Abstract
To explore the effect of fluoride (F) on the expression of purine-rich element-binding protein (PURA) gene and calmodulin (CaM) gene in osteoblasts of newborn rats, parietal calvaria bone osteoblast cultures of 48-hr-old rats were treated for 48 hr with sodium fluoride (NaF) at concentrations of 0 (control), 0.5, 2, and 8 mg/ L. The expression of PURA gene and CaM gene was determined by reverse transcription polymerase chain reaction (R T-PCR). The results indicated that F significantly enhanced (p<0.05 to p<0.01) the expression levels of the two genes in the osteoblast cultures with increasing F concentrations compared with the control group
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Neuroligin-3 activates Akt-dependent Nrf2 cascade to protect osteoblasts from oxidative stress.
Excessive oxidative stress will cause significant injury to osteoblasts, serving as one major pathological mechanism of osteoporosis. Neuroligin-3 (NLGN3) is a postsynaptic cell adhesion protein and is expressed in the bone. We here explored its potential activity against hydrogen peroxide (H2O2)-induced oxidative injury in cultured osteoblasts. In primary murine and
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Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.
Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts,
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Effects of fluoride on the proliferation and activation of osteoblasts by regulating methylation of the DNA repair genes MGMT and MLH1.
Introduction Fluoride can induce the proliferation and activation of osteoblasts, resulting in skeletal fluorosis progression; however, the specific mechanism is unclear. Methods Cell proliferation was examined using the MTT assay. Flow cytometry was performed to detect the cell cycle distribution. Alkaline phosphatase (ALP) was calculated to evaluate bone formation and turnover. Gene methylation
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TGF-ß1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells.
Highlights NaF exposure significantly decreased the proliferation rate of mouse osteoblast cells in a dose dependent manner. NaF exposure induced autophagy in the osteoblast cells with an increase in TGF-ß1 expression. Overexpression of TGF-ß1 enhanced NaF-induced autophagy. Silencing of TGF-ß1 reduced NaF-induced autophagy. Abstract It is well known that excess fluoride intake
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Fluorosilicic acid and cotinine, separately and in combination, induce genotoxicity and telomeric reduction in human osteoblast cell line MG63.
Highlights DNA damage was caused by fluorosilicic acid in human osteoblast cells. DNA damage was caused by cotinine in human osteoblast cells. Fluorosilicic acid combined with cotinine increases DNA damage. Fluorosilicic acid reduces the telomere length. Oxidative stress was induced by fluorosilicic acid and cotinine. Abstract Skeletal fluorosis is a severe
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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 & Osteoclasts
It is well established that fluoride exposure can increase bone formation by increasing the proliferation of osteoblasts. Less clear is fluoride's impact on bone resorption and the cells (osteoclasts) that resorb bone. Many have assumed that fluoride's main effect on bone resorption and osteoclasts is an inhibitory one (i.e., less
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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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Fluoride Increases Osteoid Content of Bone
Fluoride's ability to increase the osteoid content of bone is now undisputed. Osteoid is an unmineralized tissue in bone that, in the normal bone remodeling process, ultimately becomes calcified. As some observers have noted, "[t]he main histological change induced by fluoride is the increase of osteoid volume." (Arnala 1985). One way fluoride
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