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A 47-year-old woman was referred for bone pain and abnormal findings on radiography. The patient reported that for the past 17 years, she has habitually consumed a pitcher of tea made from 100 to 150 tea bags daily (estimated fluoride intake, >20 mg per day). She reported a 5-year history of pain in the lower back, arms, legs, and hips. Because of brittleness, all her teeth had been extracted. Radiography of the forearm revealed interosseous membrane calcifications (Panel A, arrows), and radiography of the spine revealed a ruggerjersey appearance (striated pattern of increased density in the upper and lower zones of the vertebrae) (Panel B, arrows), suggesting skeletal fluorosis. The serum fluoride concentration was 0.43 mg per liter (23 ?mol per liter; normal concentration, <0.10 mg per liter [5 ?mol per liter]). Skeletal fluorosis is endemic in areas
with high concentrations of fluoride in the drinking water, but it is rare in other parts of the world. Brewed tea has one of the highest fluoride contents among beverages in the United States. After appropriate counseling, the patient discontinued tea consumption, with improvement in her symptoms. Since it can take years to deplete skeletal fluoride, we are considering whether to increase bone remodeling with the intermittent use of teriparatide to facilitate the elimination of skeletal fluoride.
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Matrix metallopeptidase-2 gene rs2287074 polymorphism is associated with brick tea skeletal fluorosis in Tibetans and Kazaks, China.
Brick tea skeletal fluorosis is still a public health issue in the north-western area of China. However its pathogenesis remains unknown. Our previous study reveals that the severity of skeletal fluorosis in Tibetans is more serious than that in Kazaks, although they have similar fluoride exposure, suggesting the onset of
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FRZB1 rs2242070 polymorphisms is associated with brick tea type skeletal fluorosis in Kazakhs, but not in Tibetans, China.
Skeletal fluorosis is a metabolic bone and joint disease caused by excessive accumulation of fluoride in the bones. Compared with Kazakhs, Tibetans are more likely to develop moderate and severe brick tea type skeletal fluorosis, although they have similar fluoride exposure. Single nucleotide polymorphisms (SNPs) in frizzled-related protein (FRZB) have
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A case of thick but brittle bones and instant tea
CASE DESCRIPTION A 45-year-old white male was found to have radiographic findings of a diffusely dense appendicular skeleton, mild trabecular thickening, and multiple thoracic compression fractures indicating structural weakness. Bone mineral density was above the expected range for his age on the lumbar spine and femoral neck. Social history was significant
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Endemic fluorosis with neurological complications in a Hampshire man
We describe below a case of skeletal fluorosis occurring in a Hampshire man who presented with neurological complications, and whose condition was appreciably improved by operation. We believe that this is the first case of its kind to be reported from Britain, and also the first case of skeletal fluorosis
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Skeletal fluorosis mimicking seronegative spondyloarthropathy: a deceptive presentation
Skeletal fluorosis is rarely recognized early and is amajor cause of morbidity.We report on a 40-year-old man with skeletal fluorosis mimicking seronegative spondyloarthropathy.
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Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
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Skeletal Fluorosis in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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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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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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