“…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).…”