HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text Full Text (PDF) Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Gao, Y. Articles by Lukinmaa, P.-L. Search for Related Content PubMed PubMed Citation Articles by Gao, Y. Articles by Lukinmaa, P.-L.

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

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;

View larger version (77K): [in a new window]   Figure 1. Morphology of enamel and dentin matrices after lactational TCDD exposure. Hematoxylin-eosin staining of Pn22 rat upper first (M1) and second (M2) molars. (A–C) Control. No enamel matrix is visible after 6 mos of demineralization with EDTA. The predentin layer (asterisks) is thin in comparison with the mineralized dentin. Dam exposed to 50 µg/kg TCDD (D–F) and 1000 µg/kg TCDD (G–K). A considerable amount of enamel matrix is left after 6 mos of demineralization (arrows). Matrix is more abundant after exposure to the higher dose and is also present in the erupted part of the first molar (J,K). In the exposed rats, the predentin layer (asterisks) is thicker in proportion to mineralized dentin than in control rats. The mineralization front is globular, and interglobular dentin is visible. Cleft between ameloblasts and enamel matrix is artefactual. a, ameloblasts; d, dentin; o, odontoblasts; oe, odontogenic epithelium. Scale bar shown in A represents 500 µm in A, D, and G; bar shown in B is 100 µm in B, C, E, F, H, and I; and bar shown in J is 100 µm in J and K.

View larger version (102K): [in a new window]   Figure 2. Immunohistochemical staining for AhR (A,C,E) and CYP1A1 (B,D,F) in Pn9 rat upper first/second molars. (A,B) Control. Dam exposed to 50 µg/kg TCDD (C,D) and 1000 µg/kg TCDD (E,F). No differences between controls and exposed rats are obvious in either AhR or CYP1A1 staining. AhR reactivity is more intense in ameloblasts than in odontoblasts. a, ameloblasts; d, dentin; e, enamel; o, odontoblasts. Bar: 100 µm in A-F.

View larger version (86K): [in a new window]   Figure 3. Effect of lactational TCDD exposure on immunohistochemical staining for AhR (A–F) and CYP1A1 (G–L) in Pn22 rat upper first/second molars. (A,B,G,H) Control. Dam exposed to 50 µg/kg TCDD (C,D,I,J) and 1000 µg/kg TCDD (E,F,K,L). (A,B) AhR expression is still strong in ameloblasts and less intense in odontoblasts (see Figs. 2A, 2B). (C,D) AhR expression is clearly decreased in ameloblasts and odontoblasts. (E,F) AhR expression has virtually disappeared in both ameloblasts and odontoblasts. Some expression is still present in the papillary layer (arrowheads). (G,H) CYP1A1 expression in ameloblasts and odontoblasts is at the same level as at Pn9. (I,J) The expression has decreased considerably in all cell types. (K,L) No CYP1A1 expression is visible in any dental tissues. a, ameloblasts; d, dentin; e, enamel; o, odontoblasts. Bar: 100 µm in A-L.