Retention and plaque-inhibiting effect in man of chlorhexidine after multiple mouth rinses and retention and release of chlorhexidine after toothbrushing with a chlorhexidine gel.
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OBJECTIVES: Chlorhexidine, the gold-standard mouthwash, has several disadvantages, like promotion of antimicrobial resistance. Herbal mouthwashes are emerging as alternatives to chlorhexidine. However, its impact on antimicrobial resistance remains unclear. The aim of the study was to compare the clinical efficacy and the expression of antimicrobial resistance genes of chlorhexidine with a novel herbal mouthwash. DESIGN: Sixty patients with generalised gingivitis were randomly assigned to two groups using block randomisation. After professional mechanical plaque removal patients were instructed to use either chlorhexidine or a novel herbal mouthwash (patented composition) for two weeks. Tetracycline resistance (tetM) and macrolide efflux (mefI) gene expression in subgingival plaque were analysed using real-time polymerase chain reaction. Intragroup comparisons were performed with a paired t-test and Wilcoxon signed-rank test for parametric and nonparametric data. Intergroup comparisons employed unpaired t-test, chi-square test, and Mann-Whitney test. RESULTS: A significant reduction in bleeding, plaque, pocket depth and and patient reported outcomes were noticed in both groups. But reduction in plaque was more significant in chlorhexidine group. tetM and mefI genes significantly upregulated in the chlorhexidine group, while it was downregulated with herbal mouthwash (fold change 1.79 ± 0.74 and 0.60 ± 0.43 for tetM, and 1.83 ± 0.87 and 0.51 ± 0.44 for mefI). However, patients' perception of taste, freshness, and overall satisfaction was better in the chlorhexidine group. CONCLUSIONS: The increased expression of antimicrobial resistance genes following chlorhexidine use warrants careful consideration. Herbal mouthwash is an effective, safer alternative with comparable clinical benefits and less impact on antimicrobial resistance.
The binding of some selected food dyes to hydroxyapatite with and without a coating of chlorhexidine was studied. The apatite had bound 0.6 mumol chlorhexidine per g dry weight. The bound chlorhexidine was in equilibrium with a free concentration of 115 microgram ml (128 micron). The dyes investigated were brilliant blue (FD&C Blue No. 1), indigo carmine (FD&C Blue No. 2), tartrazine (FD&C Yellow No. 5), sunset yellow (FD&C Yellow No. 6), amaranth (FD&C Red No. 2), and riboflavin. Riboflavin did not bind to either chlorhexidine-treated apatite or untreated apatite, whereas the other dyes showed a considerable affinity for chlorhexidine-treated apatite as compared with untreated apatite. Because the dyes with binding ability possess two or three acidic groups, and because riboflavin has none, it was suggested that the binding of the dyes is mediated by an interaction between the anionic groups of the dye molecules and the cationic groups of the chlorhexidine molecules. The results are discussed and related to the formation of the brownish discolorations seen on the teeth of patients using chlorhexidine mouthrinses. A mechanism to explain the development of tooth stains is proposed.
The intention of the present experiment was to study the effects of a possible interaction between fluoride and chlorhexidine when both agents were incorporated in the same vehicle. The amount of fluoride extractable from dentrifrices containing 0.1% NaF and the fluoride ion activity were not reduced by the addition of 2% chlorhexidine digluconate. Less than 50% of the added chlorhexidine was available when the dentifrices were dissolved in deionized water. This was not affected by the presence of fluoride. The in vitro antibacterial activity of the chlorhexidine-containing dentifrices was not reduced by the addition of fluoride. Approximately 40% of the chlorhexidine was retained in the human oral cavity after brushing for 1 min with both the chlorhexidine- and the chlorhexidine/fluoride-containing dentifrice. Thus the binding of chlorhexidine to vehicle ingredients when dissolved in water is probably too weak to affect the retention in the mouth.
