Richard H. Nagelberg, DDS
The new model of periodontal disease, called polymicrobial synergy and dysbiosis (PSD), was developed after research into the activity of the bacteria from progressing sites of periodontal disease were compared to stable sites in periodontal patients.
The research focused on analysis of the bacterial mRNA, which identifies metabolic activity, as opposed to DNA analysis, which reveals the identity of the bacteria. Research revealed, to no one's surprise, that the perio pathogens were upregulating a bunch of virulence factors and perio tissue-destroying enzymes. What was a surprise, however, was the activity of the other, nonpathogenic bacterial community members, or so we thought. The others were upregulating a boatload of toxic, virulent compounds, all of which led to tissue destruction. So there we have it-the entire bacterial community has joined the gum tissue destruction party, rather than a select few periodontal pathogens.
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As if that isn't bad enough, new research indicates that Porphyromonas gingivalis (P. gingivalis) impairs host immunity, enabling the survival of all the bacterial community members. P. gingivalis also affects the gene expression of the other bacteria, allowing them to churn out all manner of toxic compounds. Furthermore, it is now apparent that P. gingivalis in low levels can wreak the havoc noted above. P. gingivalis is now known as a keystone pathogen rather than a periopathogen.
The PSD model does provide insight into some of the clinical characteristics of periodontal disease that are currently observed. For example, the PSD model may explain the variable bacterial population in diseased sites in the same individual. It may also explain the presence of pathogens in the absence of disease as well as the episodic nature of the disease. In addition, the PSD model may explain the failure of P. gingivalis to cause periodontitis without the presence of other bacteria.
What does all this mean to clinicians? It means that periodontally healthy sites populated by bacteria that are currently understood to be associated with health are actually at risk for destruction of the gingiva and alveolar bone. If P. gingivalis starts to impair host gingival immunity and gene expression of the bacteria in healthy sites, all heck can break loose. Exactly what causes P. gingivalis to convert from a quiescent state to an active state is not yet well understood. Some of the possibilities include diet, antibiotics, and immune deficiencies.
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Novel therapeutic options are under consideration that leverage the PDS model. Targeting P. gingivalis directly to reduce the population of this species may seem intuitively like a reasonable approach; however, P. gingivalis is very difficult to completely eliminate and it acts like a keystone pathogen at low levels. The ability of P. gingivalis to survive inside gingival epithelial cells also hinders elimination. Community manipulation may be a promising therapeutic option. In this case, elevating numbers of microbes that constrain P. gingivalis and reducing those that are synergistic with P. gingivalis would prevent the conversion of a commensal, nondisease-causing microbiota into a pathogenic community.1 Another therapeutic option that may be worth exploring is the targeting of host cell processes, such as enhancing protective innate immunity and influencing complement pathways to lock the host response, among others.
The need for maximal bacterial population reduction is currently understood. The PSD model requires greater urgency to do so. Bacterial identification through salivary diagnostics also has greater urgency, especially in refractory cases of periodontal disease, patients with a strong family history of periodontal disease, and with every diagnosis of periodontal disease. Evaluation of pre- and postop salivary diagnostic tests may reveal important information in view if the PSD model of periodontal disease. Attention should be paid to the shift in bacterial populations as shown in the test report and correlated to the clinical resolution of disease, since the before-and-after test may reveal which commensal bacteria are turned on by P. gingivalis.
Research is making a paradigm shift in our understanding of periodontal disease. Advances in research always enhance knowledge. It is likely that as the mechanisms of the PSD model of disease are unraveled, effective therapeutic options will emerge. For now, we need to keep reminding patients that the fuzzy end of the stick is the working end.
1. Hajishengallis G, Lamont RJ. Breaking bad: Manipulation of the host response by Porphyromonas gingivalis. Eur J Immunol. 2014;44(2):328-338. doi: 10.1002/eji.201344202.
Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact Dr. Nagelberg at [email protected]