Skeletal effects of growth hormone and IGF-I in adults

Three processes occur in the skeleton; modelling during growth, fracture repair and remodelling. Remodelling is bone resorption coupled to bone formation, and alterations in the remodelling balance are the final pathway to bone loss. Therapeutic agents are now available to minimize the normal phenomenon of age-related bone loss and protect against osteoporotic fracture. These agents reduce the rate of bone resorption, have positive effects on bone mass and some reduce fracture rates. None, however, restore bone mineral to normal levels. GH has been considered for this role due to its positive effects in vitro and in vivo. GH-deficient adults have low BMD compared to healthy controls, and the reasons for this finding are discussed. A neglected factor is a measurement artefact from the use of DXA. Long-term GH therapy can lead to clinically important increases in BMD in GH-deficient adults. The results from studies of GH administration to healthy elderly populations are also presented. The small rise of lumbar BMD or maintenance of BMD at the hip seen in these studies are no better than results achieved with cheaper, easier to administer therapies. Investigation of other agents in the somatotrophic axis, are, however, potentially promising and warrant further investigation.