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RESEARCH REPORT |
1 Department of Pedodontics and Orthodontics, Institute of Dentistry, University of Helsinki, Finland;
2 Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Finland;
3 Department of Food and Environmental Hygiene, Faculty of Veterinary Medicine, University of Helsinki, Finland;
4 Kuopio Department, National Veterinary and Food Research Institute, Finland;
5 Department of Environmental Health, National Public Health Institute, Kuopio, Finland;
6 Department of Oral Pathology, Institute of Dentistry, University of Helsinki, Finland;
7 Department of Pathology, Helsinki University Central Hospital, Finland;
10 corresponding author, Institute of Dentistry, Biomedicum Helsinki, PO Box 63, FIN-00014 UNIVERSITY OF HELSINKI, Finland, carin.sahlberg{at}helsinki.fi
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.
KEY WORDS: TCDD • enamel maturation • dentin mineralization • AhR • CYP1A1
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