PPARγ mRNA expression is down regulated in human OA chondrocytes treated with IL-1, and both PPARγ and PPARα ligands also inhibited IL-1-induced MMP and nitric oxide production in human chondrocytes, suggesting that these receptors may play an important role in IL-1-mediated cartilage breakdown and inflammation in arthritis.21,22,24,27 In addition, PPARγ cartilage-specific knockout (KO) mice exhibit spontaneous OA, and mice with inducible cartilage-specific PPARγ KO, subjected to the DMM model of OA, experienced more rapid development of OA than control mice.43,44. This evidence concerns the gene PPARG and arthritic joint disease.