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BMP2 expression in chondrocytes is essential for early fracture healing


Fracture healing in Bmp2 knockout mice, which lacked the gene either in their chondrocytes or their osteoblasts, was assessed using a range of techniques including X-rays, micro-CT scanning, histology, biomechanical testing and assays of gene expression.

Clear differences in fracture healing were observed. The mice that did not express Bmp2 in osteoblasts showed a similar pattern of fracture healing to wild-type mice, with consolidated bridging of the fracture gap by day 14, complete mineralized bridging by day 21 and mineralized replacement by day 28.

In mice that did not express Bmp2 in chondrocytes, healing was slower, with consolidated bridging occurring between day 21 and day 28. Cartilage callus formation was prolonged and mineralization was delayed, leading to a healed fracture with significantly less biomechanical strength. These mice also showed significantly lower levels of Col2a1 and Col10a1 expression by day 10, compared to wild-type mice and osteoblast-specific Bmp2 knockout mice. The authors suggest that endogenous Bmp2 expression in chondrocytes plays an essential role in the early stage of fracture healing, promoting maturation of the cartilage callus.

Editor’s comment: BMP2, considered to be a potent bone anabolic agent, is currently one of the few approved topical drugs to enhance fracture healing. This study now shows that the effects of BMP2 on fracture healing may occur predominantly through the regulation of the endochondral repair process.

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