The Effects of Manuka Honey on Plaque and Gingivitis
Research has shown that Manuka honey has superior antimicrobial properties that can be used...
Research has shown that Manuka honey has superior antimicrobial properties that can be used with success in the treatment of wound healing, peptic ulcers and bacterial gastro-enteritis. Studies have already shown that Manuka honey with a high antibacterial activity is likely to be non-cariogenic. The current pilot study investigated whether or not Manuka honey with an antibacterial activity rated UMF 15 could be used to reduce dental plaque and clinical levels of gingivitis. A chewable "honey leather" was produced for this trial. Thirty volunteers were randomly allocated to chew or suck either the Manuka honey product, or sugarless chewing gum, for 10 minutes, three times a day, after each meal. Plaque and gingival breeding scores were recorded before and after the 21-day trial period. Analysis of the results indicated that there were statistically highly significant reductions in the mean plaque scores 10.99 reduced to 0.65; p=O.OO1J, and the percentage 01 bleeding sites (48% reduced to 17%; p=O.OOl), in the Manuka honey group, with no significant changes in the control group. Conclusion: These results suggest that there may be a potential therapeutic role for Manuka honey confectionery in the treatment of gingivitis and periodontal disease.
For over one hundred years, the healing qualities and therapeutic properties of honey have been recognized, and it has been used as a medicine since ancient times in many cultures. It has now been 'rediscovered' by the medical profession, and there are numerous reports in modern medical journals that document the effectiveness of honey in wound dressings, treatment of peptic ulcers, bacterial gastro-enteritis, and eye infections.
These properties are due to hydrogen peroxide which is produced enzymatically in honey. The glucose oxidase enzyme is secreted from the hypopharyngeal gland of the bee into the nectar to assist in the formation of honey. This in turn produces hydrogen peroxide by the reaction Glucose + 02 to Gluconic acid + H2O2 to give honey its antimicrobial potency. However, different types of honey vary greatly in their antimicrobial properties.
Manuka honey is found exclusively in New Zealand and made from the Dowers of the Manuka bush (Leptospermum scoparium), which grows uncultivated throughout the country. It has been demonstrated that Manuka honey has antibacterial properties different from other types of honey, due to it containing an additional antibacterial component that is Active to honey coming from some Leptospermum species of plant. This as yet unidentified component has been called the 'Active Manuka Factor' (UMF), and provides resistance to the action of the catalase present in the tissues and serum of the body which breaks down some of the hydrogen peroxide produced in honey, thus reducing the antibacterial efficacy of the honey. UMF thus enhances the potency of Manuka honey against infection. It is also capable of diffusing into tissues to clear deep-seated infection.
As with all types of honey, there is a large variation from sample to sample, therefore the activity of all Manuka honey is not equal The UMF number was devised in order to rate the potency of the antibacterial activity of Manuka honey. This is determined by a standard laboratory test of antibacterial activity whereby honey is compared with phenol, a standard antiseptic, in an agar well diffusion. For example, a honey with a UMF rating of 6 would be equivalent to the antiseptic potency of a 6% solution of phenol. Manuka honey with a UMF rating of 12 was used in the various cases of chronic infection successfully' healed by dressing with honey, that have been reported in the medical literature. 'UMF' has been registered as a trademark by the New Zealand honey industry in order to prevent any misrepresentation of antibacterial activity, and only Manuka honey with a UMF of >10 is allowed to be labeled with a UMF rating. In order to alleviate any concern over the potential risk of introducing infection (e.g. from clostridia spores) from a natural product, Manuka honey sterilized by gamma irradiation, is available, This does not cause any loss of antibacterial activity.
When contemplating the use of honey against infection in the mouth, the question arises as to whether or not Manuka honey is likely to cause dental decay? Conflicting findings on the carcinogenicity of honey in general have been reported. However, research has demonstrated that Manuka honey selected to have high antibacterial activity (rated UMF 12) is likely to be non-carcinogenic. This in vitro study showed that the manuka honey can inhibit the growth and production of lactic acid from oral bacteria, namely Streptococcus sobrinus Streptococcus mitis and Lactobacillus casein, and stop the production of the extra cellular polysaccharide dextrin by the streptococci. These are all oral bacteria which are thought to be the major species responsible for dental caries. It has therefore been proposed that by manufacturing confectionery from selected honey instead of sugar, it should be possible to eat confectionery without the development of cariogenic plaque.
