Abstract
Dental enamel is one of the most remarkable examples of matrix-mediated biomineralization. Enamel crystals form de novo in a rich extracellular environment in a stage-dependent manner producing complex microstructural patterns that are visually stunning. This process is orchestrated by specialized epithelial cells known as ameloblasts which themselves undergo striking morphological changes, switching function from a secretory role to a cell primarily engaged in ionic transport. Ameloblasts are supported by a host of cell types which combined represent the enamel organ. Fully mineralized enamel is the hardest tissue found in vertebrates owing its properties partly to the unique mixture of ionic species represented and their highly organized assembly in the crystal lattice. Among the main elements found in enamel, Ca(2+) is the most abundant ion, yet how ameloblasts modulate Ca(2+) dynamics remains poorly known. This review describes previously proposed models for passive and active Ca(2+) transport, the intracellular Ca(2+) buffering systems expressed in ameloblasts and provides an up-dated view of current models concerning Ca(2+) influx and extrusion mechanisms, where most of the recent advances have been made. We also advance a new model for Ca(2+) transport by the enamel organ.