OSTEOARTHRITIC CARTILAGE FIBRILLATION IS ASSOCIATED WITH A DECREASE IN CHONDROCYTE ADHESION TO FIBRONECTIN

Ojective: Cartilage destruction in osteoarthritis (OA) is generally ac cepted as a failed repair process. Cell adhesion is implicated in tiss ue repair. Therefore, adhesion of OA chondrocytes to extracellular mat rix proteins was investigated. Design: Using chondrocytes from human O A femoral head cartilage, adhesion to fibronectin and type II collagen of cells from distinct areas showing an intact cartilage surface or a fibrillated cartilage surface was studied. Modulation of chondrocyte adhesion by both protein kinase C (PKC) inhibitors and glucosamine sul fate (CS) was also investigated. Results: A significant (P < 0.05) dec rease in adhesion to fibronectin of chondrocytes from fibrillated cart ilage, relative to those from grossly normal OA cartilage, was demonst rated. Adhesion to type II collagen was not modified by the chondrocyt e origins (either from normal or fibrillated OA cartilage). Adhesion t o fibronectin of cells from grossly intact cartilage was decreased by the addition of PKC and calmodulin-dependent kinase inhibitors, W7 and sphingosine, to the cell culture. Adhesion to fibronectin of chondroc ytes from fibrillated cartilage was significantly (P < 0.05) increased after glucosamine sulfate treatment. Conclusion: Fibrillation of cart ilage from OA femoral head is associated with a defective adhesion of chondrocytes to fibronectin. The process is suggested to be dependent of PKC and/or calmodulin-dependent kinases and potentially reversible. Conceivably, it could play a role in OA cartilage destruction.