Eckardt H, Ding M, Lind M, Hansen E S, Christensen K S, Hvid I
Department of Orthopaedic Surgery, Aalborg Hospital, Box 365, 9100 Aalborg, Denmark.
J Bone Joint Surg Br. 2005 Oct;87(10):1434-8. doi: 10.1302/0301-620X.87B10.16226.
The re-establishment of vascularity is an early event in fracture healing; upregulation of angiogenesis may therefore promote the formation of bone. We have investigated the capacity of vascular endothelial growth factor (VEGF) to stimulate the formation of bone in an experimental atrophic nonunion model. Three groups of eight rabbits underwent a standard nonunion operation. This was followed by interfragmentary deposition of 100 microg VEGF, carrier alone or autograft. After seven weeks, torsional failure tests and callus size confirmed that VEGF-treated osteotomies had united whereas the carrier-treated osteotomies failed to unite. The biomechanical properties of the groups treated with VEGF and autograft were identical. There was no difference in bone blood flow. We considered that VEGF stimulated the formation of competent bone in an environment deprived of its normal vascularisation and osteoprogenitor cell supply. It could be used to enhance the healing of fractures predisposed to nonunion.
血管重建是骨折愈合过程中的早期事件;因此,血管生成的上调可能会促进骨形成。我们在实验性萎缩性骨不连模型中研究了血管内皮生长因子(VEGF)刺激骨形成的能力。三组,每组八只兔子接受了标准的骨不连手术。随后在骨折断端间分别植入100微克VEGF、单纯载体或自体骨移植。七周后,扭转失效试验和骨痂大小证实,接受VEGF治疗的截骨已愈合,而接受载体治疗的截骨未愈合。接受VEGF和自体骨移植治疗的组的生物力学特性相同。骨血流量没有差异。我们认为,VEGF在缺乏正常血管化和骨祖细胞供应的环境中刺激了有功能的骨形成。它可用于促进易发生骨不连的骨折的愈合。