The literature about the effects of systemically administered calcitonin on fracture healing and in the prevention of disuse osteoporosis after fracture are reviewed in this study. Fracture healing is a biological process of great importance for the survival of the injured animal. Endochondral ossification is augmented in the fracture site followed by fast remodeling of the produced woven bone. There is strong evidence of the direct effects of calcitonin on cartilage proliferation as well as the vascularization of the callus. Calcitonin is found to promote the cartilaginous phase of fracture healing. On the other hand, the innervation of callus reveals an extensive distribution of sensory fibers containing a calcitonin gene-related peptide, a neuropeptide with potent vasodilatory actions. From several experimental studies, salmon calcitonin administration has been found to have a beneficial effect on fracture healing. Studies in humans also concur that calcitonin may speed up the time of fracture repair and facilitate early mobilization of the injured limb. Finally, calcitonin prevents post-fracture bone loss due to increased post-injury remodeling and lowers hydroxyproline and calcium excretion of patients who underwent internal fixation of fracture on the hip.
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