Abstract
Analytic chemical studies of similar human skeletal tissues obtained at autopsy from two comparable women were conducted to determine the effect of a prolonged exposure to drinking water containing 8.0 ppm of fluoride on the chemistry of human bones.
As a result of the prolonged .use of this fluoride drinking water, the fluoride in dry, fat-free skeletal tissues ranged from 0.512 to 0.653 percent, as compared with 0.062 to 0.092 percent fluoride in the skeletal tissues of a subject, comparable in age, height, weight, and sex, with no unusual water-fluoride exposure.
There was some indication that the prolonged use of drinking water containing 8.0 ppm fluoride accounted for an increase in the ash and a slight increase in the calcium content of the skeletal tissues.
The absence of any gross of systemic findings, or of any impairment of the skeletal tissues, or malfunction generally in the one subject studied, indicates that human bone may not be affected by as much as 0.5 to 0.6 percent fluoride. These findings compare favorably with other previous evidence pertinent to human bone as well as fluorosed animal bones.
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Skeletal fluorosis: histomorphometric analysis of bone changes and bone fluoride content in 29 patients
Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 +/- 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric
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The effect of fluoride on bone
Conclusions Although it is well known that the ingestion of high levels of fluoride can give rise to severe lesions in the skeletal tissues, such effects have never been found radiographically in persons using a water supply, containing less than 4 p.p.m fluorlde throughout life. A histological study of thirty ribs taken
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Association between fluoride, magnesium, aluminum and bone quality in renal osteodystrophy
INTRODUCTION: Trace elements are known to influence bone metabolism; however, their effects may be exacerbated in renal failure because dialysis patients are unable to excrete excess elements properly. Our study correlated bone quality in dialysis patients with levels of bone fluoride, magnesium, and aluminum. A number of studies have linked
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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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Industrial fluorosis [Franke et al.]
This is a review of findings on workers in an aluminum plant with industrial fluorosis. Early signs of the disease are nocturnal back pains and restriction of the rotation of the trunk. Stage I of the disease usually occurs after 10 years, stage II after 15 years and stage III
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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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Fluoride & Osteopetrosis
One of the most common radiological findings in skeletal fluorosis is osteosclerosis - a hardening of bones with a blurring of the trabecular structure. In advanced cases, the osteosclerotic form of fluorosis may closely resemble the appearance of osteopetrosis, a "marble bone" disease in which the bones are dense, but fragile and prone to fracture.
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X-Ray Diagnosis of Skeletal Fluorosis
In 1937, Kaj Roholm published his seminal study Fluorine Intoxication in which he described three phases of bone changes that occur in skeletal fluorosis. (See below). These three phases, which are detectable by x-ray, have been widely used as a diagnostic guide for detecting the disease. They describe an osteosclerotic bone disease that develops first in the axial skeleton (the spine, pelvis, and ribs), and ultimately results in extensive calcification of ligaments and cartilage, as well as bony outgrowths such as osteophytes and exostoses. Subsequent research has found, however, that x-rays provide a very crude measure for diagnosing fluorosis since the disease can cause symptoms and effects (e.g., osteoarthritis) before, and in the absence of, radiologicaly detectable osteosclerosis in the spine.
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