Cell biology of stress fractures: activation of remodelling at sites of non-union

应力性骨折是一种使人衰弱的损伤。我们描述了大鼠尺骨应力性骨折的模型，了解到它们通过激活重塑愈合，关键基因以时间模式表达，部分骨折仍未愈合，与许多临床病例相似。现在，我们将检查重塑所必需的重要基因的细胞定位，并测试不同生长因子在骨折未愈合部分激活愈合反应的功效。

Stress fractures are debilitating injuries. We characterised a model of stress fractures in rat ulnae, learning that they heal by activated remodelling, that key genes are expressed in a temporal pattern, and that part of the fracture remains un-healed, similar to many clinical cases. Now, we will examine cell localisation of important genes necessary for remodelling, and test the efficacy of different growth factors to activate a healing response in the non-healed section of the fracture.