The purpose of this investigation was to evaluate the effect of 0.2% chlorhexidine gluconate mouthrinse following gingivectomy on plague under the dressing and on healing. Twenty-eight patients with indications for gingivectomy were selected. Coe-Pak was used as surgical dressing. In addition to unsual home care, the patients rinsed twice daily with chlorhexidine or placebo for 21 d after surgery. The study followed a cross-over double-blind design. Gingival exudate was assessed and Pl I and G I were registered at 7, 14, and 21 d postsurgically. The study indicated that chlorhexidine did not influence the amount of plaque under the dressing, and it was uncertain whether chlorhexidine had any effect on the healing process when the surgical area was covered by Coe-Pak. However, (1) after the surgical dressing was removed, the chlorhexidine maintained plaque scores at the same low level as under the dressing, (2) healing was was promoted when chlorhexidine was used, and (3) the presence of a dressing in one side of the mouth did not prevent the patient from maintaining good oral hygiene.
The qualitative and semiquantitative changes in the aerobic microbial flora of normal skin with the prolonged use of a chlorhexidine scrub (6 months) were investigated. More samples in the chlorhexidine scrub group had gram-negative bacilli in their axilla (63 of 96, 66%) and groin (36 of 96, 38%) than the controls (32 of 66, 49%, for axilla and 7 of 66, 11%, for groin; P = 0.01). Klebsiella and Enterobacter were the predominant organisms in the control and chlorhexidine groups, respectively. The chlorhexidine scrub produced a reduction in the total aerobic counts in the axilla, groin, and between the toes and the fingers. Fewer samples from the chlorhexidine-treated areas revealed the presence of lipophilic diphtheroids than did the controls. Lipophilic diphteroids were also reduced quantitatively in the groin and axilla with chlorhexidine treatment. No consistent pattern for the other major groups of bacteria was noted between the treatments.
The clinical effects of an antibacterial substance with antifungal activity (chlorhexidine) and specific antimycotic (amphotericin B) in denture stomatitis were studied in 100 patients. Five 14-day regimens of chlorhexidine, amphotericin B or placebo lozenges combined with denture immersion in 0.2% chlorhexidine or water were tested. The efficiency of amphotericin B and chlorhexidine was comparable. This indicates that chlorhexidine has a considerable antifungal effect in the oral cavity and, further, that fungi are the responsible micro-organism in denture stomatitis rather than bacteria. Chlorhexidine frequently discloured the dentures. A high incidence of local and general predisposing factors to denture stomatitis, as well as of relapse 14 days after treatment, was observed.
Clinical and laboratory studies were carried out to compare the antibacterial properties of two antiseptic mouthwashes, namely 1% povidone iodine and 0.2% chlorhexidine gluconate. In a group of 10 subjects after a single rinse with povidone iodine, an immediate mean fall in total salivary aerobes and anaerobes occurred, followed by a return to normal levels by 1-hour postrinsing. With chlorhexidine gluconate a similar but greater reduction in salivary bacterial counts was observed, which was still present up to the 7-h postrinsing period. Saliva samples obtained from the subjects 2 min after rinsing with providone iodine produced little or no inhibition to the growth of a test organism in vitro, whereas following chlorhexidine gluconate, antibacterial activity was present in the saliva specimens up to the 3-h sampling time. Using culture media containing comparable levels of soluble protein to saliva, the minimum inhibitory concentrations of povidone iodine against several standard test organisms were much higher than those of chlorhexidine gluconate. The results suggest that povidone iodine, as a mouthwash, exerts only an immediate antibacterial effect and unlike chlorhexidine, is not retained at antibacterial levels within the oral cavity after expectoration. This lack of prolonged action of povidone iodine in the oral cavity would appear to be relevant to its reported lack of antiplaque activity.
