Abstract
Goal: Determine the dose-response relationship between tea-induced osteofluorosis and brick tea intake.
Method: In two representative tea-induced fluorosis areas in the north and south of China, namely Aba County of Sichuan province and Chen Banner of Inner Mongolia Autonomous Region, osteofluorosis suffers were diagnosed by means of x-ray and a regression analysis was conducted to investigate sufferers fluoride intake from brick tea.
Result: In Aba County, level 1, 2, and 3 osteofluorosis sufferers have an average daily intake of fluoride from drinking brick tea of 6.26, 9.92, and 12.80 mg, respectively. In Chen banner, level 1 and level 2 osteofluorosis sufferers have a daily intake of fluoride from drinking brick tea of 6.26 and 10.23 mg, respectively; no level 3 sufferers were found. A linear relationship exists between disease severity and annual brick tea consumption (F = 330.23, p < 0.01), with a correlation coefficient of 0.77.
Conclusion: A dose-response relationship exists between the severity of osteofluorosis and the intake of fluoride from tea drinking.
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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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Prevention of bony fluorosis in aluminum smelter workers. A 15-year retrospective study of fluoride excretion and bony radiopacity among aluminum smelter workers -- Pt. 4
1. Fifty six aluminum smelter workers with 10 to 43 years' occupational exposure, and who had been previously studied medically, were re-x-rayed. Average urinary fluoride concentrations since 1960 were estimated to range from 2.78 mg/liter preshift and 7.71 mg/liter postshift. 2. Roentgenographic studies in 1960-66 and 1974 failed to reveal
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Roentgen diagnosis of industrial skeletal fluorosis.
This paper presents X-ray manifestations of industrial fluorosis in 100 cases. It is recognized that increasing density, bony structure changes and periosseous hyperplasia with calcification or ossification, especially the process of hyperplastic calcification of the posterior margin of tibia and interosseous membrane of radius and ulna, constitute the main criteria
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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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A clinical and biochemical study of chronic fluoride toxicity in children of Kheru Thanda of Gulbarga district, Karnataka, India
The prevalence of dental and skeletal fluorosis was determined among children of Kheru Nayak Thanda of Gulbarga district, where the fluoride concentration in drinking water ranges from 0.6 to 13.4 ppm and the water has low levels of copper and zinc. These children were investigated clinically, radiologically and biochemically. The
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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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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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