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Chlorhexidine has been used for the past 35 years in the treatment of the two primary diseases of dentistry with varying degrees of success. The purpose of this paper is to review the literature for both the caries reduction potential and the microbiologic reduction of the pathogens associated with dental caries. The literature remains mixed on the success of chlorhexidine for the reduction in dental caries. Its performance as an antimicrobial against Streptococcus mutans is more consistent and favorable.
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Chlorhexidine has been used to address the two primary diseases of dentistry since the mid-1970s. This paper examines the uses of chlorhexidine from several perspectives and is limited to chlorhexidine’s interaction with dental caries.
Because of the vast literature regarding chlorhexidine’s antimicrobial effects against many different microbial forms, this paper is limited to a review of the past 10 years of reviewed literature associated with "human," "clinical trials" and "dental caries." A search of PubMed on these parameters found 38 articles meeting the search criteria that have been published since 1966. Of these, 26 articles were judged to be relevant to this paper. This review is based on these 26 articles. The majority of these articles examine the efficacy of chlorhexidine for its antimicrobial effects or its ability to reduce dental caries.
Antimicrobial Effects
Eleven papers were reviewed with regard to antimicrobial effects.1-11 The purpose of limiting the review to "human clinical trials" was to avoid the limitations inherent in laboratory research on planktonic cells and chlorhexidine’s effects on dental caries infections that are arguably biofilm-mediated infections. Planktonic cells behave and have different characteristics than biofilm, especially with regard to resistance to antimicrobial compounds.
There was a variety of formulations, ages, and specific end-points tested. Chlorhexidine concentrations range from a high of 40 percent to a low of 0.12 percent. The delivery vehicles tested were gels, gum, varnishes and rinses. Ages tested ranged from infants to elders. The bacterial outcomes tested were vertical transmission of S. mutans, antimicrobial effects on pits and fissures, effects on the microbial population adjacent to orthodontic brackets, interproximal and root flora, and sampling for the development of chlorhexidine-resistant organisms.
Figure 1 graphically sorts the human clinical trial data on the microbial effects of chlorhexidine. In most cases, the outcomes are expressed as being an "effective" or "not effective." Where a study reported other results, these are captured according to the authors’ conclusions. For the majority of these antimicrobial studies, chlorhexidine was found to be effective in controlling or reducing the microbial challenge associated with dental caries. In general, this was an assessment of the impact on S. mutans. There is great difficulty in generalizing these studies. The protocols vary widely. While this limits the continuity of these data, it does provide a reasoned perspective of chlorhexidine’s effectiveness in controlling S. mutans through a variety of clinical applications.
Effects on Dental Caries
The data from the antimicrobial effects are generally offered as a surrogate for the effect on dental caries given the infectious nature of the disease. This section reviews the actual effect on the incidence of dental caries in tested populations. The same wide variation in testing methodologies exists in these reviewed papers as was found in the antimicrobial literature. Ten human clinical trials articles were reviewed for this section.12-21
The reviewed literature showed that chlorhexidine is effective in reducing the incidence of dental caries in the populations tested (Figure 2).
To the credit of the investigators involved, testing and analysis in recent trials have become more narrowly focused on the "at risk" surfaces in the populations being examined. In children, the primary surfaces at risk are the occlusal. In elders, the "at risk" areas are root surfaces and surfaces around existing restorations.
As a general conclusion, chlorhexidine has been shown to be effective in reducing both the number of putative dental caries pathogens and, to a lesser degree, the incidence of dental caries in the tested populations.
Meta-Analysis
Three papers have been published that use a meta-analysis approach to examining the efficacy of chlorhexidine.22-24
VanRijkom22 found the overall caries-inhibiting effect of the chlorhexidine treatment studies to be 46 percent (95 percent CI = 35 percent to 57 percent). Multiple-regression analysis showed no significant influence on the prevented fractions for the variables "application method," "application frequency," "caries risk," "fluoride regime," "caries diagnosis," or "tooth surface."
Using different selection criteria, Bader and colleagues23 found that among the 22 studies addressing the prevention of carious lesions in caries-active or high-risk individuals, the strength of the evidence was judged to be fair for fluoride varnishes and insufficient for all other methods, including chlorhexidine.
Based on his review of the published data, Kanellis24 recommends the use of chlorhexidine in Women, Infants and Children; Early Head Start; and Head Start programs as part of a more comprehensive caries control program.
The mixed results are primarily based on the selection and inclusion/exclusion criteria used by the individual authors.
Tooth Survival
A useful clinical trial was conducted with the outcome of intervention, based on tooth mortality in elders.25 Studies like this one aim at a different end point than caries, as is appropriate for the population being tested. These data are useful in planning for health care benefits and can be expanded to demonstrate the costs associated with replacement of missing teeth or the consequences to overall health incurred when there is a decision not to restore these surfaces.
General Economic Comments
The literature related to chlorhexidine is limited with regard to the economic effects of its application. The clinical trials on dental caries do not generally report the number needed to treat or other data that would be useful in policy decision-making for payers or public health programs. These are becoming increasingly important as consumerism reaches the health care markets. Purchasers and individual consumers are beginning to demand data on why specific procedures are recommended or not recommended in specific situations. In the future, it will be important for researchers to engage health care economists in the original planning or clinical trials to assist in gathering appropriate data about the economic dimensions of specific diagnostics, preventives, and therapeutics.
Conclusion
In general, chlorhexidine appears to be moderately effective in reducing the number of putative caries pathogens in specific populations when applied under the regimen tested. Chlorhexidine is also useful in reducing the consequences of these infections in that it appears to generally reduce the incidence of dental caries in the tested populations. In a majority of cases, the materials tested are not available in the United States, and the extrapolation of the positive results cannot be made to the currently available rinses. Little data are presented to justify the cost of using chlorhexidine in specific populations.
In the United States, chlorhexidine may be useful in selected caries control programs. Current U.S. products are limited to a formula of 0.12 percent chlorhexidine gluconate. This is suitable for high-risk, highly compliant adult patients who do not exhibit either sensitivity to chlorhexidine or the ethyl alcohol vehicle in which it is usually contained. It is not generally recommended for children because of the diminished likelihood of compliance due to the taste acuity exhibited by children.
The suggested protocol for these selected patients is rinsing for 30 seconds just before bed for one week, repeating the regimen every three months. This protocol limits the amount of extrinsic staining and calculus deposition while systematically suppressing the S. mutans infection.
References
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To request a printed copy of this article, please contact: Maxwell H. Anderson, DDS, MS, MEd, Washington Dental Service, 9706 Fourth Ave., NE, Seattle, WA 98115 or manderson@ddpwa.com.
