Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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Table 1.2-1 – Modified DDE Index for use in epidemiological studies 12 Code Normal 0 Demarcated opacities: White/cream Yellow/brown Diffuse opacities: Lines Patchy Confluent Confluent/patchy + staining + loss <strong>of</strong> enamel Hypoplasia: Pits Missing Enamel Any other defect Combinations: Demarcated and Diffuse Demarcated and hypoplasia Diffuse and hypoplasia All 3 defects 1 2 3 4 5 6 7 8 9 A B C D Several indices have been proposed for standardizing DDE, including enamel hypoplasia. 12,13,15,16,18 Currently, one index is preferred for recording and reporting enamel opacities and hypoplasia for epidemiological purposes although several others have also been proposed. 12 Clarkson and O’Mullane proposed two versions <strong>of</strong> their index, a simplified one for screening purposes and a more comprehensive tool for dental surveys. 16 Likewise, the World Health Organization also has an index for epidemiological surveys. 15 Unfortunately, it only records enamel defects for specific teeth in the mouth 15 and thereby underestimates the true prevalence <strong>of</strong> DDE. Finally, another proposed index for DDE does not account for qualitative changes in the translucency <strong>of</strong> enamel (i.e. opacities), and instead only focuses on enamel hypoplasia. 18 The literature contains numerous studies reporting the prevalence and risk factors for enamel hypoplasia. Expert reviews on the subject <strong>of</strong> enamel hypoplasia have also 1.2-4
een published. 3,4,17,19 The intent <strong>of</strong> this chapter is not to undertake an exhaustive systematic review <strong>of</strong> the literature, but rather provide some insight into those risk factors which have been identified as contributing to enamel hypoplasia and opacities. It is also important to distinguish between enamel hypoplasia and opacities in the primary and permanent dentitions. Both dentitions begin forming during the early childhood period and genetic conditions and stressors in utero and during periods <strong>of</strong> early childhood development can negatively alter the quality and structure <strong>of</strong> enamel. Therefore, not only will information be presented specific to enamel and other DDE in deciduous teeth but data will also be presented for factors influencing the adult dentition. Etiological risk factors for enamel hypoplasia can be ascribed to three main groupings. 17 Apart from altered enamel formation as a result <strong>of</strong> genetic conditions affecting only the teeth (e.g. amelogenesis imperfecta), inherited syndromes (e.g. ectodermal dyspalasia, ectodermal-mesodermal disorders) and inherited metabolic disorders (e.g. calcium metabolic disorders, parathyroid disease, vitamin D dependent rickets, hypophosphatasia), enamel hypoplasia may also arise from both systemic or localized factors. 17 Systemic factors include infections experienced by the mother or infant, metabolic disease, nutritional disorders and deficiencies, premature birth and low birth weight, and ingestion or exposure to chemical compounds. 17,19 In contrast, localized factors include cleft lip and palate, trauma to teeth during amelogenesis, and primary tooth infections that may harm the developing successor. 17,19 Table 1.2-2 provides some evidence for the association between some genetic, systemic and local factors that have been associated with DDE. As this paper primarily 1.2-5
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: correspond to the timing of
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
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
Page 146 and 147:
indicated that they were receiving
Page 148 and 149:
and 11 hypoplasia). DDEs were also
Page 150 and 151:
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
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
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 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
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 224 and 225:
genetic conditions, childhood medic
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
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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