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Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride’s actions on bone cells predominate as anabolic effects both in vitro and in vivo. More recently, fluoride has been shown to induce osteoclastogenesis in mice. Fluorides appear to mediate their actions through the MAPK signaling pathway and can lead to changes in gene expression, cell stress, and cell death. Different strains of inbred mice demonstrate differential physiological responses to ingested fluoride. Genetic studies in mice are capable of identifying and characterizing fluoride-responsive genetic variations. Ultimately, this can lead to the identification of at-risk human populations who are susceptible to the unwanted or potentially adverse effects of fluoride action and to the elucidation of fundamental mechanisms by which fluoride affects biomineralization. [ABSTRACT FROM PUBLISHER]

The Nmp4 gene encodes a novel family of zinc finger proteins, some of which contribute to extracellular matrix gene expression in connective tissue. A human brain partial cDNA clone TNRC1 (alias CAGH1) encodes a protein that likely is the human ortholog of Nmp4 and has been mapped to human chromosome 12p12. The researchers report the isolation of a murine genomic BAC clone containing the Nmp4 gene and the localization of mouse Nmp4 to chromosome 6 band F1, using radiation hybrid mapping and fluorescence in situ hybridization analyses.