Abstract
Chronic fluorine intoxication of puppies produced extensive systemic changes of the bones and developing teeth. The intensity depended upon the age of the animal, the dose, and the duration of the administration of sodium fluoride. In puppies fed exclusively the milk of their fluorine-poisoned mother, changes of the bones were observed prior to those of the tooth buds.
The fact that in experimental fluorosis the changes of bones and developing teeth could not be prevented nor alleviated by an antirachitic diet, and calcification of a startling amount of periosteal and endosteal bone occurred in spite of continued administration of fluorine suggests the idea that the pathogenesis of the bone and tooth lesions in rickets and fluorosis differs.
Of course, the enzymatic and protoplasmic action of fluorine produced ricketslike changes in the bones and the dentine of puppies, but its effect on the bones of the older dogs and the enamel in general differed from rickets.
These experimental studies and recent observations of dental fluorosis in children and adults associated with bone changes indicate the necessity of a thorough roentgenographic examination of the skeleton of children showing “mottled enamel” in fluorine areas in this country.
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On mild degrees of fluorosis. 2: An experimental, 2-year-study of rats drinking distilled water containing 0, 1 or 5 ppm F-
24 recently weaned Sprague-Dawley rats were divided equally into 3 groups and given distilled drinking water ad libitum containing 0, 1 or 5 ppm F- (as NaF), respectively. Among the 13 animals that received the fluoridated water and survived the 2-year experimental period, 4 developed macroradiographically demonstrable resorption cavities in
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Effect of fluoride ions on apatite crystal formation in rat hard tissues.
Fluoride is widely believed to be a useful chemical substance for preventing dental caries. However, the mechanism underlying crystal perforation in the tooth enamel and the effect of fluoride on hard tissues are unclear. To clarify the mechanism of the biological action of fluoride in the mineralization process, we examined
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Rachitomimetic effects of fluoride feeding on the skeletal tissues of growing pigs
Young pigs, fed for 30, 6o and 90 days on a diet containing 1,000 parts per million of sodium fluoride, have shown defective growth and mineralization of bones, costochondral beading, softened and deformed epiphyseal plates, and enlarged and malformed bone trabeculae. Histochemical studies of demineralized sections have revealed a decrease in
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The relationship between water-borne fluoride, dental fluorosis and skeletal development in 11-15 year old Tanzanian girls
Dental fluorosis was evaluated by a classification system, previously shown to be sensitive, and skeletal changes evaluated by bone maturity and structure. Dental fluorosis was more severe in posterior than in anterior teeth in both jaws irrespective of fluoride concentration of the drinking water. There appeared to be no dependence between fluoride content
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Mottled enamel in Oklahoma Panhandle, and its possible relations to child development
Summary and Conclusions 1. Results of surveys made in Oklahoma Panhandle on Chronic Fluorine Intoxication was stated, the endemic areas located, the mottled enamel index derived, the fluorine content of the water supply of the different areas given along with the depth of the wells, along with the findings on physical
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Diagnostic Criteria for Dental Fluorosis: The TSIF ("Total Surface Index of Fluorosis")
The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental
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Community Fluorosis Index (CFI)
The current Community Fluorosis Index for U.S. adolescents as a whole (from both fluoridated and non-fluoridated areas) is roughly 5 times higher than the CFI health authorities predicted for fluoridated areas when fluoridation first began. It is also higher than the CFI that the NIDR found in fluoridated areas back in the 1980s. It is readily apparent, therefore, that children are ingesting far more fluoride than was the case in the 1950s, and even as recently as the 1980s.
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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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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin
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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.
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