Abstract
We report a case of spinal cord compression in a Mexican immigrant due to vertebral osteosclerosis from chronic fluoride intoxication. Endemic fluorosis is acquired through drinking water. Groundwater sources with high fluoride content occur worldwide. The epidemiology, metabolism, and clinical features of fluorosis are reviewed. Greater physician awareness of this entity is important to identify correctly patients with this unusual and potentially devastating clinical disorder.
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Bone fragility of the peripheral skeleton during fluoride therapy for osteoporosis
Bone fragility during fluoride therapy for osteoporosis was observed in 24 (37.5%) of 64 patients treated with sodium fluoride, calcium, and vitamin D for 2.5 years who developed episodes of lower-limb pain during treatment. Eighteen (28%) of these patients had clinical and roentgenographic features of 41 stress fractures and 12
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The Abortive Lives of Modern Inhalation Anesthetics.
READERS of this periodical were probably intrigued when, in 1971, almost an entire issue was devoted to studies in volunteers of a new anesthetic, isoflurane (Forane), a novel and useful editorial departure. Since then, a series of reports in the Journal has cast further light on some of the more
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Effect of fluoride on expression of pura gene and CaM gene in newborn rat osteoblasts.
To explore the effect of fluoride (F) on the expression of purine-rich element-binding protein (PURA) gene and calmodulin (CaM) gene in osteoblasts of newborn rats, parietal calvaria bone osteoblast cultures of 48-hr-old rats were treated for 48 hr with sodium fluoride (NaF) at concentrations of 0 (control), 0.5, 2, and
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Adenyl cyclase activity following fluoride ingestion.
Adenyl cyclase activity and fluoride content were investigated in various tissues of adult rabbits given NaF (10 mg/kg body wt./day) orally for 6 months. The activity of adenyl cyclase increased significantly in bone, liver, and kidney, whereas it was unchanged in skeletal muscle following fluoride ingestion. The levels of fluoride
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Fluoride exposure induces lysosomal dysfunction unveiled by an integrated transcriptomic and metabolomic study in bone marrow mesenchymal stem cells.
Highlights Effects of fluoride on the transcriptome and metabolome in BMSCs were studied. Fluoride inhibited lysosomal function. Glutathione metabolism was the hub affected metabolic processes in fluoride -treated BMSCs. Palmitic acid and prostaglandin metabolisms were associated with lysosomal pathway in fluoride-treated BMSCs. Fluoride has received much attention for its predominant
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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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"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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