The interrelated effects of dietary fluorine and feed intake on bone growth, body growth, Ca45 behavior, bone pathology and feed utilization are demonstrated in young pigs.
A fluorine level of 1000 ppm in the ration reduced the appetite and caused a decrease in bone growth, body growth, and feed required per unit of skeletal growth. There was an increase in feed required per unit weight gain.
When animals were restricted to the same dietary intake, levels of 200 and 1000 ppm fluorme caused a reduction in bone growth.
Limiting the dietary intake caused a decrease in bone growth, body growth and feed required per unit of bone growth; however, it caused an increase in feed required per unit of weight gain.
Autoradiograms showed that. in the fluorine treated animals there was a process occurring which tended to remove the Ca45 originally deposited in or directly below the epiphyseal
regions. It is suggested that the fluorine intake caused an increased rate of bone resorption in the primary and secondary spongiosa.
The proportion of the epiphysis occupied by hypertrophied cartilage cells was found to be a reliable measure of the rate of bone growth under the conditions of this experiment.
Deterioration of teeth and alveolar bone loss due to chronic environmental high-level fluoride and low calcium exposure
OBJECTIVES: Health risks due to chronic exposure to highly fluoridated groundwater could be underestimated because fluoride might not only influence the teeth in an aesthetic manner but also seems to led to dentoalveolar structure changes. Therefore, we studied the tooth and alveolar bone structures of Dorper sheep chronically exposed to
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
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
Effect of combined therapy with sodium fluoride, vitamin D and calcium in osteoporosis
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
Fluoride Salts are no Better at Preventing New Vertebral Fractures than Calcium-Vitamin D in Postmenopausal Osteoporosis: The FAVOStudy.
Although fluoride salts have been shown to be capable of linearly increasing spinal bone mineral density (BMD) in postmenopausal osteoporosis, the effects of this gain in density on the vertebral fracture rate remain controversial. We conducted a 2-year multicenter, prospective, randomized, double-masked clinical trial in 354 osteoporotic women with vertebral
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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.
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.
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
Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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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