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
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,
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
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
Combined effects of diets with reduced calcium and phosphate and increased fluoride intake on vertebral bone strength and histology in rats
Ingested fluoride is incorporated into bone apatite and can affect the structural integrity of bone. Fluoride absorption in the gut and incorporation into bone is affected by the presence of other ions, including calcium. We hypothesized that a low calcium phosphate diet combined with high fluoride intake would have independent
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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,
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
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
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.
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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