Bian Qin, Wang Yong-Jun, Liu Shu-Fen, Li Yi-Ping
Department of Orthopedics and Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, No.725 South Wan-ping Road, Shanghai, China.
Front Biosci (Elite Ed). 2012 Jan 1;4(1):74-100. doi: 10.2741/361.
Osteoarthritis (OA) is the most common form of joint disease. OA frequently affects knees, hips, hands, and the spine. It is characterized by the progressive destruction of articular cartilage and subchondral bone accompanied by low-grade inflammation that together result in pain and deformity. Recent studies have shed light on the nature of OA genetic susceptibility and confirmed a number of candidate genes involved in the destruction of the synovium, articular cartilage, and subchondral bone in OA pathogenesis. During the progression of OA, there are several cellular changes in joints, including an increase in the number of activated osteoclasts and macrophages and an infiltration of the synovium by activated T-cells and B-cells. Pro-inflammatory mediators (e.g. interleukin IL-1, IL-1beta, IL-6, IL-17, and IL-18, and Tumor necrosis actor-alpha), proteinases (e.g. matrix metalloproteinase 9 and cathepsin K), and regulators of cartilage and bone formation (e.g. BMPs) have been shown to have important roles in OA progression at the molecular level. Studies have suggested that OA shares several common characteristics with rheumatoid arthritis (RA). To systematically understand OA, this review summarizes OA disease genes, mouse models of human disease experimental mouse models, mechanisms of OA pathogenesis, and current OA therapies.
骨关节炎（OA）是最常见的关节疾病形式。OA常累及膝关节、髋关节、手部和脊柱。其特征是关节软骨和软骨下骨的进行性破坏，并伴有低度炎症，共同导致疼痛和畸形。最近的研究揭示了OA遗传易感性的本质，并证实了一些参与OA发病机制中滑膜、关节软骨和软骨下骨破坏的候选基因。在OA进展过程中，关节会出现多种细胞变化，包括活化破骨细胞和巨噬细胞数量增加，以及活化T细胞和B细胞浸润滑膜。促炎介质（如白细胞介素IL-1、IL-1β、IL-6、IL-17和IL-18，以及肿瘤坏死因子-α）、蛋白酶（如基质金属蛋白酶9和组织蛋白酶K）以及软骨和骨形成调节因子（如骨形态发生蛋白）已被证明在分子水平上对OA进展具有重要作用。研究表明，OA与类风湿关节炎（RA）有一些共同特征。为了系统地了解OA，本综述总结了OA疾病基因、人类疾病实验小鼠模型、OA发病机制以及当前的OA治疗方法。
