A post-classical theory of enamel biomineralization… and why we need one

Enamel crystals are unique in shape, orientation and organization. They are hundreds of thousands times longer than they are wide, run parallel to each other, are oriented with respect to the ameloblast membrane at the mineralization front and are organized into rod or interrod enamel. The classical theory of amelogenesis postulates that extracellular matrix proteins shape crystallites by specifically inhibiting ion deposition on the crystal sides, orient them by binding multiple crystallites and establish higher levels of crystal organization. Elements of the classical theory are supported in principle by in vitro studies; however, the classical theory does not explain how enamel forms in vivo. In this review, we describe how amelogenesis is highly integrated with ameloblast cell activities and how the shape, orientation and organization of enamel mineral ribbons are established by a mineralization front apparatus along the secretory surface of the ameloblast cell membrane. Genetic research into tooth-enamel formation reveals a mineralization front along which crystals form, US and Canadian scientists report. James P. Simmer and colleagues at the University of Michigan, USA, and McGill University, Canada, reviewed recent genetic studies which suggest that enamel formation, or amelogenesis, is closely linked to the activity of ameloblasts, the cells that initiate tooth growth. Based on laboratory studies, the classical theory of amelogenesis describes crystal growth on an extracellular matrix with mineral deposition governed by proteins. However, enamel appears to behave differently within the body. Studies on rodents suggest that the first mineral present in enamel is amorphous calcium phosphate (ACP), and that the initial enamel ribbons are not crystalline but flexible. A mineralization front, sustained by the ameloblast cell membrane, shapes and orientates the ribbons before they harden into rod-shaped crystals.