Journal of Endocrinology vol:149 issue:1 pages:7-12
Growth hormone activates osteoblasts to increase local synthesis of IGF-I, which acts in an autocrine or paracrine way to enhance bone matrix apposition, suggesting a role in the preservation of bone mass. Growth hormone deficiency in the elderly may therefore be of pathogenetic significance in senile osteoporosis. However, critical evidence does not yet support the concept that the decreased activity of the growth hormone-IGF-I axis alters bone remodelling, and the extent to which geriatric hyposomatotropism contributes to the age-related femoral bone loss remains to be elucidated. Despite the fact that biochemical estimates of bone turnover indicate that (short-term) administration of rhGH and IGF-I stimulates bone metabolism in non-osteoporotic older people, no significant changes have been observed in bone mineral density at the proximal femur. Additional studies are needed to assess the therapeutic potential for rhGH in attenuating or reversing bone loss in elderly people. Moreover, data on long-term adverse side effects of rhGH therapy are not yet available. Because of the known mitogenic action of IGF-I, the neoplastic potential of long-term rhGH therapy needs to be considered.