Abstract
The concentrations of serum osteocalcin (OCN) and calcitonin (CTN) were determined in sixty male workers exposed to fluoride (F) at an aluminum plant in Danjiang city, and in thirty non-F exposed males of the same general age from the local market town Gaolou village of Jun county in Danjiang city (control group). The F-exposed workers were divided into two groups according to the levels of their urine and serum F: a high-F burden group (urine F>4.0 mg/L; serum F>0.20 mg/L) and a low-F burden group (2.0 mg/L<urine F ?4.0 mg/L; 0.10 mg/L<serum F ?0.20 mg/L). Compared with the control group, the concentrations of serum OCN and CTN were significantly higher in both the high-F and low-F burden groups (p<0.05). This study found for the first time that the concentrations of serum OCN and CTN increased concurrently in a F-exposed worker population. On the basis of these findings, we propose that serum OCN and CTN might be sensitive biomarkers for detecting early stages of F bone injuries.
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Fluorosis in horses drinking artifically fluoridated water
Quarter Horses drinking water artificially fluoridated at 0.9 to 1.1 ppm over long periods of time developed dental fluorosis. Even when the horses had not been exposed to artificially fluoridated water (AFW) during formation of enamel, brown discoloration occurred and progressed. Pronounced loss of tooth-supporting alveolar bone with recession of
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Fluorotic cervical compressive myelopathy, 20 years after laminectomy: A rare event
BACKGROUND: Spinal cord compression in flourosis is a common complication. These complications are mainly due to compression of the spinal cord by thickening and ossification of posterior longitudinal ligament and ligamentum flavum. Surgical decompression is the treatment of choice for fluorotic spinal cord compression. The recurrence of spinal cord compression
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Incidence of fluorosis and urinary fluoride concentration are not always positively correlated with drinking water fluoride level.
The aim of this study was to assess the effect of fluoride on human health, focusing on the incidence of fluorosis, urinary fluoride concentration and fluoride level in drinking water in three fluoride-affected villages of Birbhum district, West Bengal, India. In one village urinary fluoride concentration was very high along
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The spectrum of radiographic bone changes in children with fluorosis
Painful, crippling deformities in Tanzanian children from an area of endemic fluorosis are reported. Excessive fluoride ingestion in pregnant women may possibly poison and alter enzyme and hormonal systems in the fetus causing disturbances to osteoid formation and mineralization. Knock-knees, bowlegs, and saber shins develop when walking begins. Combinations of osteomalacia, osteoporosis,
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Fluoride induces hypomethylation of BMP2 and activates osteoblasts through the Wnt/B-catenin signaling pathway.
Background: Skeletal fluorosis has become a public health issue in recent years as its serious impact on patients' life expectancy. Bone morphogenetic protein 2 (BMP2) plays a key role in promoting osteogenesis. However, the mechanism of BMP2-Wnt/B-catenin axis in skeletal fluorosis needs further exploration. Methods: The RT-qPCR
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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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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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Skeletal Fluorosis Causes Bones to be Brittle & Prone to Fracture
It has been known since as the early as the 1930s that patients with skeletal fluorosis have bone that is more brittle and prone to fracture. More recently, however, researchers have found that fluoride can reduce bone strength before the onset of skeletal fluorosis. Included below are some of the
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