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Background The mechanism of osteoporosis in rheumatoid arthritis (RA) is multifactorial. However, inflammation and autoimmunity are key players in its pathogenesis. Treatment with tumour necrosis factor alpha (TNFa) blockers has been shown to be beneficial for bone metabolism and they were able to prevent bone deformities in RA. Moreover, they improved the bone mineral density (BMD) [1]. However, the role of B lymphocytes in bone turnover is still controversial. Mice models showed that B cell deficiency resulted in marked osteopenia [2]. This was explained by the marked decrease in bone marrow levels of osteoprotegerin (OPG) produced by B cells. However, treatment of 46 RA patients with rituximab revealed a marked reduction of the bone resorption marker beta-crosslaps (bCTX) after 6 months [3].

bmc musculoskeletal disorders

Changes in bone density and bone turnover in patients with rheumatoid arthritis treated with rituximab, a B cell depleting monoclonal antibody (HORUS TRIAL)