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Compendium
March 2012
Volume 33, Issue 3
Peer-Reviewed

The Durability of the Resin/Dentin Complex

Gregg A. Helvey, DDS

The success of direct and indirect tooth-colored, resin-based all-ceramic restorations is largely dependant on the durability of the adhesive interface between the restorative material and the enamel/dentin substrate. Despite advances in technology, failures begin to occur with signs of marginal discoloration and adaptation soon after exposure to the oral environment.1

The main difference between etch/rinse and self-etch adhesive systems is the use of phosphoric acid, which etches the tooth substrate and then is “rinsed away,” versus using a self-etching primer that is applied then “dried away.” Both systems create a hybrid layer that is formed as a result of resins impregnating the porous enamel/dentin substrate.2 The longevity of the hybrid layer is dependent on several factors.1

Resin Degradation

Water added to ester bonds is a main factor in the breakdown of the hybrid layer, resulting in loss of resin mass—a chemical process called hydrolysis.3 Since hydrolytic degradation only occurs in the presence of water there is a correlation between the hydrophilicity of a resin and water absorption with any adhesive system used. Tay and Pashley studied the permeability of the hybrid layer and detected pathways that allowed water to diffuse through the hybrid layer. They referred to these pathways as “water trees” and concluded that the hybrid layer was a semi-permeable membrane.4

Collagen Fibril Degradation

The goal of manufacturers is to develop bonding adhesives that completely encapsulate the conditioned collagen fibrils through total infiltration of resin. Collagen fibrils that are completely surrounded by resin are protected from degradation.

When a resin adhesive is applied after the dentin has been conditioned with a phosphoric acid etchant not all of the exposed collagen fibrils are protected. Incomplete resin infiltration was observed in self-etching adhesives in the form of nanoleakage within the hybrid layer despite simultaneous adhesive etching and priming.5 Incomplete removal of water associated with the hydrophilic monomers may be responsible for the lack of total infiltration. No matter what adhesive system is employed, there are collagen fibrils left unprotected and subject to hydrolytic degradation and other degradation processes. Studies have shown that host-derived proteinases also contribute to the breakdown of collagen matrices.6

Matrix Metalloproteinases (MMPs)

Matrix metalloproteinases (MMPs) are a family of zinc-dependent structural and functional related endopeptidases that are capable of degrading extracellular matrix proteins. They play a crucial role in malignant tumor growth, invasion, metastasis, and angiogenesis. In normal physiological conditions their activity is precisely regulated in order to prevent tissue disruption. MMPs also play a role in the pathogenesis of dentin caries and periodontal disease.6 While trapped within the dentin matrix during tooth development, MMPs can become active by weak acids in the presence of water. These acids can be derived from caries-producing bacteria and/or acidic materials used in adhesive systems (phosphoric acid and acidic monomers).Ferrari and Tay found that their study suggested the degradation of the hybrid layer in areas of incomplete resin infiltration was responsible by host-derived matrix metalloproteinases within the dentin matrix.7

Pashley et al8 have described how MMPs are bound to the collagen matrix in a mineralized state where they are covered with extrafibrillar and intrafibrillar apatite crystallites. While the MMPs remain in this mineralized state they are inactive. Self-etching adhesives remove most of the extrafibrillar and some of the intrafibrillar crystals and allow space for the infiltration of the bonding agent. When a total-etch system is employed, the 32% to 37% phosphoric acid removes all of the extrafibrillar and intrafibrillar crystals. The increase in crystal removal exposes more of the collagen, resulting in an increase of MMP activation.

Pashley et al9 found that acid-etch dentin matrices did not degrade in vitro when incubated in an aqueous solution containing 0.2% chlorhexidine (CHX). They found, however, that over time the progression of degradation without the presence of CHX did indeed occur. Presently, some dental school clinics have incorporated an adhesive bonding protocol that includes the use of CHX. After etching with 37% phosphoric acid for 15 seconds, the exposed dentin is rinsed and dried. Then 2% CHX is applied for 1 minute and dried, followed by the application of the resin.

It is not clear how long and how well the CHX remains in place. The mechanism in which CHX binds to demineralized dentin is thought to be through electrostatic means.10 Since there is no covalent bonding, it is likely that the CHX leaches from the hybrid layer over a period of 1 to 2 years, leaving the collagen to degrade.8 Sadek et al11 found adhesive bonding pretreated with CHX was only preserved between 9 to 18 months and challenged the use of electostatically bound CHX as a strategy to counter collagen degradation. The degradation of the adhesive bonding is only postponed for a short period of time. Eventually, the collagen fibrils are attacked by the host-derived proteinases, and separation or debonding occurs between the composite and the tooth substrate.

MMP Inhibition

Studies have confirmed the inhibitory effects of several other MMP inhibitors such as galardin (synthetic MMP-inhibitor),12 green tea polyphenols (especially epigallocatechin-3-gallate),13 and doxycyclines.14 There is another group of MMP inhibitors that are antimicrobial agents called quaternary ammonium compounds. These include benzalkonium chloride, METMAC (methacryloyloxy-ethyltrimethyl ammonium choride), MAPTAC ([3-(methacryloylamino)propl]-trimethylammonium chloride), and MDPB (12-methacryloyloxydodecalpyridium bromide).

