|
 
 |
| ORIGINAL RESEARCH |
|
| Year : 2021 | Volume
: 12
| Issue : 2 | Page : 59-66 |
|
Comparison of Commercially Available 0.12% And 0.2% Chlorhexidine Mouthrinses on Plaque and Gingiva: A Randomized Controlled Trial
Swarnalatha C.1, Suresh Babu J.1, Nada Nasser Almansour1, Saleh Ali Almalaq1, Fahad Abdulrahman Alnasrallah1, Tayf Naif Radhi Alshammari1, Mohammad Saafaq Alshammari2, Abhishek Singh Nayyar3
1 Division of Periodontology, Department of Preventive Dental Sciences, College of Dentistry, University of Ha’il, Ha’il, Kingdom of Saudi Arabia
2 College of Dentistry, Riyadh Elm University, Riyadh, Kingdom of Saudi Arabia
3 Department of Oral Medicine and Radiology, Saraswati Dhanwantari Dental College and Hospital and Post-graduate Research Institute, Parbhani, Maharashtra, India
| Date of Submission | 27-May-2020 |
| Date of Decision | 17-Jun-2020 |
| Date of Acceptance | 05-Jul-2020 |
| Date of Web Publication | 26-Jul-2021 |
Correspondence Address:
Abhishek Singh Nayyar
Saraswati-Dhanwantari Dental College and Hospital and Post-Graduate Research Institute, Parbhani, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/denthyp.denthyp_62_20
Introduction: Regardless of potent anti-microbial and anti-plaque properties of Chlorhexidine (CHX), its widespread and comprehensive uses are restricted by local side effects which are mostly dose dependent. Thus, by understanding the properties and limitations of the CHX molecule, consideration has been given to CHX with lower concentrations, though, this, may produce an impact on its activity emphasizing the need for further clinical trials. The present study was, thus, designed to assess and compare the efficacy of commercially available 0.12% (Periogard) and 0.2% (Hexidine) of CHX mouthrinses on dental plaque and gingiva over a period of eight weeks. Materials and Methods: A randomized control, triple blind parallel clinical trial was designed among ninety-nine subjects. The study subjects were randomly distributed into three groups with random allocation of mouthrinses to each group. Plaque and gingival indices were recorded by using Plaque and Gingival indices were recorded by using Turesky, Gilmore and Glickman’s modification of Quigley Hein Plaque Index and Loe and Silness Gingival Index. Statistical analysis was done using IBM SPSS Statistics for Windows version 21 (IBM Corp, Armonk, USA). Wilcoxon matched pairs signed rank test was applied to compare reduction in mean plaque scores and mean gingival scores at different time intervals while pair-wise comparison in between the groups was done by using Mann-Whitney U test. P < 0.05 was considered as statistically significant. Results: Both the 0.2% and 0.12% CHX mouthrinses were effective in controlling plaque and gingivitis over a period of eight weeks. These mouthrinses exhibited significant decreases in mean plaque and gingival scores during baseline to 4th week examination, however, a significant rise in mean plaque and gingival score was noted again from 4th week to 8th week examination. Conclusion: The study concluded that lower concentrations of CHX (0.12%) are as effective as 0.2% of CHX, thereby, use of lower concentrations of CHX can be recommended.
Keywords: Chlorhexidine, dental plaque, gingivitis, periodontitis
How to cite this article:
C. S, J. SB, Almansour NN, Almalaq SA, Alnasrallah FA, Alshammari TR, Alshammari MS, Nayyar AS. Comparison of Commercially Available 0.12% And 0.2% Chlorhexidine Mouthrinses on Plaque and Gingiva: A Randomized Controlled Trial. Dent Hypotheses 2021;12:59-66 |
How to cite this URL:
C. S, J. SB, Almansour NN, Almalaq SA, Alnasrallah FA, Alshammari TR, Alshammari MS, Nayyar AS. Comparison of Commercially Available 0.12% And 0.2% Chlorhexidine Mouthrinses on Plaque and Gingiva: A Randomized Controlled Trial. Dent Hypotheses [serial online] 2021 [cited 2023 Jun 5];12:59-66. Available from: http://www.dentalhypotheses.com/text.asp?2021/12/2/59/322523 |
| Introduction | |  |
Untreated chronic gingivitis can initiate destruction of the gingival tissues and periodontal attachment apparatus and tooth loss in majority of the cases.[1],[2] Constant presence of chronic inflammation and inflammatory mediators has, also, been proved to be a significant risk factor for several systemic diseases e.g. preterm low birth weight babies, coronary artery diseases, diabetes mellitus etc.[3],[4],[5],[6] Numerous studies have shown a positive correlation between supra-gingival plaque levels and chronic gingivitis[7],[8],[9] and also, implicated dental plaque as a primary etiologic factor for gingival inflammation.[10],[11],[12],[13]
