Pathogenesis of degenerative joint disease produced by in vivo freezing of rabbit articular cartilage.

Overview

In vivo freezing of rabbit lateral femoral arterial cartilage with a cryoprobe produces an osteoarthritic-like condition in 12 months. Previous studies have established that the chondrocytes are killed by the freezing process. A loss of stainable mucopolysaccharide occurs. The collagen content of the lesional tissue does not change. The present study investigates the extracellular lysosomal enzyme content, collagen type (I or II), and histologic changes which produce chondrocyte cell clusters in the frozen tissue in response to freezing or articular cartilage. The results indicate that after the initial 30 days there is no significant rise in the extracellular lysosomal enzyme content of the experimental tissue compared with controls. Type II, or cartilage, collagen remains the major constituent of the lesional tissue. Histologic examination at six- to 12-month intervals suggests that chondrocyte clones are produced by invasion by the underlying viable subchondral bone. These results provide insight into the pathogenesis of degenerative joint disease and the rationale of treatment by the use of inhibitors of vascular invasion of articular cartilage.