Imazato et al15 published the results of their synthesis of a new monomer (MDPB) in 1994, which was a combination of an antibacterial agent and a methacryloyl group. The new monomer was created by replacing the terminal phosphate group of 10-methacryloyloxydecamethylene phosphoric acid self-etching monomer (10-MDP) (Kuraray, www.kuraraydental.com) with an antibacterial pyridinium group. They found S. mutans growth was inhibited compared to the control group, and there were no adverse effects on the mechanical properties of the composite. The MDPB monomer has been placed into a self-etching primer adhesive called Clearfil™ Protect (Kuraray) (a newer version is Clearfil™ SE Protect) that has shown to have bactericidal activity while in the liquid state, similar to conventional antimicrobials.16 It then forms an antibacterial copolymer after light-polymerization that is able to kill bacteria on contact.8 Imazato described this restorative material as having a “bio-active function” in that it has a therapeutic effect on the control of caries. This is a new direction in the development of restorative materials that could control secondary caries formation.16

Biofunctional Properties

The destructive cycle of dental caries is characterized by the demineralization of the dentin matrix by an acid produced by bacteria. As the acid lowers the pH (under 5.5), host-derived MMPs are uncovered and become active, which breaks down the exposed collagen exacerbating the carious lesion. The actual progression of dental caries comes from the activation of the enzymes capable of degrading the collagen matrix.17

If a restorative material had a therapeutic effect on the control of residual bacterial growth in caries-infected dentin and at the same time could inhibit the degradation effects of MMP activity and remain in the hybrid layer for many years, it would help to inhibit secondary caries and increase the durability of resin-bonded composite restorations. That restorative material could then be considered as having a biofunctional property.

Conclusion

A greater understanding in the role that host-derived matrix metalloproteinases play in the progression of dental caries and the preservation of resin-bonded restorations has motivated a change in the direction in the manufacturing of restorative materials. Not only can restorations restore the destructive effects of carious lesions but can now actually turn off the mechanisms that cause early replacement (secondary caries) of these restorations.

References

1. Breschi L, Mazzoni A, Ruggeri A, et al. Dental adhesion review: aging and stability of the bonded interface. Dent Mater. 2008;24(1):90-101.

2. Nakabayashi N, Kojima K, Masuhara E. The promotion of adhesion by the infiltration of monomers into tooth substrates. J Biomed Mater Res. 1982;16(3):265-273.

3. Tay FR, Pashley DH, Suh BI, et al. Buonocore Memorial Lecture. Water treeing in simplified dentin adhesives–déjà vu? Oper Dent. 2005;30(5):561-579.

4. Tay FR, Pashley DH. Water treeing–a potential mechanism for degradation of dentin adhesives. Am J Dent. 2003;16(1):6-12.

5. Sano H, Yoshiyama M, Ebisu S, et al. Comparative SEM and TEM observations of nanoleakage within the hybrid layer. Oper Dent. 1995;20(4):160-167.

6. Tjäderhane L, Larjava H, Sorsa T, et al. The activation and function of host matrix metalloproteinases in dentin matrix breakdown in carious lesions. J Dent Res. 1998;77(8):1622-1629.

7. Ferrari M, Tay FR. Technique sensitivity in bonding to vital, acid-etched dentin. Oper Dent. 2003;28(1):3-8.

8. Pashley DH, Tay FR, Imazato S. How to increase the durability of resin-dentin bonds. Compend Contin Educ Dent. 2011;32(7):60-66.

9. Pashley DH, Tay FR, Yiu C, et al. Collagen degradation by host-derived enzymes during aging. J Dent Res. 2004;83(3):216-221.

10. Kim J, Uchiyama T, Carriho M, et al. Chlorhexideine binding to mineralized versus demineralized dentin powder. Dent Mater. 2010;26(8):771-778.

11. Sadek FT, Braga RR, Muench A, et al. Ethanol wet-bonding challenges current anti-degradtion strategy. J Dent Res. 2010;89(12):1499-1504.

12. Breschi L, Martin P, Mazzoni A, et al. Use of a specific MMP-inhibitor (galardin) for preservation of hybrid layer. Dent Mater. 2010;26(6):571-578.

13. Kato MT, Leite AL, Hannas AR, Buzalaf MA. Gels containing MMP inhibitors prevent dental erosion in situ. J Dent Res. 2010;89(5):468-472.

14. Kadoglou NP, Liapis CD. Matrix metalloproteinases: Contribution to pathogenesis, diag: pharmacological inhibition of MMPs. Curr Med Res Opin. 2004;20(4). https://www.medscape.com/viewarticle/475262_11. Accessed January 27, 2012.

15. Imazato S, Torii M, Tsuchitani Y, et al. Incorporation of bacterial inhibitor into resin composite. J Dent Res. 1994;13(8):1437-1443.

16. Imazato S. Bio-active restorative materials with antibacterial effects: new dimension of innovation in restorative dentistry. Dent Mater J. 2009;28(1):11-19.

17. Tjäderhane L, Larjava H, Sorsa T, et al. The activation and function of host matrix metalloproteinases in dentin matrix breakdown in caries lesions. J Dent Res. 1998;77(8):1622-1629.

About the Author

Gregg A. Helvey, DDS,
Adjunct Associate Professor
Virginia Commonwealth University School of Dentistry
Richmond, Virginia

Private Practice
Middleburg, Virginia

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