Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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A few years later, additional research would produce more data on the effect <strong>of</strong> differing doses and forms <strong>of</strong> vitamin D on the dentition <strong>of</strong> school-aged children. Children receiving daily supplementation <strong>of</strong> vitamin D from cod liver oil (either 400 units or 800 units) had significantly fewer new caries surfaces than unsupplemented controls (1.65 surfaces (800 units) and 2.48 surfaces (400 units) vs. 4.5 surfaces (controls)). 112 Similarly, the intake <strong>of</strong> viosterol (800 units or 3200 units) or vitamin D from cod liver oil (400 units or 800 units) significantly reduced the mean number <strong>of</strong> new decayed surfaces per child compared to unsupplemented controls. 112 However, 800 units and 3200 units <strong>of</strong> viosterol were not superior at reducing new caries lesions than 400 units <strong>of</strong> vitamin D derived from cod liver oil in these same children. 112 In the 1940s, government measures were introduced to increase vitamin D intakes during pregnancy and early childhood, particularly cod liver oil and the fortification <strong>of</strong> margarine. 113 This provided evidence from a natural experiment as caries was assessed in five year old school children in London over three intervals, 1943, 1945 and 1947. 113 All children examined benefited from these vitamin D and calcium policies throughout antenatal and postnatal life. 113 Coincidentally, over those years, there was a marked decline in the number <strong>of</strong> children with caries in the primary dentition. 113 By 1975 the results <strong>of</strong> an epidemiological investigation on vitamin D prophylaxis contrasted the caries rates <strong>of</strong> a cohort <strong>of</strong> preschool children in Hungary with previous data on children <strong>of</strong> the same age that was collected in 1955. 95,114 Overall, vitamin D 3 injections to prevent rickets during the first year <strong>of</strong> life, referred to as Stosstherapy, appeared to <strong>of</strong>fer little protective effects against caries rates in primary dentition and was possibly insufficient to counteract consumption <strong>of</strong> high-caries-risk carbohydrates by 1.3-28
Hungarian preschool children as no logistic regression modeling was used to control for confounding variables. 114 Recent research indicates that there was no significant difference in the number <strong>of</strong> teeth with untreated decay in elderly individuals originally enrolled into a randomized, placebo-controlled trial involving vitamin D and calcium supplementation. 45 However, longitudinal evidence from the Iowa Fluoride Study cohort revealed that lower vitamin D intake at three years <strong>of</strong> age is significantly associated with increased caries in the primary dentition. 115 The relationship was very strong as inadequate intake <strong>of</strong> vitamin D was associated with increased caries experience on logistic regression. 115 <strong>Vitamin</strong> D Receptor Polymorphisms Newer evidence has begun to uncover possible associations between dental caries and VDR gene polymorphisms. A longitudinal cohort <strong>of</strong> veterans that looked at the VDR genotype found significantly more permanent teeth with caries at baseline among those with the Apaq I VDR aa genotype compared to those with the Aa genotype (5 ± 6 vs. 3 ± 3, p=.04). 51 Meanwhile, a published abstract in 2003 provides cross-sectional evidence <strong>of</strong> a strong association between VDR Taq 1 genotype polymorphisms and adult dental caries rates. 116 Allele distribution revealed those with the presence <strong>of</strong> the t allele were nearly three times more likely to develop high DMFT rates. In addition, those with the tt genotype were more than four times more likely to develop caries than those with the TT or Tt genotype. 116 1.3-29
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Influence
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Abstract Influence
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Acknowledgements This longitudinal
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Table of Contents
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Status and Non-<st
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Table 1.1-1 - Recent studies report
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Table 1.1-2 - Previous used terms f
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The Link Between Enamel Hypoplasia
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If enamel hypoplasia results from n
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malocclusions. 145 Additional human
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Daily intakes of v
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13. Milnes AR, Rubin CW, Karpa M, T
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40. Definition of
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71. Watt RG. From victim blaming to
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97. Fearne JM, Bryan EM, Elliman AM
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124. Burt BA, Pai S. Does low birth
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151. Tinanoff N, D
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Section 2 - Risk Factors for Enamel
Page 37 and 38: correspond to the timing of
Page 39 and 40: een published. 3,4,17,19 The intent
Page 41 and 42: Table 1.2-2 - Risk factors for DDE
Page 43 and 44: Opacity 51 Implicated Risk Developm
Page 45 and 46: Implicated Risk Factor Factors asso
Page 47 and 48: o Metabolic Abnormalities and Healt
Page 49 and 50: 12 months of life.
