Normal fetuses 13‐to‐21 days of age were obtained from female Long Evans Rats maintained on a stock diet known to produce normal offspring. Cleft palate fetuses were produced from mothers fed the same diet supplemented with 100 mg of pyrimethamine per kg of diet for four days beginning on the tenth day of gestation. The heads were studied with the low‐power microscope and serial histologic sections. In normal fetuses the lateral palatine processe appeared to form the roof of the mouth by two distinct mechanisms. Palatal closure was achieved rostrally by rotation of the lateral palatine processes from a ventromedial to a horizontal position while caudally, it resulted from the fusion of outgrowths from the medial surfaces. The original free ventral edges of the lateral palatine processes in the caudal region largely underwent regression by the seventeenth day. Closure commenced in the anterior third of the palate and proceeded rostrally and caudally. In the fetuses with cleft palate induced by pyrimethamine, the lateral palatine processes were observed in various stages of rotation or transformation depending on the region of the palate examined. The narrow width of these processes suggested that the antimetabolite had suppressed their growth at a critical stage in development. The results suggested certain similarities in the mechanisms of palatal closure in rat and man.
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R.D. Coleman (1965) studied this question.
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