Dental plaque is defined clinically as a structured, resilient, yellow grayish substance that adheres tenaciously to the intra-oral hard surfaces, including removable and fixed restorations.[14] According to the classic version of the non-specific theory by Loesche,[15] the indigenous oral bacteria colonize and form the dental plaque. Inflammatory periodontal disease develops in the case of bacterial proliferation above the threshold of host resistance, caused by the combined biologic effects of the total plaque flora. All plaque bacteria are thought to have some of the various virulence factors causing gingival inflammation and periodontal destruction, and it is implied that plaque will cause disease regardless of its composition.[16] Therefore, plaque control was considered as essential to limit the production of gingival irritants which lead to gingival inflammation and periodontal destruction. There are different mechanical and chemical approaches for controlling plaque. The mainstay and most common method used for plaque control is mechanical cleaning using a toothbrush[17] but its effectiveness largely depends on dexterity and compliance of the individuals, hence, it cannot be reliable all the time.[18] From this perspective, chemotherapeutic agents have been incorporated as a complementary way to attain the effective plaque control. It may, therefore, help to achieve reduced quantity of plaque below the individual’s threshold for disease, alter the quality of plaque to a more tissue friendly composition while, also, contributing to anti-inflammatory properties.[19]
Various chemotherapeutic agents have come into market in the form of mouthrinses, gels and sprays promising good efficiency. Among them, mouthrinses are most often used. Scientific research into antiseptic mouthwashes started with Slanetz and Brown[20] and continue to date.[21] Mouthrinses have various indications such as an anti-plaque, anti-cariogenic, anti-halitosis, anti-hypersensitivity, anti-mucositis or, anti-erosive activity. In order to control gingivitis and prevent periodontal breakdown, the focus is mainly on their anti-plaque efficiency.[7],[10] There is a long list of anti-plaque agents have been developed so far such as antibiotics, enzymes, metallic salts and oxygenating agents, though, among them, chlorhexidine digluconate (CHX) has remained as the gold standard anti-plaque agent so far despite recent advances in the chemical plaque control measures.[9],[22] Its effectiveness can be attributed to its bactericidal and bacteriostatic effects and its substantivity within the oral cavity.[23],[24] Commercially available CHX mouthrinses are perhaps most commonly prescribed. The products vary in their concentrations and formulations and so is the mechanism of action that varies with the concentration. At low concentrations, CHX causes damage to the cell membrane and low molecular weight molecules escape from the microorganisms while at higher concentrations, CHX causes precipitation and coagulation of the proteins in the cytoplasm of the exposed microbes.[25] These properties interfere with biofilm formation and prevent the growth processes.[26]
Regardless of potent anti-microbial and anti-plaque properties of CHX, its widespread and comprehensive uses are restricted by local side effects which are mostly dose dependent. The most common side effects are taste alteration, excess formation of supra-gingival calculus, soft tissue lesions in young patients, allergic responses and staining of teeth and soft tissues.[27],[28],[29] This kind of discoloration especially in the interproximal areas, and tongue are often caused by a precipitation reaction between tooth-bound CHX and chromogens from food or, beverages.[30] Thus, by understanding the properties and limitations of the CHX molecule, consideration has been given to CHX with lower concentrations, though, this, may produce an impact on its activity emphasizing the need for further clinical trials. The present study was, thus, designed to assess and compare the efficacy of commercially available 0.12 % (Periogard) and 0.2% (Hexidine) of CHX mouthrinses on dental plaque and gingiva over a period of eight weeks. In the present clinical trial, 0.2% CHX (Hexidine) and 0.12% CHX (Periogard) mouthrinses were used as adjuvants to regular oral hygiene practices in an attempt to assess an efficacy on plaque accumulation and gingivitis over a period of 8 weeks.
