TY - JOUR
T1 - Dental enamel formation and implications for oral health and disease
AU - Lacruz, Rodrigo S.
AU - Habelitz, Stefan
AU - Wright, J. Timothy
AU - Paine, Michael L.
N1 - Funding Information:
This work was supported by National Institute of Dental and Craniofacial Research Grants R00 DE022799 and R01 DE025639 (to R. S. Lacruz), R01 DE025709 (to S. Habelitz), R01 DE016079 (to J. T. Wright), and R01 DE019629 and R21 DE024704 (to M. L. Paine).
Publisher Copyright:
© 2017 the American Physiological Society.
PY - 2017/7
Y1 - 2017/7
N2 - Dental enamel is the hardest and most mineralized tissue in extinct and extant vertebrate species and provides maximum durability that allows teeth to function as weapons and/or tools as well as for food processing. Enamel development and mineralization is an intricate process tightly regulated by cells of the enamel organ called ameloblasts. These heavily polarized cells form a monolayer around the developing enamel tissue and move as a single forming front in specified directions as they lay down a proteinaceous matrix that serves as a template for crystal growth. Ameloblasts maintain intercellular connections creating a semi-permeable barrier that at one end (basal/proximal) receives nutrients and ions from blood vessels, and at the opposite end (secretory/apical/distal) forms extracellular crystals within specified pH conditions. In this unique environment, ameloblasts orchestrate crystal growth via multiple cellular activities including modulating the transport of minerals and ions, pH regulation, proteolysis, and endocytosis. In many vertebrates, the bulk of the enamel tissue volume is first formed and subsequently mineralized by these same cells as they retransform their morphology and function. Cell death by apoptosis and regression are the fates of many ameloblasts following enamel maturation, and what cells remain of the enamel organ are shed during tooth eruption, or are incorporated into the tooth’s epithelial attachment to the oral gingiva. In this review, we examine key aspects of dental enamel formation, from its developmental genesis to the ever-increasing wealth of data on the mechanisms mediating ionic transport, as well as the clinical outcomes resulting from abnormal ameloblast function.
AB - Dental enamel is the hardest and most mineralized tissue in extinct and extant vertebrate species and provides maximum durability that allows teeth to function as weapons and/or tools as well as for food processing. Enamel development and mineralization is an intricate process tightly regulated by cells of the enamel organ called ameloblasts. These heavily polarized cells form a monolayer around the developing enamel tissue and move as a single forming front in specified directions as they lay down a proteinaceous matrix that serves as a template for crystal growth. Ameloblasts maintain intercellular connections creating a semi-permeable barrier that at one end (basal/proximal) receives nutrients and ions from blood vessels, and at the opposite end (secretory/apical/distal) forms extracellular crystals within specified pH conditions. In this unique environment, ameloblasts orchestrate crystal growth via multiple cellular activities including modulating the transport of minerals and ions, pH regulation, proteolysis, and endocytosis. In many vertebrates, the bulk of the enamel tissue volume is first formed and subsequently mineralized by these same cells as they retransform their morphology and function. Cell death by apoptosis and regression are the fates of many ameloblasts following enamel maturation, and what cells remain of the enamel organ are shed during tooth eruption, or are incorporated into the tooth’s epithelial attachment to the oral gingiva. In this review, we examine key aspects of dental enamel formation, from its developmental genesis to the ever-increasing wealth of data on the mechanisms mediating ionic transport, as well as the clinical outcomes resulting from abnormal ameloblast function.
UR - http://www.scopus.com/inward/record.url?scp=85019170778&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85019170778&partnerID=8YFLogxK
U2 - 10.1152/physrev.00030.2016
DO - 10.1152/physrev.00030.2016
M3 - Article
C2 - 28468833
AN - SCOPUS:85019170778
SN - 0031-9333
VL - 97
SP - 939
EP - 993
JO - Physiological Reviews
JF - Physiological Reviews
IS - 3
ER -