Abstract
Dental fluorosis is caused by chronic high-level fluoride (F–) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be reabsorbed from the hardening enamel. We show that transforming growth factor ?1 (TGF-?1) can induce Klk4 expression, and we examine the effect of F– on TGF-?1 and KLK4 expression. We found that in vivo F– inhibits Klk4 but not Mmp20 transcript levels. LacZ-C57BL/6-Klk4 +/-LacZ mice have LacZ inserted in frame at the Klk4 translation initiation site so that the endogenous Klk4 promoter drives LacZ expression in the same temporal/spatial way as it does for Klk4. KLK4 protein levels in rat enamel and ?-galactosidase staining in LacZ-C57BL/6-Klk4 +/-LacZ mouse enamel were both significantly reduced by F– treatment. Since TGF-?1 induces KLK4 expression, we tested and found that F– significantly reduced Tgf-?1 transcript levels in rat enamel organ. These data suggest that F–-mediated downregulation of TGF-?1 expression contributes to reduced KLK4 protein levels in fluorosed enamel and provides an explanation for why fluorosed enamel has a higher than normal protein content.
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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
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MiR-1a-3p Inhibits Apoptosis in Fluoride-exposed LS8 Cells by Targeting Map3k1.
Dental fluorosis is a common chemical disease. It is currently unclear how fluorosis occurs at the molecular level. We used miRNA-seq to look at the differences between miRNAs in the cell line of ameloblasts LS8 that had been treated with 3.2 mmol/L NaF. We also performed gene ontology (GO) and
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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
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Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.
Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts,
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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
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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
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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
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Dental Fluorosis: The "Cosmetic" Factor
Any condition that can cause children to be embarrassed about their physical appearance can have significant consequences on their self-esteem and confidence. Researchers have repeatedly found that "physical appearance [is] the best predictor of self-esteem" in adolescents, (Harter 2000) and that facial attractiveness, particularly the appearance of one's teeth, is a
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Moderate/Severe Dental Fluorosis
In its "moderate" and severe forms, fluoride causes a marked increase in the porosity of the enamel. After eruption into mouth, the porous enamel of moderate to severe fluorosis readily takes up stain, creating permanent brown and black discolorations of the teeth. In addition to extensive staining, teeth with moderate to severe fluorosis are more prone to attrition and wear - leading to pitting, chipping, and decay.
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Diagnostic Criteria for Dental Fluorosis: The TSIF ("Total Surface Index of Fluorosis")
The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental
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