TY - JOUR
T1 - Clinical considerations of microleakage
AU - Pashley, David H.
N1 - Funding Information:
This work was supported, in part, by Grant DE 06427 from the National Institute of Dental Research and by the Medical College of Georgia Dental Research Center.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1990/2
Y1 - 1990/2
N2 - Most dental materials permit the microleakage of bacteria and bacterial products from oral fluids to reach dentin. Thus, an understanding of the clinical consequences of microleakage demands that we analyze the permeability characteristics of dentin. The more dentin surface that is exposed during tooth preparation, the greater the potential for microleakage. Thicker dentin is less permeable than thin dentin. Dentin over pulp horns is more permeable than central dentin. Similarly, the dentin making up axial walls is more permeable than dentin forming the pulpal floor of cavities. Coronal dentin is much more permeable than root dentin. In addition to the number of tubules per unit area, tubule diameter, and the location of the dentin in a tooth, another extremely important variable is the presence or absence of a smear layer. When smear layers are created, grinding debris are forced into each tubule to form a smear plug. Smear plugs are usually 1- to 2-μm long but may be 10-μm long. They are much longer than the smear layer thickness and they reduce dentin permeability more than the overlying smear layer. Smear layers constitute a natural cavity liner that reduces the permeability of dentin far more than any cavity varnish. However, its presence limits the strength of dentin bonding agents because of the relatively low cohesive forces holding the smear layer together and to dentin. If it is removed, the bond strengths of dentin adhesive resins increases, but removal also increases the potential liability for pulpal inflammation if the bond is not uniformly perfect. There is a balance between the rate of diffusion of bacterial products permeating dentin from microleakage and the rate at which they are removed by the pulpal circulation. Decreases in pulpal blood flow can permit the concentration of these products to increase, thereby triggering pulpal inflammation.
AB - Most dental materials permit the microleakage of bacteria and bacterial products from oral fluids to reach dentin. Thus, an understanding of the clinical consequences of microleakage demands that we analyze the permeability characteristics of dentin. The more dentin surface that is exposed during tooth preparation, the greater the potential for microleakage. Thicker dentin is less permeable than thin dentin. Dentin over pulp horns is more permeable than central dentin. Similarly, the dentin making up axial walls is more permeable than dentin forming the pulpal floor of cavities. Coronal dentin is much more permeable than root dentin. In addition to the number of tubules per unit area, tubule diameter, and the location of the dentin in a tooth, another extremely important variable is the presence or absence of a smear layer. When smear layers are created, grinding debris are forced into each tubule to form a smear plug. Smear plugs are usually 1- to 2-μm long but may be 10-μm long. They are much longer than the smear layer thickness and they reduce dentin permeability more than the overlying smear layer. Smear layers constitute a natural cavity liner that reduces the permeability of dentin far more than any cavity varnish. However, its presence limits the strength of dentin bonding agents because of the relatively low cohesive forces holding the smear layer together and to dentin. If it is removed, the bond strengths of dentin adhesive resins increases, but removal also increases the potential liability for pulpal inflammation if the bond is not uniformly perfect. There is a balance between the rate of diffusion of bacterial products permeating dentin from microleakage and the rate at which they are removed by the pulpal circulation. Decreases in pulpal blood flow can permit the concentration of these products to increase, thereby triggering pulpal inflammation.
UR - http://www.scopus.com/inward/record.url?scp=0025380905&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025380905&partnerID=8YFLogxK
U2 - 10.1016/S0099-2399(06)81567-0
DO - 10.1016/S0099-2399(06)81567-0
M3 - Article
C2 - 2388021
AN - SCOPUS:0025380905
SN - 0099-2399
VL - 16
SP - 70
EP - 77
JO - Journal of Endodontics
JF - Journal of Endodontics
IS - 2
ER -