Lactational Exposure of Han/Wistar Rats to 2,3,7,8-Tetrachlorodibenzo-p-dioxin Interferes with Enamel Maturation and Retards Dentin Mineralization-Reference-Cited by-同舟云学术

Lactational Exposure of Han/Wistar Rats to 2,3,7,8-Tetrachlorodibenzo-p-dioxin Interferes with Enamel Maturation and Retards Dentin Mineralization

Published:2004-02 Issue:2 Volume:83 Page:139-144
ISSN:0022-0345
Container-title:Journal of Dental Research
language:en
Short-container-title:J Dent Res

Author:

Gao Y.¹²³⁴⁵,Sahlberg C.¹²³⁴⁵,Kiukkonen A.¹²³⁴⁵,Alaluusua S.¹²³⁴⁵,Pohjanvirta R.¹²³⁴⁵,Tuomisto J.¹²³⁴⁵,Lukinmaa P.-L.¹²³⁴⁵

Affiliation:

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;

Abstract

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.

Publisher

SAGE Publications

Subject

General Dentistry

Link

http://journals.sagepub.com/doi/pdf/10.1177/154405910408300211

Reference29 articles.

1. Exposure to 2,3,7,8-tetrachlorodibenzo-para-dioxin leads to defective dentin formation and pulpal perforation in rat incisor tooth

2. Alaluusua S, Lukinmaa PL, Torppa J, Tuomisto J, Vartiainen T -1999- Developing teeth as biomarker of dioxin exposure. Lancet 353:206.

3. Repression of cytochrome P450 1A1 gene expression by oxidative stress: mechanisms and biological implications

4. A Transmission Electron Microscope Study Using Vitrified Ice Sections of Predentin: Structural Changes in the Dentin Collagenous Matrix prior to Mineralization

5. The presence and possible functions of the matrix metalloproteinase collagenase activator protein in developing enamel matrix

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