Threats to adhesive/dentin interfacial integrity and next generation bio-enabled multifunctional adhesives

Abstract

Nearly 100 million of the 170 million composite and amalgam restorations placed annually in the United States are replacements for failed restorations. The primary reason both composite and amalgam restorations fail is recurrent decay, for which composite restorations experience a 2.0-3.5-fold increase compared to amalgam. Recurrent decay is a pernicious problem-the standard treatment is replacement of defective composites with larger restorations that will also fail, initiating a cycle of ever-larger restorations that can lead to root canals, and eventually, to tooth loss. Unlike amalgam, composite lacks the inherent capability to seal discrepancies at the restorative material/tooth interface. The low-viscosity adhesive that bonds the composite to the tooth is intended to seal the interface, but the adhesive degrades, which can breach the composite/tooth margin. Bacteria and bacterial by-products such as acids and enzymes infiltrate the marginal gaps and the composite's inability to increase the interfacial pH facilitates cariogenic and aciduric bacterial outgrowth. Together, these characteristics encourage recurrent decay, pulpal damage, and composite failure. This review article examines key biological and physicochemical interactions involved in the failure of composite restorations and discusses innovative strategies to mitigate the negative effects of pathogens at the adhesive/dentin interface. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B:2466-2475, 2019.

Keywords: adhesive/dentin interface; autonomous strengthening; dental restoration; peptide engineering; proton sponge.

Figure 1:

Schematic of the adhesive/dentin interface. Within the hybrid layer, the hydrophilic component increases and the crosslink density decreases as one traverses from composite to dentin. The hybrid layer is characterized by water-rich pockets of resin-sparse collagen fibrils.

Figure 2:

Proposed polymethacrylate-based network structure and intrinsic self-strengthening processes: (A) polymethacrylate-based network formed by free-radical initiated polymerization and limited photoacid-induced sol-gel reaction after 40 s irradiation; (B) in wet environment, self-strengthening via sol-gel reaction.

Figure 3:

Chemical structure of amine-containing monomers

Figure 4:

L-lysine structures

Figure 5:

Schematic of grafted polymer surface to inhibit MMP-8: (A) Amine-terminated polymer surfaces; (B) tether-MAP peptide grafted to amines via DSS linker chemistry; (C) MMP-8 inhibition by MAP. Figure adapted from Dixit et al. 2015

Figure 6:

Visible images and corresponding Raman spectroscopic images of adhesive/dentin (A/D) interface specimen. Visible images: (A) A/D interface specimen; (B) A/D interface specimen following additional etching; (C) peptide-mediated remineralization of deficient dentin within the A/D interface. Corresponding Raman spectroscopic images of A/D interface specimen: (a) Raman XY image of A/D interface, adhesive colored as green and mineral colored as red; (b) Raman XY image of A/D interface following additional etching; (c) Raman XY image of A/D interface following peptide-mediated remineralization, the spectral features associated with the mineral (PO₄ ^2- at 960 cm⁻¹) are colored red.