Abstract
Patients with osteoporosis were treated for two years with sodium fluoride. Fifteen received sodium fluoride in capsules, 56 in enteric coated slow release tablets (Ossin) and 20 in enteric coated tablets (Procal). Seven women treated with Procal were also treated with oestrogens. All patients had a calcium intake between 1000 and 2000 mg/day, used dihydrotachysterol for vitamin suppletion and were advised to exercise. Non-responders were arbitrarily defined as those who had an increase in serum alkaline phosphatase less than 10 U/l, those who had no increase in bone mineral content measured with CT in L4 and those who got a femoral neck fracture during the period of therapy. In the overall group of 91 patients 20% were non-responders based on a serum alkaline phosphatase increase less than 10 U/l. Based on the changes in bone mineral content 40% were non-responders during the first year of treatment, 45% during the second year and 23% over the first plus second year. The impression is that patients with a femoral neck fracture have a higher increase in serum parathyroid hormone concentration than patients without fractures. The urinary excretion of fluoride has a better predictive value than the change in serum alkaline phosphatase concentration for the prediction of an increase in bone mineral content.
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Renal osteodystrophy in patients on long-term hemodialysis with fluoridated water
Serum and bone fluoride concentrations of ten patients maintained on long-term hemodialysis with fluoridated water (1 ppm, i.e., 50uM) were correlated with duration of treatment and the occurrence of clinical, radiological, and histological manifestations of bone disease. Two patients had symptomatic renal osteodystrophy when accepted on the program, whereas six
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Prolactin rs1341239 T allele may have protective role against the brick tea type skeletal fluorosis
OBJECTIVE: Prolactin (PRL) has been reported to be associated with increased bone turnover, and increased bone turnover is also a feature of skeletal fluorosis (SF). Autocrine/paracrine production of PRL is regulated by the extrapituitary promoter and a polymorphism in the extrapituitary PRL promoter at -1149 (rs1341239) is associated with disturbances
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Fluoride reduces bone strength in older rats
In response to recent concerns about the effect of water fluoridation on hip fracture rates, we studied the influence of fluoride intake on bone strength. Four groups of rats were fed a low-fluoride diet ad libitum and received 0, 5, 15, or 50 ppm of fluoride in their drinking water.
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Comparison of two village primary schools in northern Tanzania affected by fluorosis
High fluoride levels in drinking water sources are a problem throughout the East African Rift Valley and can lead to dental fluorosis (DF) and skeletal fluorosis (SF) in exposed local populations. Two villages in the Hai District of northern Tanzania in which fluoride has been identified as a problem were
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Vitamin D deficiency, rickets, and fluorosis in India
Data on the vitamin D status of the populations in a tropical country like India have seldom been documented. Vitamin D deficiency is presumed to be rare. Population studied by the author and others in the country has proved otherwise. Studies were carried out to document the dietary habits, serum
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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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"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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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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Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
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