Abstract
Fluor osteopathy, as the authors suppose, is a morphologic repetition of phylogenesis early stages in osteogenesis. Thus, osteosclerosis and osteoporosis demonstrated by X-ray should be considered as manifestation of bone fluorosis. Fluor-induced changes of bone tissue could not be adequately termed as “osteoporosis” and “osteosclerosis”, so is defined as “fluor osteopathy”.
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Clinical aspects of fluorosis in horses
Horses grazing in areas where cattle and sheep had developed severe fluorosis were examined clinically. Of those examined, 12 horses of different ages and with various degrees of fluorosis were selected for necropsy. Selected tissues were examined grossly, histologically, and radiographically. Major fluorotic lesions occurred only when the horses ingested
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Neurological complications of endemic skeletal fluorosis, with special emphasis on radiculo-myelopathy
The results of surveys carried out between 1976 and 1985 in the fluorosis-endemic area of the Ethiopian Rift Valley is summarised, with emphasis on the neurological complications resulting from the crippling osteofluorosis. The neurological manifestations in the forms of myelopathy with and without radiculopathy (respectively 72% and 28%) occurred after exposure
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Fluoride induces hypomethylation of BMP2 and activates osteoblasts through the Wnt/B-catenin signaling pathway.
Background: Skeletal fluorosis has become a public health issue in recent years as its serious impact on patients' life expectancy. Bone morphogenetic protein 2 (BMP2) plays a key role in promoting osteogenesis. However, the mechanism of BMP2-Wnt/B-catenin axis in skeletal fluorosis needs further exploration. Methods: The RT-qPCR
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Endemic fluorosis with neurological complications in a Hampshire man
We describe below a case of skeletal fluorosis occurring in a Hampshire man who presented with neurological complications, and whose condition was appreciably improved by operation. We believe that this is the first case of its kind to be reported from Britain, and also the first case of skeletal fluorosis
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Bone and joint pathology in fluoride-exposed workers
Clinical and radiological investigations were performed for 2,258 aluminum workers exposed to fluoride for an average of 17.6 yr (standard deviation = 7.6). Changes in bone and joints were presented in detail in three groups: (1) exposed up to 5 yr (135 cases), (2) exposed from 6-32 yr (1,463 cases),
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Variability in Radiographic Appearance of Skeletal Fluorosis
Osteosclerosis (dense bone) is the bone change typically associated with skeletal fluorosis, particularly in the axial skeleton (spine, pelvis, and ribs). Research shows, however, that skeletal fluorosis produces a spectrum of bone changes, including osteomalacia, osteoporosis, exostoses, changes resulting from secondary hyperparathyroidism, and combinations thereof. Although the reason for this radiographic variability is not yet fully understood, it is believed to relate to the dose of fluoride consumed, the individual's nutritional status, exposure to aluminum, genetic susceptibility, presence of kidney disease, and area of the skeleton examined.
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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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"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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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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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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