Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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Both dietary interventions and supplementation during pregnancy and infancy can improve the integrity <strong>of</strong> enamel <strong>of</strong> primary teeth. A longitudinal cohort that provided expectant women with 400 IU <strong>of</strong> vitamin D beginning in the 12 th week <strong>of</strong> pregnancy reported that infants developed significantly less enamel hypoplasia in the primary dentition compared with controls taking placebos. 87 However, this only involved a small sample <strong>of</strong> the total cohort. Meanwhile, a longitudinal investigation studied the influence <strong>of</strong> vitamin D supplementation (500 IU or 1000 IU/day) for six months in preterm children on the development <strong>of</strong> enamel hypoplasia in the primary and permanent dentitions, up to 11 years <strong>of</strong> age. 88 Results from this study indicated that there was no significant difference in the prevalence <strong>of</strong> enamel defects in primary or permanent teeth between those receiving 500 IU vitamin D daily or those receiving twice the dose. 88 In essence, there was no additional benefit found by doubling the dosage <strong>of</strong> vitamin D. Likewise, the benefits <strong>of</strong> vitamin D supplementation during the prenatal period and infancy do not continue beyond this point to aid in the development <strong>of</strong> enamel in the permanent dentition. A recent report was unable to demonstrate that such supplementation was associated with a decreased prevalence <strong>of</strong> molar incisor hypomineralization among children at 12 years <strong>of</strong> age. 89 On the other hand, a longitudinal study <strong>of</strong> children in Mexico investigated the influence <strong>of</strong> supplementation during pregnancy, infancy, and childhood with vitamins and protein, including 20,000 IU vitamin D. 90 A significant difference in the prevalence <strong>of</strong> linear enamel hypoplasia was found with children in the control group having nearly twice as much enamel hypoplasia as those who benefited from this high dose supplementation. 90 1.3-18
A 1958 review on the topic <strong>of</strong> caries prophylaxis even concluded that there is sufficient work to prove that the quality <strong>of</strong> enamel structure is determined by vitamin D and mineral salts. 91 Caries Rickets As previously mentioned, enamel hypoplasia is the phenotypic presentation <strong>of</strong> children with rickets. Likewise, caries is also common in these children. The early twentieth century caries literature reported clear associations between rickets and dental decay. For instance, longitudinal observations <strong>of</strong> children diagnosed with rickets during early life revealed that they were more likely to suffer from a higher prevalence <strong>of</strong> caries in their primary and permanent dentitions than those without rickets. 80,92 Similarly, Lady Mellanby concluded that caries was more prevalent in those with a history <strong>of</strong> severe manifestations <strong>of</strong> rickets than healthy children <strong>of</strong> the same socioeconomic class. 36 In fact, those with rickets as a result <strong>of</strong> vitamin D deficiency had more extensive forms <strong>of</strong> decay. 36 Likewise, Hess and Abramson provided observational evidence <strong>of</strong> a connection between rickets and dental caries in the primary dentition. 93 Specifically, dental caries was more prevalent among those with rickets than children protected from rickets with cod liver oil during infancy. 93 However, a case control investigation only reported a slightly higher prevalence <strong>of</strong> caries in the primary and permanent dentitions <strong>of</strong> schoolaged children with rickets compared to controls without the disease. 82 Similarly, Shelling and Anderson were unable to demonstrate that rickets predisposed children to a greater 1.3-19
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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
Page 25 and 26:
40. Definition of
Page 27 and 28: 71. Watt RG. From victim blaming to
Page 29 and 30: 97. Fearne JM, Bryan EM, Elliman AM
Page 31 and 32: 124. Burt BA, Pai S. Does low birth
Page 33 and 34: 151. Tinanoff N, D
Page 35 and 36: 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 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 88 and 89: A few years later, additional resea
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
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References 1. Combs GF. Vit
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27. Seow WK, Amaratunge A, Bennett
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Table 3.2 - Self-declared heritage
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Question Number Valid % Do you take
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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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