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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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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[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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Histomorphometric analysis of iliac crest bone biopsies in placebo-treated versus fluoride-treated subjects
In a 4-year controlled, prospective trial, histomorphometric analysis was used to compare the tissue-level skeletal effects of fluoride therapy in 43 postmenopausal women (75 mg NaF/day) with those of 35 matching placebo subjects; all subjects received 1500 mg/day elemental calcium supplement. In addition to an initial, baseline biopsy, a second
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[Experimental studies of pathogenesis of chronic fluoride intoxication].
The article presents the results of studies of occupational fluorosis pathogenesis on experimental model of chronic fluoride intoxication (CFI). In early fluoride intoxication, fluoride and calcium in the body are in compensatory relations. Later, they are disturbed. High reaction ability of fluoride in CFI is associated with hypocalciemia which triggers
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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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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 & 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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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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