Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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<strong>Vitamin</strong> D may be defined as a vitamin and a hormone, in that it can be obtained exogenously as a nutrient or synthesized endogenously in the skin on exposure to ultraviolet (UV) radiation <strong>of</strong> the appropriate wavelength. 3,4 As much as 90% <strong>of</strong> the total vitamin D requirement for humans comes from endogenous synthesis. 5 The serum half life <strong>of</strong> 25(OH)D is reported to be between 12 to 19 days. 6 Although 1,25- dihydroxyvitamin D is the most active form <strong>of</strong> vitamin D 3,4 , 25(OH)D is the main circulating form. <strong>Vitamin</strong> D is involved in mineral homeostasis ensuring that serum calcium and phosphorus levels are sufficient for the mineralization <strong>of</strong> bones and other calcified tissues, including teeth, in addition to neuromuscular functions. 4,5,7 Several physiologic, environmental and cultural factors affect vitamin D availability and thus vitamin D status in the population. 8 Due to our northern latitude, endogenous synthesis <strong>of</strong> vitamin D in Manitoba, Canada is negligible from October to March. Further, vitamin D production might be diminished due to increasing calls to limit summer sun exposure in order to reduce the <strong>of</strong> risk <strong>of</strong> skin cancer. This has led to greater usage <strong>of</strong> sunscreen and protective clothing, and perhaps a reduction <strong>of</strong> outdoor summertime activities. Dietary Sources <strong>of</strong> <strong>Vitamin</strong> D Apart from endogenous production <strong>of</strong> 25(OH)D, the other ways humans acquire vitamin D comes from exogenous sources, either from diet or dietary supplements. 3,9 Apart from dietary supplements, foods known to contain vitamin D include fatty fish and fish oils 4 , liver, eggs 10 , vitamin D fortified milk and dairy products 11,12 (e.g. fortified milk products and margarines), in addition to some cereals 4,13,14 . Exogenous vitamin D can be derived 1.3-2
from two forms: 1) animals (D 3 or cholecalciferol from endogenous origin) frequently contained in fatty fish and fish oils, or 2) from plants (D 2 or ergocalciferol). 4,9,15 <strong>Vitamin</strong> D supplements were usually in the form <strong>of</strong> ergocalciferol (D 2 ), but now most supplements contain cholecalciferol (D 3 ) as it is more effective in bolstering serum concentrations. 6,16 Evidence now indicates that our present intakes <strong>of</strong> vitamin D fall short <strong>of</strong> recommendations. 1,17,18 Insufficient data exist for an established recommended dietary allowance (RDA) for vitamin D. Therefore, an adequate intake (AI) has been adopted, as it represents the level <strong>of</strong> intake sufficient to maintain healthy blood levels <strong>of</strong> an active form <strong>of</strong> vitamin D. However, emerging research would suggest that current adequate intakes (AI) for vitamin D are set too low for many groups as they were originally set at or above 25 – 30 nmol/L (concentrations known to prevent rickets and osteomalacia). 2,17- 20 For instance, the AI for children and adolescents is only 200 IU, even though children undergo considerable growth and development during these stages <strong>of</strong> life. 21 The Canadian Paediatric Society has recently recommended higher AIs for infants, expectant and lactating mothers, and children and have stated that research on the vitamin D requirements for toddlers and older children should be encouraged (recommendation grade A). 22 Assessment <strong>of</strong> <strong>Vitamin</strong> D <strong>Status</strong> 25(OH)D is the primary form <strong>of</strong> vitamin D in circulation and is regarded to be the best indicator <strong>of</strong> vitamin D status as it is a good measure <strong>of</strong> total vitamin D received from both endogenous and exogenous sources. 3,4,6,9,14,15,23-25 Different investigative methods 1.3-3
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 and 14: Table 1.1-2 - Previous used terms f
Page 15 and 16: The Link Between Enamel Hypoplasia
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 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
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References 1. Combs GF. Vit
Page 132 and 133:
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
Page 142 and 143:
Table 3.6- Prenatal</strong
Page 144 and 145:
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
Page 152 and 153:
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
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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
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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
Page 180 and 181:
The next series of
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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
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
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vitamin D deficiency, and rickets)
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to obtain it. Health literacy may b
Page 214 and 215:
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
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
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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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