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Supported through an educational grant from A New Approach to the Classification of Periodontal Diseases Panos N. Papapanou, DDS, PhD Gingival Health dialogue Investigations and Insights in Gingival Health Research For the past decade, our research group at the Division of Periodontics, Columbia University College of Dental Medicine, has focused on the study of gene expression signatures in gingival tissues, having as overall aims to (1) gain a better understanding of the pathobiology of periodontal diseases, and (2) provide the foundation for the development of a new classification of periodontitis based on pathobiology rather than on clinical symptomatology. Gene Expression Profiling Gene expression profiling refers to the systematic cataloguing of messenger–RNA (mRNA) molecules in a cell or tissue sample. As the readers of the Gingival Health Dialogue certainly recall from their basic biology courses, DNA in the nucleus is first transcribed into mRNA, before ultimately translated into protein. Protein expression is what decides the cell’s or the organ’s phenotype, i.e., it determines its characteristics and behavior. It is important to realize that although all cells in our body share the same genetic information, they produce vastly different proteins depending on their specific functions. By examining which particular mRNAs are being transcribed at a given time point in a specific cell population, we can get a rough idea of which particular proteins are about to be translated in these cells and, thereby, an estimate of their expected phenotype. One way that this can be studied in the lab is as follows: First, total RNA is extracted by a cell or tissue sample and is then transcribed in vitro to recombinant DNA and also labeled with specific tracer molecules. These labeled fragments are then allowed to hybridize (i.e., to bind according to DNA-base complementarity) with specific probes (i.e. , nucleotide sequences) that have been immobilized on a slide, a so-called “gene chip.” Gene chips that are commercially available today carry probes that correspond to all known genes in our body. The intensity of the hybridization signal provides us with an estimate of gene expression, i.e., the amount of mRNA that corresponds to each particular gene that is being transcribed in the sample. By studying the expression of thousands of genes simultaneously, the transcriptional profile, alternatively termed “gene expression signature,” of the particular cell or tissue sample is obtained. Class Validation Gene expression profiling studies generate large amounts of data and have required the development of specific bioinformatics techniques in order to be successfully analyzed. Two principal analytic approaches are being used in this context. The first is termed “class validation,” and is used when a given classification scheme that is based on a traditional diagnostic method (e.g., “healthy” and “diseased” tissue, histological type 1 versus histological type 2 tumor) is explored at the level of gene expression. These studies can provide support for, or refute, the biological relevance of the original diagnostic A Message from Our Guest Editor … Nada Naaman, DDS, PhD Professor, Department of Periodontology Dean, Faculty of Dental Medicine Saint-Joseph University Beirut, Lebanon Dear Reader … I hope you will find this new issue of Gingival Health Dialogue as interesting as I did. The papers enclosed summarize recent discoveries in the field of periodontology, but reach the global dental profession and demonstrate the array of approaches available for maintaining healthy periodontal tissues. The issue begins with a brilliant review by Dr. Panos Papapanou on gene expression and disease classification. Based on earlier studies published by his group, he suggests a new pathobiology-based classification of periodontal disease that will implement future approaches. The next paper, written by the Distinguished Professor Sebastian Ciancio, is a review on the clinical efficacy of triclosan/copolymer- containing fluoride toothpastes. The author offers the latest information on this subject. The third paper, by Christine Hovliaras, presents a methodological view of tooth brushing and ergonomics, showing how an electric toothbrush can be an added value for improving oral hygiene. Next, Emily Boge presents novel and important data on an oral rinse and its active ingredients for controlling gingival inflammation. Dr. S.G. Damle then introduces the readers to the field of Ayurveda medicine, and shows how the application of this different medical approach can be effective in treating some diseases. The author then developed the data regarding oil pulling and oral health. Finally, we present the updated Second Edition of the textbook Periodontal Disease and Overall Health: A Clinician’s Guide (R.J. Genco and R.C. Williams, Editors), which is now available. On behalf of the program sponsor – the Colgate-Palmolive Company – I thank you for your readership. I am confident this important work is an added value for spreading scientific data to our profession. Sincerely, Volume 3 Number 2

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Page 1: Gingival Health - iowadha.com · Class Discovery The second analytical approach of such genomic data is collectively described as “class discovery.” In these analyses, a set of

Supported through an educational grant from

A New Approach to the Classification ofPeriodontal Diseases

Panos N. Papapanou, DDS, PhD

Gingival Healthdialogue

I n v e s t i g a t i o n s a n d I n s i g h t s i n G i n g i v a l H e a l t h R e s e a rc h

For the past decade, our research group at the Division of Periodontics,Columbia University College of Dental Medicine, has focused on the study ofgene expression signatures in gingival tissues, having as overall aims to (1)gain a better understanding of the pathobiology of periodontal diseases, and(2) provide the foundation for the development of a new classification ofperiodontitis based on pathobiology rather than on clinical symptomatology.

