Abstract
Chronic fluoride toxicosis caused lameness, dental lesions and illthrift in an extensive beef cattle herd in northern Australia. Up to 15% of the herd was lame and the disease forced the culling of large numbers of cows. The source of fluoride was fertiliser-grade monoammonium and diammonium phosphate fed as part of a mineral supplement. Large quantities of mineral supplement were provided to the cattle because lameness was attributed to phosphorus deficiency, which is endemic in the area. Most lameness developed in the late dry season in the post-lactation phase. Severe lameness was caused by fractured pedal bones.
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Associations of fluoride intake with children's bone measures at age 11.
BACKGROUND: Relationships between fluoride intake and bone health continue to be of interest, as previous studies show conflicting results. OBJECTIVES: The purpose is to report associations of fluoride intake with bone measures at age 11. METHODS: Subjects have been participating in the ongoing Iowa Fluoride Study/Iowa Bone Development Study. Mothers were recruited
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[Osteofluorosis caused by excess use of toothpaste].
BACKGROUND: Osteofluorosis is caused by chronic fluoride intoxication. Fluoride is used in toothpaste for the prevention of dental caries, and dental fluorosis has often been reported among children and attributed to ingestion of fluoride toothpaste. We report a case of chronic fluoride intoxication caused by excess use of toothpaste in
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Skeletal fluorosis from instant tea
INTRODUCTION: Skeletal fluorosis (SF) can result from prolonged consumption of well water with >4 ppm fluoride ion (F(-); i.e., >4 mg/liter). Black and green teas can contain significant amounts of F(-). In 2005, SF caused by drinking 1-2 gallons of double-strength instant tea daily throughout adult life was reported in
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Voriconazole
A 57-year-old man, who was receiving immunosuppressive therapy after liver transplantation, began receiving broad-spectrum antibiotics and antifungals (including amphotericin B liposomal) for a suspected fungal infection of the brain. Four days later, brain biopsy and subsequent culture led to identification of Scedosporium boydii/apiosperumum as the causative pathogen, and voriconazole [dosage
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Fluorine and Fluorosis [June 1944].
Excerpt The first account of mottled enamel in human beings was given in 1902 by Eager of the United States Public Health Service who noticed its frequency among Italian emigrants from Naples. Black and McKay (1916) found it occurring in various parts of the U.S.A. and described it more fully in
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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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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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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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