INTRODUCTION: Osteochondritis dissecans (OCD) within the weight-bearing femoral condyle carries a high risk of osteoarthritis. The definitive pathogenetic cause is unclear. Therefore biochemical and cellular features of OCD were analyzed and compared to macroscopically normal cartilage of the same joint surface.
MATERIALS AND METHODS: Dissected fragments from 14 patients and biopsies of normal cartilage from the intercondylar notch as controls were harvested at arthroscopy. Staining with safranin O to monitor proteoglycan content, alkaline phosphatase activity, and immunohistochemistry with mouse monoclonal antibodies to collagen types I, II, and X. Chondrocytes were isolated for RT-PCR to detect GAPDH, collagen types I, II, X, aggrecan, TGF-beta, BMP-7, bFGF, VEGF and IL-1. RESULTS: The dissected cartilage displayed significant variability. Apart from normal cartilage matrix components also atypical molecules such as collagen type X and alkaline phosphatase were detected at the tidemark but also across the entire dissecate, suggesting chondrocyte hypertrophy. Extended fibrous degeneration associated with collagen type I deposition was observed at the surface and may indicate chondrocyte dedifferentiation. Viable cells could be extracted from OCD and notch. Both expressed similar mRNA levels for matrix molecules, growth factors, and interleukin-1 (IL-1), however significantly more Col X mRNA was detected in dissecates.
CONCLUSION: Histology suggests focal alteration of cartilage matrix originating from the basis of the joint cartilage, potentially the mineralized layer or subchondral bone. The molecular analysis indicates a disorganization of cartilage homeostasis across the joint accompanied by embryogenetic processes. The surprisingly high viability and quality of the extracted cells suggests a still preserved intrinsic repair capacity of those vital dissecates. Pubmed