颞下颌关节紊乱综合征(temporomandibular joint disorders,TMD)是口腔疾病中常见难治病。除炎症、应力等已知的致病因素外，近些年研究发现表观遗传因素在口腔疾病发展中发挥重要作用，但目前尚不清楚蛋白乙酰化修饰改变是否与TMD有关。组蛋白去乙酰化酶Sirtuins在多种大骨关节的软骨退化与修复中发挥关键作用，但SIRT3介导的蛋白乙酰化与线粒体功能改变在TMD发生发展中的分子机制尚不清楚。本研究拟采用乙酰化蛋白质组学技术研究颞下颌关节软骨及滑膜细胞的差异蛋白与乙酰化修饰位点，分析与SIRT3调控相关的信号通路；进一步在炎性刺激细胞模型及整体动物模型上，揭示SIRT3介导的乙酰化修饰及线粒体功能变化在TMD发生发展中的作用，进而探索微囊化靶向SIRT3抑制TMD的效果。该研究不仅促进深入了解TMD发生发展机制，也为发展新的临床治疗手段提供了科学依据。

Temporomandibular joint disorders(TMD) are common and difficult to treat in oral diseases. Including all known pathogenic factors such as inflammation and stress, recent studies have found that epigenetic factors play an important role in the development of oral diseases, but it is not clear whether the changes in protein acetylation modification are related to TMD. Histone deacetylase Sirtuins plays a key role in cartilage degeneration and repair of various large bone joints, but the molecular mechanism of SIRT3 mediated protein acetylation and mitochondrial function changes in the development of TMD is unclear. In this study, the differential protein and acetylation modification sites of cartilage and synovial cells distracted from temporomandibular joint were studied by acetylation proteomics technique, and the signaling pathways related to SIRT3 regulation were analyzed. Further in the inflammatory stimulation cell model and the animal model. The proposal reveals the role of SIRT3-mediated acetylation modification and mitochondrial function change in the development of TMD, and then explores the effect of microencapsulated targeted SIRT3 to inhibit TMD progress. This study not only promotes the in-depth understanding of TMD pathogenic factors and development mechanism, but also provides a scientific basis for the development of new clinical treatment strategies.