Reed A A C, Joyner C J, Isefuku S, Brownlow H C, Simpson A H R W
Botnar Research Centre, Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, University of Oxford, Headington, England, UK.
J Bone Joint Surg Br. 2003 May;85(4):604-10. doi: 10.1302/0301-620x.85b4.12944.
Our aim was to develop a clinically relevant model of atrophic nonunion in the rat to test the hypothesis that the vessel density of atrophic nonunion reaches that of normal healing bone, but at a later time-point. Atrophic nonunion is usually attributed to impaired blood supply and is poorly understood. We determined the number of blood vessels at the site of an osteotomy using immunolocalisation techniques in both normally healing bones and in atrophic nonunion. At one week after operation there were significantly fewer blood vessels in the nonunion group than in the healing group. By eight weeks, the number in the atrophic nonunion group had reached the same level as that in the healing group. Our findings suggest that the number of blood vessels in atrophic nonunion reaches the same level as that in healing bone, but at a later time-point. Diminished vascularity within the first three weeks, but not at a later time-point, may prevent fractures from uniting.
我们的目标是建立一种大鼠萎缩性骨不连的临床相关模型，以验证以下假说：萎缩性骨不连的血管密度在后期可达到正常愈合骨的水平。萎缩性骨不连通常归因于血供受损，目前对此了解甚少。我们运用免疫定位技术，测定了正常愈合骨和萎缩性骨不连中截骨部位的血管数量。术后一周，骨不连组的血管数量显著少于愈合组。到八周时，萎缩性骨不连组的血管数量已达到愈合组的水平。我们的研究结果表明，萎缩性骨不连的血管数量在后期可达到愈合骨的水平，但时间较晚。前三周血管减少，但后期不会，这可能会阻碍骨折愈合。
