In rheumatoid arthritis (RA), the chronically inflamed joint undergoes profound phenotypical changes. Aside synovial inflammation and cartilage degeneration, subchondral bone erosions emerge early in the course of disease and are associated with functional impairment in RA patients. Chronic joint inflammation injures the bone as consequence of two key pathophysiological mechanisms: On the one hand, the proliferative synovial tissue (“pannus”) attracts monocytes/macrophages to migrate into the joint and provides specific signals for these cells to differentiate into bone-resorbing osteoclasts. These cells are activated by pro-inflammatory cytokines and resorb mineralized tissue. Second, the injured bone attempts to counteract bone resorption by attracting osteoblasts at the site of erosion. However, the inflammatory local environment prevents significant repair by overproduction of osteoblast-inhibitory mediators and facilitation of osteoblast apoptosis. Until now, osteoimmunology research in arthritis primarily focused on the mechanism of joint destruction and the effects of inhibiting osteoclasts. However, recent experimental studies imply that fostering bone formation in chronic erosive arthritis could potentially reverse joint destruction with induction of repair phenomena. This review discusses the pathomechanisms leading to impaired bone turnover and potential mediators that could be targeted to reverse bone loss in RA.
Keywords: Rheumatoid arthritis (RA), bone erosion, osteoclast, osteoblast, cytokines
Rights & PermissionsPrintExport