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RESEARCH REPORT |
1 Department of Restorative Dentistry and Endodontology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka 565-0871, Japan; and
2 Department of Restorative Dentistry, Dental School, University of Newcastle upon Tyne, Newcastle upon Tyne, UK;
* corresponding author, imazato{at}dent.osaka-u.ac.jp
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: root-surface caries • demineralization • adhesive system • antibacterial effects • artificial caries
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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An antibacterial monomer, 12-methacryloyloxydodecylpyridinium bromide (MDPB), is a polymerizable biocide and has strong bactericidal activity against oral bacteria (Imazato et al., 1994). Additionally, the antibacterial agent is immobilized in the polymer network by polymerization of MDPB, and the cured resin containing MDPB exhibits an inhibition of bacterial growth (Imazato et al., 1998a). Therefore, a dentin bonding system incorporating MDPB can show antibacterial effects before and after the curing process (Imazato et al., 1997, 1998b, 2003), so that it has the potential to exert a benefit in caries management if absorbed into demineralized dentin or when present on the tooth surface. Previously, we have reported that the MDPB-containing primer was capable of penetrating artificial demineralized lesions and of killing bacteria in dentin (Imazato et al., 2002). In this study, using an in vitro caries model, we examined the hypothesis that progression of root-surface caries can be inhibited by the application of an MDPB-containing adhesive system.
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MATERIALS & METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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Effects on Progression of Demineralized Lesion by Acid-Gel
The study was performed under a protocol approved by the ethics committee of Osaka University Graduate School of Dentistry. Extracted human premolars were obtained from patients with their informed consent, and organic debris was removed from the root surfaces. The teeth were sectioned at the cement-enamel junction, and the apex and aperture of the root were sealed with glass-ionomer cement (Fuji II LC, GC, Tokyo, Japan). The entire root surface was coated with nail varnish, apart from buccal and lingual windows 4 mm in diameter. Each tooth was immersed in 100 mL of sodium carboxymethylcellulose gel made up with lactic acid buffer at pH 4.0 for 2 wks at 37°C to produce demineralized lesions. The surface of the lesion was washed with sterile water, blot-dried, and then treated with each adhesive system as previously reported (Imazato et al., 2002). Application of LB primer or the experimental primer was performed for 30 sec. For PB and SB, the adhesive agent was directly applied without usage of etchant or primer. Buccal and lingual lesions on one root were allocated to different treatment groups.
Each specimen was again immersed in acid-gel and stored for 2 wks at 37°C. After being embedded in epoxy resin, the roots were sectioned longitudinally through the center of the demineralized area and abraded to give a specimen 100 µm thick. A contact microradiograph was recorded with a soft x-ray source (Softex CMR, Softex Co., Tokyo, Japan) at 15 kV and 3 mA, and viewed under a stereomicroscope. The depth of lesion, defined as the distance from the root surface to the base of the demineralized area, was measured with the use of image-analyzing software (WinROOF, MITANI, Fukui, Japan). Since the lesion surface was concave, due to demineralization and shrinkage during specimen preparation, a line was drawn between the sound tissue surfaces on either side of the lesion on the digital image to act as a baseline for depth measurement. The measurement was performed at 5 points in the area of the demineralization front for each specimen. The specimen to which no adhesive was applied after 2 wks of demineralization, and the specimen demineralized for 4 wks totally without application of adhesive, served as two- and four-week controls, respectively. Five samples were tested for each group. One further specimen treated with each system and demineralized for 4 wks was cut perpendicularly and observed by means of a scanning electron microscope.
Effects on Progression of Caries Lesions by Streptococcus mutans
For the bacterial demineralization test, the root specimen with the window was immersed in 40 mL of Brain Heart Infusion (BHI, Becton Dickinson, NJ, USA) broth containing 1% sucrose. A 30-µL quantity of Streptococcus mutans NCTC10449 suspension, cultured overnight in BHI broth supplemented with 0.5% yeast extract (Becton Dickinson), was added to the broth. The specimens were incubated at 37°C for 2 wks, the medium being changed every 3 to 4 days. Each adhesive was applied as in the acid-gel method, and the specimens were incubated in bacterial suspension for a further 2 wks at 37°C. The pH values of the culture after incubation were confirmed to be 4.0–5.0 at every replacement. After the specimens had been incubated for 4 wks, contact microradiographs were recorded, and the depth of the demineralized area was measured. Nine specimens were tested for each group.
The data were analyzed by ANOVA and Fisher’s PLSD test at a significance level of 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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, Fig. 1).
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, 2B). In contrast, a 30-µm-thick layer of adhesive resin could be clearly observed on the lesion treated with LB2 and the experimental system (Figs. 2C, 2D).
