Abstract
Dental fluorosis and osteofluorosis from using drinking water contaminated with the fluoride ion (F) have been reported from many countries including the People’s Republic of China and India. Because fluoride is excreted by the kidney and the toxic effects of F are more severe when renal failure is present, Imprinting control region (ICR)-derived glomerulonephritis (ICGN) mice, which have been used as a model of renal failure, could be a useful model for osteofluorosis. In the present study, ICGN mice and ICR mice were administered F at 0, 25, 50, 100, and 150 ppm in their drinking water for 4 weeks. The femurs of the mice were photographed and analyzed by microdensitometry. The teeth were stained with hematoxylin and eosin. While no significant differences in any bone indexes were found in the ICGN groups, the mean values for bone mineral content and bone mineral density of the left femur from the male ICR 150 ppm group were significantly higher than those of the control group mice (p<0.001). Partial heterogeneous calcification of the tooth dentine was observed in the ICGN mice exposed to 150 ppm. ICGN mice may be used as a model for dental fluorosis. However, ICR mice, particularly males, with an exposure period of 2–4 mo, may be a better animal model for osteofluorosis.
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Fluoride osteosclerosis from drinking water
1. A case of osteosclerosis, exhibiting in addition mottled enamel, severe anemia showing no response to anti-anemic therapy, and bilateral renal lesions is reported. 2. The diagnosis of fluoride osteosclerosis was proved by the history of a long residence in areas of endemic fluorosis and by fluorine analysis of the patient's
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Effects of fluoride on bone metabolism in patients with hemodialysis
The maior pathway of fluoride elimination from the human body is the kidney. The discharge of fluoride into urine depends on the clearance of the kidney. Fluoride in serum of hemodialysis patients is higher than that of healthy subjects. Fluoride is not reduced sufficiently with hemodialysis. Those patients are in
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Fluoridation and bone disease in renal patients
About the Authors: William J Johnson, director of the Mayo Artificial Kidney Center and professor of medicine with the Division of Nephrology at the Mayo Clinic, has been involved in the study of calcium and phosphorus metabolism and renal osteodystrophy, potassium metabolism, and uremic neuropathy. He is past chairman of the Minnesota
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Medical aspects of excessive fluoride in a water supply
A 10-year study of 116 persons in Bartlett and 121 in Cameron, Tex., was conducted to determine if prolonged exposure to fluoride in the water supply of Bartlett had produced detectable physiological effects. Bartlett's water contained about 8 p.p.m. F until 1952, when an experimental defluoridation unit was installed, reducing the
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Subacute fluorosis
A young woman presented with a novel multisystem disease: painful periostitis, osteosclerosis, hypertension, and renal dysfunction. The similarity of some of this clinical picture to fluoride intoxication led to the discovery of massively elevated fluoride levels in serum, urine, and bone. Although initially an enigma, the source of fluoride was
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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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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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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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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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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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