Schett Georg
Department of Internal Medicine 3, University of Erlangen-Nurnberg, Erlangen, Germany.
Autoimmunity. 2008 Apr;41(3):224-9. doi: 10.1080/08916930701694717.
Cytokine expression in the inflamed synovial membrane of patients with rheumatoid arthritis and other forms of chronic inflammatory arthritis and other forms of chronic inflammatory arthritis leads to formation of osteoclasts. These cells are primarily involved in the resorption of mineralized cartilage and bone and thus participate in joint damage in the course of chronic arthritides. Osteoclastogenesis in the synovial membrane is driven by cytokines such as RANKL, MCSF but also classical proinflammatory mediators such as TNF, IL-1 and IL-6. Inhibition of osteoclast formation has proven as an effective approach to inhibit structural damage in experimental arthritis and preliminary data suggest that such approaches are also effective in human RA.
类风湿关节炎及其他形式的慢性炎症性关节炎患者炎症滑膜中的细胞因子表达会导致破骨细胞形成。这些细胞主要参与矿化软骨和骨的吸收,从而在慢性关节炎病程中参与关节损伤。滑膜中的破骨细胞生成由RANKL、MCSF等细胞因子驱动,但也由TNF、IL-1和IL-6等经典促炎介质驱动。在实验性关节炎中,抑制破骨细胞形成已被证明是抑制结构损伤的有效方法,初步数据表明,此类方法在人类类风湿关节炎中也有效。