Abstract
Histomorphometric study was made on a series of sections of undecalcified epiphyseal femoral specimens from rats with experimental fluorosis. The results revealed osteosclerosis in Group A (5 ppm) being more severe than that in Group B (25 ppm). With the increase of fluoride dose, the parameters fell down instead of increased in parallel. There is seemingly a threshold over which osteosclerosis in fluorosis becomes less severe. In contrast to Bely’s conclusion the authors proposed that, fluoride toxicity, besides decreasing the number of osteoblasts, may also activate the osteoblasts. The number of osteoblasts may be increased with relative lower dose of fluoride also. The net outcome is the increment in bone volume. When toxic dose of fluoride is higher enough (higher than the proposed threshold), however, the number of osteoblasts and its activity are inhibited. So are the osteocytes. This interpretation may be the cytological basis for osteosclerosis in the experimental fluorosis.
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Experimental fluorosis in rats: NaF induced changes of bone and bone marrow
The results of our experiments suggest that increased doses of NaF cause more extensive osteosclerosis due to the decrease in number and/or activity of osteoclasts. Therefore oateosclerosis is caused primarily, not by increased bone formation but, by the inhibition of bone resorption. This view is supported by the fact that
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Aberrant methylation-induced dysfunction of p16 is associated with osteoblast activation caused by fluoride.
Chronic exposure to fluoride continues to be a public health problem worldwide, affecting thousands of people. Fluoride can cause abnormal proliferation and activation of osteoblast and osteoclast, leading to skeletal fluorosis that can cause pain and harm to joints and bones and even lead to permanent disability. Nevertheless, there is
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Suppression of Sclerostin and Dickkopf-1 levels in patients with fluorine bone injury
Evidence has been accumulating for the role of Sclerostin and Dickkopf-1 as the antagonists of Wnt/B-Catenin signaling pathway, which suppresses bone formation through inhibiting osteoblastic function. To get deep-inside information about the expression of the antagonists in patients with fluorine bone injury, a case-control study was conducted in two counties
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Sodium fluoride induces hypercalcemia resulting from the upregulation of both osteoblastic and osteoclastic activities in goldfish, Carassius auratus
The influence of sodium fluoride (NaF) on calcium metabolism was examined in goldfish (fresh water teleost). At 2days after administration of NaF (500ng/g body weight; 5?g/g body weight) (around 10-5 to 10-4M in goldfish), we indicated that plasma calcium levels upregulated in both doses of NaF-treated goldfish. To examine the
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The effects of fluoride on bone and implant histomorphometry in growing rats
The effects of fluoride at concentrations of 2.0 and 4.5 mM in drinking water on growth rate, vitamin D, water and mineral metabolism, bone histomorphometry, and osteoinduction of demineralized allogenic bone matrix (DABM) were compared in the rat. Whereas fluoride did not influence fluid intake or growth rate at the
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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's Effect on Osteoblasts (Bone-Forming Cells)
As noted by the National Research Council, "[p]erhaps the single clearest effect of fluoride on the skeleton is its stimulation of osteoblast proliferation." (NRC 2006). Osteoblasts are bone-forming cells. "Stimulatory effects of fluoride on osteoblasts result in formation of osteoid, which subsequently undergoes mineralization." (Fisher RL, et al. 1989). If the new
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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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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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