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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Roentgen diagnosis of industrial skeletal fluorosis.
This paper presents X-ray manifestations of industrial fluorosis in 100 cases. It is recognized that increasing density, bony structure changes and periosseous hyperplasia with calcification or ossification, especially the process of hyperplastic calcification of the posterior margin of tibia and interosseous membrane of radius and ulna, constitute the main criteria
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Intraosseous schwannoma of the cervical spine associated with skeletal fluorosis
Intraosseous Schwannoma of the cervical spine is very rare. Its association with skeletal fluorosis is also extremely rare. A case of successfully treated intraosseous neurofibroma of the cervical spine associated with skeletal fluorosis causing tetraparesis is reported. The clinical features, diagnostic aspects and the management is described and the literature
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The effects of fluoride on the bones and teeth from ICR-derived glomerulonephritis (ICGN) mice and ICR mice after subacute exposure
Dental fluorosis and osteofluorosis from using drinking water contaminated with the fluoride ion (F) have been reported from many countries including the People’s Republic of China and India. Because fluoride is excreted by the kidney and the toxic effects of F are more severe when renal failure is present, Imprinting
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Nutritional and metabolic rickets
Nutritional rickets is caused by vitamin D deficiency due to lack of exposure to sunlight. Neonatal rickets occurs only in infants born to mothers with very severe osteomalacia. Calcium deficiency alone does not cause mineralisation defects. It only causes osteoporosis and secondary hyperparathyroidism with raised plasma, 1,25 (OH)2D and osteocalcin.
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Quantitative epidemiological research on the relationship between fluoride concentration of drinking water and endemic fluoride poisoning.
The present study analyzes the dose-response relationship that exists between the concentration of fluoride in drinking water and the clinical symptoms of fluoride poisoning. A positive correlation is observed between the fluoride content of water and the rate of dental fluorosis, skeletal x-ray change frequency, skeletal x-ray change index, and
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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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"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 & 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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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