The present results indicate that the clinical outcomes obtained with all four approaches can be maintained over a period of 10 years.

Within their limits, the present results indicate the following: 1) the clinical improvements obtained following treatment with EMD or GTR can be maintained over a period of 8 years; and 2) further studies of much higher power need to be performed to support equivalence.

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.