Abstract: Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B₁₂ has been shown to antagonize the teratogenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B₁₂ on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on embryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B₁₂. The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B₁₂-treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B₁₂ group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B₁₂ prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.

Key words: Dexamethasone, Vitamin B₁₂, Organ culture, Cleft palate, Medial edge epithelial cells

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