Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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incidence <strong>of</strong> caries in the primary dentition than children who benefited from additional vitamin D as a prophylactic approach for rickets. 78 A few studies have attempted to curb the onset <strong>of</strong> caries in patients with rickets. Providing vitamin D in the form <strong>of</strong> cod liver oil during infancy has been shown to lower the incidence <strong>of</strong> caries. 81 In addition, the combination <strong>of</strong> both cod liver oil and sunbathing during infancy and early childhood also appeared to lessen the extent <strong>of</strong> decay. 80 Observations <strong>of</strong> a group <strong>of</strong> children with rickets in India were not able to corroborate the findings <strong>of</strong> these other investigations as those with vitamin D deficient diets did not appear to have a greater risk for dental caries. However, considering the number <strong>of</strong> children was very small, the findings are not definitive. 72 Another study examined the influence <strong>of</strong> a combined caries and rickets prophylaxis approach including both fluoride and vitamin D tablets among children six to 48 months <strong>of</strong> age. 94 Children who received the fluoride and vitamin D tablets for more than 12 months and who were breastfed for ≤ 3 months were more likely to be free from caries in primary dentition. 94 However, the reduction in caries exhibited in this trial was probably due to fluoride instead <strong>of</strong> the addition <strong>of</strong> vitamin D. The introduction <strong>of</strong> vitamin D Stosstherapy as a rickets prevention strategy did not appear to have a pr<strong>of</strong>ound effect on caries rates. 95 Results suggested that there was no significant difference in caries rates or prevalence between young children receiving vitamin D Stosstherapy three times during the first two years <strong>of</strong> life, Stosstherapy once before the first birthday and one or two additional times in the second year, and those who did not receive such vitamin D treatment. 95 1.3-20
Gedicke’s paper examined the influence <strong>of</strong> a public health approach to eradicate rickets through vitamin D supplementation on the oral health <strong>of</strong> children three to 18 years <strong>of</strong> age between the years 1952 and 1957. 96 This article provided evidence <strong>of</strong> the possibility <strong>of</strong> preventing caries and improvements in dental health through vitamin D preparations intended to prevent rickets. 96 A similar approach was undertaken as a means to prevent rickets in a Northern Manitoba community where a modified form <strong>of</strong> Stosstherapy was administered during pregnancy or infancy. 97 Unfortunately, no significant differences in caries rates were found between children who benefited from additional vitamin D and those who did not. 97 The findings are confounded by the fact that the majority <strong>of</strong> children examined had undergone aggressive rehabilitative dental surgery. While children with VDRR have an increased prevalence <strong>of</strong> enamel hypoplasia, they are also prone to dental caries. The introduction <strong>of</strong> 1α-hydroxyvitamin D 3 during infancy and childhood to manage VDRR has lead to improvements in oral health. 98 Those who received vitamin D and continued to receive supplementation at the time <strong>of</strong> dental examination had lower caries rates in the permanent dentition than adults who either did not receive or who only received supplementation until adulthood (DMFT = 2.4 ± 2.4 vs. 20.4 ± 6.4). 98 Supplementation and Dietary Interventions There are several studies that point to the potential influence <strong>of</strong> vitamin D on the development and progression <strong>of</strong> dental caries. Unfortunately, much <strong>of</strong> this evidence has been overlooked by the dental community. The majority <strong>of</strong> these studies have examined the benefit <strong>of</strong> fortifying the diet with vitamin D or foods and compounds containing this 1.3-21
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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 78 and 79: Both dietary interventions and supp
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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