Abstract
The ossification of the posterior longitudinal is always responsible of cervical myelopathy. Radiological study and the CT scan, are able to precise the level, the morphologic and associated abnormalities of this lesion. Two cases of ossification of the posterior longitudinal ligamentum with cervical myelopathy are reported. The radiologic studies determined the etiology, in the first case, it was fluorosis and the second DISH disease.
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Bone disease in hemodialysis patients with particular reference to the effect of fluoride
Forty-one patients on our chronic hemodialysis program were assessed for the degree of progression of bone disease over an average period of 46 months. Seven patients were using a fluoridated dialysate. Four of these seven patients developed a marked increase in osteoid as judged by bone biopsy, while in the
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Developmental toxicity of sodium fluoride in rats.
Despite the chronic exposure of the US population to fluoridated drinking water since the 1940s, existing studies have been judged inadequate to determine any potential reproductive or developmental hazard. This study was conducted to determine the effects of sodium fluoride (NaF) on foetal development. Sperm-positive female rats were given 0,
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Industrial fluoride pollution: Chronic fluoride poisoning in Cornwall Island cattle.
An aluminum plant on the south bank of the St. Lawrence river, southwest of Cornwall Island, Ontario, Canada, has emitted 0.816 metric tons of fluoride daily since 1973; considerably higher amounts were emitted from 1959 to 1973. The plant has been designated as the "major source of fluoride emissions impacting
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Posttraumatic pseudomenigocoele of cervical spine in a patient with skeletal fluorosis. Case report
A case of fluorotic cervical compressive myelopathy precipitated by trauma is reported. The delayed neurological deterioration was due to a posttraumatic pseudomenincocele, the prompt treatment of which resulted in recovery. Posttraumatic pseudomeningocele is very rate; and certainly so in fluorosis, and thus has not been reported in the literature to date.
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Femoral fractures in fluoride-induced osteoporosis: an update
In 1984, we reported 16 postmenopausal patients with osteoporotic vertebral fractures treated with Na fluoride (NaF), calcium (Ca) and vitamin D (D). We noted relative freedom from vertebral fractures during treatment, but a disturbing incidence of femoral fractures. We now report the current status of 17 pts followed closely on
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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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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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