EXPERIMENTAL STUDIES ON THE CLEFT PALATE INDUCTION BY GULCOCORTICOIDS IN MICE

Abstract

This inivestigation was intiated to study ; 1) the cleft palate induction potencies of glucocorticoids ; 2) the effects of the period or of the route of administration of glucocorticoids on the incidence of cleft palate. ddN mice were received a single or successive doses of cortisone (aqueous suspension), prednisolone (aqueous suspension and solution), dexamethasone (aqueous suspension and solution) and triamcinolone acetonide (aqueous suspension), respectively. The results obtained were as follows. 1. In the offsprings of the females administered subcutaneously with aqueous suspension of glucocorticoids on days 11 to 14 of gestation, the relative potencies of various glucocorticoids to cortisone in inducing cleft palate were 3. 7 in prednisolone, 33. 4 in triamcinolone acetonide, 53.9 in dexamethasone, respectively. The relative potencies of glucocorticoids were similar to the relative liver glycogen deposition potencies reported by Ringler et al. 2. When the females were received a single subcutaneous injection of four days' doses on 11 day of gestation, cleft palates were induced in the fetuses treated with aqueous suspension of glucocorticoids, but no cleft palate with aqueous solution of 2. 4 mg of prednisolone and 0.32 mg of dexamethasone. 3. A single intravenous injection of four days' doses of aqueous solution and suspension of prednisolone on day 11 of gestation was not effective in inducing cleft palate respectively, although effective in mice injected intravenously for four days on days 11 to 14 gestation. 4. 17-OHCS level in the blood of the mother 24 hours after a single subcutaneous injection of 10 mg of cortisone was approximately 4 times more in the treated mice than in the control. 5. In the 13 and 14 days old fetuses showing the palatal shelves in vertical position, the mitotic cells in the epithelial tissues were located to the oral side (outer side) of the palatal shelves. There was no evidence for growth retardation of the palatal process due to cortisone treatment until after the time of palate closure, but shelf movement was sufficiently delayed in cortisone-treated fetuses.