Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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genetic conditions, childhood medical disorders (e.g. inherited disorders <strong>of</strong> calcium metabolism), or infections during pregnancy and infancy (e.g. infant infection during the first 35 days <strong>of</strong> life, cytomegalovirus infection, maternal rubella, and postnatal measles). When controlling for other variables in our final logistic regression model, serious childhood medical problems was not significantly associated with hypoplasia. This differs from others who did find a clear relationship (as reviewed in Chapter 1, Section 2). In hindsight, it would have been useful to ask about specific medications infants received (e.g. antibiotics including amoxicillin) and whether the child was intubated following delivery as these have been identified as contributors to DDEs. Results <strong>of</strong> the final logistic regression model revealed that maternal levels <strong>of</strong> calcium were significantly associated with enamel hypoplasia. It appeared that participants with lower calcium levels were more likely to have infants with detectable enamel hypoplasia. Despite the fact that none <strong>of</strong> the mothers in this prospective study were found to have extremely low or elevated calcium levels (range 2.01 – 2.57, median 2.24), results at the bivariate level revealed that mothers who had infants with enamel hypoplasia had significantly lower calcium levels during pregnancy than those whose infants had no enamel defects (2.23 ± 0.10 mmol/L vs. 2.27 ± 0.10, p=.036). Further, it does concur with findings <strong>of</strong> other groups that hypocalcemia is a risk factor for enamel hypoplasia. 50,51 Some <strong>of</strong> these relationships were confirmed through logistic regression analysis. Those who had heard <strong>of</strong> vitamin D, consumed margarine <strong>of</strong>ten, and drank milk <strong>of</strong>ten were significantly less likely to have an infant with enamel hypoplasia while controlling 6-16
for additional factors such as the child’s medical history and prenatal 25(OH)D concentration. An interesting finding from the bivariate analysis was the fact that participants who had a previous child undergo pediatric dental surgery in hospital to treat ECC had significantly lower vitamin D levels. These same participants were also significantly more likely to have infants with noticeable enamel hypoplasia. While we are unaware <strong>of</strong> these participants’ vitamin D status during their previous pregnancies it is possible that their vitamin D levels would not differ greatly from one pregnancy to the next. Their dietary and lifestyle choices may be static over time. Low levels <strong>of</strong> vitamin D during a past pregnancy may have resulted in their older child having enamel hypoplasia that placed them at increased risk for dental surgery under GA because <strong>of</strong> ECC. However, this hypothesis cannot be substantiated in this current investigation. In addition to enamel hypoplasia, statistical analyses also explored associations with the presence <strong>of</strong> both ECC and caries rates, namely the decayed tooth rate (dt score). Several small regression models were constructed for ECC. The first involved the measures <strong>of</strong> serum metabolites obtained from the blood sample provided by participants during pregnancy. No one metabolite emerged to be significantly associated with ECC; although vitamin D levels were significantly associated with ECC at the bivariate level. However, results <strong>of</strong> the backwards logistic regression including all four serum metabolites did suggest that low 25(OH)D levels during pregnancy were associated with an increased risk for ECC (p=.063). No other study has attempted to correlate maternal prenatal levels <strong>of</strong> these metabolites with ECC development in <strong>of</strong>fspring. Another regression model for ECC controlled for factors known to have a direct influence on 6-17
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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
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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
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correspond to the timing of
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een published. 3,4,17,19 The intent
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Table 1.2-2 - Risk factors for DDE
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Opacity 51 Implicated Risk Developm
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Implicated Risk Factor Factors asso
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o Metabolic Abnormalities and Healt
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12 months of life.
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Other Factors Some uncommon risk fa
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devastating problem of</str
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13. An epidemiological index <stron
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54. Seow WK, Perham S. Enamel hypop
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82. Berdal A, Papagerakis P, Hotton
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Vitamin D may be d
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have been used to prof</str
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health’. In addition, articles we
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36 month trial had ended. 45 The nu
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Recently, a cross-sectional study <
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andomized, placebo-controlled study
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Further, amelogenin and enamelin, p
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A study of Austral
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Both dietary interventions and supp
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incidence of carie
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important nutrient. However, many <
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caries, and more hardening
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controls. 106 Interestingly, childr
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A few years later, additional resea
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Delayed Tooth Eruption Vita
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Description of Pop
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Influence
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D has an effect on the dentition, p
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14. Utiger RD. The need for more vi
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42. Spiller WF, Jr. A clinical eval
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67. Itota T, Tashiro Y, Torii Y, Ni
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95. Bruszt P. Kariesuntersuchungen
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121. Seow WK, Needleman HL, Holm IA
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Chapter 2 - Methods for a Prospecti
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Each participant also completed an
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Table 2.2 - Recognized case definit
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Population The target population fo
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allowed the project to suffer some
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women of limited m
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involving the surface of</s
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and training cup. In addition, each
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The questionnaire was administered
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statistics including frequencies an
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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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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
Page 184 and 185: Table 5.6 - Multiple regression sta
Page 186 and 187: vitamin D. However, it did suggest
Page 188 and 189: significant at the bivariate level
Page 190 and 191: Table 5.12(a) - Logistic regression
Page 192 and 193: III. Multivariate Regression Analys
Page 194 and 195: Table 5.14 - Logistic regression fo
Page 200 and 201: Table 5.19(b) - Backwards logistic
Page 202 and 203: 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)
Page 212 and 213: to obtain it. Health literacy may b
Page 214 and 215: vitamin D from the diet as dietary
Page 216 and 217: home environment can be determinant
Page 218 and 219: hormone, calcium absorption and bon
Page 220 and 221: important nutrient. For many, this
Page 222 and 223: this potential relationship with ac
Page 226 and 227: vitamin D status including milk int
Page 228 and 229: y cariogenic oral flora. 49 Since e
Page 230 and 231: (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
Page 236 and 237: scientific evidence linking prenata
Page 238 and 239: cognizant that children who undergo
Page 240 and 241: preventive program would need to be
Page 242 and 243: makers in the formative stages. As
Page 244 and 245: Surprisingly, the final regression
Page 246 and 247: 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
Page 258: esiding in disadvantaged communitie
Page 271 and 272: If you are taking vitamins during t
Page 273 and 274: 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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