Abstract
A/J and 129P3/J mouse strains have different susceptibilities to dental fluorosis, due to their genetic backgrounds. This study tested whether these differences are due to variations in water intake and/or F metabolism. A/J (susceptible to dental fluorosis) and 129P3/J mice (resistant) received drinking water containing 0, 10, or 50 ppm F. Weekly F intake, excretion and retention, and terminal plasma and femur F levels were determined. Dental fluorosis was evaluated clinically and by quantitative fluorescence (QF). Data were tested by two-way ANOVA. Although F intakes by the strains were similar, excretion by A/J mice was significantly higher due to greater urinary F excretion, which resulted in lower plasma and femur F levels. Compared with 129P3/J mice given 50 ppm F, significantly higher QF scores were recorded for A/J mice. In conclusion, these strains differ with respect to several features of F metabolism, and amelogenesis in the 129P3/J strain seems to be unaffected by high F exposure.
*Full-text study online at https://europepmc.org/article/MED/19828896#free-full-text
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Dental fluorosis and a polymorphism in the COL1A2 gene in Mexican children.
Highlights Dental fluorosis is a public health problem in the communities evaluated. The rs 412777 polymorphism in the COL1A2 gene was found in Mexican children. An association between the COL1A2 gene polymorphism and dental fluorosis was found. The genetic variant evaluated represents a risk factor to develop dental fluorosis. OBJECTIVE:
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Environmental and physiological factors affecting dental fluorosis
In addition to differences in fluoride intake and possibly to calcium deficiency or malnutrition, there are several factors which may account for individual differences in the occurrence of dental fluorosis. Disorders in acid-base balance affect the renal handling of fluoride such that, in acidosis, the excretion rate is diminished and,
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Possible Association Between Polymorphisms in ESR1, COL1A2, BGLAP, SPARC, VDR, and MMP2 Genes and Dental Fluorosis in a Population from an Endemic Region of West Bengal.
Dental fluorosis (DF) is the most prevalent form of fluorosis in India affecting millions of people all over the country. As estrogen receptor 1 (ESR1), collagen type 1 alpha 2 (COL1A2), bone ?-carboxyglutamic acid protein (BGLAP), secreted protein acidic and cysteine-rich (SPARC), vitamin D receptor (VDR), and matrix metallopeptidase 2
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Low-to-moderate fluoride exposure, relative mitochondrial DNA levels, and dental fluorosis in Chinese children.
Highlights Circulating mtDNA content is negatively related to low-to-moderate fluoride exposure. Dental fluorosis (DF) prevalence is positively related to fluoride exposure. Circulating mtDNA content is negatively associated with the DF prevalence. Gender modifies the associations of DF prevalence with mtDNA and fluoride exposure. mtDNA content partly mediates association of
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Polymorphisms in genes involved in enamel development are associated with dental fluorosis
OBJECTIVE: To evaluate the association between polymorphisms in DLX1, DLX2, MMP13, TIMP1 and TIMP2 genes with dental fluorosis (DF) phenotype. DESIGN: Four hundred and eighty one subjects (108 with DF and 373 DF free) from 6 to 18 years of age were recruited. This population lived in Rio de Janeiro, a
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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.
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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