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Updated: May 10, 2026

Micro-dissection of Enamel Organ from Mandibular Incisor of Rats Exposed to Environmental Toxicants
Published on: March 29, 2018
Enamel defects reflect perinatal exposure to bisphenol A
Katia Jedeon1, Muriel De la Dure-Molla, Steven J Brookes
1Laboratory of Molecular Oral Pathophysiology, INSERM UMRS 872, Cordeliers Research Center, Paris, France.
Bisphenol A (BPA), an endocrine-disrupting chemical, causes enamel defects similar to molar incisor hypomineralization (MIH) in developing rats. This study identifies BPA as a potential cause of MIH, highlighting a critical developmental window for enamel sensitivity.
Area of Science:
- Environmental Science
- Developmental Biology
- Toxicology
Background:
- Endocrine-disrupting chemicals (EDCs) like bisphenol A (BPA) are widespread pollutants linked to health issues.
- Molar incisor hypomineralization (MIH) prevalence is rising, with anecdotal links to EDC exposure.
- The impact of BPA on amelogenesis, the process of enamel formation, requires investigation.
Purpose of the Study:
- To investigate the effects of BPA exposure on amelogenesis in a rat model.
- To determine if BPA exposure can induce enamel hypomineralization similar to human MIH.
- To explore the molecular mechanisms underlying BPA's effects on enamel development.
Main Methods:
- Rats were exposed to BPA from conception to postnatal day 30 or 100.
- Enamel hypomineralization was assessed using scanning electron microscopy and elemental analysis.
- Gene and protein expression related to amelogenesis (enamelin, kallikrein 4) were analyzed via qPCR, Western blotting, and luciferase assays.
Main Results:
- BPA exposure by day 30 resulted in enamel hypomineralization and abnormal organic material accumulation, including exogenous albumin.
- Expression of enamelin increased, while kallikrein 4 decreased, indicating disrupted protein removal during enamel maturation.
- Enamel development was unaffected in rats exposed until day 100, suggesting a critical developmental window for sensitivity.
Conclusions:
- BPA exposure during a specific developmental window can cause enamel defects mimicking human MIH.
- BPA disrupts amelogenesis by interfering with the removal of enamel matrix proteins.
- This study presents the first experimental model for MIH and implicates BPA as a potential causative agent, with MIH potentially serving as a biomarker for early EDC exposure.
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