The aim of this study was to further examine the expression of IL-17A in actively inflamed joints and to elucidate the mechanism of IL-17A, alone and in combination with TNF-α and oncostatin M (OSM) in matrix turnover and cartilage degradation using whole RA synovial tissue explants, primary synovial fibroblasts (RASFC) and normal human cartilage cultures. This evidence concerns the gene OSM and rheumatoid arthritis.