Abstract: The purpose of this study was to investigate the effect of vitamin B₁₂ on palatal development by co-administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX). We examined the morphological and histological features of the palatal shelf and expression levels of key signaling molecules (transforming growth factor-β3 (TGF-β3) and TGF-β type I receptor (activin receptor-like kinase 5, ALK5)) during palatogenesis among a control group (Group A), TCDD+DEX exposed group (Group B), and TCDD+DEX+vitamin B₁₂ exposed group (Group C). While we failed to find that vitamin B₁₂ decreased the incidence of cleft palate induced by TCDD+DEX treatment, the expression levels of key signaling molecules (TGF-β3 and ALK5) during palatogenesis were significantly modulated. In TCDD+DEX exposed and TCDD+DEX+vitamin B₁₂ exposed groups, palatal shelves could not contact in the midline due to their small sizes. Our results suggest that vitamin B₁₂ may inhibit the expression of some cleft palate inducers such as TGF-β3 and ALK5 in DEX+TCDD exposed mice, which may be beneficial against palatogenesis to some degree, even though we were unable to observe a protective role of vitamin B₁₂ in morphological and histological alterations of palatal shelves induced by DEX and TCDD.

Key words: Cleft palate, Transforming growth factor-β3 (TGF-β3), Activin receptor-like kinase 5 (ALK5), Vitamin B₁₂, 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin, Dexamethasone

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