Page 51 and 52: Other Factors Some uncommon risk fa
Page 53 and 54: devastating problem of</str
Page 55: 13. An epidemiological index <stron
Page 58 and 59: 54. Seow WK, Perham S. Enamel hypop
Page 60 and 61: 82. Berdal A, Papagerakis P, Hotton
Page 62 and 63: Vitamin D may be d
Page 64 and 65: have been used to prof</str
Page 66 and 67: health’. In addition, articles we
Page 68 and 69: 36 month trial had ended. 45 The nu
Page 70 and 71: Recently, a cross-sectional study <
Page 72 and 73: andomized, placebo-controlled study
Page 74 and 75: Further, amelogenin and enamelin, p
Page 76 and 77: A study of Austral
Page 78 and 79: Both dietary interventions and supp
Page 80 and 81: incidence of carie
Page 82 and 83: important nutrient. However, many <
Page 84 and 85: caries, and more hardening
Page 86 and 87: controls. 106 Interestingly, childr
Page 90 and 91: Delayed Tooth Eruption Vita
Page 92 and 93: Description of Pop
Page 94 and 95: Influence
Page 96 and 97: D has an effect on the dentition, p
Page 98 and 99: 14. Utiger RD. The need for more vi
Page 100 and 101: 42. Spiller WF, Jr. A clinical eval
Page 102 and 103: 67. Itota T, Tashiro Y, Torii Y, Ni
Page 104 and 105: 95. Bruszt P. Kariesuntersuchungen
Page 106 and 107: 121. Seow WK, Needleman HL, Holm IA
Page 108 and 109: Chapter 2 - Methods for a Prospecti
Page 110 and 111: Each participant also completed an
Page 112 and 113: Table 2.2 - Recognized case definit
Page 114 and 115: Population The target population fo
Page 116 and 117: allowed the project to suffer some
Page 118 and 119: women of limited m
Page 120 and 121: involving the surface of</s
Page 122 and 123: and training cup. In addition, each
Page 124 and 125: The questionnaire was administered
Page 126 and 127: statistics including frequencies an
Page 128 and 129: elationship between the two. Poisso
Page 130 and 131: References 1. Combs GF. Vit
Page 132 and 133: 27. Seow WK, Amaratunge A, Bennett
Page 134 and 135: Table 3.2 - Self-declared heritage
Page 136 and 137: Question Number Valid % Do you take
Page 138 and 139:
Maternal Awareness
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time of recruitmen
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Table 3.6- Prenatal</strong
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A total of 77 care
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indicated that they were receiving
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and 11 hypoplasia). DDEs were also
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Caries rates for children in this p
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Table 3.12 - Frequency of</
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Chapter 4 - Results: Associations <
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II. Relationship Between 25(OH)D Le
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Pregnancy & Health Prof</st
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The frequency of v
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did not (42.9 ± 21.2 nmol/L vs. 49
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Early Childhood Caries (ECC) Pr<str
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likely to have vitamin D levels at
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did not statistically differ from v
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Figure 4.4 - Predicted number <stro
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Table 4.7 - Relationship between ds
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frequently, and less likely to have
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health as average or poor, and more
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tail (p=.034) suggesting that early
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The next series of
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Results from the second model appea
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Table 5.6 - Multiple regression sta
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vitamin D. However, it did suggest
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significant at the bivariate level
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Table 5.12(a) - Logistic regression
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III. Multivariate Regression Analys
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Table 5.14 - Logistic regression fo
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Page 198 and 199:
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Table 5.19(b) - Backwards logistic
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Table 5.20(a) - Logistic regression
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Table 5.21 - Poisson regression for
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If enamel hypoplasia is present and
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Since maternal calcium levels were
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vitamin D deficiency, and rickets)
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to obtain it. Health literacy may b
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vitamin D from the diet as dietary
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home environment can be determinant
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hormone, calcium absorption and bon
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important nutrient. For many, this
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this potential relationship with ac
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genetic conditions, childhood medic
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vitamin D status including milk int
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y cariogenic oral flora. 49 Since e
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(49.8 ± 26.3 nmol/L vs. 45.1 ± 20
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pregnancy, which may have influence
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observed and it allowed multiple ou
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scientific evidence linking prenata
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cognizant that children who undergo
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preventive program would need to be
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makers in the formative stages. As
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Surprisingly, the final regression
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13. First Nations IaMHCCPS. <strong
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38. Hollis BW. Circulating 25-hydro
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65. Li Y, Navia JM, Bian JY. Caries
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91. Brownell MD, Guevremont A, Au W
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Chapter 7 - Conclusions This thesis
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This study provided an interesting
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esiding in disadvantaged communitie
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If you are taking vitamins during t
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Do you Eat? Never Rarely (less than
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What problems can early childhood c
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Prenatal Nutrition
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Did you ever add sugar to the bottl
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Enamel Hypoplasia Enamel Hypoplasia
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Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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