Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Department of Medicine, University of Oklahoma Health Sciences Center, 975 N.E. 10th St, BRC 256, Oklahoma City, OK, 73104, USA.
Curr Osteoporos Rep. 2017 Dec;15(6):593-600. doi: 10.1007/s11914-017-0411-y.
Mounting evidence supports a role of low-grade inflammation in the pathophysiology of osteoarthritis (OA). We review and discuss the role of synovitis, complement activation, cytokines, and immune cell population in OA.
Using newer imaging modalities, synovitis is found in the majority of knees with OA. Complement activation and pro-inflammatory cytokines play a significant role in the development of cartilage destruction and synovitis. Immune cell infiltration of OA synovial tissue by sub-populations of T cells and activated macrophages correlates with OA disease progression and pain. The innate and acquired immune system plays a key role in the low-grade inflammation found associated with OA. Targets of these pathways my hold promise for future disease-modifying osteoarthritis drugs (DMOADs).
越来越多的证据表明低度炎症在骨关节炎（OA）的病理生理学中起作用。我们综述并讨论了滑膜炎、补体激活、细胞因子和免疫细胞群在 OA 中的作用。
使用更新的成像方式，大多数 OA 膝关节中都存在滑膜炎。补体激活和促炎细胞因子在软骨破坏和滑膜炎的发展中起重要作用。OA 滑膜组织中 T 细胞亚群和活化巨噬细胞的免疫细胞浸润与 OA 疾病进展和疼痛相关。先天和获得性免疫系统在与 OA 相关的低度炎症中起关键作用。这些途径的靶点可能为未来的骨关节炎疾病修饰药物（DMOADs）提供希望。
