Sharaf Sara, Hijazi Karolin
Institute of Dentistry, University of Aberdeen, Aberdeen AB25 2ZR, UK.
Microorganisms. 2022 Dec 21;11(1):15. doi: 10.3390/microorganisms11010015.
The pathogenesis of periodontitis depends on a sustained feedback loop where bacterial virulence factors and immune responses both contribute to inflammation and tissue degradation. Periodontitis is a multifactorial disease that is associated with a pathogenic shift in the oral microbiome. Within this shift, low-abundance Gram-negative anaerobic pathobionts transition from harmless colonisers of the subgingival environment to a virulent state that drives evasion and subversion of innate and adaptive immune responses. This, in turn, drives the progression of inflammatory disease and the destruction of tooth-supporting structures. From an evolutionary perspective, bacteria have developed this phenotypic plasticity in order to respond and adapt to environmental stimuli or external stressors. This review summarises the available knowledge of genetic, transcriptional, and post-translational mechanisms which mediate the commensal-pathogen transition of periodontal bacteria. The review will focus primarily on .
牙周炎的发病机制取决于一个持续的反馈循环，其中细菌毒力因子和免疫反应都会导致炎症和组织降解。牙周炎是一种多因素疾病，与口腔微生物群的致病转变有关。在这种转变过程中，低丰度的革兰氏阴性厌氧致病共生菌从龈下环境的无害定植菌转变为一种致病状态，这种状态会导致先天免疫和适应性免疫反应的逃避和颠覆。反过来，这又推动了炎症性疾病的进展和牙齿支持结构的破坏。从进化的角度来看，细菌已经发展出这种表型可塑性，以便对环境刺激或外部应激源做出反应并适应。本综述总结了介导牙周细菌共生菌-致病菌转变的遗传、转录和翻译后机制的现有知识。本综述将主要关注于……
