Oligohydramnios and Cortisone-induced Cleft Palate

Abstract

IT has been suggested¹ that cortisone disturbs the closure of the secondary palate of mouse embryos by interfering with the development of an intrinsic motive force within the palatal processes. The force is thought to be dependent on the accumulation in the palatal mesenchyme of substances which give positive results with histochemical reactions for acid mucopolysaccharides. The marked variation in the incidence of cleft palate induced in different strains of mice by similar doses of cortisone has been attributed to differences in the rate at which the intrinsic force develops². Subsequent workers^3,4 have been unable to detect histochemical differences between palatal tissues of control and cortisonetreated embryos. Although cortisone diminishes the incorporation of 35S-labelled sulphate in the tissues of treated embryos, it has proved impossible to distinguish between autoradiographs of palatal tissue from strains with a high and those with a low incidence of cortisoneinduced cleft palate⁴. At the time of palatal closure, there is a marked similarity between the distribution of acid mucopolysaccharides in the palatal mesenchyme of mouse and rat embryos, but cleft palate has not been observed in the progeny of cortisone-treated rats³.