Rheumatoid arthritis is among the most frequent autoimmune diseases and is a proto - type of an osteoimmune disease. Bone manifestations of the disease include erosions and systemic osteoporosis. Animal models and clinical studies consistently demonstrate that bone destruction in rheumatoid arthritis is predominantly due to excessive osteoclast activity. Proinflammatory cytokines play an important role in the destruction of inflamed joints; in rheumatoid arthritis RANKL, tumour necrosis factor- , interleukin-1, interleukin-6 and interleukin-17 increase osteoclast generation and activation and thus mediate bone destruction. Recent data suggest that anti - bodies against citrullinated peptides directly induce bone resorption. In contrast to bone resorption, bone formation at the sites of erosions typically is suppressed; this is mediated by antagonists of the wnt pathway, e. g. an upregulation of dickkopf-1. Targeting osteoimmune pathways thus appears to be a promising future treatment strategy for rheumatoid arthritis.
ASJC Scopus subject areas
- Medicine (all)