their limitations the authors suggest that since enormous variation in the composition of the oral microflora has been observed even between patients with the same disease , it is best to approach the etiology of periodontitis from a community - as - pathogen  model , as opposed to the traditional  single - pathogen  model . environmental microbiology , just like oral microbiology , must cope with the presence of bacteria that can not be cultivated . in the case of oral microbiology , bacterial communities from healthy and diseased periodontal samples could be screened for  pathogenic genes  using functional gene arrays , and correlations between the presence of pathogenic genes and periodontitis could be established . the rigid nature of koch 's postulates makes it difficult or impossible to satisfy them for many chronic conditions . the causal link between helicobacter pylori infection and peptic ulcer disease is almost universally accepted , not because it fulfills koch 's postulates , but because it fulfills hill 's criteria of causality . in order for causation to be established , hill 's criteria require that most of the following conditions are fulfilled : biological plausibility , dose response , strength of association , specificity of association , consistency , and temporality . given the current obstacles , it appears that the etiology of periodontitis might be more readily established if current research combines the pathogenic microbial community concept with hill 's criteria of causality . hill 's criteria of causality applied to periodontitis ( adapted from lowe et al . ) despite the difficulty in defining the precise etiology of periodontitis , one thing that is certain is the striking difference in the immune status of periodontal tissue between healthy and diseased patients . essentially , clinically healthy periodontal tissue maintains a highly ordered , mild state of inflammation . for example , e - selectin expression and an established interleukin-8 gradient constantly guide neutrophils toward the junctional epithelium that borders the normal oral microflora , which is thought to provide the stimulus for this mild inflammatory response . for instance , expression of inflammatory molecules normally present in small amounts ( such as toll - like receptor 2 ) is greatly increased , other inflammatory molecules ( such as toll - like receptor 4 ) are also expressed , and the highly ordered state of mild inflammation is replaced by a disordered state of severe inflammation . thus , it is proposed that the shift from a symbiotic microflora to a dysbiotic pathogenic community triggers the potent host inflammatory response that contributes to the tissue destruction and alveolar bone loss that are characteristic of periodontitis . as multiple etiologies are involved in development of periodontitis [ figure 2 ] , choosing appropriate treatment options can be quite difficult . despite these complications , recent advances host modulation therapy , photodynamic therapy , and probiotic therapy may provide advantages that are not observed when antibiotics or antiseptics are used . most importantly , well - designed and large - scale randomized clinical trials are required to compare the  gold standard  of scaling and root planing to the new therapies used alone or adjunctively with scaling and root planing . just as entire microbial communities can be associated with health ; current research also indicates that entire microbial communities can be associated with disease . since more than one bacterial species may be associated with a particular disease , the traditional concept of  one germ , one disease  can be rejected or may need modification . the idea that the lack of a beneficial organism in a biofilm may be just as important as the presence of a pathogen in the contribution to disease , a hypothesis has been developed linking certain diseases to a shift in membership of the local microbiota called  microbial shift  hypothesis [ figure 1 ] . microbial shift , more commonly known as dysbiosis , refers to the concept that some diseases are due to a decrease in the number of beneficial symbionts and an increase in the number of pathogens . the long - standing paradigm is that , as periodontitis develops , the oral microbiota shifts from one consisting primarily of gram - positive aerobes to one consisting primarily of gram - negative anaerobes . the development of oral dysbiosis is likely to occur over an extended period of time , gradually changing the symbiotic host , the oral health of the host deteriorates until a state of clinical disease occurs . the first such complex that has been associated with disease is the so - called orange complex , which consists of gram - negative anaerobic species such as prevotella intermedia , p. nigrescens , p. micros , and fusobacterium nucleatum . as the disease worsens , the microbiota shifts to the so - called red complex , which consists of the periodontal pathogens p. gingivalis , tannerella forsythia , and treponema denticola . examples of human diseases associated with shift in microbial flora however , recent research has challenged this paradigm . for instance , riep et al . discovered that periodontal pathogens such as p. gingivalis and t. forsythia could also be frequently isolated from healthy controls . directly contradicted the existing pattern when they observed that the gram - negative bacterium veillonella was associated with periodontal health , while the gram - positive anaerobe filifactor alocis was associated with disease . to complicate matters even further , it