The role of B cells in bone turnover in rheumatoid arthritis

Recent research has focused on the link between the immune and skeletal systems leading to the emergence of a new discipline named osteoimmunology, which incorporates the complex interactions and overlap between the two systems. The effect of B lymphocytes on bone metabolism is still poorly understood, although recent evidence suggests that B cells may be implicated in the pathogenesis of bone loss in patients with rheumatoid arthritis. Mature B cells have the potential to both inhibit and stimulate osteoclastogenesis via the secretion of specific cytokines; they have the ability to produce RANKL, a pro-osteoclastogenic cytokine, osteoprotegerin, an antiosteoclastogenic cytokine, and TGF-β, a cytokine that has the ability to both induce and inhibit osteoclast formation. It is, therefore, not surprising that the existing evidence from both in vitro and in vivo studies is inconsistent. This review critically examines the role of B lymphocytes and key cytokines in the regulation of osteoblasto-and osteoclasto-genesis in rheumatoid arthritis.