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, Fig. 3). However, lesion depths for PB, SB, and LB2 were significantly greater than that for the two-week control, and no significant difference was obtained between the experimental system and the two-week control.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS & METHODSRESULTSDISCUSSIONREFERENCES |
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The application of LB2 or the experimental system resulted in complete inhibition of the progression of demineralization in the acid-gel technique, while no inhibitory effects were observed with PB and SB. The lesion surface was covered with a thick layer of resin when LB2 and the experimental system were applied (Figs. 2C, 2D). This suggests that the combination of LB primer and LB bond, the resin components used in LB2 and the experimental system, was effective in penetrating the lesion and sealing its surface to prevent further demineralization. In contrast, PB and SB did not produce a substantive physical barrier against demineralization. In the present study, etchant was not used prior to the application of PB and SB, as in our previous report, we evaluated penetration of the adhesives into demineralized root dentin (Imazato et al., 2002). The rationale for this protocol is that the lesion produced has already been deeply demineralized, so that additional etching for short periods by the etchant would have a marginal effect on impregnation of the adhesives. In fact, deep penetration of PB and SB without the use of the etchant has previously been shown (Imazato et al., 2002), and formation of a cured layer of PB and SB on the lesion surface was confirmed by scanning electron microscopy (data not shown). We consider that such a method for arresting active caries lesions is beneficial for the management of root-surface caries, especially for institutionalized, disabled, or frail patients. LB bond is more viscous than PB or SB, and forms a thicker layer after being cured. In addition, a bonding system which uses the same catalyst as used for LB bond has been reported to show greater curing ability than SB (Miyazaki et al., 2003). It is assumed that the thin resin layer produced by PB and SB peeled away from the lesion surface during the second period of demineralization, allowing the acid to invade the lesion.
The model that used an S. mutans culture is considered to be a milder acidic challenge, since a gradual decrease in pH occurs after the broth is changed (Bradshaw and Marsh, 1998). Within this model, all of the adhesives were able to inhibit the progression of demineralization. However, the effects of PB and SB were relatively minor, and complete inhibition of demineralization was observed only with the MDPB-containing system. The limited protection offered by PB and SB could be due either to some early protection of the lesion until the resin film was disrupted, or to their limited antimicrobial action as a consequence of their low pH. Application of LB2 demonstrated greater inhibition compared with these two products. The main component of inhibition by LB2 is likely to be its ability to seal the lesion, as shown in the acid-gel model, to prevent the ingress of acid and nutrients for any bacteria in the lesion. Nevertheless, a 50-µm advance in lesion depth was observed after LB2 application. This is likely to be due to acid production by the bacteria, which had already impregnated the lesion before it was sealed by the bonding resin. In addition, it is possible that curing of the bonding resin was hampered by organic material within the body of the demineralized lesion, and that complete seal, as in the acid-gel model, may not have been established.
Lesions managed with the MDPB-containing primer did not differ, in depth, from those in the two-week controls. We have demonstrated previously that the MDPB-containing primer was capable of deeply penetrating demineralized dentin and showed a strong bactericidal effect in that situation (Imazato et al., 2002). The results we have reported above are indicative of the ability of this resin to inactivate bacteria in the lesion, preventing further advancement of demineralization. This effect was greater than that of all of the other resins, since this experimental system is both low in pH and contains an effective antimicrobial agent. The low pH of the resin alone would not account for this complete inhibition of further demineralization (Imazato, 2003).
An antimicrobial varnish containing chlorhexidine has been reported to be effective in reducing root caries activity (Wicht et al., 2003). However, such varnishes can penetrate demineralized root dentin only up to 40% of the total lesion depth, due to their hydrophobic nature (Arends et al., 1997). The MDPB-containing primer can penetrate more than 140 µm into demineralized root lesion (Imazato et al., 2002), and its penetration ability can be calculated to be more than 70%, based on the results in the present study. Therefore, application of the experimental system, which uses the antibacterial MDPB-containing primer and the adhesive resin for sealing the lesion, is advantageous over other management options.
Although the bacterial species associated with the initiation and progression of root caries are not fully understood, it is well-known that actinomyces or lactobacilli, as well as S. mutans, are frequently isolated from root caries lesions (Bowden, 1990; Ozaki et al., 1994; Schüpbach et al., 1996; Brailsford et al., 2001). MDPB-containing primers show antibacterial activity against various bacteria, including these 3 species, and obligate anaerobes (Imazato et al., 1997, 2001), and they are expected to be effective when applied to natural lesions. However, bacteria in the natural caries lesion may be more resistant to biocides than in this in vitro study, since it is possible that they are covered by metabolic products (such as extracellular matrix) that may interfere with the method of action of the antimicrobial agent. Therefore, further research is needed to investigate the effects of the application of MDPB-containing antibacterial adhesive systems in inhibiting the progression of caries lesions in more clinically relevant situations.
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ACKNOWLEDGMENTS |
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Received July 6, 2003; Last revision September 23, 2004; Accepted October 13, 2004
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REFERENCES |
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