Abstract

Fluorosed enamel is caused by exposure to fluoride during tooth formation. The objective of this study was to determine whether epithelial ameloblast-lineage cells, derived from the human enamel organ, are directly affected by micromolar concentrations of fluoride. Cells were cultured in the presence of fluoride, and proliferation was measured by BrdU incorporation. The effect of 0, 10, or 20 microM fluoride on apoptosis was determined by the flow cytometry apoptotic index. The effects of fluoride on gene expression were investigated by SuperArray microarray analysis and real-time PCR. Fluoride had a biphasic effect on cell proliferation, with enhanced proliferation at 16 microM, and reduced proliferation at greater than 1 mM F. Flow cytometry showed that both 10 microM and 20 microM NaF significantly increased the apoptotic index of ameloblast-lineage cells. There was no general effect of fluoride on gene expression. These results indicate multiple effects of micromolar fluoride on ameloblast-lineage cells.

• Related Studies :

  • LS8 cell apoptosis induced by NaF through p-ERK and p-JNK - a mechanism study of dental fluorosis

    OBJECTIVE: To investigate the possible biological mechanism of dental fluorosis at a molecular level. MATERIAL AND METHODS: Cultured LS8 were incubated with serum-free medium containing selected concentrations of NaF (0???2?mM) for either 24 or 48?h. Subcellular microanatomy was characterized using TEM; meanwhile, selected biomolecules were analysed using various biochemistry techniques. Transient

  • Protective effect of lycopene on fluoride-induced ameloblasts apoptosis and dental fluorosis through oxidative stress-mediated Caspase pathways

    Fluoride is an environmental toxicant and induces dental fluorosis and oxidative stress. Lycopene (LYC) is an effective antioxidant that is reported to attenuate fluoride toxicity. To determine the effects of LYC on sodium fluoride (NaF) -induced teeth and ameloblasts toxicity, rats were treated with NaF (10 mg/kg) and/or LYC (10 mg/kg) by

  • Fluoride induced endoplasmic reticulum stress and calcium overload in ameloblasts

    OBJECTIVE:  The aim of the study was to evaluate the involvement of endoplasmic reticulum stress and intracellular calcium overload on the development of dental fluorosis. METHODS:  We cultured and exposed rat ameloblast HAT-7 cells to various concentrations of fluoride and measured apoptosis with flow cytometry and intracellular Ca2+ changes using confocal

  • High-fluoride promoted phagocytosis-induced apoptosis in a matured ameloblast-like cell line

    Endocytosis and phagocytosis are important physiologic activities occurring during ameloblast differentiation. We have previously found that excess fluoride inhibited ameloblasts endocytotic functions. Here, we hypothesized that increasing amounts of fluoride may affect ameloblast phagocytotic function during their differentiation. Using cell culture, we first induced maturation of the mouse ameloblast-like LS8

  • In vitro effect of sodium fluoride on antioxidative enzymes and apoptosis during murine odontogenesis.

    Excessive fluoride ingestion has been identified as a risk factor for fluorosis and oxidative stress. The oxidative stress results from the loss of equilibrium between oxidative and antioxidative mechanisms that can produce kinase activation, mitochondrial disturbance and DNA fragmentation, resulting in apoptosis. Actually many people are exposed to no-adverted fluoride

• Related FAN Content :

  • Mechanisms by Which Fluoride Causes Dental Fluorosis Remain Unknown

    When it comes to how fluoride impacts human health, no tissue in the body has been studied more than the teeth. Yet, despite over 50 years of research, the mechanism by which fluoride causes dental fluorosis (a hypo-mineralization of the enamel that results in significant staining of the teeth) is not

  • Dental Fluorosis Is a "Hypo-mineralization" of Enamel

    Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin

  • Racial Disparities in Dental Fluorosis

    In 2005, the Centers for Disease Control published the results of a national survey of dental fluorosis conducted between 1999 and 2002. According to the CDC, black children in the United States have significantly higher rates of dental fluorosis than either white or Hispanic children. This was not the first time that black children were found to suffer higher rates of dental fluorosis. At least five other studies -- dating as far back as the 1960s -- have found black children in the United States are disproportionately impacted by dental fluorosis.

  • "Mild" Dental Fluorosis: Perceptions & Psychological Impact

    The vast majority of research has found that patients, parents, and the general public alike view mild fluorosis (TF score 3) as a significant blemish of the teeth, one that is likely to embarrass the affected child to a degree that cosmetic treatment would be warranted.

  • Dental Fluorosis Impacts Dentin in Addition to Enamel

    Dental fluorosis is a mineralization defect of tooth enamel marked by increased subsurface porosity. The enamel, however, is not the only component of teeth that is effected. As several studies have demonstrated, dental fluorosis can also impair the mineralization of dentin as well. As noted in one review: "The fact that