Figure 1

Targeting joint destruction in rheumatoid arthritis requires the inhibition of several pathways. Apart from interrupting the effect of macrophage-derived proinflammatory cytokines that stimulate the rheumatoid arthritis synovial fibroblasts (RA-SFs), the specific properties of these cells need to be targeted. This comprises the inhibition of cellular activation of RA-SFs, their attachment to the cartilage, the invasion into the cartilage through the release of matrix-degrading enzymes, altered apoptosis and angiogenesis.