Abstract
Currently, the mechanism behind the development of dental fluorosis remains unclear, but it is known that fluorotic enamel has higher protein content and is therefore softer than nonfluorosed enamel. Previously it was demonstrated that fluoride induces phosphorylation of the eIF2α ribosomal component, which significantly decreases protein synthesis. This occurs during the maturation stage of development when proteins are normally removed from the hardening enamel. By combining these data with current knowledge of ameloblast function during enamel development, we can hypothesize a potential mechanism in which excess fluoride results in increased protein levels and softened enamel via decreased protease secretion during the maturation stage. Briefly, this hypothesis states that phospho-eIF2α-mediated inhibition of protein production induced by intracellular fluoride results in decreased secretion of the enamel protease kallikrein-4 (KLK4) during the enamel maturation phase. This in turn results in decreased protein breakdown and higher protein content within the enamel matrix.
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Sierant, M.L., Bartlett, J.D. (2012). A Potential Mechanism for the Development of Dental Fluorosis. In: Sasaki, K., Suzuki, O., Takahashi, N. (eds) Interface Oral Health Science 2011. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54070-0_114
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DOI: https://doi.org/10.1007/978-4-431-54070-0_114
Publisher Name: Springer, Tokyo
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