Abstract
It has been reported that sodium fluoride suppressed proliferation and induced apoptosis in osteoblasts. However, the details about the mechanism at work in bone metabolism are limited. In this study, we further investigated the mechanisms of NaF on proliferation and apoptosis in the primary cultured mouse osteoblasts, which were exposed to different concentration of NaF (10(-6)-5 × 10(-4) M). We examined the effect of NaF on proliferation, cell cycle, apoptosis, oxidative stress, and the protein level of insulin-like growth factor-I (IGF-I) in osteoblasts. All the tested NaF inhibited proliferation and arrested cell cycle at S phase in osteoblasts, and further demonstrated to induce apoptosis in osteoblasts. On the other hand, we found that NaF increased oxidative stress and decreased protein expression of IGF-I. Our study herein suggested that NaF caused proliferation suppression, and apoptosis may contribute to decrease IGF-I expression and increased oxidative stress damage by NaF in the primary mouse osteoblasts.
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Fluoride-induced oxidative stress in three-dimensional culture of OS732 cells and rats.
Exposure to excessive fluoride poses a threat to human health, including increased susceptibility to developing the skeletal fluorosis. Despite its recognized importance as an endemic disease, little is known about how fluoride directly impacts on osteoblasts. We previously reported that fluoride-stimulating monolayer-cultured osteoblast proliferation or inhibiting cell viability depended on
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Simultaneous administration of fluoride and selenite regulates proliferation and apoptosis in murine osteoblast-like MC3T3-E1 cells by altering osteoprotegerin.
The receptor activator nuclear factor kappa-B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), are important for maintaining the balance between bone formation and resorption. However, the regulation of microelements on these factors remains unclear. In this study, we used murine osteoblast-like MC3T3-E1 cells to examine the impact of sodium
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Role of oxidative stress in osteoblasts exposed to sodium fluoride
We investigated the relationship between oxidative stress and osteoblasts viability in osteoblasts exposed to various concentrations of fluoride in this study. Primary calvarial osteoblasts from neonatal Kunming mice were cultured and subcultured to the third generation. Osteoblasts were incubated with sodium fluoride (0, 0.5, 1, 2, 4, 8, 12, and
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Expression of autophagy-related factors LC3A and Beclin 1 and apoptosis-related factors Bcl-2 and BAX in osteoblasts treated with Sodium Fluoride.
Objective: This study aims to analyze the expressions of autophagy-related factors light chain 3 alpha (LC3A) and Beclin 1 and apoptosis-related factors B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (BAX) in primary osteoblasts treated with sodium fluoride (NaF). Methods: Osteoblasts were extracted from Sprague-Dawley rats and treated with 0, 2.5, 5,
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Sodium fluoride modulates caprine osteoblast proliferation and differentiation
The cellular and molecular pathways of fluoride toxicity in osteoblasts are not very well understood. Therefore, the objective of the present study was to evaluate the effects of sodium fluoride (NaF) on caprine osteoblasts cultured in vitro. Caprine osteoblasts at 2.0 x 10(-4) cells/ml were incubated in vitro with NaF
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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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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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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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