Effects of diabetes and steroids on fracture healing

Fracture healing is largely controlled by local regulatory interactions among cells and tissues near the site of injury; however, many systemic hormones including insulin, the glucocorticoids, and the gonadal steroids also can influence the course of tissue repair, particularly in the case of pathologic hormone excess or deficiency. Using well-defined animal models, recent studies have established that deficiencies in insulin and estrogen impair fracture healing, but data from this type of experiment are limited. Still, the similarities between morphogenetic events in fracture healing and those found in normal bone development and remodeling suggest that testable predictions can be made concerning hormonal effects on the progress of fracture healing. One concept that has received some direct experimental support in fracture healing model studies is that systemic hormones exert pleiotropic effects on callus tissue by regulating the expression and activity of local growth factors. Further verification of this and other predicted hormone effects should increase our understanding of the fundamental mechanisms underlying fracture repair, and may aid development of means to improve fracture healing in states of altered endocrine function.