Cellular and chemical events during enamel maturation.
This review focuses on the process of enamel maturation, a series of events associated with slow, progressive growth in the width and thickness of apatitic crystals. This developmental step causes gradual physical hardening and transformation of soft, newly formed enamel into one of the most durable mineralized tissues produced biologically. Enamel is the secretory product of specialized epithelial cells, the ameloblasts, which make this covering on the crowns of teeth in two steps. First, they roughly "map out" the location and limits (overall thickness) of the entire extracellular layer as a protein-rich, acellular, and avascular matrix filled with thin, ribbon-like crystals of carbonated hydroxyapatite. These initial crystals are organized spatially into rod and interrod territories as they form, and rod crystals are lengthened by Tomes' processes in tandem with appositional movement of ameloblasts away from the dentin surface. Once the full thickness of enamel has been formed, ameloblasts initiate a series of repetitive morphological changes at the enamel surface in which tight junctions and deep membrane infoldings periodically appear (ruffle-ended), then disappear for short intervals (smooth-ended), from the apical ends of the cells. As this happens, the enamel covered by these cells changes rhythmically in net pH from mildly acidic (ruffle-ended) to near-physiologic (smooth-ended) as mineral crystals slowly expand into the "spaces" (volume) formerly occupied by matrix proteins and water. Matrix proteins are processed and degraded by proteinases throughout amelogenesis, but they undergo more rapid destruction once ameloblast modulation begins. Ruffle-ended ameloblasts appear to function primarily as a regulatory and transport epithelium for controlling the movement of calcium and other ions such as bicarbonate into enamel to maintain buffering capacity and driving forces optimized for surface crystal growth. The reason ruffle-ended ameloblasts become smooth-ended periodically is unknown, although this event seems to be crucial for sustaining long-term crystal growth.
Smith
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Faculty of Dentistry, and Department of Anatomy & Cell Biology, McGill University, Montreal, Quebec, Canada.
D000565:Ameloblasts / Q000166:cytology* / Q000378:metabolism / Q000502:physiology; D000566:Amelogenesis / Q000502:physiology*; D001031:Apatites / Q000378:metabolism; D001639:Bicarbonates / Q000378:metabolism; D001692:Biological Transport; D001834:Body Water / Q000378:metabolism; D002021:Buffers; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology / Q000648:ultrastructure; D002465:Cell Movement; D003460:Crystallization; D003743:Dental Enamel / Q000166:cytology / Q000254:growth & development / Q000378:metabolism*; D003804:Dentin / Q000033:anatomy & histology; D017886:Durapatite / Q000378:metabolism; D010450:Endopeptidases / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism / Q000502:physiology / Q000648:ultrastructure; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D014074:Tooth Calcification / Q000502:physiology; D019228:Tooth Crown / Q000166:cytology / Q000254:growth & development / Q000378:metabolism
D001031:Apatites; D001639:Bicarbonates; D002021:Buffers; D016326:Extracellular Matrix Proteins; D017886:Durapatite; D010450:Endopeptidases; D002118:Calcium