Gingivitis results from the accumulation of supragingival plaque beyond the critical mass for any individual. Stagnation of plaque is associated with a shift in the constituent proportions of the organisms in plaque, with predominance towards Gram negative anaerobes. Therefore, it was hypothesized that regular use of confectionery made from antibacterial Manuka honey might inhibit oral plaque, resulting in a reduction in gingivitis. The aim of the research reported in this paper was to test this hypothesis in a clinical pilot study.
Materials and Methods
Thirty volunteers who gave their informed consent were recruited from University of Otago School of Dentistry patients as participants in this study, after the protocol was approved by the Otago Ethics Committee. Inclusion criteria for the study recruited those volunteers who were greater than 18 years of age, who had at least 20 natural teeth with measurable plaque evident, and who would normally-include some confectionery in their diet. Exclusion criteria excluded people with diabetes, and those requiring antibiotic cover for dental procedures. Although allergy to honey is rare, people with a known hypersensitivity to pollen, bee products or honey were also excluded. Any subjects who received any antibiotic therapy or periodontal treatment during the course of the trial were also eliminated from the study.
A brief questionnaire detailing age, gender, and smoking habits of each participant was recorded. Plaque levels were then assessed at three sites (mesio-buccal, disto-buccal and mid-lingual) of every tooth in one upper quadrant and one diagonally opposite lower quadrant using the Plaque Index criteria developed by Loe and Silness. Also recorded for each tooth was the presence or absence of buccal and lingual gingival bleeding when the entrance to the gingival crevice was gently stroked with a blunt periodontal probe.
Research at the University of Waikato has devised a method of gelling honey to give it the physical form of commercially available fruit leathers. The product consists of honey, with a small proportion of a common gelling agent used in confectionery. For this trial, the chewable 'honey leather' was developed by Bee & Herbal Ltd., Cambridge, New Zealand. The honey leather was manufactured from UMF 15 Manuka honey, and each piece of honey leather was approximately 109 in weight. Wrigley's Extra sugarless chewing gum was chosen for use by the control group.
Each volunteer was randomly allocated to either the Manuka honey test group or the control group for the 21 day trial period. Participants were instructed to chew or suck the 'honey leather' or chew the chewing gum for 10 minutes, three times each day (each immediately after a main meal), for the duration of the study, in conjunction with their normal oral hygiene routine. At the end of the trial period, the plaque and gingival bleeding scores were recorded again.
Before the commencement of the study, the sale examiner was calibrated in the use ofthe Plaque Index and the criteria for recording the bleeding score, by the senior author. The examiner was unaware as to which product each subject had used during the experimental period.
Following collection of all data the confidential code was broken and results were analyzed statistically using SPSS.
Random allocation of volunteers to either the honey-or control group resulted in 14 subjects chewing honey leather, and 16 chewing sugarless gum. The mean age of participants was very similar between the two groups, and although there were slightly more males in the honey group, this was not statistically significant. The mean number of sites recorded from the half-mouth screening was 24.9 (sd, 3.1) for those participants in tbe honey group, and 26.1 (sd, 2.5) for the control group. Regarding smoking habits, only 36% of the subjects chewing honey, and 56% of subjects in the control group described themselves as either smokers or former smokers. However, this difference was found not to be statistically significant (p>0.05). At completion of the final clinical examination, subjects were asked about compliance, and all except one who withdrew from the study, indicated that instructions had been followed.
The mean changes in plaque status from baseline. The mean number of sites where plaque levels improved in the Manuka honey group was considerably greater than in the control group, although the controls did show some improvement in plaque levels. A greater mean number of sites remained unchanged in the control group, and twice the number of sites worsened on average in the control group than did in the Manuka honey group. T-test analysis showed that the mean number of sites that demonstrated improved plaque status in the Manuka honey group was highly statistically significant (p=0.02) by comparison with the control group. A statistically significant number of sites worsened in the control group compared with the Manuka honey group (p=0.049). The mean number of sites that did not show any change in plaque status was not significant between the two groups.
