Abstract
After predominant theories on the causes of fluorosis are described and remarks made about the metabolism of fluoride, an observation of bone fluorosis in a 64-year-old patient is reported. Because, despite painstaking research, none of the known causes of bone fluorosis could be found in our patient, a new pathomechanism is being offered for discussion, i.e., increased renal or intestinal absorption or an increase of fluoride deposited in the bone; i.e., an inborn or acquired error of fluoride metabolism. We recently observed a similar case with none of the well-known origins.
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Association between vitamin D receptor gene FokI polymorphism and skeletal fluorosis of the brick-tea type fluorosis: a cross sectional, case control study
Background Brick-tea type fluorosis is a public health concern in the north west area of China. The vitamin D receptor (VDR)-FokI polymorphism is considered to be a regulator of bone metabolism and calcium resorption. However, the association of VDR-FokI polymorphism with the risk of brick-tea type fluorosis has not been
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[Dermatoglyphic indices in assessing the predisposition to occupational fluorosis].
Dermatoglyphic investigations which prove the existence of genetic predisposition to occupational fluorosis in workers of aluminum and criolite plants were carried out. Mathematical methods of pattern recognition were used for the multifactorial analysis. It was found that the complex analysis of ten the most informative dermatoglyphic parameters permits to prognosticate
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Comparison of two village primary schools in northern Tanzania affected by fluorosis
High fluoride levels in drinking water sources are a problem throughout the East African Rift Valley and can lead to dental fluorosis (DF) and skeletal fluorosis (SF) in exposed local populations. Two villages in the Hai District of northern Tanzania in which fluoride has been identified as a problem were
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[Genetic markers of occupational susceptibility to fluorosis].
To determine markers showing propensity to occupational fluorosis, the authors studied prevalence of ABO, Rh, MN, ABH and Lewis phenotypes, systemic rhesus haplotypes in 229 workers engaged into aluminum production. Propensity to occupational fluorosis was marked by P (+), O (ABO) phenotypes. P (-) phenotype appeared to be a marker
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Preliminary screening of fluorine-stained osteoblastic apoptosis-related microRNA.
This article has been accepted for publication and undergone full peer review but has not been through the copy editing, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ar.24709. Endemic fluorosis is a chronic systemic
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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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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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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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