Department of Biochemistry, Faculty of Dental Medicine, "Carol Davila" University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Department of Agricultural, Food and Environmental Sciences, Università Politecnica delle Marche, Via Ranieri 65, 60131 Ancona, Italy.
Molecules. 2020 Sep 22;25(18):4338. doi: 10.3390/molecules25184338.
Periodontitis represents a complex inflammatory disease that compromises the integrity of the tooth-supporting tissue through the interaction of specific periodontal pathogens and the host's immune system. Experimental data help to outline the idea that the molecular way towards periodontitis initiation and progression presents four key steps: bacterial infection, inflammation, oxidative stress, and autophagy. The aim of this review is to outline the autophagy involvement in the pathogenesis and evolution of periodontitis from at least three points of view: periodontal pathogen invasion control, innate immune signaling pathways regulation and apoptosis inhibition in periodontal cells. The exact roles played by reactive oxygen species (ROS) inside the molecular mechanisms for autophagy initiation in periodontitis still require further investigation. However, clarifying the role and the mechanism of redox regulation of autophagy in the periodontitis context may be particularly beneficial for the elaboration of new therapeutic strategies.
牙周炎是一种复杂的炎症性疾病,通过特定的牙周病原体和宿主免疫系统的相互作用,破坏牙齿支持组织的完整性。实验数据有助于阐明这样一种观点,即牙周炎发生和进展的分子途径有四个关键步骤:细菌感染、炎症、氧化应激和自噬。本综述的目的是从至少三个方面概述自噬在牙周炎发病机制和演变中的作用:牙周病原体入侵的控制、先天免疫信号通路的调节以及牙周细胞凋亡的抑制。在牙周炎中自噬起始的分子机制中,活性氧(ROS)所起的确切作用仍需要进一步研究。然而,阐明自噬在牙周炎背景下的氧化还原调节作用及其机制可能特别有利于制定新的治疗策略。