Springer Online Journal Archives 1860-2000
Summary Chronic glucocorticoid excess is associated with the development of osteoporosis and, in human subjects, there is histomorphometric evidence of increased bone resorption. Paradoxically, most in vitro studies have suggested that glucocorticoids inhibit bone resorption but recently two groups have demonstrated increased osteolysis in glucocorticoid-treated bone organ cultures. The present study reexamines the effect of cortisol on basal bone resorption in neonatal mouse calvaria with particular emphasis on the effect of serum supplementation of the media. In the absence of serum, 45Ca release was significantly stimulated by 10-7 M cortisol (treatment/control 1.37+-0.06, P〈0.005) and by 10-6 M cortisol (treatment/control 1.27+-0.08, P〈0.005). The stimulation of resorption by 10-7 M hydrocortisone was progressive from 24 to 96 hours of incubation. In contrast, when calvaria were incubated in the presence of 5% serum, bone resorption was not increased by cortisol (10-8 M-10-6 M). In the presence of 5% charcoal-stripped, heat-inactivated serum, there was a small stimulation of 45Ca release at 10-6 M hydrocortisone only (treatment/control 1.19 +-0.06, P〈0.01). Incubation of bones with indomethacin did not modify the effect of cortisol in either the presence or absence of serum. In serum-free conditions, cortisol 10-8 M significantly inhibited the rate of thymidine incorporation, though at higher concentrations this effect was not seen. Cortisol produced a dose-related inhibition of serumstimulated thymidine incorporation. It is concluded that the presence of serum substantially modifies the effect of cortisol on basal bone resorption. The cortisol-induced stimulation of bone resorption which is seen in serum-free conditions is sustained over time and is not mediated by alterations in prostaglandin synthesis.
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