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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Effects of Fluoride on Oxidative Stress Markers of Lipid, Gene, and Protein in Rats.
Endemic fluorosis is a systemic chronic disease caused by excessive intake of fluoride. It is widely accepted that oxidative stress is closely related to fluorosis; however, molecular mechanism of oxidative stress in fluorosis remains unclear. This study investigated the effects of fluoride (F) on oxidative stress markers of lipid, gene,
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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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Fluoride Alters Signaling Pathways Associated with the Initiation of Dentin Mineralization in Enamel Fluorosis Susceptible Mice.
Fluoride can alter the formation of mineralized tissues, including enamel, dentin, and bone. Dentin fluorosis occurs in tandem with enamel fluorosis. However, the pathogenesis of dentin fluorosis and its mechanisms are poorly understood. In this study, we report the effects of fluoride on the initiation of dentin matrix formation and
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Histone acetyltransferase promotes fluoride toxicity in LS8 cells.
Previously we demonstrated that fluoride increased acetylated-p53 (Ac-p53) in LS8 cells that are derived from mouse enamel organ epithelia and in rodent ameloblasts. However, how p53 is acetylated by fluoride and how the p53 upstream molecular pathway responds to fluoride is not well characterized. Here we demonstrate that fluoride activates
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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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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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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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Severe Dental Fluorosis: Perception and Psychological Impact
[caption id="attachment_8879" align="aligncenter" width="550"] Severe fluorosis - Photograph by David Kennedy, DDS[/caption] In its severe forms, dental fluorosis causes highly disfiguring brown and black staining of the teeth, which can cause chronic embarrassment and social anxiety for the impacted child. In 1984, a panel from the National Institute of Mental Health (NIMH) warned
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Diagnostic Criteria for Dental Fluorosis: The Thylstrup-Fejerskov (TF) Index
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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