Department of Oral Biology, School of Dental Medicine, University at Buffalo, The State University of New York, Buffalo, NY.
Department of Oral Health and Diagnostic Sciences, Division of Periodontology, UConn Health, Farmington, CT.
J Periodontol. 2021 Aug;92(8):1071-1078. doi: 10.1002/JPER.21-0120. Epub 2021 May 18.
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.
这篇评论提供了背景、历史背景和对微生物失调驱动牙周病发病机制这一概念的批判性评估。长期以来，人们一直认为牙周病的发病机制依赖于牙齿携带的微生物生物膜（牙菌斑），这些生物膜会引发宿主炎症，导致一些患者的牙周破坏和牙齿丧失。控制菌斑生物膜发展的生态原则以及局部宿主反应都源于进化。对现有证据的解释表明，在大多数患者中，牙槽骨丧失是由高度多样化的共生微生物群与宿主相互作用引起的，而不是由导致“失调”的少数“条件致病菌”过度生长引起的。例如，大多数以前描述的失调性慢性疾病，如炎症性肠病和皮炎，其特征是微生物多样性减少（可能是由于一种或几种微生物类群的明显过度生长）。大多数常见形式的牙周炎似乎不符合这一总体原则，相关的微生物组实际上与牙周健康相比，几乎总是显示出更高的细菌多样性。这种多样性是由遗传和环境因素在特定时间窗口内协同作用的相互作用驱动的。牙周病发病机制可能是“个性化病理”的结果，因为每个患者可能都有不同的微生物组合和宿主危险因素，这些因素会影响疾病发生的特定组织部位，并在有限的时间窗口内（组织破坏性的“爆发”）发生。本文还讨论了牙周病发病机制中较高丰度共生菌的协同毒力概念，这与其他疾病中观察到的失调模式不一致。
