Bone necrosis secondary to avascularity may not only delay or inhibit consolidation of a fracture, it may also be a cause of refracture. Both initial trauma und surgical insult will determine the extent of necrosis. Only the latter is under the surgeon's control; it can be reduced by gentle soft tissue handling and by minimizing periosteal stripping. While the impact of avascular necrosis on fracture healing is well recognized, its role in the pathogenesis of refractures has received less attention. Cortical necrosis delays bridging of gaps; these gaps act as stress risers which, following resumption of full activity or after implant removal, can lead to refracture. Evaluation of 28 refractures in 25 patients, with biopsies in 14 patients, suggests that the duration of fracture immobilization through external or internal means must be sufficiently long to allow vascular invasion of necrotic areas, their substitution by new bone and bridging of the fracture. These processes must be followed by radiographic studies prior to implant removal. Special attention needs to be paid to adequate visualization of the fracture gap on successive radiographs.
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