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Cartilage destruction in osteoarthritis (OA) is thought to be mediated by two main enzyme families; the matrix metalloproteinases (MMPs) are responsible for cartilage collagen breakdown, whereas enzymes from the 'a disintegrin and metalloproteinase domain with thrombospondin motifs' (ADAMTS) family mediate cartilage aggrecan loss. Tissue inhibitors of metalloproteinases (TIMPs) regulate the activity of these enzymes. Although cartilage destruction in OA might be driven by the chondrocyte, low-grade synovitis is reported in patients with all grades of this disease.  Our earlier work profiling these gene families in cartilage identified a number of genes that are regulated in OA, which are hence implicated in the disease process. Because the synovium might contribute to cartilage-matrix destruction in OA, we have extended the screening in the current study. We have profiled  MMP ,  ADAMTS  and  TIMP  genes in both cartilage and synovium from patients with either OA of the hip or a fracture to the neck of femur (NOF), giving a more complete picture of proteolysis in this disease.  The four most significantly upregulated genes ( P  < 0.0001) in OA synovium compared to the fractured NOF are  MMP28 ,  ADAMTS16 ,  ADAMTS17  and  TIMP2 . For  MMP9 ,  MMP10 ,  MMP12 ,  MMP17, MMP23 ,  MMP28 ,  ADAMTS4 , and  ADAMTS9 , there is a significant correlation between expression levels in the synovium and cartilage, suggesting similar mechanisms of regulation. Additionally, we have shown that in cartilage the median level of steady-state mRNA for  MMP13  is approximately 20-fold higher than  MMP28  and approximately 1,500-fold higher than  ADAMTS16 , with expression of this latter gene approximately 150-fold higher in synovium than cartilage.  This study is the most comprehensive analysis of the metzincin family of proteinases in the joint to date and has identified several proteinase genes not previously reported to be expressed or regulated in synovium.

Expression profiling of metalloproteinases and their inhibitors in synovium and cartilage.