The effect of daily toothbrushing with 0.5% chlorhexidine-containing gel for 12 months was evaluated in a double-blind study in 37 dental students. The active gel did not markedly influence plaque formation, gingival conditions, or caries as compared with placebo gel treatment. Salivary bacterial counts were performed on subgroups of six subjects using chlorhexidine gel and on six using placebo gel. No differences in the effect of treatment on the microorganisms studied in the two subgroups could be detected except for S. sanguis. The percentage of this species decrease in the placebo group and increased in the chlorhexidine group. The difference became significant after 2 weeks. A tendency to a greater reduction of S. mutans noted in the chlorhexidine group was most marked in individuals who had high initial counts of this species. The proportion of S. sanguis, which could grow on chlorhexidinei-containing mitis salivarius medium, increased and after 12 months of chlorhexidine treatment averaged 34% of cultivable S. sanguis compared with 0.002% prior to treatment. The number of less sensitive S. sanguis decreased in the 12 months following termination of treatment. There was no observed tendency for the selection or proliferation of other streptococci, gram-negative rods, yeasts, or staphylococci.
The purpose of the present study was to evaluate the effect of fluoride upon the stain-inducing capacity of chlorhexidine. Ninety-one children, 13 years of age, volunteered for the experiment. Three test dentifrices were used, containing 0.1% NaF, 0.1% NaF + 2% chlorhexidine, and 2% chlorhexidine respectively. The experiment was carried out as a double-blind test, and the degree of staining was recorded after 1 and 2 years. Four methods were used for stain scoring. The results after 1 year showed that chlorhexidine induced less stain when applied together with fluoride than when applied alone. After 2 years this difference disappeared, indicating that fluoride only retarded chlorhexidine-induced staining of teeth.
A gloved-hand wash method was used to compare the antimicrobial effect of chlorhexidine gluconate alcohol emollient hand wash (HIBISTAT) with that of 70% isopropyl alcohol on the normal flora of the hands (81 subjects) under conditions designed to mimic use by surgeons. Results of the immediate postwash effects on the bacterial counts for all 3 tests days showed that chlorhexidine significantly reduced the normal flora of the hands. When compared with the base line bacterial counts, there was 85, 96, and 98% reduction with chlorhexidine treatment and 84, 93, and 90% reduction with alcohol treatment on days 1,2, and 5, respectively. The difference between chlorhexidine and alcohol treatments was not statistically significant on days 1 and 2, but was significant on day 5 (P less than 0.01). For delayed postwash bacterial counts (for persistent antimicrobial effects), the overall log means were 4.9943 and 5.4684 for chlorhexidine and alcohol treatments, respectively. The difference between the two treatments was significant (P less than 0.01). After the chlorhexidien treatment, there was no significant growth of bacteria over a period of 6 h when compared with the base line bacterial counts.
The effectiveness of a 1% chlorhexidine-containing dental gel on dental plaque and gingival health was evaluated over a period of 6 months using a double-blind procedure. One hundred and seventeen mentally retarded subjects aged between 10-17 years resident in an institution were divided into two groups. One group was assigned daily brushing with the 1% chlorhexidine gel, the other group a placebo quinine sulfate-containing gel. No other form of oral hygiene was used during the experimental period. Assessment of dental plaque accumulation and gingivitis was made at 0, 1, 3, and 6 months. An assessment was also made 2 months after the gel was withdrawn from use and normal toothbrushing procedures resumed. No clinical or statistical advantage was noted in plaque or gingivitis scores in the group receiving chlorhexidine treatment during the 6-month period. This group showed a higher prevalence of tooth staining. It was concluded that periodontal severity and poor oral hygiene exceeded the plaque- and gingivitis-preventing potential of chlorhexidine.
The susceptibility to chlorhexidine of bacteria in aerobic, facultatively anaerobic and anaerobic isolates from clinical specimens of wounds, urine, saliva, and dental plaque was studied. Agar diffusion tests using 50 microng chlorhexidine discs and agar dilution tests were performed and the MIC values correlated with inhibition zone diameters. Anaerobic plaque strains were isolated and tested by the agar dilution method in an anaerobic glove box. Regression lines obtained for five agar media demonstrated a good correlation between zone diameters and MIC values. There was a broad range of susceptibility to chlorhexidine among both Gram-positive and Gram-negative strains. Low MIC values were noted for staphylococci, S. mutans, S. salivarius and E. coli, while strains of Proteus, Pseudomonas and Klebsiella were less susceptible. S. sanguis showed intermediate susceptibility with both low and high MIC values. Among the anaerobic isolates tested, the strains most susceptible to chlorhexidine were Propionibacterium and Selenomonas, While the least susceptible strains were Gram-negative cocci resembling Veillonella.
