Rheumatology 2003; 42: II11-II16
© 2003 British Society for Rheumatology
Original Article |
Pathogenesis of bone and cartilage destruction in rheumatoid arthritis
Harvard Medical School, New England Baptist Bone and Joint Institute, Boston, MA, USA.
Correspondence to:
Correspondence to: S. R. Goldring, Beth Israel Deaconess Medical Center, Department of Medicine, 110 Francis Street, #5A, Boston, MA 02215, USA. E-mail: sgoldrin{at}caregroup.harvard.edu
Proinflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF
), have been implicated in the dysregulation of bone and cartilage remodelling characteristic of rheumatoid arthritis (RA). With respect to bone remodelling, both of these cytokines have been shown to up-regulate the production of the receptor activator of nuclear factor-
B ligand, which acts to enhance osteoclastic bone resorption. TNF stimulates differentiation of osteoclast progenitors into mature osteoclasts and IL-1 acts directly on osteoclasts to increase the bone-resorbing capacity of these cells. IL-1 and TNF also adversely affect cartilage remodelling, although IL-1 is more potent on a molar basis. This cytokine not only increases production of factors that stimulate cartilage matrix degradation, but also inhibits the synthesis of type II collagen and proteoglycans. Enhanced understanding of the mechanisms underlying the processes of joint destruction will allow more selective and specific application of therapeutic agents that target these pro-inflammatory cytokines and, thus, more effective management of patients with RA and other inflammatory disorders.
KEY WORDS: Bone, Cartilage, Cytokines, Interleukin-1, Osteoclast, Receptor activator of nuclear factor-B ligand, Rheumatoid arthritis, Tumour necrosis factor alpha
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