Prevalence and age at development of enamel hypoplasias in Mexican children.

@article{Goodman1987PrevalenceAA,
  title={Prevalence and age at development of enamel hypoplasias in Mexican children.},
  author={Alan H. Goodman and Lindsay H Allen and Gabriela Hernandez and Armando Amador and Larraitz Arriola and A Ch{\'a}vez and Gretel H Pelto},
  journal={American journal of physical anthropology},
  year={1987},
  volume={72 1},
  pages={
          7-19
        }
}
Enamel hypoplasias, deficiencies in enamel thickness resulting from disturbances during the secretory phase of enamel development, are generally believed to result from nonspecific metabolic and nutritional disruptions. However, data are scare on the prevalence and chronological distributions. of hypoplasias in populations experiencing mild to moderate malnutrition. The purpose of this article is to present baseline data on the prevalences and chronological distributions of enamel hypoplasias… 
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The prevalence of enamel defects in this study group is comparable to that seen in other studies of normally developed children except that the primary tooth types most commonly affected with enamel hypoplasia or isolated opacities were mandibular second molar and maxillary second molars, respectively.
Enamel hypoplasia in an early medieval population of Prząsław ( 11-12 th century )
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The retrospective analysis of stress episodes in early childhood revealed the increased frequency of factors disturbing ameloblast metabolism, mainly in the post-weaning period, which indicated that the mean age of enamel hypoplasia occurrence was at over 3 years.
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The results indicate that the stress associated with weaning probably occurred earlier in incipient industrial societies than in prehistoric hunter/gatherers and agriculturalists, yet not as early as in modern industrial groups.
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The results do not support the view that peak ages of occurrence of hypoplastic defects are associated with the cessation of breast‐feeding or the weaning process in general, and are not consistent with separate studies, demographic, isotopic and historical.
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  • 1989
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Social and biological correlates of localized enamel hypoplasia of the human deciduous canine tooth.
TLDR
The defect appears to be due to minor physical trauma to the face approximately 6 months after birth occasioned by normal motor development, involving handling and mouthing objects, which damages the developing tooth crown through deficient cortical bone over the canine crypt.
Enamel Hypoplasia in the Deciduous Teeth of Edo Japanese
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Results suggest that people in Edo City lived under highly stressful environment, with most of the enamel hypoplasia detected occurred postnatally, few occurring prenatally and perinatally.
Epidemiology of enamel hypoplasia in deciduous teeth: Explaining variation in prevalence in western india
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The association between low birth weight and EH is strong and well documented clinically, but the association between childhood stature and LHPC is more variable across groups and may reflect inter‐group variation in the duration and intensity of environmental stress.
Macroscopic dental enamel hypoplasia in deciduous teeth: health conditions and socio-economic status in nineteenth- to twentieth-century Granada, Spain
TLDR
The analysis of dental enamel hypoplasia provides an excellent index of developmental stress levels in the past and two peaks of occurrence of stressful events were observed in the decades of the late 1930s and the mid-1940s, and in the early 1970s.
Macroscopic enamel defects of primary anterior teeth--types, prevalence, and distribution.
TLDR
Exfoliated primary anterior teeth from children who were healthy products of uneventful pregnancies exhibited at least one macroscopic enamel defect, and developmental enamel defects (DED) occurred with increased frequency on maxillary teeth, facial surfaces, and the middle third of affected surfaces.
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Differences in hypoplasia frequencies among teeth are not solely due to variation in time of crown development, as is usually reported, and there is evidence for biological gradients in susceptibility to ameloblastic disruption.
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TLDR
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