颞下颌关节骨关节炎软骨退变:机制及再生的挑战  

Cartilage degeneration in temporomandibular joint osteoarthritis:mechanisms and regenerative challenges

作　　者：杨肖 白月辉 赵甜甜 王东昊 赵琛[1] 袁硕[1] Yang Xiao;Bai Yuehui;Zhao Tiantian;Wang Donghao;Zhao Chen;Yuan Shuo(Department of Prosthodontics,Stomatological Hospital of Hebei Medical University,Hebei Provincial Key Laboratory of Stomatology,Hebei Provincial Oral Health Technology Innovation Center,Shijiazhuang 050017,Hebei Province,China)

机构地区：[1]河北医科大学口腔医院·口腔医院修复科·河北省口腔医学重点实验室·河北省口腔健康技术创新中心,河北省石家庄市050017

出　　处：《中国组织工程研究》2026年第4期926-935,共10页Chinese Journal of Tissue Engineering Research

基　　金：2022年河北省政府资助临床医学优秀人才培养和基础课题研究项目(361029),项目负责人:赵琛;2023年河北省医学科学研究指令性课题(20230184),项目负责人:赵琛;河北省财政厅河北省卫生健康委2024年政府资助临床优秀人才项目(ZF2024154),项目负责人:袁硕。

摘　　要：背景:目前颞下颌关节骨关节炎的发病机制不明确,传统临床治疗策略是缓解疼痛和减少炎症等对症治疗,可在一定程度上阻止疾病的进展,但无法逆转软骨的破坏。软骨退变作为颞下颌关节骨关节炎发生最主要的病理特征之一,越来越多的研究集中在其发生机制,旨在为颞下颌关节的再生提供理想的治疗方案。目的:对颞下颌关节骨关节炎软骨退变机制的研究进展进行综述。方法:以“颞下颌关节骨关节炎,软骨基质降解,滑膜炎,氧化应激,软骨细胞肥大,软骨细胞凋亡,铁死亡,自噬,软骨血管生成,细胞外囊泡”为中文检索词,以“temporomandibuar joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidativestress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles”为英文检索词,分别在PubMed数据库和中国知网进行文献检索,检索时限为2004年1月至2024年10月。通过分析和阅读文献进行筛选,按照纳入排除标准最终纳入81篇文献进行综述。结果与结论:(1)软骨基质降解酶分泌增加,引起软骨基质的降解,导致软骨退变;(2)滑膜炎通过巨噬细胞M1型极化及炎性递质的产生促进软骨退变;(3)氧化应激通过活性氧的过度产生加重炎症反应促进软骨退变;(4)软骨细胞表型变化及死亡,导致软骨基质合成的减少,导致软骨退变;(5)软骨下骨的血管穿透钙化软骨层到达软骨浅层,破坏软骨的结构,致软骨退变;(6)炎症状态下血清来源的细胞外囊泡携带的生物活性物质也会促进颞下颌关节骨关节炎软骨退变。BACKGROUND:The exact pathogenesis of temporomandibular joint osteoarthritis is currently unclear.Traditional clinical treatment strategies for temporomandibular joint osteoarthritis are symptomatic treatments such as pain relief and reduction of inflammation,which can stop the progression of the disease to a certain degree but cannot reverse the destruction of the cartilage.Cartilage degeneration,as one of the most prominent pathologic features in the development of temporomandibular joint osteoarthritis,has been the subject of an increasing number of studies that focus on its pathogenesis.Consequently,we hope to provide an ideal radical solution for the regeneration of the temporomandibular joint.OBJECTIVE:To review the progress of research on cartilage degeneration in temporomandibular joint osteoarthritis.METHODS:The search terms were“temporomandibular joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidative stress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles”in Chinese and English.Literature search was conducted in PubMed database and CNKI,and the time limit for the search was from January 2004 to October 2024.Screening was performed by analyzing and reading the literature,and according to the inclusion and exclusion criteria,81 papers were finally included for review.RESULTS AND CONCLUSION:(1)Increased secretion of cartilage matrix degrading enzymes causes degradation of the cartilage matrix,leading to cartilage degeneration.(2)Synovitis promotes cartilage degeneration through macrophage M1-type polarization and production of inflammatory mediators.(3)Oxidative stress promotes cartilage degeneration by exacerbating the inflammatory response through overproduction of reactive oxygen species.(4)Chondrocyte phenotypic changes and death lead to the decrease of cartilage matrix synthesis,resulting in cartilage degeneration.(5)Blood vessels of subchondral bone penetrate the calcified cartilage layer to reach the superficial cartilage la

关 键 词：颞下颌关节骨关节炎 软骨基质降解 滑膜炎 氧化应激 软骨细胞肥大 软骨细胞调亡 铁死亡 血管生成 细胞外囊泡 工程化组织构建 

分 类 号：R459.9[医药卫生—治疗学] R318[医药卫生—临床医学] R78