Gene Expression ProfilingGene expression profiling refers to the systematic cataloguing of

messenger–RNA (mRNA) molecules in a cell or tissue sample. As the readersof the Gingival Health Dialogue certainly recall from their basic biology courses,DNA in the nucleus is first transcribed into mRNA, before ultimately translatedinto protein. Protein expression is what decides the cell’s or the organ’s phenotype,i.e., it determines its characteristics and behavior. It is important to realizethat although all cells in our body share the same genetic information, theyproduce vastly different proteins depending on their specific functions. Byexamining which particular mRNAs are being transcribed at a given time pointin a specific cell population, we can get a rough idea of which particular proteinsare about to be translated in these cells and, thereby, an estimate of their expectedphenotype. One way that this can be studied in the lab is as follows: First,total RNA is extracted by a cell or tissue sample and is then transcribed invitro to recombinant DNA and also labeled with specific tracer molecules.These labeled fragments are then allowed to hybridize (i.e., to bind accordingto DNA-base complementarity) with specific probes (i.e., nucleotide sequences)that have been immobilized on a slide, a so-called “gene chip.” Gene chipsthat are commercially available today carry probes that correspond to all knowngenes in our body. The intensity of the hybridization signal provides us withan estimate of gene expression, i.e., the amount of mRNA that corresponds toeach particular gene that is being transcribed in the sample. By studying theexpression of thousands of genes simultaneously, the transcriptional profile,alternatively termed “gene expression signature,” of the particular cell or tissuesample is obtained.

Class ValidationGene expression profiling studies generate large amounts of data and have

required the development of specific bioinformatics techniques in order to besuccessfully analyzed. Two principal analytic approaches are being used inthis context. The first is termed “class validation,” and is used when a givenclassification scheme that is based on a traditional diagnostic method (e.g.,“healthy” and “diseased” tissue, histological type 1 versus histological type 2tumor) is explored at the level of gene expression. These studies can providesupport for, or refute, the biological relevance of the original diagnostic

A Message from Our Guest Editor …Nada Naaman, DDS, PhDProfessor, Department of PeriodontologyDean, Faculty of Dental MedicineSaint-Joseph UniversityBeirut, Lebanon

Dear Reader …

I hope you will find this new issue of Gingival Health Dialogue asinteresting as I did. The papers enclosed summarize recent discoveriesin the field of periodontology, but reach the global dental professionand demonstrate the array of approaches available for maintaininghealthy periodontal tissues.

The issue begins with a brilliant review by Dr. Panos Papapanouon gene expression and disease classification. Based on earlier studiespublished by his group, he suggests a new pathobiology-basedclassification of periodontal disease that will implement futureapproaches.

The next paper, written by the Distinguished Professor SebastianCiancio, is a review on the clinical efficacy of triclosan/copolymer-containing fluoride toothpastes. The author offers the latestinformation on this subject.

The third paper, by Christine Hovliaras, presents a methodologicalview of tooth brushing and ergonomics, showing how an electrictoothbrush can be an added value for improving oral hygiene.

Next, Emily Boge presents novel and important data on an oralrinse and its active ingredients for controlling gingival inflammation.

Dr. S.G. Damle then introduces the readers to the field of Ayurvedamedicine, and shows how the application of this different medicalapproach can be effective in treating some diseases. The authorthen developed the data regarding oil pulling and oral health.

Finally, we present the updated Second Edition of the textbookPeriodontal Disease and Overall Health: A Clinician’s Guide (R.J.Genco and R.C. Williams, Editors), which is now available.

On behalf of the program sponsor – the Colgate-Palmolive Company –I thank you for your readership. I am confident this important work isan added value for spreading scientific data to our profession.

