Post-Eruptive Maturation of Dental Enamel: Development of an in vitro Model

Abstract

Dental caries is a highly prevalent chronic disease, the treatment of which, forms a significant financial burden. Furthermore, due to the invasive nature and relatively high long-term failure rate of established treatments, focus has been placed on effective prevention strategies in order to instead circumvent the problem before it occurs. Prevalence of dental caries is particularly high in adolescents due to the increased susceptibility of newly erupted teeth to acid dissolution. A transient vulnerability that is gradually lost with time through a post-eruptive maturation process. Post-eruptive maturation (PEM) refers to chemical and physical changes that occur in the outer enamel layers following exposure of newly erupted teeth to the oral environment. Whilst little is known about the underlying mechanism, it is believed to be a result of the natural fluctuation between de- and remineralising states within the oral cavity. To date, most literature regarding PEM places focus on measuring the outcomes of the process (Which include increased surface hardness, decreased porosity and a decrease in susceptibility to acid dissolution) as opposed to investigating the reasoning behind such changes. One reason for this focus is the difficulties faced when initially approaching the study of PEM, as there is currently no established model or protocol for recreating the process in vitro. In order to address this problem, the current work outlines the development process of a proposed pH-cycling model for use in the study of PEM. The efficacy of the model was initially assessed though its ability to reduce acid dissolution and then also through its effect on surface microhardness. The often speculated role of repeated sub-clinical caries events as the basis to PEM was confirmed through the observation of significantly reduced mineral loss in enamel previously exposed to plaque-fluid-relevant pH-cycling conditions. Further to this, the ability of Fluoride, Zinc and Strontium to supplement this effect was demonstrated, in addition their ability to replicate the increased surface microhardness observed during PEM. The 20-day, plaque-fluid-relevant, pH-cycling model proposed within this work has the potential to allow much greater insight into the underlying chemical mechanisms underpinning PEM, particularly the potential incorporation of ions such as F and Zn, in addition to allowing the testing and identification of agents to enhance the observed effects. As such, this work provides a much-needed springboard from which the clinical potential of PEM can be unlocked.