Wei Yingjun, Xie Xingwen, Li Dingpeng, Hou Xuan, Ren Ling, Wan Kangwei
Gansu University of Chinese Medicine, Lanzhou, China.
Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, China.
Front Med (Lausanne). 2025 Aug 20;12:1643285. doi: 10.3389/fmed.2025.1643285. eCollection 2025.
Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic synovial inflammation, autoantibody production and progressive joint destruction. One of the main pathological features is irreversible damage and dysfunction of bone and joints, and the core pathological link is osteoclast-mediated imbalance of bone metabolism. With the advances in immunology, molecular biology and cytology, different types of cells, including T cells, B cells, macrophages, natural killer cells, synovial fibroblasts and vascular endothelial cells, activate osteoclasts in rheumatoid arthritis, leading to bone metabolism imbalance in RA and causing bone and joint damage. In this paper, we will systematically summarize the effects and mechanisms of different cell types on osteoclast differentiation in rheumatoid arthritis bone metabolism, which will provide theoretical basis and practical guidance for the precise treatment and targeted intervention of RA bone metabolism abnormalities.
类风湿关节炎是一种全身性自身免疫性疾病，其特征为慢性滑膜炎症、自身抗体产生和进行性关节破坏。主要病理特征之一是骨骼和关节的不可逆损伤及功能障碍，核心病理环节是破骨细胞介导的骨代谢失衡。随着免疫学、分子生物学和细胞学的发展，包括T细胞、B细胞、巨噬细胞、自然杀伤细胞、滑膜成纤维细胞和血管内皮细胞在内的不同类型细胞在类风湿关节炎中激活破骨细胞，导致类风湿关节炎中骨代谢失衡并引起骨骼和关节损伤。在本文中，我们将系统总结不同细胞类型在类风湿关节炎骨代谢中对破骨细胞分化的影响及机制，这将为类风湿关节炎骨代谢异常的精准治疗和靶向干预提供理论依据和实践指导。
