Abstract
A population of eastern grey kangaroos (Macropus giganteus) inhabiting heathland and farmland surrounding an aluminum smelter at Portland, Victoria, Australia, exhibited clinical signs of lameness. An investigation was undertaken to determine the cause of this lameness. Hematology, necropsy, histopathology, fecal egg count, total worm count, reproductive status, and the population age range were examined and failed to reveal any additional underlying disease state. The specific problem of lameness was addressed with bone histopathology, radiography, quantitative ultrasonography, microradiography, and multielement analysis of bone ash samples. The significant lesions observed were: osteophytosis of the distal tibia and fibula, tarsal bones, metatarsus IV, and proximal coccygeal vertebrae; osteopenia of the femur, tibia, and metatarsus IV; incisor enamel hypoplasia; stained, uneven, and abnormal teeth wear; abnormal bone matrix mineralization and mottling; increased bone density; and elevated bone fluoride levels. Microradiography of affected kangaroos exhibited “black osteons,” which are a known manifestation of fluorosis. Collectively, these lesions were consistent with a diagnosis of fluorosis.
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When less is more: a comparison of models to predict fluoride accumulation in free-ranging kangaroos.
Highlights Exposure models can predict toxic effects of fluoride consumption in wildlife. Exposure models that vary in intensity of field data collection warrant comparison. Simple spatial metrics can predict fluoride accumulation in a free-ranging mammal. Complex exposure models may not perform better than simple spatial metrics. Vegetation contaminated by industrial fluoride
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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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Industrial Fluorosis [Carnow et al.]
SUMMARY: In 1242 apparently healthy and actively employed workers of a Canadian aluminum facility, the history of musculoskeletal symptoms, of the incidence of fractures, of neck and back surgery, as well as the x-ray findings were reviewed. A highly significant relationship of exposure to fluoride was established with the frequency
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Silencing GSK3ß instead of DKK1 can inhibit osteogenic differentiation caused by co-exposure to fluoride and arsenic.
Highlights Wnt signaling is involved in the osteogenic differentiation caused by co-exposure to F and As. Silencing GSK3ß can inhibit osteogenic differentiation caused by co-exposure to F and As. Silencing DKK1 cannot inhibit osteogenic differentiation caused by co-exposure to F and As. The interaction between F and As of the
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Effects of smoking, use of aluminum utensils, and tamarind consumption on fluorosis in a fluorotic village of Andhra Pradesh, India
A field study was undertaken to determine effects of tamarind, the use of aluminium (Al) cooking utensils, and smoking on dental and skeletal fluorosis in the randomly selected fluoride (F) endemic village of Buttlapally in the Nalgonda District, Andhra Pradesh, India, where the F level in the drinking water is
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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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