牙周炎与活性氧致病机制的研究进展  

Research progress of pathogenic mechanism of periodontitis and active oxygen

作　　者：方慧[1] 刘琪[1] 

机构地区：[1]遵义医学院附属口腔医院牙周科,贵州遵义563003

出　　处：《中国医药导报》2018年第5期22-26,共5页China Medical Herald

基　　金：国家自然科学基金资助项目(81360168)

摘　　要：近年研究认为,氧化应激的直接和间接参与也是导致牙周组织破坏的关键因素。活性氧(ROS)是机体氧化应激的产物,它已成为近年牙周炎发病机制的研究热点。生理水平的ROS能作为第二信使参与调控细胞内环境稳态、信号转导、凋亡等生理活动,而过量ROS则发挥细胞毒性,对蛋白质、脂质、DNA造成氧化损伤,干扰细胞生长和细胞周期进程,并诱导牙龈成纤维细胞凋亡。ROS的这些作用共同对牙周组织造成了不可逆转的直接损伤。此外,ROS还能通过激活炎性因子、核因子κB(NF-κB)、c-Jun氨基末端激酶(JNKs)及自噬改变牙周微环境而对牙周组织造成间接的严重破坏。本文概述了目前ROS的过量生成及其所激活的相关信号通路与牙周炎的关系,为进一步探索ROS与牙周炎发生发展的相关性提供依据。Recent studies suggest that the direct and indirect participation of oxidative stress is also a key factor in the destruction of periodontal tissue. Reactive oxygen species （ROS） is a product of oxidative stress in the body. It has become a hot research topic in the pathogenesis of periodontitis in recent years. Physiological levels of ROS can participate in physiological activities such as homeostasis, signal transduction and apoptosis in cells as second messengers. Excessive ROS play a cytotoxic role, causing oxidative damage to proteins , lipids and DNA, interfering with cell growth and cell cycle progression , and induce gingival fibroblast apoptosis. These effects of ROS together cause irreversible and direct damage to the periodontal tissue. In addition, ROS can also indirectly cause serious damage to periodontal tissues by activating inflammatory factors, nuclear factor κB （NF-κB）, c-Jun N-terminal kinases and au- tophagy. This article summarizes the relationship between the excessive production of ROS and its activated signal transduction pathway and periodontitis, so as to provide evidence for further exploration of the correlation between ROS and periodontitis.

关 键 词：牙周炎 活性氧 炎性因子 核因子ΚB C-JUN氨基末端激酶 自噬 

分 类 号：R781.4[医药卫生—口腔医学]