The effects of dihydrotestosterone (DHT) on glucocorticoid-pretreated fetal rat long bone were studied in an in vitro culture system. First, dose-response curves of corticosterone, hydrocortisone, and dexamethasone were studied at several concentrations. Then, hydrocortisone (H) at 10–5 M was selected for the second part of the study, as it slackened rudiment mineralization (104 ± 16% of the initial dark zone vs. 141 ± 9% in control bones), as well as its lengthening (140 ± 4% of the harvesting day length vs. 160 ± 1% in control bones), by both inhibition of cell proliferation and stimulation of resorption. On the contrary, in H-pretreated metatarsal bones, DHT (10–7 M) partly limited slackening of mineralization (124 ± 5%) and lengthening (153 ± 2%). Moreover, a control-like cell proliferation was re-established and resorption holes were filled in. Thus, in this study, DHT partly limited hydrocortisone-induced impairment of fetal rat metatarsal bone development.

Keywords:
Dihydrotestosterone, Glucocorticoids, Osteopenia
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© 2000 S. Karger AG, Basel
2000
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