Immunohistochemical Localization of Fam83h During Fluorosis-induced Mouse Molar Development.

The clinical and pathological features of fluorosis are similar to amelogenesis imperfecta (AI) caused by FAM83H mutations, suggesting that excess fluoride could have effects on the expression of Fam83h. Our previous study found that Fam83h was downregulated by fluorosis induction in ameloblasts; the purpose of this study was to underline the importance of understanding the relationship between fluoride administration and Fam83h expression in vivo. A total of 80 healthy female adult Kunming mice were randomly divided into control group or F group that induced the clinical features of fluorosis. Immunohistochemical staining on sections of the embryo mandible regions was performed at different developmental stages. Mouse primary ameloblast-like cells of the two groups at E13.5, E15.5, and E18.5 were cultured and examined for the expression of Fam83h. The expression of Fam83h in the F group was significantly lower than that in the control group; however, Fam83h was observed clearly in the whole enamel organ in the control group. Our findings shed new light on the potential effects of Fam83h in fluorosis using a mouse model and revealed that high fluoride decreased the expression of Fam83h. This may be one of the reasons for the occurrence of fluorosis.