Abstract

Purpose: Cartilage degradation in OA is due to the overproduction of secreted proteases by chondrocytes, including the matrix metalloproteinases (MMPs). Synoviocytes can also contribute to this activity by releasing mediators that exacerbate joint destruction. Cross-talk between synovial cells and chondrocytes mediated by proinflammatory factors could intensify catabolic signaling activity in both cell populations to contribute to joint tissue destruction. Protease cleavage of matrix proteins generates matrix fragments that include fibronectin fragments (FN-f) found in OA cartilage and synovial fluid.

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