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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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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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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Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.
Background: Oxidative stress plays an important role in the pathogenesis of endemic fluorosis. We analyzed associations between oxidative stress-related gene polymorphisms (PON1 rs662, CAT rs769217, rs2300182, and SOD2 rs11968525) and skeletal fluorosis, and examined potential gene–environment interactions with dietary vitamin C, vitamin E, zinc, and selenium intake. Methods: A cross-sectional study
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Fluoride's effects on the formation of teeth and bones, and the influence of genetics.
Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride's actions on bone cells predominate
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The dose-time effects of fluoride on the expression and DNA methylation level of the promoter region of BMP-2 and BMP-7 in rats.
Highlights Fluoride has a dose-time effect on Bone Morphogenetic Protein-2 expression. Fluoride increases the expression of Bone Morphogenetic Protein-2 and 7. DNA methylation may be involved in fluoride regulation of target protein expression. Skeletal fluorosis is a chronic metabolic bone disease caused by excessive exposed to fluoride. Recent studies have
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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 & Rheumatoid Arthritis
The symptoms of skeletal fluorosis can closely resemble rheumatoid arthritis (RA), and thus individuals with fluorosis can "easily be mistaken" as having RA. In addition, clinical research on fluoride-treated osteoporosis patients has found that fluoride exposure can exacerbate pre-existing RA, and recent research shows that the levels of fluoride found in the blood of the general population (19-57 ppb) are sufficient to effect an enzyme (15-lipoxygenase) implicated in the inflammatory process of RA.
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Estimated "Threshold" Doses for Skeletal Fluorosis
For over 40 years health authorities stated that in order to develop crippling skeletal fluorosis, one would need to ingest between 20 and 80 mg of fluoride per day for at least 10 or 20 years. This belief, however, which played an instrumental role in shaping current fluoride policies, is now acknowledged by the National Academy of Sciences (NAS) and other US health authorities to be incorrect.
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