Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Department of Physical Medicine, Rehabilitation and Occupational Medicine, Medical University of Vienna, 1090 Vienna, Austria.
Int J Mol Sci. 2022 Aug 5;23(15):8740. doi: 10.3390/ijms23158740.
Rheumatoid arthritis (RA), an autoimmune disease, is characterized by the presence of symmetric polyarthritis predominantly of the small joints that leads to severe cartilage and bone destruction. Based on animal and human data, the pathophysiology of osteoporosis, a frequent comorbidity in conjunction with RA, was delineated. Autoimmune inflammatory processes, which lead to a systemic upregulation of inflammatory and osteoclastogenic cytokines, the production of autoantibodies, and Th cell senescence with a presumed disability to control the systemic immune system's and osteoclastogenic status, may play important roles in the pathophysiology of osteoporosis in RA. Consequently, osteoclast activity increases, osteoblast function decreases and bone metabolic and mechanical properties deteriorate. Although a number of disease-modifying drugs to treat joint inflammation are available, data on the ability of these drugs to prevent fragility fractures are limited. Thus, specific treatment of osteoporosis should be considered in patients with RA and an associated increased risk of fragility fractures.
类风湿关节炎（RA）是一种自身免疫性疾病，其特征为主要累及小关节的对称性多关节炎，可导致严重的软骨和骨破坏。基于动物和人类数据，RA 常见的合并症——骨质疏松症的病理生理学已经得到阐明。自身免疫炎症过程导致全身性炎症和破骨细胞生成细胞因子的上调、自身抗体的产生以及 Th 细胞衰老，可能对 RA 患者骨质疏松症的病理生理学中发挥重要作用。因此，破骨细胞活性增加，成骨细胞功能下降，骨代谢和力学特性恶化。尽管有许多治疗关节炎症的疾病修饰药物，但这些药物预防脆性骨折的能力的数据有限。因此，RA 患者和脆性骨折风险增加的患者应考虑进行骨质疏松症的特异性治疗。
