Abstract
A study is reported of DNA damage by fluoride to primary calvarial osteoblasts of newborn rats isolated by enzymic digestion. Sodium fluoride at concentrations of 0, 0.5, 1, 2, and 3 mmol/L was administered to the isolated osteoblast cells for 24 hr, and damage to DNA was determined by single cell gel electrophoresis assay (SCGE = Comet assay). Breakage of DNA strands occurred at 2 mmol /L NaF and above. Compared with the control group, the comet tail length was significantly increased, indicating that, at sufficient concentrations, fluoride can induce DNA damage in osteoblasts.
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Investigation of the genotoxic effects of fluoride on a bone tissue model .
Fluorides are thought to be a major cause of osteocarcinogenesis, due to their widespread industrial use, ability to accumulate in bone tissue, and genotoxic and probable carcinogenic properties. In vitro experiments investigating the genotoxic potential of fluorides in bone tissue models can provide valuable indirect information on their involvement in
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DNA damage induced by fluoride in rat kidney cells.
DNA damage by fluoride to newborn rat kidney cells isolated by enzymic digestion is reported. The cells were exposed for 24 hr to sodium fluoride at NaF concentrations of 0, 0.2, 0.4, 0.8, and 1.0 mM. Damage to DNA was determined by single cell gel electrophoresis assay (Comet assay). Significant breakage of DNA strands
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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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Influence of calcium supplementation against fluoride-mediated osteoblasts impairment in vitro: Involvement of canonical Wnt/B-catenin signaling pathway.
Fluoride (F) is capable of promoting abnormal proliferation and differentiation in primary cultured mouse osteoblasts(OB cells), although; the underlying mechanism responsible remain rare. This study aimed to explore the roles of Wingless and INT-1(Wnt) signaling pathways and screen appropriate doses of calcium (Ca2+) to alleviate the sodium fluoride (NaF)-induced OB
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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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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 & Liver Cancers in NTP Bioassay
On October 28, 1988, Battelle Columbus Laboratories submitted its Final Report to the NTP concerning the results of the Mouse study. The principal finding of Battelle's report was that a dose-dependent increase of a rare liver cancer (hepatocholangiocarcinoma) had occurred in the fluoride-treated male and female mice.
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Fluoride's Mutagenicity: The "Oral Health Research Institute's" Studies
Although many in vitro and in vivo studies have detected mutagenic effects from fluoride exposure, the Oral Health Research Institute at Indiana University's School of Dentistry has repeatedly failed to find any such effect in multiple studies on the subject.
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Fluoride/Osteosarcoma Link Is Biologically Plausible
The "biological plausiblility" of a fluoride-osteosarcoma link is widely acknowledged in the scientific literature. The biological plausibility centers around three facts: 1) Bone is the principal site of fluoride accumulation, particularly during the growth spurts of childhood; 2) Fluoride is a mutagen when present at sufficient concentrations, and 3) Fluoride can stimulate the proliferation of osteoblasts (bone-forming cells).
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NTP Bioassay on Fluoride/Cancer (1990)
In 1977, the U.S. Congress requested that animal studies be conducted to determine if fluoride can cause cancer. The result of the Congressional request was an extensive animal study conducted in the 1980s by the National Toxicology Program (NTP) and published in 1990. The main finding of NTP's study was a dose-dependent increase in osteosarcoma (bone cancer) among the fluoride-treated male rats.
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