The Embryology of Cortisone-induced Cleft Palate

IN the past, the sporadic, unpredictable occurrence of cleft palate made the study of its embryological origins difficult. The discovery by Fraser et al. (1954) that large doses of cortisone injected into pregnant strain A/ Jax females would cause cleft palate in 100 per cent, of the offspring, provided a means for studying cleft palate in all stages of its development. Also, the lower incidence (17 per cent.) of this defect in strain C57BL after cortisone treatment supplied an additional tool for detecting differences between normal and abnormal palate development. Thus, a study of the embryology of cortisone-induced cleft palate was undertaken. However, to understand the abnormal it is usually necessary first to understand the normal. Since the literature on normal palate development was incomplete and controversial, this subject was re-examined and the results have been presented previously (Walker & Fraser, 1956). In summary, this study showed that the palatine shelves, which initially lie in a vertical plane lateral to the tongue, move into a horizontal plane extending across the tongue dorsally, where they meet in the midline and fuse. This movement is accomplished by a protrusion of the dorso-medial wall of each palatine shelf and a compensating regression of the ventral ridge, with the movement of shelf tissue and depression of the tongue being accomplished by some force within the shelves. It is recommended that the reader refer to Walker & Fraser (1956) before reading the following account of cleft palate.