The effect of chlorhexidine on the proportions of Streptococcus mutans and Streptococcus sanguis in plaque was studied in hamsters fed a diet containing 28% sucrose. In animals given chlorhexidine in their drinking water for 10 d a decrease in the population of S. mutans and an increase of S. sanguis occurred in the plaque. Following the removal of chlorhexidine the population of S. mutans increased again in the presence of sucrose and the number of S. sanguis returned to initial values. When animals were given a sucrose-free diet the low proportion of S. mutans observed following the short-term chlorhexidine period persisted. These data indicate that there is an inverse relationship between the number of S. sanguis and S. mutans in plaque and that the sensitivity in vivo of S. mutans to chlorheximide can be used to suppress the population of S. mutans with a concomitant rise in the proportion of S. sanguis.
In order to evaluate the effect of chlorhexidine on the acidogenicity of dental plaque, pH changes in plaque were measured in situ after sucrose applications. The results showed that a 0.2% chlorhexidine mouthrinse inhibited acid production for a period of 24 h, whereas a 0.05% chlorhexidine rinse showed an inhibitory effect for 4 h. It is suggested that the mechanism involved may be related to the retention of chlorhexidine in the mouth and in plaque providing a bacteriostatic milieu which may be of importance in the observed long-term effect.
The inhibitory effect of chlorhexidine and other bis-biguanides on the formation of dental plaque is not fully understood. The present paper describes the effect of chlorhexidine and some selected detergents on the activity of dextransucrase (EC 2.4.1.5.), an enzyme involved in the formation of important components of dental plaque. All detergents examined exerted an inhibitory effect on dextransucrase activity, to some degree dependent on the presence of charged groups and their characters. The high concentrations of chlorhexidine necessary to inhibit dextransucrase activity seem to exclude the possibility that chlorhexidine exerts its plaque inhibiting effect by means of an effect on dextransucrase.
It was the purpose of the study to test the efficacy of brushing with a 1% chlorhexidine gel or a commercial solution cleanser (Steradent) in preventing formation of plaque on the fitting surface of new dentures. The study group consisted of 74 denture wearers with denture stomatitis who were assigned randomly to one of four treatment groups, testing either the chlorhexidine gel, a placebo gel, Steradent, or a placebo solution. The experiment was started immediately after denture treatment was completed. The experimental period was 1 month. The amount of denture plaque, the clinical condition of the palatal mucosa, and the concentration of yeasts in mucosal and denture smears were recorded while the patients used their original dentures and after the experimental period. Plaque had formed on all new dentures but to a smaller extent in the groups testing the chlorhexidine gel or the placebo gel. The study does not provide any obvious evidence of a chemical effect of chlorhexidine gel or Steradent as a means to prevent formation of microbial plaque on the mucosal surface of maxillary complete dentures.
A trial was conducted to compare the effectiveness of povidone iodine and chlorhexidine gluconate with buffered peroxyborate in the treatment of acute ulcerative gingivitis. After 20 patients had entered the trial and 11 had required additional therapy with metronidazole to control their symptoms, the study was terminated. Those patients receiving peroxyborate all showed a satisfactory improvement in clinical signs and symptoms. One patient each receiving povidone iodine or chlorhexidine reported a symptomatic improvement, although gingival ulceration was still apparent at 1 week. The remaining patients all required metronidazole therapy to control their symptoms. Povidone iodine and chlorhexidine gluconate therefore cannot be recommended for the treatment of acute ulcerative gingivitis.