Sincerely,

Volume 3 Number 2

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classification scheme, and can also identify specific genes that arerelevant to the distinction between classes. An example of successfulimplementation of a genomic approach with significant translationalvalue in patient care is work in breast cancer by a research group inthe Netherlands.1 These investigators examined gene expression intwo groups of malignant breast tumors, one of which was often associatedwith lymph node involvement, metastasized rapidly, and frequentlyresulted in death within a five-year period from diagnosis; the othergroup behaved much less aggressively, i.e., was associated with infrequentlymph node involvement, metastasis, or death. Gene expression profilingof these tumors showed significant differential expression between thetwo groups with respect to 70 specific “reporter genes.” Theseobservations resulted in the development of a diagnostic tool for tumorbehavior,2 which was used in subsequent studies to predict the outcomechemotherapy3 and to study genes that mediated metastasis of breasttumor into the brain.4

Class DiscoveryThe second analytical approach of such genomic data is collectively

described as “class discovery.” In these analyses, a set of samples withno previous diagnostic distinctions is examined for evidence of newclassifications, which can then be related to relevant clinical variables.For example, diffuse large B-cell lymphomas have been classified intwo groups based on gene expression data, and these groups differedin long-term prognosis.5 Otherwise heterogeneous breast cancers6 couldbe classified into a small number of distinct groups characterized bymajor differences in gene expression. Importantly, successful applicationof gene expression profiling in the study of human diseases has notbeen restricted to cancer; it has also included diseases of multifactorialetiology, such as Alzheimer’s disease,7 arthritis,8 and asthma.9

Application of Gene Expression in Classifying Periodontal DiseaseInspired by the publications above, our group initiated similar studies

targeting periodontal diseases. We hypothesized that the study of geneexpression in gingival tissues would identify the molecular underpinningsof periodontal homeostasis and pathology, and would ultimately facilitatethe development of a novel classification of periodontitis based onpathobiology. In this project, we recruited a sample of 120 periodontitispatients, including men and women with either chronic or aggressiveperiodontitis (63 and 57 patients, respectively). From each of theseindividuals, we harvested at least two interproximal gingival papillaefrom areas with deep pockets, attachment loss, and bleeding on probing,as well as one control healthy tissue sample (with no signs of clinicalinflammation, pocketing, or attachment loss), if available. Prior toharvesting these tissue samples, we also obtained samples of subgingivalplaque from both the mesial and distal aspect of the harvestedinterproximal gingival papilla. In all, our completed database consistedof 311 tissue samples (240 from diseased and 71 from healthy sites)that were analyzed with respect to the level of expression of > 38,500well-characterized genes. The database also included the correspondingsubgingival plaque samples that were analyzed with respect to thelevel of each of 11 bacterial species, as well a sample of peripheral bloodfrom each participant that was analyzed with respect to the presenceof IgG antibodies to each of the 11 bacterial species.Our first publication originating from this database10 provided the

first comprehensive description of gene expression signatures in thegingival tissues in states of periodontal health and disease, and identified

those genes and molecular pathways that are differentially expressedbetween the two conditions. The full listings of these genes and pathwaysare available online and provide a valuable resource to researchers inthe scientific community. Our next aim was to explore whether the bacterial content of the

periodontal pocket facing the gingival tissues was a significant determinantof gene expression. This work11 demonstrated that the levels of certainbacteria, including Campylobacter rectus, Porphyromonas gingivalis,and Tannerella forsythia are strong regulators of gene expression inthe adjacent gingiva, while levels of other bacteria were only weaklyassociated with differential gene expression in the tissues. Subsequently,we proceeded with a formal class validation step, and comparedexpression patterns in gingival tissue lesions originating from patientswith either chronic or aggressive periodontitis.12 This work demonstratedthat the differences in the transcriptomes of the two main forms ofperiodontitis are relatively limited, and did not provide any supportfor the commonly believed notion that there are fundamental differencesin the molecular makeup of lesion-form chronic and aggressiveperiodontitis. In other words, the gingival tissues forming a deep pocketobtained from a chronic periodontitis patient expressed largely similarmRNA patterns as gingival tissues from a pocket of an aggressiveperiodontitis patient with similar clinical characteristics. However, when we proceeded with a class discovery approach,13

i.e., first pooled together all chronic and aggressive periodontitis patientsand asked the transcriptomes to identify novel groups based on commongene expression patterns, we identified two robust clusters based onthe molecular patterns (Figure 1). Interestingly, these two clustersalso displayed significant phenotypic differences. Thus, patients in

Figure 1. Transcriptomes identify two molecular clusters. Green colors indicate lowgene expression; red colors indicate high expression.

