Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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feeding, either bottle or breast, has little influence on ECC. 74-77 Bottle-use for nutritive purposes must be distinguished from pacification, where inappropriate bottle use increases the risk for caries. 12,37,38,78 Other evidence concludes that “at-will breastfeeding” and enamel hypoplasia may predispose a child to ECC. 79 Further, a recent systematic review suggests that there is also insufficient scientific evidence that a strong association between breastfeeding and ECC exists. 80 Promising prevention efforts include the use <strong>of</strong> fluoride varnishes, chemotherapeutics, and motivational interviewing techniques to assist parents in adopting healthy early childhood oral health practices. 21,81- 83 ECC is an important and <strong>of</strong>ten overlooked pediatric health issue. Caries prevention is crucial for this age group as preschool children who exhibit primary tooth decay at young ages, are more likely to have an increased caries burden along the continuum <strong>of</strong> childhood 4-6,84,85 Therefore, efforts to reduce caries among the very young may have a broader impact. Treatment alone is not the appropriate solution for this devastating pediatric dental syndrome as the risk <strong>of</strong> recurrent caries following complex restorative care is considerable. 86-88 Rather, more attention needs to be spent on effective preventive strategies during key periods <strong>of</strong> early childhood development such as bolstering prenatal nutrition, reducing maternal levels <strong>of</strong> streptococcus mutans, reducing the vertical transmission <strong>of</strong> cariogenic microorganisms from mothers to infants, early screening <strong>of</strong> infants and toddlers, promoting regular infant oral hygiene, and applying fluoride varnish or other chemotherapeutic agents (i.e. silver fluoride, chlorhexidine, betadine). 12 1.1-7
The Link Between Enamel Hypoplasia and Early Childhood Caries The integrity <strong>of</strong> the primary tooth enamel (host resistance) is an important aspect in ECC development. Enamel hypoplasia results from defective amelogenesis, and is clinically identified by absences <strong>of</strong>, pitting, grooves, or other irregularities <strong>of</strong> enamel. 89-93 These structural defects may place an infant’s primary teeth at greater risk for bacterial colonization, specifically, by Mutans streptococci, resulting in dental caries. 94,95 These and other cariogenic oral bacteria convert dietary carbohydrates into acids, which can lead to the demineralization <strong>of</strong> tooth enamel and subsequent decay. Therefore, the calcification process <strong>of</strong> primary teeth, when enamel formation is occurring is crucial to understanding the significance <strong>of</strong> enamel hypoplasia. The primary maxillary anterior teeth begin to calcify during the second trimester, specifically between weeks 13 and 17 in utero, and this process does not end until 3 months postnatal. 96,97 Therefore, it is important to investigate the possible etiologies in utero that can disrupt normal enamel formation, as enamel hypoplasia is consistent with the period <strong>of</strong> amelogenesis, documented to originate in utero and end soon after birth. Causes <strong>of</strong> Enamel Hypoplasia and the Potential Link with <strong>Vitamin</strong> D Primary tooth enamel defects have been correlated with several factors ranging from genetic disorders to difficulties arising during prenatal and early postnatal periods. 66 Such disorders include low birth weight, malnourishment, prematurity, and metabolic difficulties. 66 Deficiencies <strong>of</strong> vitamin D in utero are also believed to be associated with enamel hypoplasia, because <strong>of</strong> metabolic insult to ameloblasts 98-103 , a theory first proposed by Lady May Mellanby in the 1920s. 104,105 1.1-8
Page 1 and 2: Influence
Page 3 and 4: Abstract Influence
Page 5 and 6: Acknowledgements This longitudinal
Page 7 and 8: Table of Contents
Page 9 and 10: Status and Non-<st
Page 11 and 12: Table 1.1-1 - Recent studies report
Page 13: Table 1.1-2 - Previous used terms f
Page 17 and 18: If enamel hypoplasia results from n
Page 19 and 20: malocclusions. 145 Additional human
Page 21 and 22: Daily intakes of v
Page 23 and 24: 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 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
Page 130 and 131:
References 1. Combs GF. Vit
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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
Page 140 and 141:
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</
Page 154 and 155:
Chapter 4 - Results: Associations <
Page 156 and 157:
II. Relationship Between 25(OH)D Le
Page 158 and 159:
Pregnancy & Health Prof</st
Page 160 and 161:
The frequency of v
Page 162 and 163:
did not (42.9 ± 21.2 nmol/L vs. 49
Page 164 and 165:
Early Childhood Caries (ECC) Pr<str
Page 166 and 167:
likely to have vitamin D levels at
Page 168 and 169:
did not statistically differ from v
Page 170 and 171:
Figure 4.4 - Predicted number <stro
Page 172 and 173:
Table 4.7 - Relationship between ds
Page 174 and 175:
frequently, and less likely to have
Page 176 and 177:
health as average or poor, and more
Page 178 and 179:
tail (p=.034) suggesting that early
Page 180 and 181:
The next series of
Page 182 and 183:
Results from the second model appea
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Table 5.6 - Multiple regression sta
Page 186 and 187:
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
Page 196 and 197:
Page 198 and 199:
Page 200 and 201:
Table 5.19(b) - Backwards logistic
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Table 5.20(a) - Logistic regression
Page 204 and 205:
Table 5.21 - Poisson regression for
Page 206 and 207:
If enamel hypoplasia is present and
Page 208 and 209:
Since maternal calcium levels were
Page 210 and 211:
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
Page 232 and 233:
pregnancy, which may have influence
Page 234 and 235:
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
Page 244 and 245:
Surprisingly, the final regression
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13. First Nations IaMHCCPS. <strong
Page 248 and 249:
38. Hollis BW. Circulating 25-hydro
Page 250 and 251:
65. Li Y, Navia JM, Bian JY. Caries
Page 252 and 253:
91. Brownell MD, Guevremont A, Au W
Page 254 and 255:
Chapter 7 - Conclusions This thesis
Page 256 and 257:
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
Page 275 and 276:
What problems can early childhood c
Page 277 and 278:
Prenatal Nutrition
Page 279 and 280:
Did you ever add sugar to the bottl
Page 281 and 282:
Enamel Hypoplasia Enamel Hypoplasia
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Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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