Abstract
Fluoride administration in both man and animals has been shown to stimulate new bone formation. However, the bone is poorly mineralized, and osteomalacia and secondary hyperparathyroidism frequently occur. In this study we investigated the effect of variable levels of fluoride and calcium intake, accompanied by vitamin D, on osteoporosis in eleven patients treated for one year. Bone biopsies indicated an increase in new bone formation in all patients receiving 45 mg of sodium fluoride per day, whereas SOO mg of calcium per day prevented both osteomalacia and any increase in bone resorption. In order to restore bone mass in osteoporotic subjects without producing roentgenographic or microscopic: evidence of fluorosis, a therapeutic regimen of 50 mg of sodium fluoride and at least 900 mg of calcium per day and 50,000 units of vitamin D twice weekly is recommended.
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Severe bone deformities in young children from vitamin D deficiency and fluorosis in Bihar-India
A case-control study was undertaken to understand the etiopathology of the bone deformities among young children in a fluoride-affected village of the Bihar State. Two villages were selected: one village with high fluoride in drinking water (7.9 +/- 4.15 ppm), and the other village with normal levels of fluoride (0.6
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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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Nutritional bone disease in Indian population
Syndromes of bone disease and deformities consequent to disorders of nutrition, bone and mineral metabolism constitute a serious national health problem. The studies on this subject are scanty. Data on nutritional bone disease are described and discussed. We had surveyed 337.68 million population residing in 0.39 million villages in 22
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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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Effect of variations in calcium intake on the skeleton of fluoride-fed kittens
Kittens were fed fluoride (2.5 mg. per kilogram of body weight) for 2 months. In one group of animals the addition of calcium (20 mg. per kilogram) to an otherwise calcium-deficient diet resulted in a depressed serum calcium, abnormally wide osteroid tissue, and increased formation and resorption of bone. In
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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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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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Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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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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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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