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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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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Chronic fluorine intoxication from drinking water
Summary The case of ? 35-year-old woman is described presenting stiffness and severe pain in the spine, gastric disturbances, stomatitis, paresthesias in legs and arms, especially in the u1nar nerve area, loss of mental acuity, visual disturbances and extreme general malaise. On1y ? few clear-cut objective findings were noted, namely: decreased muscular
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Fluoride's effects on the formation of teeth and bones, and the influence of genetics.
Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride's actions on bone cells predominate
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Calcium deficiency in fluoride-treated osteoporotic patients despite calcium supplementation
To test the hypothesis that the osteogenic response to fluoride can increase the skeletal requirement for calcium, resulting in a general state of calcium deficiency and secondary hyperparathyroidism, we assessed calcium deficiency, spinal bone density, by quantitative computed tomography, and serum PTH in three groups of osteoporotic subjects. Two of
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Exposure to natural fluoride in well water and hip fracture: a cohort analysis in Finland
In the retrospective cohort study based on record linkage, the authors studied a cohort of persons born in 1900-1930 (n = 144,627), who had lived in the same rural location at least from 1967 to 1980. Estimates for fluoride concentrations (median, 0.1 mg/liter; maximum, 2.4 mg/liter) in well water in
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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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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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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Fluoridation, Dialysis & Osteomalacia
In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on
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