Liu Chengcheng, Mo Longyi, Niu Yulong, Li Xin, Zhou Xuedong, Xu Xin
State Key Laboratory of Oral Disease, West China Hospital of Stomatology, Sichuan UniversityChengdu, China.
Department of Periodontics, West China Hospital of Stomatology, Sichuan UniversityChengdu, China.
Front Physiol. 2017 Jun 23;8:439. doi: 10.3389/fphys.2017.00439. eCollection 2017.
Periodontitis is a chronic inflammatory disease that causes damage to periodontal tissues, which include the gingiva, periodontal ligament, and alveolar bone. The major cause of periodontal tissue destruction is an inappropriate host response to microorganisms and their products. Specifically, a homeostatic imbalance between reactive oxygen species (ROS) and antioxidant defense systems has been implicated in the pathogenesis of periodontitis. Elevated levels of ROS acting as intracellular signal transducers result in autophagy, which plays a dual role in periodontitis by promoting cell death or blocking apoptosis in infected cells. Autophagy can also regulate ROS generation and scavenging. Investigations are ongoing to elucidate the crosstalk mechanisms between ROS and autophagy. Here, we review the physiological and pathological roles of ROS and autophagy in periodontal tissues. The redox-sensitive pathways related to autophagy, such as mTORC1, Beclin 1, and the Atg12-Atg5 complex, are explored in depth to provide a comprehensive overview of the crosstalk between ROS and autophagy. Based on the current evidence, we suggest that a potential linkage between ROS and autophagy is involved in the pathogenesis of periodontitis.
牙周炎是一种慢性炎症性疾病，会对牙周组织造成损害，牙周组织包括牙龈、牙周膜和牙槽骨。牙周组织破坏的主要原因是机体对微生物及其产物的不适当反应。具体而言，活性氧（ROS）与抗氧化防御系统之间的稳态失衡与牙周炎的发病机制有关。作为细胞内信号转导分子的ROS水平升高会导致自噬，自噬在牙周炎中通过促进细胞死亡或阻止感染细胞的凋亡发挥双重作用。自噬还可以调节ROS的产生和清除。目前正在进行研究以阐明ROS与自噬之间的相互作用机制。在此，我们综述了ROS和自噬在牙周组织中的生理和病理作用。深入探讨了与自噬相关的氧化还原敏感途径，如mTORC1、Beclin 1和Atg12-Atg5复合物，以全面概述ROS与自噬之间的相互作用。基于目前的证据，我们认为ROS与自噬之间的潜在联系参与了牙周炎的发病机制。
