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The Oral Microbiome: A New View of Plaque Biofilm

Course Number: 676


The primary learning objective for this course is to increase your general knowledge of the various ways that dental professionals have viewed plaque throughout the years, highlighting its evolution from a sticky mass of microorganisms to a plaque biofilm that is now recognized as an important part of the oral microbiome. Learnings from the 10-year Human Microbiome Project funded by the National Institutes of Health (NIH) from 2008-2017,1 have created a major paradigm shift in terms of the way we now view dental plaque, plaque biofilm, and its relationship to the oral microbiome. The oral microbiome is second only to the gut microbiome in the number of microbial inhabitants with over 700 different species listed in the Human Oral Microbiome Database.2

The oral microbiome has been identified as an integral part of our well-being when considered to be in a state of symbiosis where both commensal microbial species co-exist with those who have the potential to be disease producing. These commensal microorganisms are responsible for the smooth running of our initial food digestion, play a critical role in maintaining oral homeostasis, and protecting the oral cavity from disease.3 However, if this symbiotic balance is disrupted and more disease-producing microbes overpower the beneficial species, an immune response is triggered, dysbiosis of the oral microbiome occurs, and periodontal disease ensues. Understanding the mechanisms that cause this state of dysbiosis is integral to how we as dental professionals can help our patients in both maintaining and/or returning the periodontium into a symbiotic state.

Dental researchers have attempted to understand the microbial nature of oral diseases over the past 130 years. Their view of plaque and its constituent microorganisms has shifted numerous times from a non-specific plaque hypothesis, to a specific plaque hypothesis and then back again to a non-specific theory that led to first the ecological plaque hypothesis, the keystone pathogen hypothesis and finally the currently introduced IMPEDE model (Inflammation-Mediated Polymicrobial-Emergence and Dysbiotic-Exacerbation).4 At this time, no one microbe has yet been shown to be responsible for causing periodontal disease, rather host-related factors such as genetic variations, inflammatory-immune response to pathogens, environmental factors all contribute to the initiation and progression of periodontal disease.5 More specifically, local environmental conditions have been shown to impact the microbial composition, and the impact of inflammation on the microbiome has been shown to be modifiable. Echoed by the new classification of periodontal disease in 2017, created by the American Academy of Periodontology in partnership with the European Federation of Periodontology, periodontitis was redefined as: “a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus”.6 This shifting view of plaque has important implications for future efforts in research, treatment and prevention.