Abstract
OBJECTIVE: To detect, diagnose and treat for endemic fluorosis earlier.
METHODS: Six kinds of indices, such as environmental fluoride level, were collected from the population in epidemic and non-epidemic areas of endemic fluorosis with a 1:1 paired-match design. A discriminant analysis model was established by multivariate analysis. Levels of fluoride in environment and biological materials were determined by fluoride electrode method. Living condition of the subjects were measured and interviewed. Function of skeletons and joints was measured. Biochemical and enzyme indices were measured with reagent kits and gel electrophoresis. Other indices were measured by interview. All data collected were analyzed by SAS and MDAS computer software.
RESULTS: There was significant overall difference between four kinds of discriminant functions, with an overall agreement of 85.78% (83.33% to 98.86%), based on resubstitution with sampled data. Posterior probabilities for new classification of sampled data automatically and randomly produced from a computer were 86.39% to 99.99%.
CONCLUSION: The discriminant functions mentioned above, except for the third one with a too small sample size, can be used in early discrimination of endemic fluorosis caused by exposure to coal burning, or in evaluation for the effectiveness of pharmaceutical therapy, with a power of 95%.
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Skeletal fluorosis from brewed tea.
BACKGROUND: High fluoride ion (F(-)) levels are found in many surface and well waters. Drinking F(-)-contaminated water typically explains endemic skeletal fluorosis (SF). In some regions of Asia, however, poor quality "brick tea" also causes this disorder. The plant source of brick, black, green, orange pekoe, and oolong tea, Camellia
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Skeletal fluorosis from instant tea
INTRODUCTION: Skeletal fluorosis (SF) can result from prolonged consumption of well water with >4 ppm fluoride ion (F(-); i.e., >4 mg/liter). Black and green teas can contain significant amounts of F(-). In 2005, SF caused by drinking 1-2 gallons of double-strength instant tea daily throughout adult life was reported in
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[Genetic markers of occupational susceptibility to fluorosis].
To determine markers showing propensity to occupational fluorosis, the authors studied prevalence of ABO, Rh, MN, ABH and Lewis phenotypes, systemic rhesus haplotypes in 229 workers engaged into aluminum production. Propensity to occupational fluorosis was marked by P (+), O (ABO) phenotypes. P (-) phenotype appeared to be a marker
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Osteoporosis--an early radiographic sign of endemic fluorosis.
Radiological investigation of skeletal fluorosis was carried out among the inhabitants from two areas where the fluoride content of water was high, using both conventional radiography and radiographic measurements of bone mineral content (BMC). Of 139 cases in the first group, 68 presented bone abnormalities while 21 of 54 cases in the
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Excessive ingestion of fluoride and the significance of sialic acid: glycosaminoglycans in the serum of rabbit and human subjects
The levels of sialic acid and glycosaminoglycans were explored in the sera of rabbit and human subjects who ingested fluoride and had clinical manifestation of fluorosis. Changes observed in the level of these chemical constituents in sera possibly reflect changes occurring in calcified and noncalcified tissues due to fluoride intoxication. The
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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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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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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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Fluoride Magnifies Impact of Repetitive Stress on Joints
Research has repeatedly found that fluoride's effect on the skeleton is most pronounced in the bones and joints that undergo the greatest strain. Indeed, both the symptoms of fluorosis (i.e., joint pain and stiffness) as well as the radiological findings (e.g., exostoses, interosseuous membrane calcification) have been found to occur earliest, and most severely, in the joints
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