Excerpt:
Summary
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.
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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
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Fluoride and nutritional osteoporosis: Physicochemical data on bones from an experimental study in dogs
Osteoporosis was induced by feeding a low calcium-high phosphorus diet for 41 weeks to adult beagles. The effect of fluoride to modify this condition was examined by adding increasing levels to the purified diet; daily intake of fluoride was about 0, 25, 85, 300 and 1,000 /ug/kg body weight. Radiographic
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Treatment of postmenopausal osteoporosis with slow-release sodium fluoride. Final report of a randomized controlled trial
OBJECTIVE: To test whether slow-release sodium fluoride inhibits spinal fractures and is safe to use. DESIGN: Placebo-controlled randomized trial. INTERVENTIONS: Slow-release sodium fluoride, 25 mg twice daily, in four 14-month cycles (12 months receiving sodium fluoride followed by 2 months not receiving it) compared with placebo. Calcium citrate, 400 mg calcium twice daily, continuously in
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Effects of dialysate calcium and fluoride on bone disease during regular hemodialysis
A previous study indicated that, in patients maintained by hemodialysis, clinically and roentgenographically apparent bone disease appeared almost exclusively when the dialystate calcium concentration was less than 5.7 mg per 100 ml. In the present study, bone biopsy specimens from the iliac crest were studied at the beginning and end
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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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"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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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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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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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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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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