| Materials and Methods | | |
A randomized control, triple blind parallel clinical trial was designed to assess and compare the efficacy of commercially available 0.12 % (Periogard) and 0.2% (Hexidine) CHX mouthrinses on dental plaque and gingiva over a period of eight weeks. Sterile distilled water was used as control. Each step in present randomized controlled trial was followed by Consolidated Standards of Reporting Trials (CONSORT 2010) guidelines.[31] Prior to the commencement of the study, the study protocol was approved from the Institutional Ethics Committee via Institutional Letter approval no. SDDC/IEC/01-33-2018. The study included subjects within an age between 18 and 22 years with a minimum of twenty natural teeth including at least two molars and with minimum Plaque and Gingival Index Score of < 1.5 and no history of dental visit in the past three months while the subjects who had existing soft tissue damage due to ill-fitting appliances or, who were with periodontal disease with pocket depth of > 3 mm or, with > 2mm loss of attachment, subjects with of any systemic conditions that could lead to an alteration in the production and/or composition of the saliva (Eg. Sjogren’s syndrome, drug history, surgical removal of salivary glands etc.), those with habit of tobacco chewing/smoking, pregnant women, subjects with a history of allergy to oral CHX, subjects who had used any antibiotics in past three months or, with any dental conditions which needed prompt professional attention (Eg. pain, abscess, swellings etc.) were excluded from the study. Sample size was calculated based on data observed from small-scale pilot study with 95% confidence interval and 5% of chance of error, and also, according to Chow and Liu[32] and Mahajan,[33], sample size of greater than 30 is considered large enough to obtain statistical significance. Hence, in this study each group comprised of thirty three study subjects to ensure that the difference obtained was, also, statistically significant. All eligible study subjects were given information about the products and the purpose of the study. After screening for suitability, study subjects were requested to give their written informed consent. The study procedure was explained to study subjects prior to the beginning of the study and written informed consent was obtained from them. Commercially available 0.12% CHX mouthrinse (Periogard), 0.2% CHX mouthrinse (Hexidine) and distilled water in case of controls were used in the study. The solutions were transferred to sterile amber-colored containers and labeled as A, B, C and given to the investigator. The subjects, the investigator and statistical analyst were blinded in this study. All the examinations were conducted by a single pre-trained and pre-calibrated investigator. The scorings were recorded by pre-trained recorder. In the present study, in order to eliminate selection bias, simple random sampling by lottery method was employed to distribute the study subjects into three groups. The study subjects were randomly distributed into three groups and categorized as Group A, Group B and Group C by a second year post-graduate student from Department of Public Health Dentistry. Each group comprised of thirty-three study subjects and random allocation of mouthrinses was done to each group. The study was conducted for a period of eight weeks with clinical examination being carried out at baseline (Day 0), 4th week and 8th week of mouthrinses use. Plaque and Gingival indices were recorded by using Turesky, Gilmore and Glickman’s[34] modification of Quigley Hein Plaque Index and Loe and Silness’s[35] Gingival Index. The study subjects were asked to gargle 10 ml of the provided mouthrinse two times a day for 30 seconds and expectorate (morning after brushing and night before going to bed) while not to consume tea/coffee and/or, any food stuff at least half an hour after using mouthrinse and report immediately if any adverse reactions were noticed. Subjects were, also, instructed to continue with their routine oral hygiene practices. The study subjects were made to sit comfortably on an ordinary chair and Type III American Dental Association clinical examination was carried out under natural light.
Statistical Analysis Used
Statistical analysis was done using IBM SPSS Statistics for Windows version 21 (IBM Corp, Armonk, USA). Wilcoxon matched pairs signed rank test was applied to compare reduction in mean plaque scores and mean gingival scores at different time intervals while pair-wise comparison in between the groups was done by using Mann-Whitney U test. P < 0.05 was considered as statistically significant.
| Results | | |
Of the 99 subjects included in the clinical study, there were no dropouts. Equal number of subjects was allocated in each group (Total − 33). At the end of the study, mouthrinses were decoded and was found that Group A used 0.12% CHX, Group B used 0.2% CHX and Group C used sterile distilled water. The study was conducted among 99 subjects aged between 18 −22 years in Omega Degree College, Hyderabad with mean age of 19.3 ± 1.4. Of the total of ninety-nine, forty-nine male (49.5%) and fifty female (50.5%) study subjects were randomly distributed into three groups, coded as Group A, Group B and Group C. Among them, Group A and Group B comprised of seventeen males (51.5%) and sixteen females (48.5 %), while fifteen males (45.5%), eighteen females (54.5%) were distributed in Group C. Significant differences were not observed between three groups with respect to age and gender distribution. The mean plaque scores in Group A at baseline, 4th week and 8th week examinations were 2.98± 0.3, 0.58 ± 0.2, 1.25 ± 0.4 respectively [Table 1]. Among Group B mean plaque scores at baseline examination, 4th week and 8th week examinations were 2.93 ± 0.5, 0.58 ± 0.2 and 1.21 ± 0.4. In Group C the mean plaque scores at baseline was 3 ± 0.4, at 4th week was 2.77 ± 0.6 and at 8th week examination was at 2.84 ± 0.6 respectively. Significant differences were found between the groups at three intervals except at baseline examination (P = 0.00). While comparing the reduction in mean plaque scores at baseline, 4th week and 8th week examinations, in Group A, 2.39 ± 0.4 and 1.73 ± 0.6 reduction in mean plaque scores were noticed from baseline to 4th week (80.4%), and baseline line to 8th week examination (58.1%) respectively (P = 0.00). On the contrary significant rise in mean plaque scores (–0.66 ± 0.4) were observed from 4th week to 8th week (−113.5%). Likewise in Group B, 2.34 ± 0.5 reductions in mean plaque scores observed from baseline to 4th week examination (80.1%) and 0.71 ± 0.6 mean plaque score reduction found from baseline to 8th week examination (58.5%). While significant