Abstract
Introduction: Collagen type X is secreted by hypertrophic chondrocytes during fracture repair. Its precise role is uncertain. This study uses a knockout mouse model in which the collagen X gene is removed to examine its function.
Method: Bilateral femoral fractures were created in type X collagen knockout mice (mutant) and normal mice (wild type), and were stabilized using an external fixator. The mice were sacrificed 7, 10, 14, 21, 28 and 60 days after fracture. Fracture healing was followed by x-rays, histology, gene expression studies, immuno-histochemistry and mechanical testing.
Results: In the mutant mice, bony union was delayed, there was abnormal persistence of aggrecan up to 60 days after fracture. Histology reviewed amorphous acellular areas surrounded by osteoclasts at 21 and 28 days, while mechanical testing revealed that at 14 days after fracture, mutant callus was stiffer than the wild type, but the trend is reversed at 28 and 60 days.
Discussion: This study contributes to the understanding of the basic mechanisms involved in fracture repair. The data suggest that collagen type X plays a significant role in bone remodeling during fracture healing. Its absence results in delayed union and abnormalities within the fracture callus.
The abstracts were prepared by Professor Jegan Krishnan. Correspondence should be addressed to him at the Flinders Medical Centre, Bedford Park 5047, Australia.
