Objectives
In rheumatoid arthritis (RA), tumor necrosis factor (TNF) alpha is a major inductor of the proinflammatory/pro-destructive functions of synovial fibroblasts (SFB). These effects are predominantly mediated via the TNF receptor-1 (TNFR1). In addition to the NF-κB pathway, the p38 MAP kinase seems to play a central role for the underlying signal transduction. In the present study, RA-SFB were compared with osteoarthritis (OA)-SFB concerning the TNF-α/TNFR1/2-induced secretion of IL-6, IL-8, prostaglandin E2 (PGE2), and matrix metalloproteinase-1/tissue inhibitor of matrix metalloproteinase-1 (MMP-1/TIMP-1), as well as the sensitivity to p38 MAP-kinase inhibition.