Exposure to environmental dioxins via mother’s milk may
be one causative factor of mineralization defects in children’s teeth. A prerequisite
for the completion of enamel mineralization is the removal of enamel matrix. To test
the hypothesis that dioxins interfere with enamel maturation, we administered
lactating Han/Wistar rats a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 50 or 1000 μg/kg) on the day after delivery
and analyzed tissue sections of the pup heads at post-natal days (Pn) 9 and 22. By
Pn22, the first and second molars of the exposed pups, but not controls, showed
retention of enamel matrix. Predentin was thicker than normal. Immunostaining for the
aryl hydrocarbon/dioxin receptor (AhR) and cytochrome P4501A1 (CYP1A1) in ameloblasts
and odontoblasts was reduced, suggesting that TCDD interferes with tooth
mineralization via AhR. Extinction of AhR may lead to
abolition of CYP1A1 expression as a sign of impaired dental cell function.
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