rise in mean plaque scores (−0.63 ± 0.4) were detected from 4th week to 8th week examination (−108.6%). Pertaining to Group C, significant reduction in mean plaque scores noticed from baseline to 4th week (0.22 ±0.4) (7.43%) and to 8th week examination (0.15 ± 0.4) (5.17%) (p=0.00). Moreover significant increase in mean plaque scores (−0.07 ± 0.3) were prominent from 4th week to 8th week examination (−2.44%) (P = 0.00). While comparing between-group comparisons with respect to mean plaque scores, statistically significant differences were not found between the groups except at baseline examination (P = 0.000). Between Group A and Group B, no statistically significant difference was evident at 4th week and 8th week examinations. In contrast Group C exhibited significant difference with Group A and Group B at 4th week and 8th week examinations. Pair-wise comparisons between the study groups in reduction of mean plaque scores at baseline, 4th week and 8th week examination, Group A and Group B were not significantly different in their mean reduction in plaque scores at baseline to 4th week, baseline to 8th week and from 4th week to 8th week examinations. On the other hand Group C showed significant difference with Group A and Group B in reduction of mean plaque scores at baseline to 4th week, baseline to 8th week and from 4th week to 8th week examinations. In Group A, mean gingival scores at baseline, 4th week and 8th week examinations were 2.01 ± 0.3, 0.6 ± 0.2 and 1.22 ± 0.3 respectively [Table 2]. With respect to Group B mean gingival scores at baseline, 4th week and 8th week examination were 2.08 ± 0.3, 0.48 ± 0.2 and 1.22 ± 0.3 respectively and corresponding mean scores in Group C were 2.05 ± 0.3, 2.02 ± 0.3, and 2.07 ± 0. Significant differences were, also, found between three groups at three intervals except at baseline examination (P = 0.00). While comparing the reduction in mean gingival scores at baseline, 4th week and 8th week examinations between three groups, with respect to Group A, 1.4 ± 0.3 mean reduction from baseline to 4th week (69.9%), 0.78 ± 0.4 from baseline to 8th week (39.1%) and −0.62 ± 0.3 found from 4th week to 8th week examination (-102.5%) was found (p= 0.00). Whereas for Group B, 1.6 ± 0.3 mean reduction from baseline to 4th week (77%), 0.78 ± 0.4 from baseline to 8th week (41.6%) and −0.74 ± 0.3 found from 4th week to 8th week examination (−154.2%). In Group C, 0.03 ± 0.2, −0.02 ± 0.2 and −0.05 ± 0.1 mean gingival score reductions were apparent from baseline to 4th week (1.57%), baseline to 8th week (−0.79%) and 4th week to 8th week examinations (−2.39%) respectively. Between groups comparisons with respect to mean gingival scores at baseline, 4th week and 8th week examinations, all three groups were not significantly different at baseline examination, but they were significantly different at 4th week examination. Group A and Group B exhibited similar results at 8th week examination (P = 0.9). On the other hand, Group A and Group B revealed significant difference with Group C at 8th week examination (P = 0.00). Comparison of reduction in mean gingival scores at three intervals between three groups, significant difference was noticeable from baseline to 4th week, baseline to 8th week and 4th week to 8th week examination between Group A, Group B and Group C except for Baseline to 4th week and 4th week to 8th week examinations between Group A and Group B. | Table 1 Comparison between three groups at different time intervals with respect to Plaque Index scores
Click here to view |
 | Table 2 Comparison between three groups at different time intervals with respect to Gingival Index scores
Click here to view |
| Discussion | | |
The results of the present study showed that the mean plaque scores exhibited similar trends in all three groups (Group A, Group B and Group C). There was a significant reduction in the scores from baseline to 4th week and baseline to 8th week examination with significant rise from 4th week to 8th week examination (P = 0.000). Similar findings were noticed for mean gingival scores in Group A (0.2% CHX) and Group B (0.12% CHX) (P = 0.000). However, in Group C (sterile distilled water), significant reduction was found from baseline to 4th week examination and significant rise from baseline to 8th week and 4th week to 8th week examination was observed (P = 0.000).
The existence of the micro-organisms as poly-species in oral cavity has profound implications in the etiology of dental caries, periodontal disease and other systemic diseases.[36] Control of oral microbiota by antimicrobial mouthrinses as an adjunctive to mechanical plaque control has been an effective method of preventing dental diseases. Mouthrinses have been used for centuries for medicinal and cosmetic purposes, but it is only in recent years that the rationale regarding their ingredients has been subjected to scientific research and clinical trials.[37]
Mouthrinses are solutions used to rinse the mouth for a number of purposes: (a) prevent the biofilm formation (b) inhibition of early microbial colonization on tooth surfaces (c) the alteration of pathogenic plaque into non-pathogenic plaque and (d) to have a therapeutic effect by relieving periodontal infections or, preventing dental caries.[38] Evidence in dental literature support and recognize CHX as the gold standard against which other anti-plaque and anti-gingivitis agents are measured.[9] The success of CHX is based on high intra-oral substantivity of this product and its bactericidal and bacteriostatic actions.[11],[26],[38]
The inhibitory action of CHX on the plaque formation on teeth may occur via different mechanisms: (i) immediate bactericidal effect, (ii) prolonged bacteriostatic effect by surface bound CHX, (iii) blockage of the acidic groups from the salivary glycoproteins that form the pellicle, (iv) binding to the bacterial surface in sub-lethal amounts so that initial adhesion to the surface is inhibited, (v) disturbing the plaque formation by precipitation of agglutination factors in saliva and by displacing calcium from the plaque matrix.[39],[40] Also, it has been demonstrated that gingivitis can be resolved due to the plaque inhibitory action of CHX.[41]
Unfortunately, CHX as the most-used mouthrinse has some dose dependent disadvantages.[28] Hence to reduce the local side effects, commercially available CHX mouthrinses are made available in different concentrations. This varied concentrations of CHX may have an impact on plaque inhibiting activity, therefore, the study was undertaken to assess and compare the efficacy of commercially available 0.12 % (Periogard) and 0.2% concentrations (Hexidine) of CHX mouthrinses on dental plaque and gingiva over a period of eight weeks.
