EGF-R and erbB-2 in murine tooth development after ethanol exposure

Alcohol consumption during pregnancy can frequently lead to a congenital disorder known as fetal alcohol syndrome (FAS); however, not all children born to alcoholic women develop FAS. Alcohol consumption may affect diverse organs and systems during embryonic development, including craniofacial structures. Small teeth, enamel alterations, and delayed eruption have been observed after ethanol exposure. Epidermal growth factor receptors (EGF-Rs) participate in dental proliferation and differentiation, and changes in these receptors were considered here to be a likely mechanism associated to the dental anomalies observed in this syndrome. Epidermal growth factor receptor type 1 (EGF-R) and epidermal growth factor receptor type 2 (erbB-2) immunoexpression during the lower first molar morphogenesis was investigated in mouse fetuses exposed to ethanol during gestation.

Pregnant female mice were divided into groups, consuming either 5, 10, 15, 20, or 25% ethanol solutions, or water (control group). Heads were obtained from 16.5- and 18.5-day fetuses. Immunohistochemistry was applied to EGF-R and erbB-2.

At days 16.5 and 18.5, fetuses from 15%, 20%, and 25% ethanol groups showed delayed differentiation, degenerative changes in dental epithelial tissues and reduced dental size; additionally, they displayed an enhanced immunoreactivity to EGF-R and erbB-2.

Our results suggest that ethanol consumption during pregnancy affects the expression of EGF receptors and induces a delay in murine fetal dental morphogenesis. Dental development is a process that involves a number of growth factors; hence we consider that further research is required to show whether the changes in glycosylation and growth-factor signaling pathways observed in other cells are also involved in the alterations observed in this study.