Abstract
Female rats were given 150 ppm fluoride in the drinking water during three successive pregnancy and lactation periods; the femoral diaphyses were then examined for morphological alterations by light and scanning electron microscopy to determine the influence of fluoride ingestion during multiple pregnancies and lactations. The periosteal surface was dominated by areas of woven bone formation with some prolonged resting areas around osteocyte lacunae. The endosteal surface consisted mainly of areas of active bone resorption with some areas of bone formation. The interior of the cortex was characterized by numerous resorption cavities and remodeling in secondary Haversian systems. Fluoride, by the nature of its incorporation into bone crystals and by its direct cytotoxic effect on bone resorbing cells, reduces the availability of calcium from bone. It appears that fluoride ingestion during lactation created a heightened state of calcium homeostatic stress. As a result, bone mineral was mobilized by resorption of the endosteal surface and by cavitation of the interior of the cortex. Secondary hyperparathyroidism is thought to play an integral part in an attempt to maintain calcium homeostasis.
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Normal ionized calcium, parathyroid hypersecretion, and elevated osteocalcin in a family with fluorosis
Sera from five patients with skeletal fluorosis were investigated for total calcium, ionized calcium, phosphate, alkaline phosphatase, 25 hydroxyvitamin D (25 OHD), 1,25 dihydroxyvitamin D (1,25[OH]2D), parathyroid hormone, and osteocalcin concentrations. Total and ionized calcium concentrations were normal in four and subnormal in one, but PTH concentration was elevated in all five.
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[Effects of excess fluoride on bone turnover under conditions of diet with different calcium contents].
OBJECTIVE: To study the effects of excess fluoride on bone turnover under conditions of diet containing different amount of calcium. METHODS: The experiment was performed on rats raised on a balanced diet with adequate calcium or a monotonous diet with low calcium and given amount of fluoride in their drinking water
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Endemic skeletal fluorosis in children: hypocalcemia and the presence of renal resistance to parathyroid hormone
Although endemic skeletal fluorosis has been reported in children, hypocalcemia has not been previously noted. In a prevalence study of 260 schoolchildren living in an endemic fluorosis area in South Africa (water fluoride content 8-12 ppm), hypocalcemia was documented in 23%. Furthermore in a separate study of nine children with skeletal symptoms due to
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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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Effect of fluoride and low versus high levels of dietary calcium on mRNA expression of osteoprotegerin and osteoprotegerin ligand in the bone of rats
The ratio of osteoprotegerin ligand (OPGL) to osteoprotegerin (OPG) determines the delicate balance between bone resorption and synthesis. The main objective of the present study is to investigate the possible role of OPGL and OPG in the bone metabolism of rats exposed to fluoride and the protective or aggravating effect
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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 Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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Fluoride & Osteocytes
The osteocyte is a type of bone cell which is increasingly believed to play an important role in repairing defects that arise in bone, thereby maintaining the bone’s structural integrity. Because osteocytes are engulfed in fluoride-rich bone mineral and help resorb the bone as part of the remodeling process, they
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Fluoride & Osteoclasts
It is well established that fluoride exposure can increase bone formation by increasing the proliferation of osteoblasts. Less clear is fluoride's impact on bone resorption and the cells (osteoclasts) that resorb bone. Many have assumed that fluoride's main effect on bone resorption and osteoclasts is an inhibitory one (i.e., less
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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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