Fracture Repair: Update on Mechanism and Antagonists

Abstract

Fracture healing is a complex biologic process that involves specific regenerative patterns and changes in the expression of several gene pathways. After the initial trauma, bone heals by a direct intramembranous or an indirect fracture-healing process, which consists of intramembranous and endochondral bone formation. These two processes involve a series of four temporally defined phases of repair: inflammatory, early callus, mature callus, and remodeling. Many factors influence the inflammatory phase, including the arachidonic acid metabolism and Wnt pathway agonists and antagonists. The early callus, late callus, and remodeling phases are modulated by factors that affect the receptor activator of the nuclear factor-kappa B ligand pathway. These factors include denosumab, osteoprotegerin, parathyroid hormone, strontium ranelate, and estrogen. Parathyroid hormone indirectly affects this pathway by binding to the osteoblasts. Binding stimulates the osteoblasts to increase their expression of receptor activator of nuclear factor-kappa B ligand and inhibits their expression of osteoprotegerin. Diphosphonates directly modify the effects of bone resorption by acting on the osteoclast, thus modulating the remodeling phase of fracture healing. It is important to review the specific pathways of fracture healing modification along with risk factors for impaired bone healing in fractures classified as patient dependent, or modifiable, and patient independent, or nonmodifiable.

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