Cleft palate formation: a role for pyridoxine in the closure of the secondary palate in mice.

Abstract

AbstractDietary pyridoxine deprivation in mice throughout pregnancy produced 20% cleft palate (CP). This frequency was significantly increased when either 4‐deoxypyridoxine or cortisone was administered during the period of palate closure. A low dose of cortisone given to pregnant mice fed a pyridoxine‐deficient diet produced a CP frequency greater than the sum of those produced by each teratogen alone. At a higher dose the interaction between cortisone and pyridoxine deficiency was additive. The effects of cortisone and pyridoxine deprivation were mitigated when pyridoxine was given during the time of palate shelf movement. Clearing arid staining for bone formation revealed general delay of ossification but no visible skeletal defects. Exencephaly, with a frequency of 0.4 %, was the only other gross defect seen after maternal pyridoxine deprivation.