Abstract
The prevalence of dental and skeletal fluorosis was determined among children of Kheru Nayak Thanda of Gulbarga district, where the fluoride concentration in drinking water ranges from 0.6 to 13.4 ppm and the water has low levels of copper and zinc. These children were investigated clinically, radiologically and biochemically. The study revealed that 89% of the children had dental fluorosis and 39% exhibited skeletal fluorosis. Serum samples of these children showed elevated levels of alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), and decreased levels of total protein, albumin, and potassium. Radiographic changes suggestive of osteoporosis, osteosclerosis, and genu valgum were observed.
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A Brief and Critical Review of Chronic Fluoride Poisoning (Fluorosis) in Domesticated Water Buff aloes (Bubalus bubalis) in India: Focus on its Impact on Rural Economy.
In the rural areas of India, fl uoridated drinking water, industrial fluoride pollution and fluoride rich feed phosphate supplements are the major sources of fluoride exposure for domesticated water buffaloes (Bubalus bubalis). However, the fluoridated drinking groundwater is the commonest and principal source of fluoride exposure for these ruminants. Chronic
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Multiple painless masses: periostitis deformans secondary to fluoride intoxication
Diagnosis The differential diagnosis based on the imaging findings included ossification of subperiosteal hematomas, ectopic calcification in the setting of a connective tissue disorder, and periostitis deformans secondary to fluoride intoxication. Laboratory assays were requested by the patient’s rheumatologist, which were notable for a mildly elevated alkaline phosphatase level (216 U/L,
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Industrial fluorosis [Franke et al.]
This is a review of findings on workers in an aluminum plant with industrial fluorosis. Early signs of the disease are nocturnal back pains and restriction of the rotation of the trunk. Stage I of the disease usually occurs after 10 years, stage II after 15 years and stage III
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Skeletal fluorosis in a resettled refugee from Kakuma refugee camp.
“I suspected some contamination of the water of the much-frequented street pump in Broad Street, near the end of Cambridge Street”, said John Snow, about the contaminated water pump of the cholera outbreak of 1854, in London, UK.1 In September, 2015, a Somalian man aged 46 years presented to a refugee
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Association of Dietary Calcium Intake with Dental, Skeletal and Non-Skeletal Fluorosis among Women in the Ethiopian Rift Valley.
Fluorosis is a major public health problem in the Rift Valley of Ethiopia. Low calcium (Ca) intake may worsen fluorosis symptoms. We assessed the occurrence of fluorosis symptoms among women living in high-fluoride (F) communities in South Ethiopia and their associations with dietary Ca intake. Women (n = 270) from
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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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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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Estimated "Threshold" Doses for Skeletal Fluorosis
For over 40 years health authorities stated that in order to develop crippling skeletal fluorosis, one would need to ingest between 20 and 80 mg of fluoride per day for at least 10 or 20 years. This belief, however, which played an instrumental role in shaping current fluoride policies, is now acknowledged by the National Academy of Sciences (NAS) and other US health authorities to be incorrect.
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