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Previous studies on the development of cleft lip, alveolus, palate, and velum and neural tube defects have revealed several shared multifactorial causes. Both anomalies emerge at different times during embryonic development and are not associated with each other unless there is a genetic component to the etiology. Vitamin deficiency disorders are one of several factors contributing to the etiology of these anomalies.Vitamins B6, folic acid and B12 play an essential role in the methylation cycle. A lack of or deficiency in these vitamins thus has severe consequences for the organism, especially the unborn child. Due to its short half-life, vitamin B6 is particularly important for undisturbed embryogenesis and should be taken along with folic acid as a periconceptional supplement to prevent embryonic deformities. This paper is intended to provide the orthodontist (as a member of the interdisciplinary cleft team) with an overview of the issues and etiological significance of vitamin B deficiencies as possible inducers of these embryopathies. This may encourage comprehensive counselling, particularly of parents of children born with deformities who wish to have more children.

Objective: In this study, folic acid was tested for its antiteratogenic effects on experimentally induced cleft palate in animals. Design: Eleven pregnant Lew 1 A dams (75 fetuses) received 200 mg/kg procarbazine via gastric tubing on postconception (p.c.) day 14 to induce a cleft palate (CP); seven of the pregnant dams (45 fetuses) were additionally given 4 mg/kg folic acid subcutaneously from the 14th to the 17th day p.c. As a control group, three more pregnant dams (24 fetuses) were not treated with the drugs mentioned above. All fetuses were delivered by Caesarian section on day 20 p.c. Outcomes measured: All fetuses were weighed and examined macroscopically with a stereomicroscope. Each fetal head was cut into 35 frontal sections and scrutinized histologically. Results: None of the control fetuses (n = 24) exhibited a cleft. Without folate administration, 90% of the fetuses (27 of 30) that received procarbazine exhibited a CP. After additional prenatal folate administration, this rate remained virtually unchanged (91%; 41 of 45). However, the proportion of complete (total) CP (4%) was significantly (p < .0001) lower than in the group without folate (53%). Cleft-associated microgenia and microglossia were also significantly less frequent when folate was administered prenatally: microgenia was reduced by 22% (p = .029) and microglossia by 24% (p = .032). Conclusions: On the basis of these results, folate has a partial ameliorating effect on the teratogenicity of procarbazine given to pregnant rats. Additional studies are necessary on the effect of folate in different species, also taking cleft lip and CP into consideration.

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