Abstract
In June of 2011, the Puyehue–Cordon Caulle volcanic eruption deposited large amounts of ashes in Chile and Argentina. Although ashes were initially considered innoxious based on water leachates, we found clinical cases of fluoride intoxication in red deer (Cervus elaphus) and domestic herbivores in Argentina. The diagnosis was corroborated by high bone fluoride concentrations. The dynamics of temporal accumulation of fluoride suggested an average increase of 1,000 ppm per year of fluoride in the bone. However, a few deer had fluoride levels, suggesting an accumulation rate of about 3,700 ppm per year. Via recent sampling of deer, we now confirm that bone levels have reached up to 10,396 ppm of fluoride after about 28 months of exposure. Tephra across various sites averaged 548 ppm of fluoride, and due to dry conditions and eolic redeposition of ashes particularly east of the continental divide, clinical fluorosis is expected to continue to intensify. The described impact will reverberate through several aspects of the ecology of the deer, including effects on population dynamics, morbidity, predation susceptibility, as well as other components of the ecosystem, including other herbivores, scavengers, and plant communities.
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Insights into material and structural basis of bone fragility from diseases associated with fractures: how determinants of the biomechanical properties of bone are compromised by disease.
Minimal trauma fractures in bone diseases are the result of bone fragility. Rather than considering bone fragility as being the result of a reduced amount of bone, we recognize that bone fragility is the result of changes in the material and structural properties of bone. A better understanding of the
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Why did the ancient inhabitants of Palmyra suffer fluorosis?
The skeletal remains uncovered from the 2nd and 3rd century underground tombs of Palmyra, Syria, retain traces of arthritis and mottled enamel. A brown discoloration was also observed in the teeth. In order to clarify that these facts can be related to fluorosis, the teeth excavated from Tomb C and
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Skeletal fluorosis: an unusual metabolic bone complication for HPN patients
Rationale: Prevalence and pathophysiology of HPN-associated metabolic bone disease (MBD) xe patially unknown. Therefore, we began a systematic review of 0ur patients in order to increase our knowledge in this paticular field. Here, we report two cases of skeletal fluorosis, an unusual HPN-related bone abnormality. Method: Until now, 12 patients (6
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Effects of fluoride on the proliferation and activation of osteoblasts by regulating methylation of the DNA repair genes MGMT and MLH1.
Introduction Fluoride can induce the proliferation and activation of osteoblasts, resulting in skeletal fluorosis progression; however, the specific mechanism is unclear. Methods Cell proliferation was examined using the MTT assay. Flow cytometry was performed to detect the cell cycle distribution. Alkaline phosphatase (ALP) was calculated to evaluate bone formation and turnover. Gene methylation
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Equine dental and skeletal fluorosis induced by well water consumption.
Two horses that consumed well water with high fluoride content exhibited clinical signs of chronic dental and skeletal fluoride toxicosis and were later euthanized and autopsied. Both horses had degenerative disease of multiple joints and multiple dental defects. Elevated fluoride concentrations were found in bone and tooth samples of both
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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 & 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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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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Similarities between Skeletal Fluorosis and Renal Osteodystrophy
It is quite possible, and indeed likely, that some kidney patients diagnosed with renal osteodystrophy are either suffering from skeletal fluorosis or their condition is being complicated/exacerbated by fluoride exposure.
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