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Updated: Mar 14, 2026
Micro-dissection of Enamel Organ from Mandibular Incisor of Rats Exposed to Environmental Toxicants
Published on: March 29, 2018
Androgen Receptor Involvement in Rat Amelogenesis: An Additional Way for Endocrine-Disrupting Chemicals to Affect
Katia Jedeon1, Sophia Loiodice1, Khaled Salhi1
1Centre de Recherche des Cordeliers (K.J., S.L., K.S., M.L.N., S.H., J.C., A.B., S.B.), INSERM Unité Mixte de Recherche en Santé 1138, Université Paris-Descartes, Université Pierre et Marie Curie-Paris, Paris Laboratory of Molecular Oral Pathophysiology, and Unité de Formation et de Recherche d'Odontologie (K.J., S.L., K.S., S.H., J.C., A.B., S.B.), Université Paris-Diderot, F-75006 Paris, France; and Centre de Référence des Maladies Rares de la Face et de la Cavité Buccale (K.J., A.B.), Hôpital Rothschild, Assistance Publique-Hôpitaux de Paris, F-75571 Paris, France.
Abstract:
Endocrine-disrupting chemicals (EDCs) that interfere with the steroid axis can affect amelogenesis, leading to enamel hypomineralization similar to that of molar incisor hypomineralization, a recently described enamel disease. We investigated the sex steroid receptors that may mediate the effects of EDCs during rat amelogenesis. The expression of androgen receptor (AR), estrogen receptor (ER)-α, and progesterone receptor was dependent on the stage of ameloblast differentiation, whereas ERβ remained undetectable. AR was the only receptor selectively expressed in ameloblasts involved in final enamel mineralization. AR nuclear translocation and induction of androgen-responsive element-containing promoter activity upon T treatment, demonstrated ameloblast responsiveness to androgens. T regulated the expression of genes involved in enamel mineralization such as KLK4, amelotin, SLC26A4, and SLC5A8 but not the expression of genes encoding matrix proteins, which determine enamel thickness. Vinclozolin and to a lesser extent bisphenol A, two antiandrogenic EDCs that cause enamel defects, counteracted the actions of T. In conclusion, we show, for the first time, the following: 1) ameloblasts express AR; 2) the androgen signaling pathway is involved in the enamel mineralization process; and 3) EDCs with antiandrogenic effects inhibit AR activity and preferentially affect amelogenesis in male rats. Their action, through the AR pathway, may specifically and irreversibly affect enamel, potentially leading to the use of dental defects as a biomarker of exposure to environmental pollutants. These results are consistent with the steroid hormones affecting ameloblasts, raising the issue of the hormonal influence on amelogenesis and possible sexual dimorphism in enamel quality.
