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      Effects of a mouthwash with chlorine dioxide on oral malodor and salivary bacteria: a randomized placebo-controlled 7-day trial

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          Abstract

          Background

          Previous research has shown the oxidizing properties and microbiological efficacies of chlorine dioxide (ClO 2). Its clinical efficacies on oral malodor have been evaluated and reported only in short duration trials, moreover, no clinical studies have investigated its microbiological efficacies on periodontal and malodorous bacteria. Thus, the aim of this study was to assess the inhibitory effects of a mouthwash containing ClO 2 used for 7 days on morning oral malodor and on salivary periodontal and malodorous bacteria.

          Methods/Design

          A randomized, double blind, crossover, placebo-controlled trial was conducted among 15 healthy male volunteers, who were divided into 2 groups. Subjects were instructed to rinse with the experimental mouthwash containing ClO 2 or the placebo mouthwash, without ClO 2, twice per day for 7 days. After a one week washout period, each group then used the opposite mouthwash for 7 days. At baseline and after 7 days, oral malodor was evaluated with Organoleptic measurement (OM), and analyzed the concentrations of hydrogen sulfide (H 2S), methyl mercaptan (CH 3SH) and dimethyl sulfide ((CH 3) 2S), the main VSCs of human oral malodor, were assessed by gas chromatography (GC). Clinical outcome variables included plaque and gingival indices, and tongue coating index. The samples of saliva were microbiologically investigated. Quantitative and qualitative analyses were performed using the polymerase chain reaction-Invader method.

          Results and Discussion

          The baseline oral condition in healthy subjects in the 2 groups did not differ significantly. After rinsing with the mouthwash containing ClO 2 for 7 days, morning bad breath decreased as measured by the OM and reduced the concentrations of H 2S, CH 3SH and (CH 3) 2S measured by GC, were found. Moreover ClO 2 mouthwash used over a 7-day period appeared effective in reducing plaque, tongue coating accumulation and the counts of Fusobacterium nucleatum in saliva. Future research is needed to examine long-term effects, as well as effects on periodontal diseases and plaque accumulation in a well-defined sample of halitosis patients and broader population samples.

          Trial registration

          ClinicalTrials.gov NCT00748943

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          Most cited references51

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          PERIODONTAL DISEASE IN PREGNANCY. II. CORRELATION BETWEEN ORAL HYGIENE AND PERIODONTAL CONDTION.

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            Polymerase chain reaction detection of 8 putative periodontal pathogens in subgingival plaque of gingivitis and advanced periodontitis lesions.

            A 16S rRNA-based polymerase chain reaction (PCR) detection method was used to determine the prevalence of Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Eikenella corrodens, Porphyromonas gingivalis, Prevotella intermedia. Prevotella nigrescens and Treponema denticola in subgingival specimens of 50 advanced periodontitis, 50 adult gingivitis and 50 pediatric gingivitis subjects. The optimal PCR conditions were determined for each study species. Agarose gel electrophoresis of PCR products from each study species revealed a single band of the predicted size. Restriction enzyme digestion of amplicons confirmed the specificity of the amplification. PCR detection limits were in the range of 25-100 cells. No cross-reactivity with other oral micro-organisms or nonspecific amplification was observed. The prevalence by PCR in advanced periodontitis, adult gingivitis and pediatric gingivitis subjects was 30%, 14% and 14% for A. actinomycetemcomitans, 86%, 18% and 8% for B. forsythus, 74%, 52% and 78% for C. rectus, 80%, 70% and 66% for E. corrodens, 70%, 10% and 14% for P. gingivalis, 58%, 12% and 18% for P. intermedia, 52%, 20% and 22% for P. nigrescens, and 54%, 16% and 16% for T. denticola, respectively. The prevalence was higher in the advanced periodontitis group than in both adult gingivitis and pediatric gingivitis for A. actinomycetemcomitans, B. forsythus, P. gingivalis, P. intermedia, P. nigrescens and T. denticola at P < 0.01, and for E. corrodens at P < 0.05. The prevalence of C. rectus was significantly higher in the advanced periodontitis group than in the adult gingivitis group at P < 0.01. Matching results between PCR and culture occurred in 28% (B. forsythus) to 71% (A. actinomycetemcomitans) of the samples; the major discrepancy occurred in the PCR-positive/culture-negative category. Matching results between PCR and DNA probe methods were found in 84% of the subjects (B. forsythus) and 70% (P. gingivalis). Odds ratio analysis revealed statistically significant positive associations between 17 of the 28 possible combinations (P < 0.01). This study demonstrated the utility of a 16S rRNA-based PCR detection method for identifying important subgingival microorganisms. The results indicated a strong association between the study species and periodontitis. Several previously unreported symbiotic relationships were found between the 8 species tested.
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              Production and origin of oral malodor: a review of mechanisms and methods of analysis.

              Organoleptic studies indicate that the oral cavity is usually the principal source of physiologic malodor associated with the early morning halitosis. In all individuals, regardless of the age or health status of the oral tissues, the most intense oral malodor is exhibited after prolonged periods of reduced saliva flow and abstinence from food and liquid. This results from normal metabolic activity in the oral cavity and is accentuated in cases with periodontal involvement. Physiologic oral malodor is transient in duration as it can be controlled to varying degrees in most individuals by oral hygiene measures, such as tooth brushing, dental prophylaxis, tongue scraping and rinsing with antiseptic mouth washes. Experimental evidence strongly suggests that putrefaction of sulphur-containing proteinaceous substrates by predominantly gram-negative oral microorganisms is the primary cause of oral malodor. Optimum putrefactive activity occurs in low carbohydrate environment, physiological pH, and anaerobic conditions. Salivary sediment containing the exfoliated epithelial cells is the primary source of substrate which exists in a disulphide state. Proteolysis and reduction of disulphide bonds precedes the formation of odor. The odor intensity of putrescent saliva and plaque head-space vapor has been correlated with the concentration of volatile sulphur compounds consisting of hydrogen sulphide, methyl mercaptan, dimethyl sulphide and dimethyl disulphide. Except for dimethyl disulphide, the same sulphur-containing compounds have been found in mouth air of all tested individuals. Hydrogen sulphide and methyl mercaptan emanate an offensive putrid odor and account for approxiamtely 90% of the total sulphur content of mouth air. In half of the population tested, methyl mercaptan and hydrogen sulphide content of early morning mouth air is sufficiently high to account for the oral malodor. Brushing studies indicate that both plaque and tongue are important sources of malodor with most of the odor emanating from the dorso-posterior surface of the tongue. None of the gas chromatographic or mass spectrometric analyses have detected the presence of amines, indole, or skatole in the head-space, mouth air, or breath vapor samples.
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                Author and article information

                Journal
                Trials
                Trials
                BioMed Central
                1745-6215
                2010
                12 February 2010
                : 11
                : 14
                Affiliations
                [1 ]Department of Oral Health Promotion, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan
                [2 ]Centre for Oral Health Strategy, NSW, Australia
                Article
                1745-6215-11-14
                10.1186/1745-6215-11-14
                2831889
                20152022
                0b29f34c-2d09-4f84-ab18-678f6f0a4717
                Copyright ©2010 Shinada et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 October 2009
                : 12 February 2010
                Categories
                Research

                Medicine
                Medicine

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