An investigation on the effect of FGF-2 for the induction of chondrogenesis in full-thickness articular cartilage defects.

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We investigated the effect of shorter exposure of fibroblast growth factor (FGF)-2 on the repair of die fufl-thickness defects of articular cartilage of rabbits. Five-mm full-thickness articular cartilage defects, which are not repaired spontaneously, were created in the femoral trochlea, and FGF-2 (150 pg/h) was administered into the joint cavity with an osmotic delivery system for 1 day, 3 days, 1 week or 2 weeks. By the treatment with FGF-2 for only 1 day, the defects were resurfaced wife cartilaginous matrix as successfully as those treated for 2 weeks. Immunohistochemical analyses using anti-proliferating cell nuclear antigen demonstrated high proliferative activity of mesenchymal cells in the reparative tissues at 1 week in all FGF-2 treated groups. Clearance of FGF-2 administered into the defect was monitored by a radiotope study. Half-life of FGF-2 in the defect cavity was estimated to be 【less than or equal】 30 min. We also examined in vitro the FGF-2 action on the migration of rabbit marrow-derived mesenchymal cells and found a chemotactic response of those cells to FGF-2. These results indicate that FGF-2 signals participate in mobilization and recruitment of actively replicating mesenchymal cells from bone marrow into the defect cavities.