Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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A study <strong>of</strong> Australian infants who were premature and diagnosed, both clinically and radiographically, with rickets in the neonatal period reported that all children exhibited developmental defects <strong>of</strong> enamel in the primary dentition, with 47% having enamel opacities and hypoplasia, 20% with only opacities, and the remainder with enamel hypoplasia (33%). 77 Meanwhile, an early case-controlled study provided evidence that children with rickets were more likely to have enamel hypoplasia in both primary and permanent dentitions than children without rickets who received vitamin D prophylaxis (viosterol) during the early childhood period. 78 Specifically, those with rickets were more likely to have both marked hypoplasia and slight hypoplasia than ricket-free controls who received vitamin D prophylaxis in the form <strong>of</strong> viosterol. 78 There were further case reports <strong>of</strong> children with acute rickets having enamel hypoplasia in their dentitions. 79 There is long-standing longitudinal evidence too, showing that children who experienced rickets during the early childhood period were more likely to have enamel defects in their permanent dentitions. 80,81 In fact, the more severe the case <strong>of</strong> rickets, the greater the prevalence and the more severe the enamel defects. 80,81 Another study contrasted dental findings <strong>of</strong> children with rickets and controls. 82 This case-control study revealed that children with rickets were nine times more likely to have hypoplasia in the permanent dentition than healthy controls. 82 There are several classifications <strong>of</strong> rickets, including dietary, transport, matrix defect and metabolic. 77 One type <strong>of</strong> metabolic rickets is VDDR, where the synthesis <strong>of</strong> 1,25(OH) 2 D is impaired. 83 Case study reports have confirmed that children with VDDR are highly prone to enamel hypoplasia. 38,83,84 Even those who were diagnosed with 1.3-16
vitamin D resistant rickets (VDRR) and received vitamin D 3 and phosphate therapy before 12 months <strong>of</strong> age displayed some manifestations <strong>of</strong> isolated enamel hypoplasia in the permanent dentition. 85 Those diagnosed and treated by 18 months <strong>of</strong> age also demonstrated isolated enamel hyoplastic lesions in the permanent dentition. 85 Supplementation & Dietary Interventions Knowing that vitamin D deficiencies and altered vitamin D metabolism can result in enamel hypoplasia, it is plausible that vitamin D supplementation during periods <strong>of</strong> enamel formation can reduce the incidence <strong>of</strong> hypoplastic defects. Much <strong>of</strong> Mellanby’s work on the effect <strong>of</strong> diet on dental structure and disease in man is summarized in her final report to the Medical Research Council published in 1934. 36 While most <strong>of</strong> this report focused on the relationship between diet and caries, she did conclude that vitamin D in the prenatal diet and during periods <strong>of</strong> dental development after birth results in a reduction <strong>of</strong> enamel hypoplastic defects. 36 Another <strong>of</strong> her reports on the influence <strong>of</strong> diet on caries in children’s teeth would also support the theory that the addition <strong>of</strong> vitamin D to the diet during enamel development improves the structure <strong>of</strong> permanent first molars. Mellanby’s early observations were that normal enamel and dentin structure were more frequent among children benefiting from cod liver oil in their diets compared to children whose diets contained little vitamin D. 86 Supplementing infants with rickets with cod liver oil has been documented to reduce the incidence <strong>of</strong> enamel hypoplasia. 81 Further, this antirachitic therapy, which included cod liver oil and sunbathing during infancy and early childhood has also shown to be effective in decreasing the incidence <strong>of</strong> enamel hypoplasia in the permanent dentition. 80 1.3-17
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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
Page 21 and 22:
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 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 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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