Abstract
A comparative study of bone mineral density (BMD) and bone fracture was conducted in a fluorotic and a nonfluorotic area of the Nalgonda District, Andhra Pradesh, India. BMD measured by dual X- ray absorptiometry (DXA) of L2–L4 vertebrae, femoral neck, hip, and whole body was significantly higher by 112%, 43%, 57%, and 50%, respectively, in 12 fluorotic subjects than in 14 nonfluorotic subjects (p<0.01). However, there was an 11% decrease, although not statistically significant, in forearm BMD in the fluorotic subjects compared to the nonfluorotic subjects. Serum levels of total and bone specific alkaline phosphatase in the fluorotic subjects were significantly elevated by 219 and 313% , respectively (p<0.01), whereas serum Ca, protein, and phosphorus were 10, 12, and 32% lower, respectively (p<0.01). On the other hand, serum creatinine, urea, and zinc levels in the two groups of subjects were not significantly different. In the fluorotic village, with a 34% lower average consumption unit intake of calcium, the overall bone fracture rate of 6.3% was significantly higher than the 2.1% rate in the nonfluorotic village (p<0.05).
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Fluoride-related bone disease associated with habitual tea consumption
Acquired osteosclerosis is a rare disorder of bone formation but an important consideration in adults with sclerotic bones or elevated bone density results. In such patients, malignancy, hepatitis C, and fluorosis should all be considered when making a diagnosis. We describe 4 patients evaluated at our Metabolic Bone Disease Clinic
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[Generalized osteopathy with pathological fractures in a patient with long-term exposure to fluorine-containing plastics].
In a 68-year-old man with a painful syndrome of the lower extremities which began at the age of 64 years, workup revealed a generalized osteopathy with sclerosis of the axial skeleton and osteopenia at the extremities associated with pathologic fractures. The occupational history showed exposure to several synthetics such as
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Fluoridation and bone disease in renal patients
About the Authors: William J Johnson, director of the Mayo Artificial Kidney Center and professor of medicine with the Division of Nephrology at the Mayo Clinic, has been involved in the study of calcium and phosphorus metabolism and renal osteodystrophy, potassium metabolism, and uremic neuropathy. He is past chairman of the Minnesota
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Industrial Fluorosis [Carnow et al.]
SUMMARY: In 1242 apparently healthy and actively employed workers of a Canadian aluminum facility, the history of musculoskeletal symptoms, of the incidence of fractures, of neck and back surgery, as well as the x-ray findings were reviewed. A highly significant relationship of exposure to fluoride was established with the frequency
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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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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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Fluoride Reduces Bone Strength Prior to Onset of Skeletal Fluorosis
The majority of animal studies investigating fluoride's impact on bone strength have found that fluoride has either no effect, or a detrimental effect, on bone strength. Importantly, several of the animal studies that have found fluoride reductes bone strength have reported that this reduction in strength occurs before signs of skeletal fluorosis
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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 & Spontaneous Hip Fractures in Osteoporosis Patients
Due to its ability to increase vertebral bone mass, fluoride has been used as an experimental treatment for osteoporosis (doses > 20 mg/day). Fluoride treatment, however, proved far more harmful than beneficial. Not only was fluoride therapy shown to increase fracture rates among the treated patients, it was also found to
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