Abstract
Damage to collagen protein and its gene expression caused by excessive fluoride (F) ingestion plays an important role in the etiology of skeletal fluorosis. Recently we found that industrial F pollution significantly increased the expression level of type II collagen gene (COL2A1) in rib cartilage of Inner Mongolia cashmere goats. With the same goats and methods, we have now quantified another important collagen gene, the rib COL1A2 gene, which encodes an ?2(I) polypeptide chain assembled into collagen molecules. The results showed that the expression level of COL1A2 and COL1A2/?-actin increased by 88% and 81%, respectively.
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Periarticular calcifications containing giant pseudo-crystals of francolite in skeletal fluorosis from 1,1-difluoroethane 'huffing".
Highlights Diagnosing inhalant use disorder can be lifesaving. Chronic inhalation of F--containing vapors can cause skeletal fluorosis (SF). SF can elevate bone density and cause periostitis and ectopic calcification. Francolite is a carbonate-rich fluorapatite. Periarticular calcification in SF can comprise giant pseudo-crystals of francolite. Inhalant use disorder is a psychiatric
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Experimental fluorosis in rats: NaF induced changes of bone and bone marrow
The results of our experiments suggest that increased doses of NaF cause more extensive osteosclerosis due to the decrease in number and/or activity of osteoclasts. Therefore oateosclerosis is caused primarily, not by increased bone formation but, by the inhibition of bone resorption. This view is supported by the fact that
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Is the severity of osteosclerosis of fluorosis proportional to the dose of fluoride intake?
Histomorphometric study was made on a series of sections of undecalcified epiphyseal femoral specimens from rats with experimental fluorosis. The results revealed osteosclerosis in Group A (5 ppm) being more severe than that in Group B (25 ppm). With the increase of fluoride dose, the parameters fell down instead of
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Progress of Signaling Pathways, Stress Pathways and Epigenetics in the Pathogenesis of Skeletal Fluorosis.
Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in
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Expression of core-binding factor a1 and osteocalcin in fluoride-treated fibroblasts and osteoblasts
To study the effects and importance of fluoride on FBs in the development of extraperiosteal calcification and the ossification of skeletal fluorosis, the presence of the osteogenic phenotype, which is indicated by the expression of core-binding factor a1 (Cbfa1) and osteocalcin (OCN), in an FB cell line (L929) and in
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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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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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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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Fluoride & DISH (Diffuse Idiopathic Skeletal Hyperostosis)
Among individuals with skeletal fluorosis, the fluoride-induced changes to the spine, and the accompanying symptoms, can bear a close resemblance to DISH (Forestier's Disease). Some authors report that skeletal fluorosis can so closely resemble that DISH that the only way to distinguish the two would be to conduct an invasive bone biopsy. No studies have ever been conducted to determine what role, if any, fluoride plays in the development of DISH.
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Fluoride & Spinal Stenosis
Spinal stenosis is a narrowing of the spaces in the spine that results in pressure being placed on the spinal cord and/or nerve roots. Although stenosis can develop without symptoms, it may produce numbness, tingling, pain and difficulty in walking, as well as a heavy/tired feeling in the legs. It is estimated that 250,000 to 500,000 Americans currently have symptoms of spinal stenosis. Skeletal fluorosis is one cause of stenosis.
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