Cleft beak induced by hydrocortisone in the chick is prevented by increased cell division after experimental reduction of amniotic fluid

Abstract

 Hypoplasia of the medial nasal process has been reported in chick embryos on embryonic day (ED) 5, 24 h after their exposure to hydrocortisone (HC). As a result, the cleft beak occurs in 80–100% of specimens on ED 9. In order to analyze its influence on cell proliferation, HC was injected intra-amniotically into embryos on ED 4, and the mitotic index and number of BrdU-positive cells were evaluated 24 h later, both in the epithelium and mesenchyme of the medial nasal processes, on serial frontal histological sections. Two hours after BrdU administration, there were 50% of labeled mesenchymal cells in the embryos exposed to HC and only 23% in the control group. The mitotic index of mesenchymal cells was significantly lower in the HC group than in the controls. The epithelium showed no significant difference. HC seemed to prevent the mesenchymal cells from entering mitosis. The cleft beak in the embryos exposed to HC on ED 4 was totally eliminated by tearing open the amnion (amniotomia) and allowing fluid to leak out on ED 5. In some of specimens exposed to HC, the mitotic index was investigated at six time intervals from 15 to 120 min after amniotomia. A significant increase in the mitotic index was detected in the mesenchymal cells of the medial nasal processes during the first hour after amniotomia. Such a prompt increase of the mitotic activity may be hypothetically explained by release of the HC from its receptor binding as a consequence of outflow of the amniotic fluid together with the HC pool, and freeing of the mesenchymal cells, blocked in the G₂ phase, to enter mitosis. As a result, the hypoplasia of the medial nasal process might be compensated and the development of the cleft beak prevented.