The present clinical trial was so planned that the investigator, the study subjects and the person who conducted the statistical analysis were unaware of the group allocation (Group A, Group B and Group C) which ensured that subjective bias, observer bias and bias in evaluation were eliminated (triple blind). Sterile distilled water (Group C) was used to evaluate whether routine swishing action had an effect on plaque accumulation and gingivitis, thereby, acting as a control. No adverse reactions were noticed among the study subjects during study period.
In the present study, Turesky, Gilmore and Glickman’s[34] modification of Quigley Hein Plaque Index was used to record plaque while Gingival index by Loe and Silness[35] was used to record qualitative changes of the gingival tissues. These indices are considered as reliable indicators for measuring plaque and the condition of gingival tissues by estimating the extent of plaque on the buccal as well as the lingual surfaces covered on an ordinal scale. These indices have been used frequently in clinical trials for evaluating therapeutic agents as they have high sensitivity and reproducibility than the other similar methods used to assess plaque and gingival health. Clinical examination was carried at baseline, 4th week and 8th week in order to provide adequate time for anti-plaque and anti- gingivitis effect of study mouthrinses. Oral prophylaxis was not carried out prior to commencing the study since the primary intention was to evaluate efficacy of 0.12% and 0.2% CHX with existing plaque and gingival status. The study subjects were instructed to continue their routine oral hygiene practices to avoid the impact of altered oral hygiene practices on plaque accumulation and gingivitis.
The results of the present study showed that 0.12% and 0.2% CHX mouthrinse exhibited similar clinical efficacy when used twice daily in accordance with the findings of the study conducted by Rath and Singh[42] who obtained comparable results while taking into consideration plaque accumulation and gingival changes with the said concentrations of CHX mouthrinse. Segreto et al.[43], also, obtained similar results in their double blind parallel study comprising of six hundred adults and reported that 0.12% CHX mouthrinses offers similar clinical benefits as 0.2% CHX mouthrinses when used twice daily. Likewise, Najafi et al.[44], also, did not find any significant differences between 0.12%and 0.2% CHX in terms of plaque index and gingival index in their 14 day observation made in the study.
In another study conducted by Neto et al.[45], no significant difference was found between 0.12% and 0.2% concentrations of CHX in relation to plaque accumulation and gingival bleeding. Smith et al.[27], also, stated that the two concentrations of CHX mouthrinses showed similar efficacy in plaque inhibition. Similar findings were obtained in other studies conducted by Jenkins et al.[46]and Greenstein et al.[47] as well suggesting lower concentration of CHX can safely be recommended to achieve similar clinical efficacy and results.
There have been few studies contradicting the said studies, too, including the studies conducted by Addy et al.[30] and Cousido et al.[41] wherein it was demonstrated that 0.2% CHX produced a significantly greater anti-bacterial effect than 0.12% CHX in all the saliva samples obtained after mouthrinse. Likewise, Thomas et al.[48], also, stated from the findings of their study that the antimicrobial activity of 0.2% CHX was significantly greater than that of 0.12% CHX when the salivary flora was assessed at 30s and 1h after the mouthrinse.
Stoeken et al.[49], also, did not find 0.12% CHX as effective as 0.2% CHX. This difference in the efficacy of the said two concentrations of CHX might be explained on the basis of the difference in the forms in which it would have been used in the said experimental designs like in the said study, 0.2% CHX was applied in form of mouthrinse while 0.12% CHX was used in the form of spray which might have affected the retention of the drug and its substantivity with the passage of time.
