Abstract
Background: Vitamin D is important for increasing absorption of calcium and phosphate, reducing phosphate excretion, and improving bone mineralisation. Deficiency of maternal vitamin D during pregnancy, as measured by 25-hydroxyvitamin D (25(OH)D), is common in New Zealand and associated with lower newborn 25(OH)D levels. 25(OH)D reserves at birth are important; a postnatal drop in calcium and phosphate signals synthesis of 25(OH)D into active vitamin D, enhancing mineralisation potential. Teeth are at a critical stage of mineralisation during pregnancy and at birth; disturbances during this time can lead to a reduction in enamel or dentine quality. Developmental enamel defects and dental caries have been associated with severe 25(OH)D deficiency in early life. However, the impacts of milder 25(OH)D deficiency during pregnancy and early postnatal life on future oral health outcomes are still unclear.
Aim: The aim of this study was to investigate the dental consequences of vitamin D deficiency, as measured by maternal 25(OH)D during pregnancy, and infant 25(OH)D at birth.
Methods: All participants from a Dunedin vitamin D study conducted in 2012 (n=126) were invited to participate. Background data were collected, and a comprehensive dental assessment, with posterior bitewing radiographs, were undertaken when participants were six years of age. Baseline demographic information was available through the 2012 vitamin D study. Oral health data were collected to determine caries risk status and update participants’ medical history. Participants completed a dental questionnaire and were assessed for caries and developmental defects. Dental caries was classified using the International Caries Detection and Assessment System (ICDAS), and dental enamel defects were classified using both the European Academy of Paediatric Dentistry index for Molar Incisor Hypomineralisation (EAPD for MIH) and the Developmental Defects of Enamel (DDE) index. Participants were invited to donate an exfoliated primary incisor tooth when one became available. Donated teeth were cleaned and and scanned by micro-CT, then embedded in resin and sectioned. One half of each sample was used for EDX analysis, and the other half for Raman spectroscopy.
Results: Eighty-one children participated in this study and 63 provided an exfoliated primary tooth for laboratory analysis. The mean age was 6.6 years, 52% were male, and 80% resided in areas of low or medium deprivation. Two-thirds of participants had at least one tooth affected by an enamel defect, and half had experienced dental caries. Early life 25(OH)D insufficiency was not associated with enamel defect prevalence but was associated with a greater caries risk IRR of 3.55 (CI 1.15-10.92) by age six. No differences in mineral or protein content by 25(OH)D status were identified. Raman spectroscopy data revealed structural differences in enamel crystallinity, with higher crystalline content in enamel observed in participants with sufficient levels of 25(OH)D at birth.
Conclusion: Vitamin D insufficiency during early life may be associated with increased caries risk for children; however, there was a lack of clear evidence regarding the association with developmental enamel defects. Vitamin D sufficiency at birth may improve enamel crystallinity of developing teeth.
Future Research: Further dental assessment for this cohort at age 10 to 12 years would be of interest as the primary second molars will be due to exfoliate, and most of the permanent teeth should have erupted. Primary second molars would be of particular interest as mineralisation for these teeth occur pre- and-postnatally; a neonatal line in enamel should therefore be visible in ground sections of these teeth. It is possible that the postnatal drop in calcium and phosphate, and any delay in vitamin D synthesis after birth, may be identifiable.