Abstract
Fluoride contents of water and food, collected from the subjects of five selected areas of Tamil Nadu in South India, were determined. Surveys were conducted to ascertain dental fluorosis prevalences among children of the areas, and dental and skeletal fluorosis prevalences in the adult populations. Dean’s “Community Fluorosis Index” (CFI) for dental fluorosis was calculated, from the children’s survey, and was found to be correlated with the prevalence and severity of fluorosis in the areas. A direct correlation was also confirmed between the mean fluoride level in drinking water and the percentage incidence of dental fluorosis. The dominant role of fluoride from drinking water, when compared with that from food, was established.
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Fluorosis with report of an advanced case.
It is quite possible that endemic centres [of skeletal fluorosis] exist but that the cause of the disabling spondylitis or other joint affections has not been determined, and a diagnosis of chronic arthritis has resulted. Few cases in Canada or the United States will be found to be as dramatic
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Bovine calves as ideal bio-indicators for fluoridated drinking water and endemic osteo-dental fluorosis
Relative susceptibility to fluoride (F) toxicosis in the form of osteo-dental fluorosis was observed in an observational survey of 2,747 mature and 887 immature domestic animals of diverse species living in areas with naturally fluoridated (>1.5 ppm F) drinking water. These animals included buffaloes (Bubalus bubalis), cattle (Bos taurus), camels (Camelus dromedarius),
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Endemic skeletal fluorosis
Endemic skeletal fluorosis is described in 6 children aged 11 or over. Four cases were crippled with severe deformities in the spine, hips, and knees. All showed positive phosphorus, magnesium, and nitrogen balances and excessively positive calcium balances. The skeletal x-rays, histology, and chemical composition of the bones revealed diagnostic
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Fluoride osteosclerosis
1. Twenty-three cases of fluoride osteosclerosis are presented. 2. These cases were gathered from 170,000 roentgenographic examinations of the spine and pelvis of patients living in Texas and Oklahoma where many communities have excessive fluoride content in their drinking water. 3. In each case, adequate clinical examination failed to establish any relationship
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The relationship between Alu I polymorphisms in the calcitonin receptor gene and fluorosis endemic to Chongqing, China
OBJECTIVE: This study explored the association between an Alu I polymorphism at position 1,377 of the calcitonin receptor (CTR) gene and endemic fluorosis. SUBJECTS AND METHODS: A case-control study of 321 participants was conducted in regions with high fluorosis rates (Wushan and Fengjie counties) and those without high fluorosis rates (Yubei
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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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"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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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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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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