Sreenivasan and Gittins[50] and Jayaprakash et al.,[51] also, compared the efficacy of different concentrations of CHX on plaque accumulation and gingivitis and found that the anti-microbial efficacy and substantivity of CHX was concentration dependent. In the present study, 0.12% (Periogard) and 0.2% CHX (Hexidine) mouthrinses showed significantly greater efficacy than control group (sterile distilled water) during the study period. The present study showed a significant rise in mean plaque and mean gingival scores from 4th week to 8th week examination among Group A and Group B study subjects. This might be due to the ‘Hawthorne effect’ amongst the study subjects which refers to any ‘unexplained result in an experiment on human subjects on assumption that the result occurred simply because the subjects were in an experiment and thereby, experienced something that otherwise would not have affected them.[52],[53]
Limitations of the Present Study
The present study had certain inherent shortcomings, too, in the form of the study being restricted only to the age group of 18-22 years. Furthermore, only immune-competent subjects were included in the study which puts forth another limitation of the study in the form of variable results that might be expected in hosts with different immune-competencies. Also, a plethora of systemic conditions, also, affect the host response to any antimicrobial agent used in the body. Most importantly, the mentioned ‘Hawthorne effect’ was unavoidable in the present study and there was a possibility of subject variability since the study design was a parallel design.
Future Research Directions
Periodontitis is a group of inflammatory disease processes that affect the connective tissue attachment and supporting bone around the teeth. Its initiation and progression depend on the presence of virulent microorganisms capable of causing the disease. Also, it is considered to be a multifactorial disease process with no clear cut etiology, so, its identification and early diagnosis becomes even more challenging. The current clinical diagnostic parameters including the Plaque and Gingival indices by Turesky, Gilmore and Glickman’s modification of Quigley Hein Plaque Index and Loe and Silness Gingival Index used in the present study were introduced decades ago. Also, clinical and radiological measurements of attachment loss are not precisely accurate while individual susceptibility to periodontitis, too, has been seen to vary both genetically and over time. In addition to these inherent pitfalls in the clinical and radiological diagnostic criteria and the wide variations seen in host immune responses based on their genetic make-up, these methods, further, suffer from a major setback in that they provide an indication of disease severity rather than the disease activity. Here, comes the quintessential role of certain markers which can be used to predict the exact extent of the disease process and to validate the therapeutic strategies which are used to treat the same. A biomarker is a substance used to indicate a biologic state and is an objective measure to evaluate the present and future disease activity or, the pharmacologic responses to a therapeutic intervention. There have been numerous studies conducted in this regard that have suggested the possible presence of such markers including salivary and serum endothelin-1, malondialdehyde, asymmetric dimethylarginine (ADMA) and homocysteine (Hcy) amongst others in patients with periodontitis in the active phases of the disease process as well as in predicting the possible risk of host for an active disease.[54],[55],[56],[57],[58],[59] These biomarkers are of help not only in predicting the risk of periodontal disease but the impact that it can have on the systemic health of the host. The present clinical trial, thus, suggests future clinical trials on wide sample sizes and with inclusion of immuno-compromised hosts to assess the efficacy of the varying concentrations of chlorhexidine as well as other therapeutic interventions used in the light of such markers to come to valid conclusions.
| Conclusion | | |
The present study showed that 0.12% CHX mouthrinse (Periogard) exhibited similar clinical efficacy as 0.2% CHX (Hexidine) when used twice daily. These two mouthrinses revealed a significant advantage on plaque accumulation and gingivitis than the control group (sterile distilled water) during examination period (8 weeks). Based on the results of the present study, it can be concluded that lower concentrations of CHX (0.12%) are as effective as 0.2% of CHX (which can be considered as gold standard), thereby, use of lower concentrations of CHX can be recommended.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | American Academy of Periodontology. Diagnosis of Periodontal Diseases (Position Paper). Chicago, Ill: The American Academy of Periodontology; April 1995.  |
