| [ Summary ] |
Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by chronic synovitis and bone damage. TNF and IL-6 play pivotal roles in the pathological processes of RA. Inflammatory cytokines such as TNF are largely produced from infl amed synovia and cause activation of osteoclasts which deviate from bone remodelling cycles, resulting in joint destruction. The combinational use of MTX and biologics targeting TNF, however, has revolutionized the treatment of RA, producing significant improvements in clinical, radiographic, and functional outcomes which were not previously observed. Progression of joint destruction is remarkably suppressed and structural remission is possible for the vast majority of patients. In contrast to the use of TNF inhibitors, bisphosphonate is well known to be effective for postmenopausal osteoporosis and glucocorticoid-induced osteoporosis, but not for RA bone erosion. The anti-RANKL antibody denosumab has the potential to inhibit joint destruction as well as systemic and GC-mediated osteoporosis in RA. In this review, differential mechanisms aff ecting bone damage observed in RA will be discussed from the viewpoint of the differential efficacy of TNF-inhibitors and anti-osteoporotic drugs. |