Abstract
The involvement of fibroblast growth factor-2 (FGF-2) during the repair of rabbit full-thickness articular cartilage defects was investigated. The local administration of FGF-2 for 2 weeks in the 5-mm-diameter defects of articular cartilage, which were large enough not to repair spontaneously, resulted in successful regeneration of the articular cartilage and the subchondral bone. In contrast, the administration of a neutralizing monoclonal antibody against FGF-2 caused a significant inhibition of a chondrogenic repair response in the 3-mm-diameter defects, which were small enough to be resurfaced spontaneously by articular cartilage. The chondrogenic repair response of the defects was correlated with the high incidence of PCNA-positive undifferentiated cells in the reparative defect cavities. We then assessed the effect of shorter exposures of FGF-2, and demonstrated that even a limited exposure (1 day) was sufficient for cartilage regeneration in the 5-mm-diameter defects. We also found that FGF-2 stimulated migration of cultured rabbit marrow-derived mesenchymal cells in vitro. These results indicate that FGF-2 signals participate in mobilization and recruitment of actively replicating mesenchymal cells from bone marrow into the defect cavities.
