Abstract
OBJECTIVE: To observe the effect of overdose fluoride on the proliferation of rat’s incisor ameloblast.
METHODS: 20 Wistar rats were divided randomly into 2 groups: Group I (Control); Group II 50 mg/L F(-) were given. After 8 weeks treatment, the AgNORs stain and TUNEL technique were applied to analyze the effect of fluoride on the proliferation and apoptosis of ameloblasts.
RESULTS: The imagination analysis results showed that proliferation of pre-secretion ameloblasts were inhibited in group II as compared with the control group (P < 0.001). There was significant increase of apoptosis with the trend of migration toward secretion stage.
CONCLUSION: The mechanism of fluorosis mottled enamel may be the effect of overdose fluoride with inhibits proliferation and induces apoptosis of ameloblasts resulting in dysfunction of secretion or absorption of enamel matrix proteins.
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LS8 cell apoptosis induced by NaF through p-ERK and p-JNK - a mechanism study of dental fluorosis
OBJECTIVE: To investigate the possible biological mechanism of dental fluorosis at a molecular level. MATERIAL AND METHODS: Cultured LS8 were incubated with serum-free medium containing selected concentrations of NaF (0???2?mM) for either 24 or 48?h. Subcellular microanatomy was characterized using TEM; meanwhile, selected biomolecules were analysed using various biochemistry techniques. Transient
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Fluoride induced endoplasmic reticulum stress and calcium overload in ameloblasts
OBJECTIVE: The aim of the study was to evaluate the involvement of endoplasmic reticulum stress and intracellular calcium overload on the development of dental fluorosis. METHODS: We cultured and exposed rat ameloblast HAT-7 cells to various concentrations of fluoride and measured apoptosis with flow cytometry and intracellular Ca2+ changes using confocal
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Protective effect of lycopene on fluoride-induced ameloblasts apoptosis and dental fluorosis through oxidative stress-mediated Caspase pathways
Fluoride is an environmental toxicant and induces dental fluorosis and oxidative stress. Lycopene (LYC) is an effective antioxidant that is reported to attenuate fluoride toxicity. To determine the effects of LYC on sodium fluoride (NaF) -induced teeth and ameloblasts toxicity, rats were treated with NaF (10 mg/kg) and/or LYC (10 mg/kg) by
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MiR-1a-3p Inhibits Apoptosis in Fluoride-exposed LS8 Cells by Targeting Map3k1.
Dental fluorosis is a common chemical disease. It is currently unclear how fluorosis occurs at the molecular level. We used miRNA-seq to look at the differences between miRNAs in the cell line of ameloblasts LS8 that had been treated with 3.2 mmol/L NaF. We also performed gene ontology (GO) 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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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin
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Mechanisms by Which Fluoride Causes Dental Fluorosis Remain Unknown
When it comes to how fluoride impacts human health, no tissue in the body has been studied more than the teeth. Yet, despite over 50 years of research, the mechanism by which fluoride causes dental fluorosis (a hypo-mineralization of the enamel that results in significant staining of the teeth) is not
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