Abstract
Microscopic examinations were made of 99 bones from 37 persons coming to necropsy who had resided 10 years or more in communities where the drinking water contained 1 to 4 ppm of naturally occurring or artificially added fluoride. Ninety-four bone specimens from 33 controls who had lived in areas where the drinking water contained less than 0.5 ppm fluoride were used for comparison.
In addition to the bone specimens, the lumbar intervertebral body joints of the subjects were examined.
The microscopic examinations showed no significant differences between the fluoride-exposed group and the control group that could be related to fluoride intake. Microscopic changes in the bones and joints incidental to aging and due to non-fluoride-related conditions were observed in both series.
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Human vertebral bone: relation of strength, porosity, and mineralization to fluoride content
Radiographically normal vertebral bone cylinders from 80 male subjects were tested mechanicallly by static compression and analyzed for porosity, fluoride and ash content. As a group, they had low fluoride content, suggesting little prior intake, consonent with this geographic area. Nevertheless, increasing levels of fluoride were associated with bulkier bone,
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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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Experimental osteofluorosis and arthrofluorosis in rats
OBJECTIVE: to study qualitative and quantitative changes of bone tissue and articular cartilage in rats exposed to sodium fluoride. MATERIALS AND METHODS: 75 female Wistar cats, each weighing about 200 g, were divided equally into three groups. Animals in Groups 1 and 2 received daily doses of 0.5 mg and 5
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Short-term effects of fluoride and strontium on bone formation and resorption in the mouse
The early effects of sodium fluoride (0.80 mg/kg/d) and strontium chloride (0.27%) given alone, or in combination in drinking water, on bone metabolism were examined in the mouse using dynamic histomorphometric methods. Four weeks of oral strontium supplementation increased the osteoid surface and reduced the number of acid phosphatase-stained osteoclasts.
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Effect of fluoride on aluminum-induced bone disease in rats with renal failure
Aluminum (Al) accumulation in renal failure is an etiological factor in the pathogenesis of low turnover bone disease. Aluminum-induced impairment of mineralization has been related to a reduced extent of active bone-forming surface. The present study investigated the effect of fluoride, a potent stimulator of osteoblast number, on the toxicity
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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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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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"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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