The effects of microfracture and bone morphogenetic protein-2 on the healing of articular cartilage defect of the rabbit

Articular cartilage has a limited capacity for repair. The lack of repair in partial cartilage injury may result from the avascular nature of cartilage. Several methods have been developed to accelerate cartilage healing. Microfracture is an operative method that can facilitate access to stem cells in bone marrow and stimulate cartilage regeneration. However, microfracture has been shown to result in regeneration with fibrocartilage. The bone morphogenetic protein-2 has been shown to induce the expression of cartilage and bone marker. These findings prompted us to investigate rhBMP-2's ability to modulate the repair of full-thickness defect of articular cartilage. The full thickness articular cartilage defects of 6x3mm size were created in the trochlear groove of forty-eight rabbits. Twelve defects were left empty, and other thirty-six defects were treated with microfracture. Among those thirty-six defects, twelve defects were filled with fibrin glue, and twelve defects with fibrin glue and rhBMP-2. The animals were killed at 8 weeks after surgery. The repair tissue was examined histologically and evaluated with real time PCR to analysis collagen type. After microfracture at the cartilage defect, treatment with fibrin glue and rhBMP-2 accelerated cartilage healing and the formation of new subchondral bone, and showed more hyaline-like cartilage components than other groups on the histological findings. Real-time PCR showed higher amounts of collage type 1 and type 2 in the group filled with fibrin glue and rhBMP-2.