Abstract
The very high prevalence of dental and skeletal fluorosis in relation to the fluorine content of local coal and clay was investigated in two rural regions with low water fluoride (Hualuo Village and Majianzhuang Village) of Guizhou Province, China. The fluorine content of coal in the two regions is considerably lower than the total fluorine content of the commonly used coal-clay (a mixture of coal and clay). The fluorine released from combustion of the coal itself accounts for less than 15% of the total fluorine emissions during the combustion of coal-clay, thereby indicating that the fluorine source that contaminates the food and air is mainly from the clay rather than the coal.
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Reducing the off-target endocrinologic adverse effects of azole antifungals—can it be done?
Highlights Azole antifungals are associated with off-target endocrinologic adverse events. Skeletal fluorosis, pseudohyperaldosteronism, adrenal insufficiency, hyponatraemia and hypogonadism are reported. Clinical and biochemical monitoring may play a role in prevention and progression. Novel azoles offer therapeutic advantages due to greater selectivity of binding to fungal CYP51. Integration of pharmacogenomics
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Long-term exposure to the fluoride blocks the development of chondrocytes in the ducks: The molecular mechanism of fluoride regulating autophagy and apoptosis.
Highlights Long-term fluoride exposure blocks the development of chondrocytes. Excessive fluoride could induce chondrocytes apoptosis. Long-term excessive fluoride triggered autophagy. Fluoride-induced chondrocytes apoptosis is associated with CytC/Bcl-2/P53 pathways. Long-term exposure to excessive fluoride causes chronic damage in the body tissues and could lead to skeletal and dental fluorosis. Cartilage damage
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Effect of fluoride on osteoclast formation at various levels of receptor activator of nuclear factor Kappa-B ligand (RANKL).
Receptor activator of nuclear factor kappa-B ligand (RANKL) acting on osteoblasts is an essential cytokine for osteoclast formation. Recent studies have shown that fluoride (F) can stimulate RANKL expression of osteoblasts. However, the effect of F under various levels of RANKL on osteoclast formation is not clear. In this study,
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[A study of the genetic basis of susceptibility to occupational fluorosis in aluminum industry workers of Siberia].
The phenotype frequency distributions of several classical blood genetic markers and dermatoglyphic characters were analyzed in workers of Siberian aluminum plants who had occupational fluorosis. Comparison with healthy workers revealed significant differences in frequencies of several markers. Phenotypes B (AB0), D (Rh), MN (MN), P1 (P), Le a (Lewis), Gc
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[Exploration for an early discriminant model of non-skeletal phase in endemic fluorosis exposed to coal-burning].
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
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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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Fluoride Reduces Bone Strength Prior to Onset of Skeletal Fluorosis
The majority of animal studies investigating fluoride's impact on bone strength have found that fluoride has either no effect, or a detrimental effect, on bone strength. Importantly, several of the animal studies that have found fluoride reductes bone strength have reported that this reduction in strength occurs before signs of skeletal fluorosis
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Tea Intake Is a Risk Factor for Skeletal Fluorosis
A number of recent studies have found that heavy tea drinkers can develop skeletal fluorosis - a bone disease caused by excessive intake of fluoride.
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