ABSTRACT
Localized enamel hypoplasia of the primary canine (LHPC) is produced by a different mechanism from that causing linear enamel hypoplasia, and yet contributes disproportionately to epidemiological studies of enamel hypoplasia in childhood that do not separate the two etiological types. LHPC results from impact, probably self-inflicted by infants mouthing objects, to the unerupted primary canine crown through abnormally fenestrated cortical bone overlying the crypt. Examination of the primary teeth of ninety-six children whose mothers were enrolled in the Healthiest Babies Possible Program in Vancouver showed an average prevalence of 31 percent with LHPC (ranging from 19 percent in Vietnamese Canadians to 56 percent among Indocanadians). This is much higher than previously reported for unselected samples from Vancouver, but equivalent to studies in the USA. Mean hours of sunshine in the birth month of children with LHPC is 141.7 hours and those without is 169.4 hours; the difference is statistically significant (p = .0383). Seasonal increase in food costs and reduced availability of fresh foods containing vitamin A are thought to contribute to facial osteopenia predisposing the infant to LHPC.
