[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。

    [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

    [中图分类号] R781.4 [文献标识码] A [文章编号] 1673-7210(2018)02(b)-0022-05

    [Abstract] 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 ......