内质网应激介导的牙周炎骨改建失衡的研究进展  

Advances in endoplasmic reticulum stress-mediated bone remodeling imbalance in periodontitis

作　　者：孙鸿坤 艾虹[1] 陈正[1] Hongkun Sun;Hong Ai;Zheng Chen(Center of Stomatology,the Third Affiliated Hospital of Sun Yat-sen University,Guangzhou 510630,China)

机构地区：[1]中山大学附属第三医院口腔医学中心,广州510630

出　　处：《中华口腔医学研究杂志（电子版）》2024年第4期211-218,共8页Chinese Journal of Stomatological Research(Electronic Edition)

基　　金：国家自然科学基金(82271021);广州市科技计划(2024A03J0098);中山大学高校基本科研业务费青年教师培育项目(23qnpy143)。

摘　　要：牙周炎是以牙周组织破坏为特征的慢性感染性疾病,宿主的免疫反应是导致附着丧失、牙槽骨吸收的重要原因。蛋白合成负荷过重时,易产生未折叠或错误折叠蛋白,其在内质网内腔积聚后产生内质网应激(ERS)。虽然细胞可以通过相关通路诱发非折叠蛋白应答反应(UPR)缓解ERS,但在牙周炎病理环境下,ERS不可避免地持续存在,而与之互作的UPR会介导促炎转录程序并诱发细胞凋亡,导致骨改建失衡、牙槽骨质丢失。本文就ERS介导的牙周炎骨改建失衡及其潜在治疗靶点相关研究进行回顾,以进一步了解ERS在牙周炎骨代谢及治疗中的作用和意义。Periodontitis is a chronic infectious disease characterized by the destruction of periodontal tissue.The host's immune response is an important cause of attachment loss and alveolar bone resorption.When protein synthesis is overloaded,it is easy to produce unfolded or misfolded proteins which accumulate in the endoplasmic reticulum lumen and cause endoplasmic reticulum stress(ERS).Although the cells can induce an unfolded protein response(UPR)to mitigate ERS through related pathways,ERS inevitably persists in the pathological environment of periodontitis,and the interacting UPR can mediate pro-inflammatory transcriptional procedures and induce apoptosis,leading to the imbalance of bone remodeling and alveolar bone loss.This article reviewed the studies on ERS mediated bone remodeling imbalance in periodontitis and its potential therapeutic targets in order to further understand the role and significance of ERS in bone metabolism and treatment of periodontitis.

关 键 词：牙周炎 内质网应激 非折叠蛋白应答 细胞凋亡 牙槽骨质丢失 

分 类 号：R781.42[医药卫生—口腔医学]