Abstract
ABSTRACT Cortisone treatment causes cleft palates by interfering with the development of the condition within the palatine shelves that forces them to change their alignment from the vertical to the horizontal plane. The consequent delay in shelf movement, the apparent inability of the shelves to grow wider without the stimulus of being fused, and the continued increase in head width, result in a palate in which the shelves are too far apart to touch and fuse when they finally become horizontal. The strain difference between C57BL and A/Jax mice in their susceptibility to the teratogenic action of cortisone is due in part to the earlier closing of the palate in C57BL embryos, and in part to the lesser inhibition of shelf movement in C57BL embryos as compared to A/Jax embryos. These differences suggest that the C57BL maternal-embryo complex has a more efficient metabolic system for developing palate shelf movement than exists in the A/Jax strain.
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