Foetal, neonatal and child vitamin D status and enamel hypomineralization.

OBJECTIVES: Recent literature suggested that higher vitamin D concentrations in childhood are associated with a lower prevalence of molar incisor hypomineralization (MIH). As tooth development already starts in utero, we aimed to study whether vitamin D status during foetal, postnatal and childhood periods is associated with the presence of hypomineralized second primary molars (HSPMs) and/or MIH at the age of six. METHODS: Our study was embedded in the Generation R Study, a population-based, prospective cohort from foetal life onwards in Rotterdam, the Netherlands. HSPMs and MIH were scored from intraoral photographs of the children at their age of six. Serum 25(OH)D concentrations were measured at three points in time, which resulted in three different samples; mid-gestational in mothers' blood (n = 4750), in umbilical cord blood (n = 3406) and in children's blood at the age of 6 years (n = 3983). RESULTS: The children had a mean (±SD) age of 6.2 (±0.5) years at the moment of taking the intraoral photographs. After adjustment for confounders, no association was found between foetal 25(OH)D concentrations and the presence of HSPMs (OR 1.02 per 10 nmol/L higher 25(OH)D, 95% CI: 0.98-1.07) or MIH (OR 1.05 per 10 nmol/L increase, 95% CI: 0.98-1.12) in 6-year-olds. A higher 25(OH)D concentration in umbilical cord blood resulted in neither lower odds of having HSPM (OR 1.05, 95% CI: 0.98-1.13) nor lower odds of having MIH (OR 0.95, 95% CI: 0.84-1.07) by the age of six. Finally, we did not find higher 25(OH)D concentrations at the age of six to be associated with a significant change in the odds of having HSPM (OR 0.97, 95% CI: 0.92-1.02) or MIH (OR 1.07, 95% CI: 0.98-1.16). CONCLUSIONS: 25(OH)D concentrations in prenatal, early postnatal and later postnatal life are not associated with the presence of HPSMs or with MIH at the age of six. Future observational research is required to replicate our findings. Furthermore, it is encouraged to focus on identifying other modifiable risk factors, because prevention of hypomineralization is possible only if the causes are known.

Neonatal Serum Phosphorus Levels and Enamel Defects in Very Low Birth Weight Infants.

BACKGROUND: Very low birth weight (VLBW) infants miss out on the period of greatest mineral accretion that occurs during the last trimester of pregnancy and are at higher risk of enamel defects. No studies have well described the relationship between neonatal nutrition and dental outcomes in preterm, VLBW infants. The objective of this study was to assess the differences in nutrition biomarkers, feeding intake, and comorbidities among VLBW infants with and without enamel defects. METHODS: A retrospective chart review of VLBW infants recruited for an ongoing longitudinal dental study between 2007 and 2010 was done. Participants were classified as cases and controls according to the presence/absence of developmental defects of enamel at 8 and/or 18-20 and/or 36 months. Demographics and medical and nutrition data were abstracted from 76 subjects' medical charts. RESULTS: Of the 76 VLBW subjects, 62% had enamel defects (hypoplasia and/or opacity). The only significant variable in the logistic regression analysis was that infants with a 1-mg/dL increase in serum phosphorus levels had a 68% reduction in the odds of having enamel hypoplasia (odds ratio, 0.322; P = .024). CONCLUSION: Neonatal lower serum phosphorus levels are significantly associated with enamel hypoplasia in VLBW infants younger than 3 years.

Effects of early vitamin D deficiency rickets on bone and dental health, growth and immunity.

Vitamin D deficiency is associated with adverse health outcomes, including impaired bone growth, gingival inflammation and increased risk for autoimmune disease, but the relationship between vitamin D deficiency rickets in childhood and long-term health has not been studied. In this study, we assessed the effect of early vitamin D deficiency on growth, bone density, dental health and immune function in later childhood to determine if children previously diagnosed with rickets were at greater risk of adverse health outcomes compared with healthy children. We measured serum 25-hydroxyvitamin D, calcium, parathyroid hormone, bone mineral density, anthropometric measures, dietary habits, dental health, general health history, and markers of inflammation in 14 previously diagnosed rickets case children at Children's Hospital Oakland Research Center. We compared the findings in the rickets cases with 11 healthy children selected from the population of CHO staff families. Fourteen mothers of the rickets cases, five siblings of the rickets cases, and seven mothers of healthy children also participated. Children diagnosed with vitamin D deficiency rickets had a greater risk of fracture, greater prevalence of asthma, and more dental enamel defects compared with healthy children. Given the widespread actions of vitamin D, it is likely that early-life vitamin D deficiency may increase the risk of disease later in childhood. Further assessment of the long-term health effects of early deficiency is necessary to make appropriate dietary recommendations for infants at risk of deficiency.

