Oelzner P, Hein G
Klinik für Innere Medizin IV, Friedrich-Schiller-Universität Jena.
Med Klin (Munich). 1997 Oct 15;92(10):607-14. doi: 10.1007/BF03044788.
Systemic osteoporosis is a common and pathogenetically heterogenous complication in rheumatoid arthritis. Various factors such as disease activity, dosage and duration of glucocorticoid treatment and immobilization are involved in pathogenesis of osteoporosis in rheumatoid arthritis.
Proinflammatory cytokines secreted by immunocompetent cells have a role in the regulation of the activity of osteoblasts and osteoclasts. The effects of these proinflammatory cytokines include the inhibition of bone formation and an increase in bone resorption. Interleukin-6 and nitric oxide induced in osteoblasts by proinflammatory cytokines are likely to be important mediators between these cytokines and the function of osteoblasts and osteoclasts. Furthermore, disease activity dependent changes in the secretion of glucocorticoids and in vitamin D metabolism may be involved in the pathogenesis of osteoporosis in this disease. Alteration of bone remodeling associated with immobilization is an important factor of systemic bone loss in rheumatoid arthritis.
The inflammatory process in rheumatoid arthritis may cause penarticular and systemic bone loss by various cytokine and hormone mediated mechanisms. Concluding from these pathogenetic mechanisms, bisphosphonates and active vitamin D metabolites are likely to be effective therapeutic options in osteoporosis associated with rheumatoid arthritis.
全身性骨质疏松是类风湿关节炎中一种常见且发病机制异质性的并发症。疾病活动度、糖皮质激素治疗的剂量和持续时间以及制动等多种因素参与类风湿关节炎骨质疏松的发病机制。
免疫活性细胞分泌的促炎细胞因子在调节成骨细胞和破骨细胞的活性中起作用。这些促炎细胞因子的作用包括抑制骨形成和增加骨吸收。促炎细胞因子在成骨细胞中诱导产生的白细胞介素-6和一氧化氮可能是这些细胞因子与成骨细胞和破骨细胞功能之间的重要介质。此外，疾病活动度依赖性的糖皮质激素分泌变化和维生素D代谢可能参与该疾病骨质疏松的发病机制。与制动相关的骨重塑改变是类风湿关节炎全身性骨质流失的一个重要因素。
类风湿关节炎中的炎症过程可能通过多种细胞因子和激素介导的机制导致关节周围和全身性骨质流失。从这些发病机制推断，双膦酸盐和活性维生素D代谢产物可能是类风湿关节炎相关骨质疏松的有效治疗选择。