| 2. | Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6. |
| 3. | Li X, Kristin M, Kolltveit XX, Olsen I. Systemic diseases caused by oral infection. Clin Microbiol Rev 2000;13:547-58. |
| 4. | Dietrich T, Garcia RI. Associations between periodontal disease and systemic disease: Evaluating the strength of the evidence. J Periodontol 2000;11:2175-83. |
| 5. | Gurenlian JR. Inflammation: The relationship between oral health and systemic disease. Access 2006;20:1-9. |
| 6. | Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K. Relationship between periodontal infections and systemic disease. Clin Microbiol Infect 2007;13:3-10. |
| 7. | Ash M, Gitlin BN, Smith NA. Correlation between plaque and gingivitis. J Periodontol 1964;35:425-9. |
| 8. | Muller HP, Heinecke A, Eger T. Site-specific association between supra-gingival plaque and bleeding upon probing in young adults. Clin Oral Invest 2000;4:212-8. |
| 9. | Jones CG. Chlorhexidine: Is It still gold standard? Periodontol 2000 1997;15:55-62. |
| 10. | Loe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol 1965;36:177-87. |
| 11. | Kornman KS. The role of supra-gingival plaque in the prevention and treatment of periodontal diseases. J Periodontal Res 1986;21:5-22. |
| 12. | Bartold PM, Cantley MD, Haynes DR. Mechanisms and control of pathologic bone loss in periodontitis. Periodontol 2000 2010;53:55-69. |
| 13. | Ten Cate JM. Biofilms: A new approach to the microbiology of dental plaque. Odontol 2006;94:1-9. |
| 14. | Bowen WH. Nature of plaque. Oral Sci Rev 1976;9:3-21. |
| 15. | Loesche WJ. Chemotherapy of dental plaque infections. Oral Sci Rev 1976;9:65-107. |
| 16. | Hancock EB. Periodontal diseases: prevention. Ann Periodontol 1996;1:223-49. |
| 17. | Hogg SD. Chemical control of plaque. Dent Update 1990;17:330-4. |
| 18. | Lindhe J, Westfelt E, Nyman S, Socransky S, Hajjajee AD. Long term effect of surgical/non-surgical treatment of periodontal disease. J Clin Periodontol 1984;11:448-58. |
| 19. | Van der Weiden GA, Hoie KP. A systematic review of effectiveness of self-performed mechanical plaque removal in adults with gingivitis using a manual tooth brush. J Clin Periodontol 2005;32:214-8. |
| 20. | Slanetz LW, Brown EA. Studies on the number of bacteria in the mouth and their reduction by the use of oral antiseptics. J Dent Res 1949;28:313-23. |
| 21. | Jiyani T. Clinical comparison of plain Chlorhexidine (0.2%) and Chlorhexidine (0.2%) in combination with Sodium Fluoride (0.05%) and Zinc Chloride (0.09%). J Chem Pharm Res 2015;7:758-64. |
| 22. | Lorenz K, Bruhn G, Heumann C, Netuschil L, Brecy M, Hoffmann T. Effect of two new chlorhexidine mouthrinses on the development of dental plaque, gingivitis and discoloration: a randomized, investigator-blind, placebo-controlled, 3-week experimental gingivitis study. J Clin Periodontol 2006;33:561-7. |
| 23. | Mathur S, Mathur T, Shrivastava R, Khatri R. Chlorhexidine: the gold standard in chemical plaque control. Natl J Physiol Pharm Pharmacol 2011;1:45-50. |
| 24. | Balagopal S, Arjunkumar R. Chlorhexidine: The Gold Standard Anti-plaque Agent. J Pharm Sci Res 2013;5:270-4. |
| 25. | Hugo WB, Longworth AR. The effect of chlorhexidine on the electrophoretic mobility, cytoplasmic constituents, dehydrogenase activity and cell walls of Escherichia coli and Staphylococcus aureus. J Pharm Pharmacol 1966;18:569-78. |
| 26. | Denton GW. Chlorhexidine. In Block SS, Ed. Disinfection, sterilization and preservation. 4th Ed. Philadelphia, PA: Lea and Febiger. 1991; pp. 274-89. |
| 27. | Smith RG, Moran J, Addy M, Doherty F, Newcombe RG. Comparative staining in-vitro and plaque inhibitory properties in-vivo of 0.12% and 0.2% chlorhexidine mouthrinses. J Clin Periodontol 1995;22:613-7. |
| 28. | Flotra L, Gjermo P, Rolla G, Waerhaug J. Side effects of chlorhexidine mouth washes. Scand J Dent Res 1971;79:119-25. |
| 29. | Quirynen M, Avontroodt P, Peeters W, Pauwels M, Cauck W, Steen Berghe D. Effect of different chlorhexidine formulations in mouthrinses on de novo plaque formation. J Clin Periodontol 2001;28:1127-36. |
| 30. | Addy M, Wade W, Goodfield S. Staining and antimicrobial properties in-vitro of some chlorhexidine formulations. Clin Prev Dent 1991;13:13-7. |
| 31. | Schulz KF, Altman DG, Moher D; CONSORT Group. Collaborators: Altman DG, Barbour V, Berlin JA, Boutron I, Devereaux PJ, Dickersin K, et al. CONSORT 2010 Statement: Updated guidelines for reporting parallel group randomized trials. BMC Med 2010;8:18. |
| 32. | Chow SC, Liu JP. Design and Analysis of Clinical Trials: Concepts and Methodologies. 2nd Ed. New York: John Wiley and Sons, 1998. |
