Reduced deposition of collagen in the degenerated articular cartilage of dogs with degenerative joint disease.

Collagen metabolism in the focal degenerated cartilage from immature dogs with degenerative joint disease was compared with that in the adjacent 'normal' cartilage of the same joint surface. The deposition of collagen into the cartilage in vitro as measured by accumulation of hydroxy[14C]proline was decreased in the early and in advanced stages of cartilage degeneration. The deposition of collagen into cartilage in vivo as measured by the accumulation of hydroxy[3H]proline (intravenously injected [3H]proline) also was reduced in the degenerated cartilages of a dog with degenerative joint disease. Gel electrophoretic analysis revealed that degenerated cartilage contained less alpha 1 II collagen chains, but increased amounts of larger proteins. Degenerated cartilage contained more water, increased amounts of unidentified, non-collagenous protein, increased collagenolytic enzyme activity and fewer chondrocytes. Decreased deposition of collagen would result in collagen depletion in the foci of degenerated cartilage in joints of dogs with degenerative joint disease.

The type of collagen made by the articular cartilage in joints of dogs with degenerative joint disease.

The collagen in the degenerated articular cartilage from dysplastic canine hip joints was characterized as to type by examining cartilage directly and also after labeling cartilage slices with 14C-proline in vitro. Collagen analysis was by sodium dodecylsulfate-polyacrylamide gel electrophoresis of 14C-labeled collagen, and of 14C-peptides which had been cleaved by cyanogen bromide. Amino acid analysis was done on hydrolysates of whole cartilage and of purified collagens to quantify the ratio of hydroxyproline to hydroxylysine. Data revealed that type II collagen was the radiolabeled product synthesized in all samples of degenerated cartilage and was the only collagen detected in biochemical tests in the cartilage of joints with degenerative joint disease as well as in disease free hip joints. Results suggested that chondrocytes in degenerated cartilage of canine joints did not switch their collagen phenotype, but continued to synthesize type II collagen. Cartilage degeneration in joints of dogs with hip dysplasia proceeded without a change in collagen phenotype.