Influence of retinyl acetate on osteochondral junction chondrocytes in C3H and balb mice.

Abstract

To establish the pathophysiology of retinoid induced hyperostosis. Radiographical, histological, ultrastructural, and immunohistochemical features of retinoid induced hyperostosis were evaluated using C3H-Heston mice and Balb mice. Dose dependent and progressive ossification was noted at extraosseous sites of both mouse strains. New bone formation was seen not only in the extraosseous tissues, but subchondral bone showed prominent proliferation. Major histopathological abnormalities appeared to take place in the chondrocytes near the osteochondral junctions, and some of the metaplastic chondrocytes near the osteochondral junction expressed osteocalcin and type I collagen, extracellular molecules normally present in bone. Species dependent responsiveness was also noted. Longterm administration of retinoids may induce an aberrant differentiation of the articular and entheseal chondrocytes near the osteochondral junctions, and the affected cells appeared to produce extracellular components including osteocalcin and type I collagen.