The Nexus Between Periodontal Inflammation and Dysbiosis

Abstract

The nexus between periodontal inflammation and the polymicrobial biofilm in the gingival sulcus is critical to understanding the pathobiology of periodontitis. Both play a major role in the etiology and pathogenesis of periodontal diseases and each reinforces the other. However, this nexus is also at the center of a significant conundrum for periodontology. For all mucosal polymicrobial biofilms, the most confounding issue is the paradoxical relationship between inflammation, infection, and disease. Despite significant advances made in both periodontal microbiology and periodontal pathobiology, the issue of which comes first, the inflammatory response or the change to a dysbiotic subgingival microbiota, is still debated. In this paper, we present a model for the pathogenesis of periodontitis based on the central role of inflammation and how this modulates the polymicrobial biofilm within the context of the continuum of health, gingivitis, and periodontitis. We propose a new model termed "Inflammation-Mediated Polymicrobial-Emergence and Dysbiotic-Exacerbation" (IMPEDE), which is designed to integrate into and complement the 2017 World Workshop Classification of Periodontitis.

Keywords: gingivitis; periodontal infection; periodontal inflammation; periodontal pathogen; periodontitis.

Figure 1

Inflammation-Mediated Polymicrobial Emergence and Dysbiotic Exacerbation (IMPEDE) Model. A proposal to demonstrate how inflammation is a principal driver of plaque-associated periodontitis. This model recognizes 5 stages (0-IV) through which health, gingivitis, and periodontitis may develop, be contained or progress. Stage 0: periodontal health; Stage I: Gingivitis (inflammation); Stage II: Initiation/early periodontitis (Polymicrobial diversity emerges); Stage III: Inflammation mediated dysbiosis and opportunistic infection and Stage IV: Late stage periodontitis.

Figure 2

IMPEDE, Periodontal Disease Classification Stages and Treatment.The IMPEDE model proposes that inflammation can manifest for each periodontitis classification stage as a principal driver of the clinical condition. In keeping within the framework of the current classification of periodontitis, the IMPEDE model identifies 5 stages (0–IV) integrating the transition from health, to gingivitis and (if untreated) ultimately to periodontitis. (A) IMPEDE stages within the new classification framework. 0 = Periodontal Health; Stage I = Gingivitis (initiation of inflammation); Stage II = Initiation/early periodontitis (Polymicrobial diversity emerges); Stage III = Advancing Periodontitis (dysregulated inflammation and pocket formation) and Stage IV = Late stage periodontitis (Inflammation mediated dysbiosis, opportunistic infection and advanced tissue destruction). (B) Inflammation-mediated polymicrobial dysbiosis and tissue damage can be exacerbated if no treatment is provided or can be driven toward resolution of inflammation and tissue repair/regeneration if treatment is provided.