Bone differs from other tissues in its capacity to self-repair after a fracture. The low bone mass and structural deterioration of bone associated with osteoporosis increases the risk of fragility fracture compared with healthy individuals. The intention of this article is to review the complex process of fracture repair and essential requirements for a successful fracture healing response summarized as the "diamond concept" in terms of aging and osteoporosis. The current preclinical and clinical evidence for a beneficial or harmful influence of anti-osteoporosis medications such as bisphosphonates, parathyroid hormone (PTH), strontium ranelate and antibodies of Wnt-inhibiting signaling proteins on bone healing is presented and discussed. Literature suggests that there are no detrimental consequences of such therapeutics on fracture repair processes. Following a fragility fracture, it seems that early start of preventive anti-osteoporotic treatment right after surgery does not delay the union of the fracture, except perhaps in the case of very rigidly fixed fracture requiring direct bone healing. There is some promising experimental and clinical evidence for possible enhancement of the bone repair process via administration of systemic agents. Further well designed studies in humans are necessary to accumulate more evidence on the positive effects and to translate this knowledge into valid therapeutic applications.
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