2009
DOI: 10.1177/0022034509343280
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The Impact of Fluoride on Ameloblasts and the Mechanisms of Enamel Fluorosis

Abstract: Intake of excess amounts of fluoride during tooth development cause enamel fluorosis, a developmental disturbance that makes enamel more porous. In mild fluorosis, there are white opaque striations across the enamel surface, whereas in more severe cases, the porous regions increase in size, with enamel pitting, and secondary discoloration of the enamel surface. The effects of fluoride on enamel formation suggest that fluoride affects the enamelforming cells, the ameloblasts. Studies investigating the effects o… Show more

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Cited by 184 publications
(157 citation statements)
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“…During amelogenesis, the tooth when chronically exposed to low-dose fluoride results in development of the double-response lines, formed at the secretory stage. Posteruptive defects after a single high plasma peak level of fluoride are deep and shallow pits that result from sub-ameloblastic cysts formed by damaged earlyand late-secretory ameloblasts [23].…”
Section: Discussionmentioning
confidence: 99%
“…During amelogenesis, the tooth when chronically exposed to low-dose fluoride results in development of the double-response lines, formed at the secretory stage. Posteruptive defects after a single high plasma peak level of fluoride are deep and shallow pits that result from sub-ameloblastic cysts formed by damaged earlyand late-secretory ameloblasts [23].…”
Section: Discussionmentioning
confidence: 99%
“…In mild cases, chalky white opaque areas are observed, in moderate cases spots may be brownish, 2 and in severe cases enamel is fragile which can lead to fracture and loss of tissue. 3 DF is observed in specific geographical areas in the world 4 showing an endemic epidemiological pattern affecting millions of people; this alteration can be considered an indicator of excessive fluoride exposure.…”
Section: Ental Fluorosis (Df) As It Was Called By Trendley Dean Inmentioning
confidence: 99%
“…Ameloblasts in the maturational phase appear to be the cellular target of chronic fluoride exposure (DenBesten and Thariani, 1992), whereas acute fluoride toxicity targets the transitional and early-secretory ameloblasts (Lyaruu et al, 2006). The mechanism(s) underlying DF remain obscure, but likely contribute to the observed retention of enamel matrix proteins and may include reduced removal of enamel matrix proteins during enamel maturation, perturbation of extracellular transport, or initiation of the ER stress-response pathway (Matsuo et al, 2000;DenBesten et al, 2002;Kubota et al, 2005;Sharma et al, 2008;Bronckers et al, 2009;Everett et al, 2009). While biological factors likely play critical roles in the pathogenesis of DF, physicochemical affects should also be considered (Robinson et al, 2004).…”
Section: Actions On Ameloblastsmentioning
confidence: 99%