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Enamel matrix derivative inhibits proteoglycan production and articular cartilage repair, delays the restoration of the subchondral bone and induces changes of the synovial membrane in a lapine osteochondral defect model in vivo

Improving the structural qualities of the new tissue that fills osteochondral defects is critical to enhance articular cartilage repair. Enamel matrix derivative (EMD) modulates chondrocyte proliferation and differentiation. In the present study, we assessed the effect of EMD on early chondrogenesis and bone repair in an osteochondral defect model in vivo. Standardized osteochondral defects were established in the trochlear groove of rabbits. EMD or the carrier substance without EMD activity was applied to the blood clot that was forming within the defect. After 3 weeks in vivo, the quality of articular cartilage repair was evaluated using a semiquantitative scoring system and biochemical assays for proteoglycan and DNA contents. The extent of formation of the subchondral bone within the original osteochondral defect was measured. Application of EMD resulted in an inferior histological articular cartilage repair. The total proteoglycan content of the repair tissue as well as the proteoglycan production standardized to the cell proliferative activities within the defects were reduced following treatment with EMD. Restoration of the subchondral bone within the osteochondral defect was delayed when EMD was applied. Significant changes of the synovial membrane were present, reflected in an increased villus thickening and changes in villus architecture. These data suggest that EMD inhibits the early repair of the osteochondral unit in vivo. Copyright © 2012 John Wiley & Sons, Ltd.