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This commentary provides background, historical context, and a critical assessment of the concept that microbial dysbiosis drives the pathogenesis of periodontal diseases. It is long known that periodontal pathogenesis is dependent on tooth-borne microbial biofilms (dental plaque) that trigger host inflammation resulting in periodontal destruction and tooth loss in some patients. Ecological principles governing plaque biofilm development, along with localized host responses, are both rooted in evolution. Interpretation of available evidence suggests that, in most patients, alveolar bone loss results from interactions of a highly diverse commensal microbiota with the host, and not from "overgrowth" of a few "pathobionts" that results in a "dysbiosis." Most previously described dysbiotic chronic diseases, for example, inflammatory bowel diseases and dermatitis, are characterized by decreased microbial diversity (likely due to frank overgrowth of one or a few microbial taxa). Most common forms of periodontitis do not appear to conform to this general principle, and the associated microbiome in fact almost always shows increased bacterial diversity compared with periodontal health. This diversity is driven by interactions of genetic and environmental factors working in concert within specific windows of time. Periodontal pathogenesis is likely the result of "personalized pathology," insofar as each patient likely has a variable constellation of microbes and host risk factors influencing specific tissue sites where disease activity occurs, and during a limited window of time (a tissue-destructive "burst"). The concept of cooperative virulence of higher abundance commensals in periodontal pathogenesis, which does not conform to the model of dysbiosis observed for other diseases, is discussed.
Scannapieco et al. (Mon,) studied this question.