Abstract
Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extracellular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.
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Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).
Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in
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Fluorosis-induced hyperparathyroidism mimicking a giant-cell tumour of the femur
We report the case of a young woman who, over a period of five years was diagnosed and treated for a giant-cell tumour of bone, osteomalacia and fluorosis. A review of the literature revealed a correlation between these three diagnoses, the primary pathology being fluorosis and the remaining symptoms being secondary manifestations. It
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Endemic skeletal fluorosis in children: hypocalcemia and the presence of renal resistance to parathyroid hormone
Although endemic skeletal fluorosis has been reported in children, hypocalcemia has not been previously noted. In a prevalence study of 260 schoolchildren living in an endemic fluorosis area in South Africa (water fluoride content 8-12 ppm), hypocalcemia was documented in 23%. Furthermore in a separate study of nine children with skeletal symptoms due to
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The spectrum of radiographic bone changes in children with fluorosis
Painful, crippling deformities in Tanzanian children from an area of endemic fluorosis are reported. Excessive fluoride ingestion in pregnant women may possibly poison and alter enzyme and hormonal systems in the fetus causing disturbances to osteoid formation and mineralization. Knock-knees, bowlegs, and saber shins develop when walking begins. Combinations of osteomalacia, osteoporosis,
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Circulating levels of immunoreactive parathyroid hormone in endemic genu valgum
Circulating levels of immunoreactive parathyroid hormone (PTH) were estimated in fifteen normal subjects and twenty-five subjects suffering from the skeletal fluorosis, ten of whom had associated endemic genu valgum. Levels of PTH were high in all the subjects with fluorosis as compared to normals, but among fluorosis subjects, those who had endemic genu valgum had
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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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Gastrointestinal Problems Among Individuals with Skeletal Fluorosis
Humans suffering from skeletal fluorosis are known to suffer from an increased occurrence of gastrointestinal disorders. When fluoride intake is reduced, these gastrointestinal problems are among the first symptoms to disappear. The following are some of the studies that have examined this issue: "It is clear from the observations presented in this article
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Skeletal Fluorosis in India & China
In India and China, scientists have repeatedly found that skeletal fluorosis occurs in populations drinking water with just 0.7 to 1.5 ppm fluoride. Although nutritional deficiencies and hot climates make populations in India and China more susceptible to fluoride toxicity than is generally the case in western countries, this fact does not remove the relevance of the Indian and Chinese experience to the situation in fluoridating countries. This is because (a) nutritional deficiencies also exist in the western world, particularly in low-income communities, and (b) some individuals, including those with kidney disease, can be just as -- if not more -- susceptible to fluoride toxicity.
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