Abstract
Endemic skeletal fluorosis is widely prevalent in India and is a major public health problem. The first ever report of endemic skeletal fluorosis and neurological manifestation was from Prakasam district in Andhra Pradesh in the year 1937. Epidemiological and experimental studies in the endemic areas suggest the role of temperate climate, hard physical labor, nutritional status, presence of abnormal concentrations of trace elements like strontium, uranium, silica in water supplies, high fluoride levels in foods and presence of kidney disease in the development of skeletal fluorosis. Neurological complications of endemic skeletal fluorosis, namely radiculopathy, myelopathy or both are mechanical in nature and till date the evidence for direct neurotoxicity of fluoride is lacking. Prevention of the disease should be the aim, knowing the pathogenesis of fluorosis. Surgery has a limited role in alleviating the neurological disability and should be tailored to the individual based on the imaging findings.
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[Histomorphometric profile of bone fluorosis induced by prolonged ingestion of Vichy Saint-Yorre water. Comparison with bone fluorine levels].
Nine transiliac bone biopsies from 7 patients with skeletal fluorosis due to prolonged ingestion of often high quantities of Vichy Saint-Yorre water were analyzed. Four of these patients also suffered from a chronic renal failure. A histomorphometric study was possible in 8 out of the 9 biopsies. The measurement of bone fluoride
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Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis
Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride (40-60 mg/day) for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case,
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Subacute fluorosis
A young woman presented with a novel multisystem disease: painful periostitis, osteosclerosis, hypertension, and renal dysfunction. The similarity of some of this clinical picture to fluoride intoxication led to the discovery of massively elevated fluoride levels in serum, urine, and bone. Although initially an enigma, the source of fluoride was
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[Genetic factors predisposing to occupational fluorosis].
Having analyzed a total amount of all systems, the authors specified the most important genetic markers predisposing to chronic flour intoxication: the patients demonstrated higher frequency of ACP1*A and PGM1*1-alleles, phenotypes of acid phosphatase AA, of phosphoglucomutase 1+1+ and 2+2+, of dry cerumen consistence--d. The results could help to improve
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Diagnostic criteria for endemic osteofluorosis (WS 192-1999)
According to the General Administration of Quality Supervision, Inspection, and Quarantine: National Standards Committee Proclamation (2005, No. 146), GB 16396-1996 “Clinical Diagnosis and Classification of Endemic Osteofluorosis” shall be repealed as of the date of implementation of these Criteria. These Criteria combine GB 16396-1996 “Clinical Diagnosis and Classification of Endemic Osteofluorosis”
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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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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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"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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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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