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This article is part of the supplement: 21st European Workshop for Rheumatology Research

Meeting abstract

The pathogenesis of osteoarthritis: potential targets for therapy

S Abramson

  • Correspondence: S Abramson

Author Affiliations

Department of Rheumatology & Medicine, Hospital for Joint Diseases, New York, USA

Arthritis Res 2001, 3(Suppl A):L020  doi:10.1186/ar165

The electronic version of this article is the complete one and can be found online at:


Received:15 January 2001
Published:26 January 2001

© 2001 2001 BioMed Central Ltd

Meeting abstract

It is likely that the excessive production of cytokines, inflammatory mediators and growth factors by the inflamed synovium and activated chondrocytes play an important role in the pathophysiology of osteoarthritis. IL-1b and TNF-a can stimulate their own production and induce chondrocytes and synovial cells to produce other cytokines such as IL-8, IL-6, LIF, as well as stimulate proteases, nitric oxide (NO) and prostaglandin E2 (PGE2) production. NO and PGE2 are spontaneously produced by human osteoarthritis-affected cartilage. The excessive production of nitric oxide inhibits matrix synthesis and promotes its degradation. Furthermore, by reacting with oxidants such as superoxide anion, nitric oxide promotes cellular injury and renders the chondrocyte susceptible to cytokine-induced apoptosis. Although PGE2 is the predominant eicosanoid produced by OA cartilage, PGI2, PGD2, TXA2 and LTB4 are also spontaneously produced. These specific eicsoanoids exert diverse effects on matrix metabolism and gene expression that require detailed elucidation. Differential gene product analysis also reveals increased expression of osteopontin (OPN) and fibronectin (FN) mRNA in human osteoarthritis-affected. Osteopontin inhibits the spontaneous production of inflammatory mediators such as NO and PGE2. Therefore, inflammatory and anti-inflammatory molecules produced by OA chondrocytes can be targeted in future therapeutic stategies of OA.