Conclusion:
1. During the treatment with a total dose of 21 grams of fluoride in a two years period further compression fractures of vertebrae were noticed in 5 or 23 cases. No conclusion can be drawn of course from further compression fractures about the effectiveness of treatment. Concerning the peripheral skeleton an average decrease of the bone mineral content of the radius was observed.
2. The histological picture of the bone biopsies show on an average a positive influence of treatment after the mentioned dose and time.
3. Taking into consideration all parameters, an analysis of the individual cases shows a progression in 4 cases, an obvious amelioration of osteoporosis in 6 cases and in 13 cases nearly unchanged findings indicate no progression of the disease.
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Long term effects of sodium fluoride in osteoporosis
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
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Femoral fractures in fluoride-induced osteoporosis: an update
In 1984, we reported 16 postmenopausal patients with osteoporotic vertebral fractures treated with Na fluoride (NaF), calcium (Ca) and vitamin D (D). We noted relative freedom from vertebral fractures during treatment, but a disturbing incidence of femoral fractures. We now report the current status of 17 pts followed closely on
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The effects of fluoride on the bones and teeth from ICR-derived glomerulonephritis (ICGN) mice and ICR mice after subacute exposure
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
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Fluoride intake and bone measures at age 5
Fluoride intake is known to affect mineralization of both teeth and bones. Few studies have comprehensively assessed fluoride intake and related findings to bone measures. Objectives: To relate fluoride intake from birth to age 4 years to bone measures (spine bone mineral content [bmc] and density [bmd], hip bmc and
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Fluoride content and mineralization of red deer (Cervus elaphus) antlers and pedicles from fluoride polluted and uncontaminated regions
Fluoride, calcium, and phosphorus content as well as ash percentage and ash density of primary antlers and pedicle bones were studied in nine yearling red deer stags from a fluoride polluted region in North Bohemia (Czech Republic) and in nine control animals from two uncontaminated areas in West Germany. Fluoride
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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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