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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Deterioration of teeth and alveolar bone loss due to chronic environmental high-level fluoride and low calcium exposure
OBJECTIVES: Health risks due to chronic exposure to highly fluoridated groundwater could be underestimated because fluoride might not only influence the teeth in an aesthetic manner but also seems to led to dentoalveolar structure changes. Therefore, we studied the tooth and alveolar bone structures of Dorper sheep chronically exposed to
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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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Association between low-to-moderate fluoride exposure and bone mineral density in Chinese adults: Non-negligible role of RUNX2 promoter methylation.
Highlights RUNX2 promotor methylation is positively related to excessive fluoride (F) exposure. Bone mineral density (BMD) is negatively related to excessive F exposure in women. BMD is negatively associated with RUNX2 promotor methylation in women. RUNX2 methylation mediates the association of excessive F exposure and BMD in women. Bone mineral density
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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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Elevated serum fluoride concentrations in women are not related to fractures and bone mineral density.
Epidemiologic studies of the relations between drinking-water fluoride levels and bone mineral density (BMD) and fracture are characterized by disparate conclusions and an absence of information about individual circulating fluoride levels. This study relates serum fluoride concentrations, which reflect individual fluoride exposures, to BMD and bone fractures. Data are from
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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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