| 33. | Mahajan BK. Methods in Biostatistics: For Medical Students and Research Workers. 7th Ed. New Delhi: Jaypee Brothers Medical Publishers (Pvt.) Ltd., 2011. |
| 34. | Turesky S, Gilmore ND, Glickman I. Reduced plaque formation by the chloromethyl analogue of vitamin C. J Periodontol 1970;41:41-3. |
| 35. | Loe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533-51. |
| 36. | Guggenheim B, Giertsen E, Schupbach P, Shapirol P. Validation of an in-vitro biofilm model of supra-gingival plaque. J Dent Res 2001;80:363-70. |
| 37. | Adams D, Addy M. Mouthrinses. Adv Dent Res 1994;8:291-301. |
| 38. | Addy M. Chlorhexidine compared with other locally delivered antimicrobials: a short review. J Clin Periodontol 1986;13:957-64. |
| 39. | Jenkins S, Addy M, Wade W. The mechanism of action of chlorhexidine: a study of plaque growth on enamel inserts in-vivo. J Clin Periodontol 1988;15:415-24. |
| 40. | Rolla G, Melsen B. On the mechanism of plaque inhibition by chlorhexidine. J Dent Res 1975;54:57-62. |
| 41. | Cousido MC, Tomas Carmona I, García-Caballero L, Limeres J, Alvarez M, Diz P. In-vivo substantivity of 0.12% and 0.2% chlorhexidine mouthrinses on salivary bacteria. Clin Oral Invest 2010;14:397-402. |
| 42. | Rath SK, Singh M. Comparative clinical and microbiological efficacy of mouthwashes containing 0.2% and 0.12% chlorhexidine. Dent Res J 2013;10:364-9. |
| 43. | Segreto VA, Collins EM, Beiswanger BB, de La Rosa M, Isaacs RL, Lang NP et al. A comparison of mouthrinses containing two concentrations of chlorhexidine. J Periodontal Res 1986;21:23-32. |
| 44. | Najafi MH, Taheri M, Mokhtari MR, Forouzanfar A, Farazi F, Mirzaee M et al. Comparative study of 0.2% and 0.12% digluconate chlorhexidine mouth rinses on the level of dental staining and gingival indices. Dent Res J 2012;9:305-8. |
| 45. | Neto CAF, Parolo CCF, Rosing CK, Maltz M. Comparative analysis of the effect of two chlorhexidine mouthrinses on plaque accumulation and gingival bleeding. Braz Oral Res 2008;22:139-44. |
| 46. | Jenkins S, Addy M, Newcombe RG. Dose response of chlorhexidine against plaque and comparison with triclosan. J Clin Periodontol 1994;21:250-5. |
| 47. | Greenstein G, Berman C, Jaffin R. Chlorhexidine: An adjunct to periodontal therapy. J Periodontol 1986;57:370-7. |
| 48. | Thomas I, Cousido MC, Tomás M, Limeres J, García-Caballero L, Diz P. In-vivo bactericidal effect of 0.2% chlorhexidine but not 0.12% on salivary obligate anaerobes. Arch Oral Biol 2008;53:1186-91. |
| 49. | Stoeken JE, Versteeg PA, Rosema NA, Timmerman MF, Van der velden U. Inhibition of “de novo” plaque formation with 0.12% chlorhexidine spray compared to 0.2% spray and 0.2% chlorhexidine mouthwash. J Periodontol 2007;78:899-904. |
| 50. | Sreenivasan PK, Gittins E. Effects of low dose chlorhexidine mouthrinses on oral bacteria and salivary microflora including those producing hydrogen sulfide. Oral Microbiol Immunol 2004;19:309-13. |
| 51. | Jayaprakash R, Sharma A, Moses A. Comparative evaluation of the efficacy of different concentrations of chlorhexidine in reducing the mutans streptococci in saliva: an in-vivo study. J Ind Soc Pedo Prev Dent 2010;28:162-6. |
| 52. | Adair JG. The Hawthorne effect: a reconsideration of the methodological artifact. J Appl Psychol 1984;69:334-45. |
| 53. | Parsons HM. Hawthorne: An early OBM experiment. J Organ Behav Manag 1992;12:27-43. |
| 54. | Khalid W, Vargheese SS, Lakshmanan R, Sankari M, Jayakumar ND. Role of endothelin-1 in periodontal diseases: a structured review. Indian J Dent Res 2016;27:323-33. [ PUBMED] [Full text] |
| 55. | Isola G, Polizzi A, Alibrandi A, Indelicato F, Ferlito S. Analysis of Endothelin-1 concentrations in individuals with periodontitis. Scientific Reports 2020;10:1652-9. |
| 56. | Isola G, Polizzi A, Santonocito S, Alibrandi A, Ferlito S. Expression of salivary and serum malondialdehyde and lipid profile of patients with periodontitis and coronary heart disease. Int J Mol Sci 2019;20:6061. |
| 57. | Hendek MK, Olgun E, Kısa U. Effect of initial periodontal treatment on cardiovascular risk markers in patients with severe chronic periodontitis. Meandros Med Dent J 2019;20:114-20. |
| 58. | Isola G, Alibrandi A, Currò M, Matarese M, Ricca S, Matarese G et al. Evaluation of salivary and serum ADMA levels in patients with periodontal and cardiovascular disease as subclinical marker of cardiovascular risk. J Periodontol 2020; doi: 10.1002/JPER.19-0446. |
| 59. | Isola G, Alibrandi A, Rapisarda E, Matarese G, Williams RC, Leonardi R. Association of vitamin D in patients with periodontitis: a cross-sectional study. J Periodontal Res 2020; doi: 10.1111/jre.12746 |
[Table 1], [Table 2]
|
Search Pubmed for