Prenatal vitamin D and dental caries in infants.

OBJECTIVES: Inadequate maternal vitamin D (assessed by using 25-hydroxyvitamin D [25OHD]) levels during pregnancy may affect tooth calcification, predisposing enamel hypoplasia and early childhood caries (ECC). The purpose of this study was to determine the relationship between prenatal 25OHD concentrations and dental caries among offspring during the first year of life. METHODS: This prospective cohort study recruited expectant mothers from an economically disadvantaged urban area. A prenatal questionnaire was completed and serum sample drawn for 25OHD. Dental examinations were completed at 1 year of age while the parent/caregiver completed a questionnaire. The examiner was blinded to mothers' 25OHD levels. A P value ≤ .05 was considered significant. RESULTS: Overall, 207 women were enrolled (mean age: 19 ± 5 years). The mean 25OHD level was 48 ± 24 nmol/L, and 33% had deficient levels. Enamel hypoplasia was identified in 22% of infants; 23% had cavitated ECC, and 36% had ECC when white spot lesions were included in the assessment. Mothers of children with ECC had significantly lower 25OHD levels than those whose children were caries-free (41 ± 20 vs 52 ± 27 nmol/L; P = .05). Univariate Poisson regression analysis for the amount of untreated decay revealed an inverse relationship with maternal 25OHD. Logistic regression revealed that enamel hypoplasia (P < .001), infant age (P = .002), and lower prenatal 25OHD levels (P = .02) were significantly associated with ECC. CONCLUSIONS: This study found that maternal prenatal 25OHD levels may have an influence on the primary dentition and the development of ECC.

Enamel defects associated with coeliac disease: putative role of antibodies against gliadin in pathogenesis.

Enamel defects in the permanent teeth of patients with coeliac disease (CD) are often reported as an atypical manifestation, sometimes being suggestive of an undiagnosed atypical disease. We proposed to explore the pathogenesis of these oral defects, which are poorly studied. Sequence analyses of proteins from gluten (gliadins) and of proline-rich enamel proteins (amelogenin and ameloblastin) suggested the presence of common antigenic motifs. Therefore, we analyzed, by ELISA and western blotting, the reactivity of sera from patients with CD against gliadin and enamel-derived peptides. Correlation analyses between the levels of specific antibodies against gliadin and enamel derived peptides and inhibition experiments confirmed the presence of cross-reactive antibodies. Immunoblot analysis revealed that the most prominent component in enamel matrix derivative (of approximately 18.6 kDa), identified by an amelogenin-specific antibody, is recognized by sera from patients with CD; in addition, several fractions of pure gliadin were recognized by amelogenin-specific antibody. In agreement, sera from mice immunized with enamel matrix-derived proteins generated antibodies that recognized a peptide (of approximately 21.2 kDa) derived from gliadin. In conclusion, antibodies against gliadin generated in patients with CD can react in vitro with a major enamel protein. The involvement of anti-gliadin serum in the pathogenesis of enamel defects in children with untreated CD can be hypothesized on the basis of these novel results.

[Some clinical-laboratory indices in children with dental dysplasia of permanent teeth]. / Niakoi klnikolaboratorni pokazateli pri detsa sus zubna displaziia na postoiannite zubi.

The authors studied some serum indices of protein and electrolyte metabolism (total protein, protein fraction, serum calcium, ionized calcium, phosphorus, potassium, sodium, osmolality, Ca/P ratio) in 26 clinically healthy children, aged fro 7 to 10, with clinically diagnosed dysplasia (hypoplasia or hypomineralization) of the permanent teeth. The mean values of the single biochemical parameters for both groups of children remain within referent limits of the respective indices for childhood, and their comparison established no statistically significant differences (p greater than 0.05). That provided grounds the authors to associate with the opinion that enamel defects, localized on a restricted part of the clinical crown of a symmetric group of teeth, could be "markers" for disorders in protein and mineral metabolism only during a certain time period coinciding with the active phases of odontogenesis. The absence of lasting changes in those two metabolisms determined the trends of the secondary prophylaxis--caries-prophylactic measures aiming at the avoidance of complications.