Abstract
The purpose of this prospective study was to investigate the quantity and quality of bone by quantitative ultrasound (QUS) measurements and to assess bone resorption by urinary excretion measurement of C-terminal telopeptide of type I collagen (CTX) in an adult Turkish population living in an endemic fluorosis area and consuming drinking water with a high fluoride (F) concentration (mean 3.57 ppm F). Excretion of urinary CTX, heel broadband ultrasound attenuation (HBUA; dB/MHz), and speed of sound (SOS; m/s) were examined in 122 Turkish adults (37 pre- menopausal, 40 post-menopausal women, and 45 men) living in the endemic fluorosis area. For comparison, the same measurements were made on 117 controls (48 pre-menopausal women, 34 post-menopausal women, and 35 men) living in a nonendemic low F water area (mean 0.4 ppm F). In the F endemic area urinary excretion of CTX was higher in all subjects, whereas calcaneal BUA was lower in post-menopausal women. In the F endemic area SOS was significantly greater among pre-menopausal women but was not significantly different in the other two groups. Although non-trauma bone fracture rates were not significantly different among any of the groups, some of the bone marker differences indicate that exposure to prolonged high concentration of F may increase the risk of bone fracture, especially in post-menopausal women.
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Fluorosis as a probable factor in metabolic bone disease in captive New Zealand native frogs (Leiopelma species)
This report describes the investigations into the cause and treatment of metabolic bone disease (MBD) in captive native New Zealand frogs (Leiopelma spp.) and the role of fluoride in the disease. MBD was diagnosed in Leiopelma archeyi and Leiopelma hochstetteri in 2008 at three institutions: Auckland Zoo, Hamilton Zoo, and
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Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).
Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in
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Fluorosis with report of an advanced case.
It is quite possible that endemic centres [of skeletal fluorosis] exist but that the cause of the disabling spondylitis or other joint affections has not been determined, and a diagnosis of chronic arthritis has resulted. Few cases in Canada or the United States will be found to be as dramatic
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Insights into material and structural basis of bone fragility from diseases associated with fractures: how determinants of the biomechanical properties of bone are compromised by disease.
Minimal trauma fractures in bone diseases are the result of bone fragility. Rather than considering bone fragility as being the result of a reduced amount of bone, we recognize that bone fragility is the result of changes in the material and structural properties of bone. A better understanding of the
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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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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 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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"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 & 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 in India & China
In India and China, scientists have repeatedly found that skeletal fluorosis occurs in populations drinking water with just 0.7 to 1.5 ppm fluoride. Although nutritional deficiencies and hot climates make populations in India and China more susceptible to fluoride toxicity than is generally the case in western countries, this fact does not remove the relevance of the Indian and Chinese experience to the situation in fluoridating countries. This is because (a) nutritional deficiencies also exist in the western world, particularly in low-income communities, and (b) some individuals, including those with kidney disease, can be just as -- if not more -- susceptible to fluoride toxicity.
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