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Review
, 62 (1), 203-17

Periodontitis: A Host-Mediated Disruption of Microbial Homeostasis. Unlearning Learned Concepts

Review

Periodontitis: A Host-Mediated Disruption of Microbial Homeostasis. Unlearning Learned Concepts

P Mark Bartold et al. Periodontol 2000.

Abstract

New concepts evolve when existing ones fail to address known factors adequately or are invalidated by new evidence. For decades periodontitis has been considered to be caused by specific bacteria or groups of bacteria and, accordingly, treatment protocols have largely been based on anti-infective therapies. However, close inspection of current data leads one to question whether these bacteria are the cause or the result of periodontitis. Good evidence is emerging to suggest that it is indeed the host response to oral bacteria that leads to the tissue changes noted in gingivitis. These changes lead to an altered subgingival environment that favors the emergence of 'periodontal pathogens' and the subsequent development of periodontitis if the genetic and external environmental conditions are favorable for disease development. Thus, it seems that it is indeed the initial early host-inflammatory and immune responses occurring during the development of gingivitis, and not specific bacteria or their so-called virulence factors, which determine whether periodontitis develops and progresses. In this review we consider these concepts and their potential to change the way in which we view and manage the inflammatory periodontal diseases.

Figures

Fig. 1
Fig. 1
(A) Traditional view of the pathogenesis of periodontitis. Gingivitis develops as a nonspecific inflammatory reaction to supragingival plaque accumulation. This leads to an altered subgingival environment owing to the release of inflammatory mediators and gingival connective tissue breakdown products into the gingival sulcus via the gingival crevicular fluid. This altered environment now favors the overgrowth of ‘periodontal pathogens’ in the subgingival biofilm. If the host immune and inflammatory responses are sufficient, and there are favorable genetic and environmental influences, the lesion may be ‘contained’ as gingivitis and not progress to periodontitis. Alternatively, inadequate, or over-responsive, host immune and inflammatory responses, together with unfavorable genetic predisposition and unfavorable environmental influences, result in progression to clinical evidence of periodontitis. (B) Revised treatment strategies for the management of periodontitis. If the inflammatory response occurring at the level of gingivitis can be controlled or resolved (through mechanical debridement and adjunctive chemotherapy) there will be a subsequent change in the subgingival environment, leading to a reduction in nutrient supply to the subgingival microflora (particularly the ‘periodontal pathogens’). The host immune and inflammatory reactions will further subside and this, together with favorable genetic predisposition and absence of adverse environmental influences, will be able to contain the infection and return it toward a commensal flora compatible with periodontal health.

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