Influence of Maternal Prenatal Vitamin D Status on Infant Oral Health

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Chapter 1 – Introduction & Review <strong>of</strong> the Literature Section 1 – Introduction Prevalence and Consequences <strong>of</strong> Early Childhood Caries Primary tooth decay during the preschool years is called Early Childhood Caries (ECC). While caries among the general population is on the decline, the same is not true among certain groups <strong>of</strong> Canadians, including young Aboriginal children. Evidence from the United States indicates that caries among preschool children is on the rise. 1 In fact, caries is the most common chronic disease <strong>of</strong> childhood. 2 Early childhood is a crucial time in a child’s development as it sets the foundation for overall long-term health, including oral health. Infant and preschool children are particularly vulnerable for developing caries in their primary dentition as they are entirely dependent on parents and caregivers for activities <strong>of</strong> daily living, including nutrition and feeding behaviours, oral hygiene, dental prevention, and access to oral health care. While not obvious to most, ECC is in fact a major public health concern. If left untreated, dental caries can progress to infections and pain and ultimately affect a child’s quality <strong>of</strong> life. 3 Further, children afflicted with ECC are significantly more likely to suffer additional dental caries in both primary and permanent dentitions throughout the continuum <strong>of</strong> childhood and may also suffer from future orthodontic malocclusions. 4-6 Like many other chronic diseases and pediatric health conditions in Canada, ECC disproportionately affects North American Aboriginal children. For example, Indigenous children are known to have higher rates <strong>of</strong> obesity and type 2 diabetes, asthma and respiratory tract infections, otitis media, and face more nutritional challenges. 7-10 There are three distinct groups <strong>of</strong> Aboriginal people in Canada, First Nations people, both 1.1-1
<strong>Status</strong> and Non-<strong>Status</strong> Indians, the Inuit, and the Métis. Several Canadian studies have revealed that the prevalence <strong>of</strong> decay among Aboriginal children and other children living in the north is high, compared with the general population, ranging from 50% to as high as 98%. 11-18 Table 1.1-1 reports published prevalence and caries rates for Canadian preschool children over the past two decades. 11,12,15-17,19-26 These studies indicate that First Nations and other Aboriginal children suffer disproportionately from ECC than other groups. Reasons for such discrepancies are generally attributed to the lower SES <strong>of</strong> these groups and their limited access to dental care. 11,12,18 Chronic diseases, like dental caries, are strongly influenced by the social determinants <strong>of</strong> health. The reality is that only <strong>Status</strong> Indians and the Inuit are recipients <strong>of</strong> dental benefits through the Non-Insured Health Benefits (NIHB) program <strong>of</strong> First Nations and Inuit Health (FNIH), Health Canada. The federal government is charged with the responsibility <strong>of</strong> providing dental care to registered First Nations and Inuit people in Canada, but regular access to dental care in rural and remote northern communities is <strong>of</strong>ten limited. Even Aboriginal peoples residing in urban centres face challenges in accessing ideal dental care. In the past, decay among preschool children has <strong>of</strong>ten been referred to as “babybottle tooth decay” and “nursing caries”. These terms have now been replaced by the term ECC, in an attempt to raise awareness <strong>of</strong> the multiple factors contributing to this disease, rather than continuing to attribute causation solely to inappropriate feeding practices. 27-31 Preventive efforts to curb improper feeding methods alone have had limited or modest success in reducing ECC. 32-35 As associations between ECC and improper feeding practices are inconsistent it is no longer considered the principle etiology. 12,27,30,31,36-38 A listing <strong>of</strong> antecedent terms appears in Table 1.1-2. 39 1.1-2
Page 1 and 2: Influence
Page 3 and 4: Abstract Influence
Page 5 and 6: Acknowledgements This longitudinal
Page 7: Table of Contents
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 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
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Further, amelogenin and enamelin, p
Page 76 and 77:
A study of Austral
Page 78 and 79:
Both dietary interventions and supp
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incidence of carie
Page 82 and 83:
important nutrient. However, many <
Page 84 and 85:
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
Page 92 and 93:
Description of Pop
Page 94 and 95:
Influence
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D has an effect on the dentition, p
Page 98 and 99:
14. Utiger RD. The need for more vi
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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
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Each participant also completed an
Page 112 and 113:
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 <
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
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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
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The next series of
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Results from the second model appea
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Table 5.6 - Multiple regression sta
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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
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Table 5.21 - Poisson regression for
Page 206 and 207:
If enamel hypoplasia is present and
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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
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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
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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
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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
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91. Brownell MD, Guevremont A, Au W
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Chapter 7 - Conclusions This thesis
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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
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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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