Department of Orthopaedic Surgery, University of California San Diego, San Diego, CA, USA.
Division of Rheumatology, Allergy and Immunology, Department of Medicine, University of California San Diego, San Diego, CA, USA.
Nat Rev Rheumatol. 2022 May;18(5):258-275. doi: 10.1038/s41584-022-00749-9. Epub 2022 Feb 14.
Osteoarthritis (OA) is a progressive degenerative disease resulting in joint deterioration. Synovial inflammation is present in the OA joint and has been associated with radiographic and pain progression. Several OA risk factors, including ageing, obesity, trauma and mechanical loading, play a role in OA pathogenesis, likely by modifying synovial biology. In addition, other factors, such as mitochondrial dysfunction, damage-associated molecular patterns, cytokines, metabolites and crystals in the synovium, activate synovial cells and mediate synovial inflammation. An understanding of the activated pathways that are involved in OA-related synovial inflammation could form the basis for the stratification of patients and the development of novel therapeutics. This Review focuses on the biology of the OA synovium, how the cells residing in or recruited to the synovium interact with each other, how they become activated, how they contribute to OA progression and their interplay with other joint structures.
骨关节炎(OA)是一种进行性退行性疾病,导致关节恶化。OA 关节存在滑膜炎症,并与影像学和疼痛进展相关。几种 OA 风险因素,包括衰老、肥胖、创伤和机械负荷,在 OA 发病机制中起作用,可能通过改变滑膜生物学。此外,其他因素,如线粒体功能障碍、损伤相关分子模式、细胞因子、代谢物和滑膜中的晶体,激活滑膜细胞并介导滑膜炎症。了解参与 OA 相关滑膜炎症的激活途径可能为患者分层和新型治疗药物的开发奠定基础。这篇综述重点介绍了 OA 滑膜的生物学特性,包括驻留在滑膜中的细胞或招募到滑膜中的细胞如何相互作用,它们如何被激活,它们如何促进 OA 的进展,以及它们与其他关节结构的相互作用。