Abstract
Effects of fluoride (as NaF) on cell cycle, DNA content, and apoptosis of mouse fetal long bone cultures were examined and analyzed by flow cytometry (FCM). The results showed that NaF at 2.5–5.0 µg/mL (2.5–5.0 ppm) had only slight effects on the DNA content and cell cycle distributions. At 10.0 µg/mL, however, NaF increased the number of cells in S phase but did not change the frequency of the G0/G1 and G2/M phase. At 20.0 µg /mL NaF not only increased the number of cells in S phase but also decreased the frequency of the G2/M phase. Cell proliferation was also influenced. At 2.5–10.0 µg/mL NaF did not induce increased apoptosis, but the number of apoptotic cells was significantly increased at 20.0 µg NaF/mL. Therefore F damage to bone may involve promoting apoptosis and disordering cell cycle distributions. Although the differences in DNA content, cell cycle distributions, and apoptosis between controls and the two lower NaF concentrations were not statistically significant, there was evidence of hormesis (paradoxical stimulatory) effects. The results indicate that F exerts a dual influence on osteocytes.
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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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Effect of fluoride on expression of pura gene and CaM gene in newborn rat osteoblasts.
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
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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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Fluorosis induces endoplasmic reticulum stress and apoptosis in osteoblasts in vivo
The present study investigated the effects of fluoride on endoplasmic reticulum (ER) stress (ERS) and osteoblast apoptosis in vivo. Forty-eight Wistar rats were randomly divided into four groups (12/group) and exposed to 0, 50, 100, and 150 mg/L of fluoride in drinking water for 8 weeks, respectively. Peripheral blood samples and bilateral
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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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"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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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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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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