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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Skeletal pathology of eastern grey kangaroos (Macropus giganteus) exposed to high environmental fluoride levels in South-Eastern Australia
Significantly elevated bone fluoride concentrations have been reported in a population of eastern grey kangaroos (Macropus giganteus) resident near a fluoride-emitting aluminum smelter in southeastern Australia. This paper describes the skeletal and synovial joint lesions observed post mortem in the same sample of kangaroos (n = 76). The prevalence and severity of
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Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis
Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride (40-60 mg/day) for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case,
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Bone resorption marker and ultrasound measurements in adults residing in an endemic fluorosis area of Turkey
The purpose of this prospective study was to investigate the quantity and quality of bone by quantitative ultrasound (QUS) measurements and to assess bone resorption by urinary excretion measurement of C-terminal telopeptide of type I collagen (CTX) in an adult Turkish population living in an endemic fluorosis area and consuming
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An epidemiological, clinical and biochemical study of endemic, dental and skeletal fluorosis in Punjab
Since 1958 the Department of Medicine, Patiala, has been actively engaged in epidemiological, clinical amd biochemical studies of endemic fluorosis in Punjab, one of the most highly endemic areas in the world. Extensive data on dental, skeletal and neurological aspects of fluorosis have been fully reported in our earlier studles
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Total hip arthroplasty for the treatment of severe hip osteoarthritis due to fluorosis
BACKGROUND: Now, total hip arthroplasty (THA) is one of the effective methods for the treatment of severe hip osteoarthritis due to fluorosis. OBJECTIVE: To investigate the strategies and efficacy of THA for the treatment of severe hip osteoarthritis due to fluorosis. METHODS: A total of five cases with severe hip osteoarthritis due
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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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X-Ray Diagnosis of Skeletal Fluorosis
In 1937, Kaj Roholm published his seminal study Fluorine Intoxication in which he described three phases of bone changes that occur in skeletal fluorosis. (See below). These three phases, which are detectable by x-ray, have been widely used as a diagnostic guide for detecting the disease. They describe an osteosclerotic bone disease that develops first in the axial skeleton (the spine, pelvis, and ribs), and ultimately results in extensive calcification of ligaments and cartilage, as well as bony outgrowths such as osteophytes and exostoses. Subsequent research has found, however, that x-rays provide a very crude measure for diagnosing fluorosis since the disease can cause symptoms and effects (e.g., osteoarthritis) before, and in the absence of, radiologicaly detectable osteosclerosis in the spine.
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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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