UPMC, Univ Paris 06, UR4 "Ageing, Stress and Inflammation", Labex Transimmunom, Inflammation- Immunopathology-Biotherapy department (I2B), F-75252, Cedex 5, Paris, France.
Curr Rheumatol Rep. 2013 Nov;15(11):375. doi: 10.1007/s11926-013-0375-6.
Osteoarthritis (OA) is a whole joint disease, in which thinning and disappearance of cartilage is a critical determinant in OA progression. The rupture of cartilage homeostasis whatever its cause (aging, genetic predisposition, trauma or metabolic disorder) induces profound phenotypic modifications of chondrocytes, which then promote the synthesis of a subset of factors that induce cartilage damage and target other joint tissues. Interestingly, among these factors are numerous components of the inflammatory pathways. Chondrocytes produce cytokines, chemokines, alarmins, prostanoids, and adipokines and express numerous cell surface receptors for cytokines and chemokines, as well as Toll-like receptors. These receptors activate intracellular signaling pathways involved in inflammatory and stress responses of chondrocytes in OA joints. This review focuses on mechanisms responsible for the maintenance of cartilage homeostasis and highlights the role of inflammatory processes in OA progression.
骨关节炎（OA）是一种全关节疾病，其中软骨变薄和消失是 OA 进展的关键决定因素。无论其原因（衰老、遗传易感性、创伤或代谢紊乱）如何，软骨稳态的破裂都会导致软骨细胞发生深刻的表型改变，进而促进一系列促软骨损伤因子的合成，并靶向其他关节组织。有趣的是，这些因子中有许多是炎症途径的组成部分。软骨细胞产生细胞因子、趋化因子、警报素、前列腺素和脂肪因子，并表达细胞因子和趋化因子的许多细胞表面受体，以及 Toll 样受体。这些受体激活细胞内信号通路，参与 OA 关节中软骨细胞的炎症和应激反应。这篇综述重点介绍了维持软骨稳态的机制，并强调了炎症过程在 OA 进展中的作用。
