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
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
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
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
Effects of sodium fluoride, vitamin D, and calcium on cortical bone remodeling in osteoporotic patients
The purpose of this histomorphometric study of iliac bone biopsies from 10 postmenopausal osteoporotic patients was to describe the effects of sodium fluoride (combined with calcium and vitamin D) on remodeling in cortical bone after 6 months and after 5 years of treatment. Biopsies had been fixed in absolute methanol,
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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
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.
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
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 & 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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