Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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163. Vieth R, Cole DE, Hawker GA, Trang HM, Rubin LA. Wintertime vitamin D insufficiency is common in young Canadian women, and their vitamin D intake does not prevent it. Eur J Clin Nutr 2001; 55(12):1091-1097. 164. Vieth R, Cole DE, Hawker GA, Trang HM, Rubin LA. Wintertime vitamin D insufficiency is common in young Canadian women, and their vitamin D intake does not prevent it. Eur J Clin Nutr 2001; 55(12):1091-1097. 165. Thomas MK, Lloyd-Jones DM, Thadhani RI, Shaw AC, Deraska DJ, Kitch BT et al. Hypovitaminosis D in medical inpatients. N Engl J Med 1998; 338(12):777-783. 166. Zeghoud F, Garabedian M, Jardel A, Bernard N, Melchior J. [Administration <strong>of</strong> a single dose <strong>of</strong> 100,000 U.I. <strong>of</strong> vitamin D3 in the pregnant woman in winter. The effect on blood calcium level <strong>of</strong> the newborn infant]. J Gynecol Obstet Biol Reprod (Paris) 1988; 17(8):1099-1105. 167. Serenius F, Elidrissy AT, Dandona P. <strong>Vitamin</strong> D nutrition in pregnant women at term and in newly born babies in Saudi Arabia. J Clin Pathol 1984; 37(4):444-447. 168. Ardawi MS, Nasrat HA, BA'Aqueel HS. Calcium-regulating hormones and parathyroid hormone-related peptide in normal human pregnancy and postpartum: a longitudinal study. Eur J Endocrinol 1997; 137(4):402-409. 1.1-27
Section 2 – Risk Factors for Enamel Hypoplasia in Young Children The previous section identified enamel hypoplasia as a key risk factor in the development <strong>of</strong> dental caries, including Early Childhood Caries (ECC). The intent <strong>of</strong> this chapter is to review our understanding <strong>of</strong> factors contributing to these enamel defects in children. Dental enamel is a unique hard tissue <strong>of</strong> ectoderm rather than connective tissue origin. 1 Ameloblasts, the cells that form enamel first secrete an enamel matrix, which is both inorganic and organic in composition. 1 Secretion and limited mineralization <strong>of</strong> the matrix continues until the enamel has reached its intended thickness. Following this process, the matrix undergoes a maturation process that results in the loss <strong>of</strong> protein and water from the matrix and the addition <strong>of</strong> minerals leading to mature enamel. 1 The primary dentition begins to form at week 6 in utero and amelogenisis, the process <strong>of</strong> enamel formation generally commences during the 18 th week. 1 The formation <strong>of</strong> hard tissues <strong>of</strong> the primary maxillary and mandibular incisors begins between 4 and 4.5 months in utero. 2 While the bulk <strong>of</strong> enamel deposition occurs during prenatal life the remainder is formed during infancy. 3 Disturbances to the developing enamel matrix (ameloblasts) are irreversible and serve as a permanent record <strong>of</strong> the insult to enamel formation in the primary and permanent dentitions. Thus, it is possible to estimate when the disturbance to developing enamel might have occurred (Figure 1.2-1). Developmental defects <strong>of</strong> enamel (DDE) serve as records <strong>of</strong> such disturbances to the amelogenesis process. DDE have been implicated as risk factors for ECC. 4,5 Specifically, these sites are preferentially colonized by cariogenic microorganisms including, Mutans streptococci. 6-10 1.2-1
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: 151. Tinanoff N, D
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
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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