Abstract
We report a case of spinal cord compression in a Mexican immigrant due to vertebral osteosclerosis from chronic fluoride intoxication. Endemic fluorosis is acquired through drinking water. Groundwater sources with high fluoride content occur worldwide. The epidemiology, metabolism, and clinical features of fluorosis are reviewed. Greater physician awareness of this entity is important to identify correctly patients with this unusual and potentially devastating clinical disorder.
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The effect of alternating administration of aluminum chloride and sodium fluoride in drinking water on the concentration of fluoride in serum and its content in bones of rats.
INTRODUCTION: Fluorine and aluminum remain a very interesting research topic due to equivocal and relatively unknown toxic action, role in the etiology of various diseases, and interactions of both elements. Fluorine and aluminum compounds are absorbed by organisms through the gastric and respiratory systems, although the latter route operates only at
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Effect of ultrastructural changes on the toughness of bone.
The ultrastructure of bone can be considered as a conjunction between the biology and the biomechanics of the tissue. It is the result of cellular and molecular activities of bone formation, and its organization dominates the mechanical behavior of bone. Following this perspective, the objective of this review is to
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Fluorosilicic acid induces DNA damage and oxidative stress in bone marrow mesenchymal stem cells.
Highlights Fluorosilicic acid is the most used additive for water fluoridation. Dental fluorosis can be caused by fluorosilicic acid present in drinking water. DNA damage was caused by fluorosilicic acid in mesenchymal stem cells. Fluorosilicic acid altered bone mineralization in mesenchymal stem cells. DNA damage caused by fluorosilicic acid
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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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Addition of monofluorophosphate to estrogen therapy in postmenopausal osteoporosis: a randomized controlled trial
INTRODUCTION: Treatment of osteoporosis with high-dose fluoride alone does not reduce fracture risk. We hypothesized that the antifracture efficacy of fluoride could be optimized by its use in low doses combined with an antiresorptive agent. EXPERIMENTAL SUBJECTS: Subjects included 80 women with postmenopausal osteoporosis who had been taking estrogen for at least 1
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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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