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    Inside Dentistry

    December 2012, Volume 8, Issue 12
    Published by AEGIS Communications


    The Durability of theResin/Dentin Complex

    Resin-bond restorations are likely to last longer when materials that retard the progression of decay are used.

    By Gregg A. Helvey, DDS

    Currently, there are two basic adhesive system strategies. One system (etch and rinse) removes the smear layer with phosphoric acid, while the other system (self-etch) incorporates the smear layer as a substrate for adhesion. The main difference between the two 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 and then “dried away.”

    Both systems create a hybrid layer, which is formed as a result of resins impregnating the porous enamel–dentin substrate. The longevity of the hybrid layer is dependent on several factors.1 Physical factors include occlusal chewing forces and thermal cycling that result in the constant development of expansion and contraction stresses.1,2 Chemical factors include acids from foods, beverages, and bacterial by-products.3,4

    Resin Degradation

    Esters of methacrylic acid and other derivatives are used to make most adhesive monomers into more hydrophilic monomethacrylates or more hydrophobic dimethacrylates.5 One of the main factors that contributes to the breakdown of the hybrid layer is the addition of water to ester bonds, which results in the loss of resin mass through a chemical process called hydrolysis.3 Because hydrolytic degradation occurs only in the presence of water, there is a correlation between the hydrophilicity of a resin and water absorption, regardless of the adhesive system used.6,7 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.8,9 In their study, Cadenaro et al found a correlation between the extent of polymerization and the permeability of dental adhesives regardless of the adhesive system used.9 An inverse correlation between polymerization and permeability was found to be evident in simplified adhesives.

    Collagen Fibril Degradation

    The goal that manufacturers strive for 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.10,11

    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. Wang and Spencer described gradually decreasing gradients of incomplete zones of resin infiltration at the bottom of the hybrid layer associated with total-etch adhesives.12 In separate studies, Armstrong13 and Hashimoto14 also had similar findings of denuded collagen fibrils in the lower portions of the hybrid layers, indicating a lack of complete resin infusion after acid-etching.

    Incomplete resin infiltration was also observed in self-etching adhesives in the form of nanoleakage within the hybrid layer despite simultaneous adhesive etching and priming.15 Incomplete removal of water associated with the hydrophilic monomers may be responsible for the lack of total infiltration.16

    No matter what adhesive system is employed, there are collagen fibrils left unprotected and, therefore, subject to hydrolytic degradation and other degradation processes.17 Studies have shown that host-derived proteinases also contribute to the breakdown of collagen matrices.18-20

    Matrix Metalloproteinases (MMPs)

    Matrix metalloproteinases (MMPs) are a family of zinc-dependent, structurally and functionally 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.21 MMPs also play a role in the pathogenesis of dentinal caries and periodontal disease.18-20 While trapped within the dentin matrix during tooth development, MMPs can become activated 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 (such as phosphoric acid and acidic monomers).16 Ferrari and Tay concluded that their study suggested that the degradation of the hybrid layer in areas of incomplete resin infiltration was responsible for host-derived matrix metalloproteinases within the dentin matrix.22

    Pashley et al23 have described how the 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 is24 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.

    Gendron et al25 evaluated the inhibitory effect of chlorhexidine on MMP-2 (gelatinase A), MMP-9 (gelatinase B), and MMP-8 (collagenase 2) activity. Their study suggested that there was a direct inhibition of the MMP activity by chlorhexidine—even at low concentrations—while still preserving the integrity of the hybrid layer.5 Pashley et al26 found that acid-etched dentin matrices did not degrade in vitro when incubated in an aqueous solution containing 0.2% chlorhexidine. They did find that, over time, the degradation progress without the presence of chlorhexidine did indeed occur. Presently, some dental-school clinics have incorporated an adhesive bonding protocol that includes the use of chlorhexidine. After etching with 37% phosphoric acid for 15 seconds, the exposed dentin is rinsed and dried; 2% chlorhexidine is then applied for 1 minute and dried, followed by the application of the resin.27

    It is not clear how long and how well the chlorhexidine remains in place. The mechanism by which chlorhexidine binds to demineralized dentin is thought to be through electrostatic means.28 Because there is no covalent bonding, it is likely that the chlorhexidine leaches from the hybrid layer over a period of 1 to 2 years, leaving the collagen to degrade.23 Sadek et al29 found adhesive bonding pre-treated with chlorhexidine was only preserved for between 9 and 18 months and challenged the use of electostatically bound chlorhexidine 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),30 green tea polyphenols (especially epigallocatechin-3-gallate),31 and doxycyclines.32 Another group of MMP-inhibitors are antimicrobial agents called quaternary ammonium compounds. These include benzalkonium chloride, METMAC (methacryloyloxy-ethyl trimethylammonium chloride, MAPTAC ([3-(methacryloylamino)propl]-trimethylammonium chloride), and MDPB (12-methacryloyloxydodecalpyridium bromide).23

    In 1994, Imazato et al33 published the results of their synthesis of a new monomer (MDPB), 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) from Kuraray Medical, Inc. (www.kuraraymedical.com), with an antibacterial pyridinium group. They found Streptococcus 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 was incorporated into a self-etching primer adhesive called Clearfil™ Protect Bond, which, while in the liquid state, was shown to have bactericidal activity, similar to conventional antimicrobials.34 (Note: An updated version of that product is called Clearfil™ SE Protect Bond.) After being light-polymerized, the product forms an antibacterial copolymer that is able to kill bacteria on contact.23 Imazato described this restorative material as having a “bioactive 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.34

    Biofunctional Restorative Material and MMP Inhibition

    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, thus exacerbating the carious lesion. The actual progression of dental caries comes from the activation of the enzymes capable of degrading the collagen matrix.35

    Conclusion

    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.

    References

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    2. DeMunck J, Van Meerbeek F, Van Landuyt K, Lambrechts P. Influence of a shock absorbing layer on the fatigue resistance of a dentin-biomaterial interface. Eur J Oral Sci. 2005;113:1-6.

    3. Tay FR, Pashley DH. Have dentin adhesives become too hydrophilic? J Can Dent Assoc. 2003;69(11):726-731.

    4. Hashimoto M, Ohno H, Kaga M, et al. In vivo degradation of resin-dentin bonds in humans over 1 to 3 years. J Dent Res. 2000;79(6):1385-1391.

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

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    18. 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.

    19. Sulkala M, Larmas M, Sorsa T, et al. The localization of matrix metalloproteinase-20 (MMP-20, enamelysin) in mature human teeth. J Dent Res. 2002;81(9):603-607.

    20. van Strijp AJ, Jansen DC, DeGroot J, et al. Host-derived proteinases and degradation of dentine collagen in situ. Caries Res. 2003;37(1):58-65.

    21. Köhrmann A, Kammerer U, Kapp M, et al. Expression of matrix metalloproteinases (MMPs) in primary human breast cancer and breast cancer cell lines: New findings and review of the literature. BMC Cancer. 2009;9:188. 

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

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

    30. 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.

    31. 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.

    32. Kadoglou NP, Liapis CD. Matrix metalloproteinases: contribution to pathogenesis, diagnosis, surveillance and treatment of abdominal aortic aneurysms. Curr Med Res Opin. 2004;20(4):419-432.

    33. Imazato S, Torii M, Tsuchitani Y, et al. Incorporation of bacterial inhibitor into resin composite. J Dent Res. 1994;73(8):1437-1443.

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

    35. 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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