Abstract
Having analyzed a total amount of all systems, the authors specified the most important genetic markers predisposing to chronic flour intoxication: the patients demonstrated higher frequency of ACP1*A and PGM1*1-alleles, phenotypes of acid phosphatase AA, of phosphoglucomutase 1+1+ and 2+2+, of dry cerumen consistence–d. The results could help to improve criteria of occupational selection and to specify practical recommendations on prophylaxis of chronic fluor intoxication.
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[Qualitative and quantitative variation of serum proteins in fluorosis patients].
Comparison between patients with occupational fluorosis, a group of healthy workers, and a sample from the general population revealed differences in concentrations of some polymorphic serum proteins. These differences depended on phenotypes of patients. TF 1-2, PI 1-2, and HP 2-1 patients exhibited a decreased concentration of transferrin (TF), a
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Aberrant DNA methylation of Cyclind-CDK4-p21 is associated with chronic fluoride poisoning.
Endemic fluorosis is a serious problem in public health, affecting thousands of people. Abnormal proliferation and activation of osteoblasts in skeletal fluorosis lesions play a leading role and osteoblast proliferation is finely regulated by the cell cycle. There are a few reports on fluoride-induced DNA methylation. However, the role of
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The spectrum of radiographic bone changes in children with fluorosis
Painful, crippling deformities in Tanzanian children from an area of endemic fluorosis are reported. Excessive fluoride ingestion in pregnant women may possibly poison and alter enzyme and hormonal systems in the fetus causing disturbances to osteoid formation and mineralization. Knock-knees, bowlegs, and saber shins develop when walking begins. Combinations of osteomalacia, osteoporosis,
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[A study of the genetic basis of susceptibility to occupational fluorosis in aluminum industry workers of Siberia].
The phenotype frequency distributions of several classical blood genetic markers and dermatoglyphic characters were analyzed in workers of Siberian aluminum plants who had occupational fluorosis. Comparison with healthy workers revealed significant differences in frequencies of several markers. Phenotypes B (AB0), D (Rh), MN (MN), P1 (P), Le a (Lewis), Gc
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Modifying role of GSTP1 polymorphism on the association between tea fluoride exposure and the brick-tea type fluorosis
BACKGROUND: Brick tea type fluorosis is a public health concern in the north-west area of China. The association between SNPs of genes influencing bone mass and fluorosis has attracted attention, but the association of SNPs with the risk of brick-tea type of fluorosis has not been reported. OBJECTIVE: To investigate the
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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: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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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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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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