Abstract
Sural nerve biopsies from 13 patients with radiologically confirmed skeletal fluorosis were studied for myelinated fibre densities, frequency distribution oftheir diameters, and single teased nerve fibre preparations. It was observed that most of the biopsies showed a marked reduction in myelinated fibre densities with more than half of them in:volving the smaller fibres of less than 7 um diameter.
Teased fibre measurements of internodal lengths and internodal diameters point to myelinated fibre dropout being due to axonal degeneration with secondary demyelination. The selective loss of small fibres is unlikely to be due to an entrapment neuropathy alone, and possibility of primary toxic injury needs to be considered.
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Studies on skeletal muscle biopsies in endemic skeletal fluorosis
Neurological manifestations of skeletal fluorosis have been attributed to compressive radiculomyelopathy. Experimental fluorosis has shown evidence of myopathic changes. Data on human muscle pathology is very scanty. This study included 22 patients with established osteofluorosis. 16 of them showed only EMG changes of neurogenic muscle disease. Histochemistry and histopathology of muscle biopsies showed
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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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Neuro-medical manifestations of fluorosis in populations living in the Main Ethiopian Rift Valley.
Prolonged exposure to higher concentrations of fluoride (> 1.5 mg/L) is associated with dental and skeletal fluorosis. The effects of fluoride on dental and skeletal system have been studied extensively; however, the neurological consequences of fluoride in population-based studies are limited. The study aims to assess the epidemiology of neurological
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Prevalence of fluorosis in Pratabpura and Surajpura villages, District Ajmer (Rajasthan).
HEEP COPYRIGHT: BIOL ABS. In a study of 357 individuals at Pratabpura and Surajpura villages in Ajmer district, Rajasthan, where (F-) contents in water were 14.3 and 13.9 mg/l, respectively, dental fluorosis was present in 280 (83.5%). Males were slightly more (87.56%) affected than females (78.66%). Of children below 15
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New data for the validation of the mean daily maximum permissible concentration of hydrogen fluoride in atmospheric air
1. Round-the-clock exposure to hydrogen fluoride concentrations of 0.10 and 0.03 mg/m3 causes inhibition in the central nervous system, decreases the activity of a number of enzymes, impairs the phosphorus-calcium metabolism, and causes the accumulation of fluorine in the body and damage to the internal organs and bone tissue. 2. A
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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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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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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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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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