Abstract
Earlier observations and a review on endemic fluorosis in the Bhatinda District of Punjab were published in 1961 [this Bulletin, 1962, v. 37, 243] and the object of the present paper “is to summarize our epidemiological work done over three years and to emphasize the importance of this work from the social and preventive aspects”.
The physiography of the Bhatinda District is described with the inclusion of a map. The method of survey is shortly stated. The district has an approximate population of 58, 000 in which 2, 282 persons over the age of 30 were critically examined for the presence of skeletal fluorosis. This condition was diagnosed in 63 persons and of these 27 showed neurological complications. In addition a high incidence of dental fluorosis in children was found. Much detail is given of the patients with skeletal fluorosis-their symptoms, clinical signs and the results of laboratory investigations of the cerebrospinal fluid and serum chemistry. There are X-ray photographs of some of the advanced cases of skeletal fluorosis.
A table presents data on the fluorine content of soil, water, blood and bone in relation to individual cases of skeletal fluorosis.
The social and preventive aspects are discussed briefly.
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Studies on fluorosis in Mehsana District of North Gujarat.
A survey was conducted in eighteen fluoride endemic villages in Mehsana District of North Gujarat (India). The individuals afflicted with fluorosis were examined for apparent mottled teeth and skeletal complications. Samples of urine and blood of these individuals along with drinking water were collected and compared with samples obtained from
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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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Fluoride exposure altered metabolomic profile in rat serum
Highlights 58 NEG and 73 POS metabolites were altered in F-treated 3 weeks rat serum. 126 NEG and 70 POS metabolites were altered in F-treated 11 weeks rat serum. Four significantly different metabolites, nicotinamide, adenosine, 1-Oleoyl-sn-glycero-3-phosphocholine, and 1-Stearoyl-sn-glycerol 3-phosphocholine were shared by two models. Urea, N2-Acetyl-l-ornithine, and betaine were
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[Relationship between fluoride exposure, orthopedic injuries and bone formation markers in patients with coal-burning fluorosis].
Chronic exposure to fluoride is a public health problem worldwide. We explored the relationship between fluoride exposure, orthopedic injuries and bone formation markers alkaline phosphatase (ALP), bone Gla protein (BGP) in participants with coal-burning fluorosis in Hehua Village (coal-burning fluorosis endemic area) in Zhijin County of Guizhou Province and Zhangguan
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ESPEN micronutrient guideline
Background Trace elements and vitamins, named together micronutrients (MNs), are essential for human metabolism. Recent research has shown the importance of MNs in common pathologies, with significant deficiencies impacting the outcome. Objective This guideline aims to provide information for daily clinical nutrition practice regarding assessment of MN status, monitoring, and prescription. It proposes
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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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Similarities between Skeletal Fluorosis and Renal Osteodystrophy
It is quite possible, and indeed likely, that some kidney patients diagnosed with renal osteodystrophy are either suffering from skeletal fluorosis or their condition is being complicated/exacerbated by fluoride exposure.
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Fluoride & Rheumatoid Arthritis
The symptoms of skeletal fluorosis can closely resemble rheumatoid arthritis (RA), and thus individuals with fluorosis can "easily be mistaken" as having RA. In addition, clinical research on fluoride-treated osteoporosis patients has found that fluoride exposure can exacerbate pre-existing RA, and recent research shows that the levels of fluoride found in the blood of the general population (19-57 ppb) are sufficient to effect an enzyme (15-lipoxygenase) implicated in the inflammatory process of RA.
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