Tanaka Yoshiya
The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1, Iseigaoka, Kitakyushu 807-8555, Japan.
J Clin Med. 2021 Mar 17;10(6):1241. doi: 10.3390/jcm10061241.
In rheumatoid arthritis, a representative systemic autoimmune disease, immune abnormality and accompanying persistent synovitis cause bone and cartilage destruction and systemic osteoporosis. Biologics targeting tumor necrosis factor, which plays a central role in the inflammatory process, and Janus kinase inhibitors have been introduced in the treatment of rheumatoid arthritis, making clinical remission a realistic treatment goal. These drugs can prevent structural damage to bone and cartilage. In addition, osteoporosis, caused by factors such as menopause, aging, immobility, and glucocorticoid use, can be treated with bisphosphonates and the anti-receptor activator of the nuclear factor-κB ligand antibody. An imbalance in the immune system in rheumatoid arthritis induces an imbalance in bone metabolism. However, osteoporosis and bone and cartilage destruction occur through totally different mechanisms. Understanding the mechanisms underlying osteoporosis and joint destruction in rheumatoid arthritis leads to improved care and the development of new treatments.
在类风湿关节炎(一种典型的系统性自身免疫性疾病)中,免疫异常及随之而来的持续性滑膜炎会导致骨骼和软骨破坏以及全身性骨质疏松。针对在炎症过程中起核心作用的肿瘤坏死因子的生物制剂和Janus激酶抑制剂已被用于类风湿关节炎的治疗,使临床缓解成为一个切实可行的治疗目标。这些药物可以预防骨骼和软骨的结构损伤。此外,由绝经、衰老、活动减少和使用糖皮质激素等因素引起的骨质疏松,可以用双膦酸盐和抗核因子κB受体活化剂抗体进行治疗。类风湿关节炎中的免疫系统失衡会导致骨代谢失衡。然而,骨质疏松以及骨骼和软骨破坏是通过完全不同的机制发生的。了解类风湿关节炎中骨质疏松和关节破坏的潜在机制有助于改善护理并开发新的治疗方法。