颞下颌关节骨关节炎(TMJOA)是口腔颌面部领域的常见病，其发病机制尚不明确，治疗效果亦不理想。以往研究表明TMJOA是一种多基因参与的复杂性疾病。近几年来表观遗传调节与骨关节炎关系的研究成为其发病机制研究中的一个新亮点。组蛋白乙酰化及去乙酰化修饰是最重要的组蛋白修饰方式之一, 是基因表达调控的主要驱动力。本研究拟通过已构建的大鼠TMJOA动物模型以及在炎症因子诱导下的髁突软骨细胞模型中，检测组蛋白去乙酰化酶（HDACs）家族的表达情况。利用HDAC抑制剂TSA观察其对大鼠TMJOA发生发展过程的影响；在模拟的骨关节炎细胞模型中探讨HDACx对髁突软骨细胞增殖和下游靶基因表达的影响。针对DNA甲基化调控、信号通路Wnt/β-catenin和MAPK P38，研究HDACx表达变化的调控机制。通过以上研究评价HDACx在TMJOA发病机制中的作用，以期为该病治疗提出新的治疗策略。

Temporomandibular joint osteoarthritis (TMJOA) is a common clinical disease in the oral and maxillofacial area. Since its pathogenesis is unclear, the treatment effect is not ideal. Our previous studies showed that TMJOA is a complex disease with multiple genes involved in. In recent years, the relationship between epigenetic regulation and osteoarthritis has become a new spotlight of osteoarthritis pathogenesis. Histone acetylation and histone deacetylation modification are one of the most important histone modifications, which is the main driving force of gene expression. In the present study, the expression status of HDACs family genes will be detected based on our previous TMJOA animal model and the osteoarthritic cell model induced by inflammatory cytokines. The influence of histone deacetylase inhibitors, TSA to the development of TMJOA was observed and the role of HDACx to the downstream gene expression in the osteoarthritic cell model was explored. The further regulation mechanism of DNA methylation, Wnt/ beta -catenin and P38 MAPK signal pathway to HDACx in TMJOA will be conducted. Based on the above study, the role of HDACx in the pathogenesis of TMJOA will evaluated and a new research strategy would be supplied for the treatment of OA.