Abstract
Fluoride is widely believed to be a useful chemical substance for preventing dental caries. However, the mechanism underlying crystal perforation in the tooth enamel and the effect of fluoride on hard tissues are unclear. To clarify the mechanism of the biological action of fluoride in the mineralization process, we examined the hard tissues of rats having received water containing a relatively low fluoride level. Electron microscopy revealed that fluoride ions could interrupt the crystal nucleation process, resulting in crystal perforation in the developing tooth enamel and the presence of amorphous minerals in bone crystals. Furthermore, the results of enzymatic analyses indicated that fluoride directly interfered with the synthesis of carbonic anhydrase by the enamel-forming cells, rather than being directly involved in the crystal formation. From the results, we would like to provide a possible mechanism of crystal perforation in the enamel induced by fluoride intake. Also, we would like to suggest that regardless of its amount, fluoride intake has harmful effects on both tooth and bone formation.
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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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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 Alters Signaling Pathways Associated with the Initiation of Dentin Mineralization in Enamel Fluorosis Susceptible Mice.
Fluoride can alter the formation of mineralized tissues, including enamel, dentin, and bone. Dentin fluorosis occurs in tandem with enamel fluorosis. However, the pathogenesis of dentin fluorosis and its mechanisms are poorly understood. In this study, we report the effects of fluoride on the initiation of dentin matrix formation and
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Histone acetyltransferase promotes fluoride toxicity in LS8 cells.
Previously we demonstrated that fluoride increased acetylated-p53 (Ac-p53) in LS8 cells that are derived from mouse enamel organ epithelia and in rodent ameloblasts. However, how p53 is acetylated by fluoride and how the p53 upstream molecular pathway responds to fluoride is not well characterized. Here we demonstrate that fluoride activates
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Fluoride affects enamel protein content via TGF-B1-mediated KLK4 inhibition
Dental fluorosis is caused by chronic high-level fluoride (F-) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be
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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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"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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Diagnostic Criteria for Dental Fluorosis: The TSIF ("Total Surface Index of Fluorosis")
The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental
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Community Fluorosis Index (CFI)
The current Community Fluorosis Index for U.S. adolescents as a whole (from both fluoridated and non-fluoridated areas) is roughly 5 times higher than the CFI health authorities predicted for fluoridated areas when fluoridation first began. It is also higher than the CFI that the NIDR found in fluoridated areas back in the 1980s. It is readily apparent, therefore, that children are ingesting far more fluoride than was the case in the 1950s, and even as recently as the 1980s.
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