Abstract
The effects of airborne fluoride from unvented indoor burning of fluoride-rich coal on the bones and teeth of residents of two rural villages in SW China were investigated and compared. In the highly polluted village of Xaochang in Sichuan Province, stage III skeletal fluorosis was found in 43 (84%) of 51 examinees. In the moderately polluted village of Minzhu in Guizhu Province, this stage was seen in 25 (51%) of 49 examinees. In the nonpolluted control village of Shucai in Jiangxi Province in SE China, none of 47 examinees showed any evidence of skeletal fluorosis. In Minzhu, but not in Xaochang, significantly more males than females were afflicted with stage III skeletal fluorosis. In contrast with Xaochang, some examinees in Minzhu had serious skeletal effects but normal teeth or minor dental fluorosis. A high frequency of extremital transverse bone growth lines was observed in Xaochang but not in Minzhu. These findings suggest that greater exposure to fluoride occurred during infancy and early childhood in Xaochang than in Minzhu.
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Recent advances in cellular effects of fluoride: an update on its signalling pathway and targeted therapeutic approaches.
Fluoride is a natural element essential in minute quantities in human’s to maintain dental and skeletal health. However, the disease fluorosis manifests itself due to excessive fluoride intake mostly through drinking water and sometimes through food. At the cellular energetics level, fluoride is a known inhibitor of glycolysis. At the
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Quantification of rib COL1A2 gene expression in healthy and fluorosed Inner Mongolia cashmere goats.
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
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Neurology of endemic skeletal fluorosis
Endemic skeletal fluorosis is widely prevalent in India and is a major public health problem. The first ever report of endemic skeletal fluorosis and neurological manifestation was from Prakasam district in Andhra Pradesh in the year 1937. Epidemiological and experimental studies in the endemic areas suggest the role of temperate
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Excessive ingestion of fluoride and the significance of sialic acid: glycosaminoglycans in the serum of rabbit and human subjects
The levels of sialic acid and glycosaminoglycans were explored in the sera of rabbit and human subjects who ingested fluoride and had clinical manifestation of fluorosis. Changes observed in the level of these chemical constituents in sera possibly reflect changes occurring in calcified and noncalcified tissues due to fluoride intoxication. The
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Industrial fluorosis [Boillat et al.]
43 potroom workers (aluminium industry) with fluorosis have been compared with 18 foundry workers of the same age, but who had never been exposed to fluorides. Clinical examination revealed a higher incidence of articular pain and limitation of motion in the exposed group. The diagnosis of fluorosis is not only
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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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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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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 Magnifies Impact of Repetitive Stress on Joints
Research has repeatedly found that fluoride's effect on the skeleton is most pronounced in the bones and joints that undergo the greatest strain. Indeed, both the symptoms of fluorosis (i.e., joint pain and stiffness) as well as the radiological findings (e.g., exostoses, interosseuous membrane calcification) have been found to occur earliest, and most severely, in the joints
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Skeletal Changes in Industrial and Endemic Fluorosis
Fluorotic changes in bones and joints were evaluated in 105 aluminum workers and 20 residents of an endemic fluorosis region in India.
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