Abstract
Genetic factors underlie the susceptibility and the resistance to dental fluorosis (DF). The A/J (DF susceptible) and 129P3/J (DF resistant) mouse strains have previously been used to detect quantitative trait loci (QTLs) associated with DF on chromosome (Chr) 2 and Chr 11. In the present study, increased marker density genotyping followed by interval mapping was performed to narrow the QTL intervals and improve the logarithm of the odds (to the base 10) (LOD) scores. Narrower intervals were obtained on Chr 2 where LOD ? 6.0 (57-84 cM or ? 51 Mb), LOD ? 7.0 (62-79 cM or ? 32 Mb), and LOD ? 8.0 (65-74 cM or ? 17 Mb); and on Chr 11 where LOD ? 6.0 (18-51 cM or ? 53 Mb), LOD ? 7.0 (28-48 cM or ? 34 Mb), and LOD ? 8.0 (31-45 cM or ? 22 Mb). Haplotype analysis between A/J and 129P3/J mice further reduced the QTL intervals. Accn1 was selected as a candidate gene based upon its location near the peak LOD score on Chr 11 and distant homology with the Caenorhabditis elegans fluoride-resistance gene, flr1. The severity of DF between Accn1(-/-) and wild-type mice was not significantly different. Hence, the loss of ACCN1 function does not modify DF severity in mice. Narrowing the DF QTL intervals will facilitate additional candidate gene selections and interrogation.
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Multiomics Analysis Revealed the Molecular Mechanism of miRNAs in Fluoride-Induced Hepatic Glucose and Lipid Metabolism Disorders.
Fluoride-induced liver injury seriously endangers human and animal health and animal food safety, but the underlying mechanism remains unclear. This study aims to explore the mechanism of miRNAs in fluoride-induced hepatic glycolipid metabolism disorders. C57 male mice were used to establish the fluorosis model (22.62 mg/L F–, 12 weeks). The
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Short exposure to high levels of fluoride induces stage-dependent structural changes in ameloblasts and enamel mineralization.
We tested the hypothesis that the sensitivity of forming dental enamel to fluoride (F-) is ameloblast developmental stage-dependent and that enamel mineralization disturbances at the surface of fluorotic enamel are caused by damage to late-secretory- and transitional-stage ameloblasts. Four-day-old hamsters received a single intraperitoneal dose of 2.5-20 mg NaF/kg body
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Uncoupling protein-2 is an antioxidant that is up-regulated in the enamel organ of fluoride-treated rats
Dental fluorosis is characterized by subsurface hypomineralization and retention of enamel matrix proteins. Fluoride (F-) exposure generates reactive oxygen species (ROS) that can cause endoplasmic reticulum (ER)-stress. We therefore screened oxidative stress arrays to identify genes regulated by F- exposure. Vitamin E is an antioxidant so we asked if a
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Utilization of ( 3 H)-serine by ameloblasts of rats receiving sub-mottling doses of fluoride.
Five-day-old Wistar rats were given three intraperitoneal injections at 2-hourly intervals of a solution of sodium fluoride in 0.9 per cent sodium chloride. Three fluoride levels were used: a mottling dose of 3 mgF/kg body weight; and two sub-mottling doses, 0.05 mg and 0.01 mgF/kg body weight. Thirty minutes after
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Enamel fluorosis related to plasma F levels in the rat.
The purpose of this long-term study was to investigate disturbances in enamel mineralization associated with low, but relatively constant, plasma fluoride levels produced by constant infusion or with fluctuating plasma fluoride levels caused by drinking fluoridated water. Weanling rats were raised for 8 weeks on low-fluoride food and water containing
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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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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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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
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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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