The effect of glucocorticoids on bone resorption was examined in a serum‐free mineralizing organ culture system derived from 20 day fetal rat parietal bones. Bone resorption was assessed by prelabeling the fetal rats in utero with ⁴⁵Ca and determining the daily release of ⁴⁵Ca into the medium of cultured bones. During the first 24 h of treatment a transient stimulation of bone resorption was found; 4.5 ± 0.3% of the total ⁴⁵Ca was released into the medium with 1 nM corticosterone and 4.1 ± 0.2% with 10 nM corticosterone compared to 2.9 ± 0.2% in control bones. Treatment with 1 and 10 nM dexamethasone for 24 h also showed an increase in ⁴⁵Ca release compared to control bones. During the same time period ⁴⁵Ca release was 6.9 ± 1.4% with 10 nM parathyroid hormone. At later time points 100 and 1000 nM corticosterone inhibited ⁴⁵Ca release, but 1 and 10 nM corticosterone values were similar to controls. At 24 h the number of osteoclasts per mm² tissue in bone lacunae was significantly elevated with 1–100 nM corticosterone and 10 nM parathyroid hormone compared to control bones. In control bones 0.10 ± 0.05 osteoclasts per mm² of tissue were found, but 0.59 ± 0.21 osteoclasts per mm² were seen with 10 nM corticosterone and 1.50 ± 0.34 with 10 nM parathyroid hormone. An additional assay of bone resorption, the release of lysosomal β‐glucuronidase into the medium was also elevated in glucocorticoid and parathyroid hormone‐treated cultures. During 0–24 h, the medium from 10 nM parathyroid hormone‐treated bones contained elevated levels of β‐glucuronidase activity, 7.5 ± 0.7 versus 6.0 ± 0.4 μg/ml in the control bones and, during 24–48 h, 10.5 ± 0.8 versus 7.7 ± 0.6 μg/ml of phenolphthalein in the controls. With 10 nM corticosterone there was a significant increase of 10.0 ± 0.5 μg/ml released at 24–48 h, but high concentrations of glucocorticoids decreased β‐glucuronidase release. We conclude that corticosterone can cause a transient increase in bone resorption by increasing osteoclast number and activity in bone.