Abstract

Several lines of evidence suggest that the insulinlike growth factors play a role in fracture healing. They promote cell proliferation and matrix synthesis by chondrocytes and osteoblasts, the two cell types largely responsible for the formation of fracture callus. Circulating levels of insulinlike growth factor I and bone mineral density decrease with increasing age, and administration of insulinlike growth factor I increases bone turnover in patients with low bone mineral density. Insulinlike growth factor I may accelerate the normal healing of intramembranous bone defects, inducing the healing of defects that otherwise would not heal. An important role of insulinlike growth factor I is to mediate many of the actions of growth hormone on the skeleton. Considerable effort has been devoted to testing the effect of growth hormone and, thereby, indirectly that of insulinlike growth factor I on fracture healing. These studies have yielded such disparate results that no general conclusions regarding the effect of growth hormone (or of growth hormone dependent insulinlike growth factor I) on fracture healing currently can be drawn. Additional studies are needed to clarify the role of the insulinlike growth factors in the fracture healing process and to determine how their anabolic actions can be enlisted in the clinical enhancement of fracture healing.

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