Growth hormone is not able to counteract osteopenia of rat cortical bone induced by glucocorticoid with protracted effect.

UNLABELLED

Osteopenia and inhibited longitudinal growth in childhood are serious side effects during glucocorticoid therapy. The effects of glucocorticoids on bone have been confirmed in animal experiments. Long-term glucocorticoid administration to rats results in reduced body weights, reduced bone growth (length and cross-sectional area), and bone strength. Glucocorticoid treatment also resulted in a reduced bending stress, indicating reduced bone quality. Growth hormone, on the other hand, increased body weights, bone dimensions, and bone strength. The aim of the present study was to evaluate if growth hormone administration would have an anabolic effect on rat bone when given to animals also receiving a high dosage of glucocorticoid. Five groups of female rats, 3.5 months old, were treated as follows: (1) saline control; (2) glucocorticoid (prednisolone: Delcortol 5 mg/kg/day); (3) growth hormone (recombinant human growth hormone 5 mg/kg/day); (4) glucocorticoid and growth hormone; and (5) food restriction, consisting of restricted access to food to reduce their weight gain to match that of the glucocorticoid injected rats. After 80 days of hormone administration the animals were sacrificed. The right femur was removed and tested biomechanically in a three-point bending procedure. The left femur was used for determination of bone dimensions. Biomechanical parameters (ultimate load and ultimate stiffness) were then normalized to diaphyseal cross-sectional diameters of the femur, giving the values of ultimate bending stress and Young's modulus.

RESULTS

administration of both hormones simultaneously could not reverse the decrease in body weights, bone length, and diameters, or the decreased bone strength induced by glucocorticoid administration. In conclusion, growth hormone cannot prevent cortical osteopenia in female rats induced by a high dose of glucocorticoid with protracted effect.