The same statistical analysis was carried out for bleeding status, and an almost identical trend was noted. An improvement in bleeding status was defined as an absence of bleeding in a site, which had previously bled at baseline. The mean number of sites that showed an improvement in bleeding was statistically significant in the Manuka honey group when compared with those in the control group (p=0.02). The increased number of sites that bled (i.e. a worsened bleeding status) in the control group was also significant (p=0.016), when compared with the honey group. There was no statistically significant difference between the number of sites that remained unchanged in the two groups.
Statistical analysis also determined the mean difference in plaque scores between the two groups from baseline to endpoint. The mean plaque score in the Manuka honey group at baseline was 0.99 (sd, 0.33) and the initial mean plaque score in the control group was 0.85 (sd, 0.35). This difference was not significant, therefore indicating that the two groups at baseline were similar. At the end of the 21 ~day trial period a highly significant drop in the mean plaque score of the Manuka honey group to 0.65 (sd, 0.37) was recorded (Wilcoxon Signed Ranks test,p=0.001). The control group also showed a slight overall reduction in mean plaque score to 0.76 (sd, 0.29), (Wilcoxon Signed Ranks test, p>0.05) However the difference between the two groups was not significant (Mann.Whitney U· test, p= 0.24) difference in the percentage of sites that bled before and after the trial period. At baseline, 48% of sites in the Manuka honey group showed bleeding on probing compared with 51% of sites in the control group. However, this initial difference was not statistically significant (p> 0.05). At endpoint, only 17% of sites in the Manuka honey group still bled, while 43% of sites in the control group bled (Independent samples t-test, (p=0.001). This shows a highly significant effect of the Manuka honey treatment on gingivitis.
Discussion and Conclusions
This pilot study demonstrates that plaque levels and bleeding scores could be significantly reduced by the antibacterial properties of Manuka honey when compared with a control group using chewing gum. These findings are consistent with the hypothesis of this research, and are explained by the actions of hydrogen peroxide and Active Manuka Factor, outlined earlier in this paper. Manuka honey has been shown to be more effective than other honeys against Helieohacler pylori, enterococci, Staphylococcus aureus, and Escherichia coli. These studies further support the results of the present research, explaining the mechanisms which are thought to be responsible for the beneficial effect of Manuka honey in reducing plaque and gingivitis.
The greater reduction seen in the bleeding scores (rather than the plaque score) in the honey group in this pilot study, may be the result of the anti-inflammatory properties of Manuka honey working in conjunction with its antibacterial action; the latter reducing the quantity of supragingival plaque. The potent anti-inflammatory action of honey has been noted in many clinical reports of its use in healing burns and other wounds.
There was also some overall improvement in both plaque levels and gingivitis in the sugarless chewing gum control group, although these differences were found not to be statistically significant. It is known that sugarless chewing gum stimulates the flow of saliva and lowers the acidity of plaque after eating, thereby reducing the possibility of dental decay. Although research has shown that the use of sugar-free chewing gum reduces occlusal plaque formation, it has been reported that it does not reduce plaque on the facial and lingual surfaces, or reduce gingivitis. Therefore, the slight improvement shown in the control group could be attributed to the Hawthorne Effect which can result in improvement due to participation in a research study, simply because subjects know that their actions are being evaluated. Alternatively, the apparent improvement in the control group could be due to a migration towards the mean because of possible examiner bias. Notwithstanding this, in a pilot study with only 14 and 16 subjects respectively in the experimental/control groups, highly significant results were found in the Manuka honey group.
This paper reports on the first clinical trial to examine the potential benefits of Manuka honey on supragingival plaque and gingivitis. However, it was only a pilot study with a small sample size, and further research is required. The present findings need to be confirmed in a larger trial, possibly a crossover randomized control study in order to ensure an even distribution of smokers and non-smokers, gender, etc.
There is also potential for further research to determine whether or not subgingival application of Manuka honey has any significant effects on organisms that cause periodontitis, and whether or not there is any potential therapeutic role for Manuka honey products in the control of periodontal diseases.