has been proposed that two herpes virus species , epstein  barr virus and human cytomegalovirus , act synergistically with bacteria in the pathogenesis of periodontitis . these findings demonstrate that , in addition to a bacterial etiology , other factors like bacterial  viral co infection , genetic and immunological factors are also likely to contribute to periodontitis . now that there is a wide consensus that periodontitis is a biofilm - associated disease , the primary goal is determining which of the 700 species or more found in the oral cavity is responsible . while koch 's postulates served medical microbiologists well for determining the causation of many human diseases , their limitations the authors suggest that since enormous variation in the composition of the oral microflora has been observed even between patients with the same disease , it is best to approach the etiology of periodontitis from a community - as - pathogen  model , as opposed to the traditional  single - pathogen  model . environmental microbiology , just like oral microbiology , must cope with the presence of bacteria that can not be cultivated . in the case of oral microbiology , bacterial communities from healthy and diseased periodontal samples could be screened for  pathogenic genes  using functional gene arrays , and correlations between the presence of pathogenic genes and periodontitis could be established . the rigid nature of koch 's postulates makes it difficult or impossible to satisfy them for many chronic conditions . the causal link between helicobacter pylori infection and peptic ulcer disease is almost universally accepted , not because it fulfills koch 's postulates , but because it fulfills hill 's criteria of causality . in order for causation to be established , hill 's criteria require that most of the following conditions are fulfilled : biological plausibility , dose response , strength of association , specificity of association , consistency , and temporality . given the current obstacles , it appears that the etiology of periodontitis might be more readily established if current research combines the pathogenic microbial community concept with hill 's criteria of causality . hill 's criteria of causality applied to periodontitis ( adapted from lowe et al . ) despite the difficulty in defining the precise etiology of periodontitis , one thing that is certain is the striking difference in the immune status of periodontal tissue between healthy and diseased patients . essentially , clinically healthy periodontal tissue maintains a highly ordered , mild state of inflammation . for example , e - selectin expression and an established interleukin-8 gradient constantly guide neutrophils toward the junctional epithelium that borders the normal oral microflora , which is thought to provide the stimulus for this mild inflammatory response . for instance , expression of inflammatory molecules normally present in small amounts ( such as toll - like receptor 2 ) is greatly increased , other inflammatory molecules ( such as toll - like receptor 4 ) are also expressed , and the highly ordered state of mild inflammation is replaced by a disordered state of severe inflammation . thus , it is proposed that the shift from a symbiotic microflora to a dysbiotic pathogenic community triggers the potent host inflammatory response that contributes to the tissue destruction and alveolar bone loss that are characteristic of periodontitis . as multiple etiologies are involved in development of periodontitis [ figure 2 ] , . host modulation therapy , photodynamic therapy , and probiotic therapy may provide advantages that are not observed when antibiotics or antiseptics are used . most importantly , well - designed and large - scale randomized clinical trials are required to compare the  gold standard  of scaling and root planing to the new therapies used alone or adjunctively with scaling and root planing . various causes and treatment for periodontitis the literature as it currently stands appears to indicate that oral dysbiosis , or a shift from beneficial symbiotic bacteria to pathogenic bacteria , is at least partially responsible for the development of periodontitis . thus , while a microbial shift is known to play a significant role in the development of periodontitis , genetic , immunological , and environmental factors must also be investigated in order for clinicians and researchers to fully understand disease progression . because of the various risk factors that contribute to periodontitis , it is possible that there will be no  magic bullet  treatment . indeed , the complexity of periodontitis emphasizes the necessity of a treatment that is highly tailored to the specific needs of the patient . overall , the goal for both researchers and clinicians is to find the best treatment . from a biological perspective , the most successful treatments need to attack the integrity of the periodontal biofilm and suppress the destructive host inflammatory response . from a clinical perspective , the best treatments are those that are simple , affordable , and able to confer a clinically relevant benefit to the patient .
periodontitis is a biofilm - associated inflammatory disease of the periodontium . 
 this disease appears to have multiple etiologies with microbial factor contributing to initiation of the disease and immunological factor of the host propagating the disease . 
 this review is on the concept of  microbial dysbiosis  and molecular nature of periodontitis , and the scope of traditional and emerging technologies for treating this disease .