Abstract
Our results demonstrate that the bone response to NaF treatment is a phase process: an increase in bone turnover is combined with an osteomalacia-like reaction during the first year of treatment. These metabolic observations are in close agreement with the histomorphometric data of Olah, Reutter and Schenk. By comparing the doses of NaF (50 and 100 mg), a 1:2 dose response relationship to the biochemical indices of bone formation and collagen turnover was observed.
Osteoarticular pains as major side effect were observed in both dose groups in about 60% of subjects, the peak of pains coinciding with the peak of alkaline phosphatase after six to twelve months of treatment. In one fifth of all subjects the NaF treatment had to be discontinued because of osteoarticular problems.
On sodium fluoride cortical bone decreased while an increase of cancellous bone, especially in the lumbar spine, was observed. After two years of treatment with 100 mg of sodium fluoride the mechanical stability of the lumbar vertebrae appeared to be improved. Therefore only a long-term treatment with sodium fluoride may be beneficial in osteoporosis.
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Long-term fluoride therapy of postmenopausal osteoporosis
The benefit of sodium fluoride (NaF) in the therapy of osteoporosis is still controversial. For 3 years we monitored patients with postmenopausal osteoporosis subjected to a continuous treatment with 80 mg NaF/day and patients without fluoride treatment. Every 3 months peripheral total and trabecular bone densities were evaluated with high-precision
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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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Fluoridation and the rheumatic diseases: a comparison of rhematism in Watford and Leigh
(1) A population sample in the town of Watford, Hertfordshire, has been examined clinically, radiologically, and serologically to determine the prevalence of chronic rheumatic diseases. A comparison has been made with a population sample in Leigh, Lancashire. The water supply in Watford had been fluoridated during the previous 5 years,
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A roentgenologic study of a human population exposed to high-fluoride domestic water; a ten-year study
As shown in Table 1, a limited number of participants from both Bartlett and Cameron showed some degree of roentgenographic bone change but, in general, these changes were minimal. There was a larger number with no observable change in the ten-year interval, a fact disregarded or unreported in most fluoride
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The effect of tamoxifen and fluoride on bone mineral density, biomechanical properties and blood lipids in ovariectomized rats
The most important aspect of therapy with fluoride and tamoxifen concerns its influence on bone tissue and lipid metabolism. The aim of the study was to evaluate the effect of tamoxifen and natrium fluoride (NaF) on bone metabolism, biochemical properties and blood lipids levels in ovariectomized rats. The study was
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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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