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Cluster #2 showed higher extent and severity of periodontitis thantheir Cluster #1 counterparts, as indicated by statistically significantlyhigher mean probing depth (PD), mean clinical attachment loss (CAL),and mean number of sites with PD ≥ 5 mm or CAL ≥ 5 mm. In addition,patients in Cluster #2 showed a higher frequency of sites with bleedingon probing, despite comparable levels of dental plaque. With respectto bacterial profiles, patients in Cluster #2 were more heavily colonizedby most “red” and “orange complex” species examined, while colonizationlevels by health-associated bacteria were significantly higher in Cluster#1. Furthermore, patients in Cluster #2 showed approximately five-fold higher mean serum IgG antibody levels to Campylobacter rectus,significantly higher IgG levels to T. denticola and Actinomyces naeslundii,and a tendency for higher IgG to P. gingivalis. Lastly, when assessing the host responsiveness to periodontal

colonization by using the ratio of antibody titer over the mean level ofcolonization by the homologous species (“infection ratio,”14 Cluster#2 patients showed significantly more robust responses to C. rectusand A. naeslundii. These findings demonstrate that gingival tissuetranscriptomes can indeed identify clusters of patients with distinctperiodontal phenotypes, and thus suggest that, after further developmentand appropriate external validation, this approach can provide thefoundation for a novel, pathobiology-based classification of periodontitis.

Application to the Study of Gingival InflammationOur laboratory has used a similar approach in the study of the

development of gingival inflammation using an experimental gingivitismodel. In this study,15 ten periodontally healthy volunteers abstainedfrom plaque control over a period of three weeks and donated gingivaltissues at baseline, 7, 14, and 21 days of plaque accumulation (“inductiongroup”). A second group comprising another 10 individuals developedexperimental gingivitis over 21 days, after which they received prophylaxisand reinstituted oral hygiene measures; they donated gingival tissuesat days 21, 25, 30, and 35 (“resolution group”). By serially examiningthe activation of genes over time, we were able to study the moleculardynamics in the gingival tissues during the induction and resolution ofexperimentally induced inflammation. As shown in Figure 2, the mosteventful period in terms of gene activation in the gingival tissues wasthe second week of gingivitis induction and the first five days afterprophylaxis and reinstitution of oral hygiene. In the same volunteers,we used a high throughput proteomic approach to identify proteinssecreted in the gingival crevicular fluid during the course of experimentalgingivitis.16 Using liquid chromatography-tandem mass spectrometry(LC-MS/MS), we identified a total of 254 human, 14 bacterial, 12 fungal,and 7 yeast proteins, several of which were reported for the first timeas involved in gingival inflammation.

The Future of Pathobiological Approaches to Periodontal DiseaseOur research group is continuing to develop an integrated systems

biology approach in the study of the pathobiology of periodontal diseases.We expect that the use of the high throughput technologies described

above will shed new light into our understanding of the complex molecularinteractions that occur in the gingival tissues.

References

1. van ‘t Veer LJ, Dai H, van de Vijver MJ, He YD, Hart AA, Mao M, PeterseHL, van der Kooy K, Marton MJ, Witteveen AT, Schreiber GJ, KerkhovenRM, Roberts C, Linsley PS, Bernards R, Friend SH. Gene expressionprofiling predicts clinical outcome of breast cancer. Nature 2002;415:530-6.

2. Schubert CM. Microarray to be used as routine clinical screen. NatMed 2003;9:9.

3. Straver ME, Glas AM, Hannemann J, Wesseling J, van de Vijver MJ,Rutgers EJ, Vrancken Peeters MJ, van Tinteren H, van’t Veer LJ,Rodenhuis S. The 70-gene signature as a response predictor forneoadjuvant chemotherapy in breast cancer. Breast Cancer Res Treat

These findings demonstrate that gingival tissue transcriptomes,after further development and appropriate external validation,can provide the foundation for a novel, pathobiology-basedclassification of periodontitis.

Dr. Papapanou is Professor and Chairman,Division of Periodontics, Section of Oral andDiagnostic Sciences, Columbia UniversityCollege of Dental Medicine, New York, NY, USA.

Continued on pg. 12

Figure 2.Number of differentially expressed genes during the induction and resolution phases.Red color indicates upregulated genes, green color indicates downregulated genes.

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In 1992, the Colgate-Palmolive Company introduced Colgate®

Total® Toothpaste, containing 0.3% triclosan — a broad spectrumantibacterial — 2.0% polyvinylmethyl ether maleic acid (PVM/MA)copolymer, and 0.243% sodium fluoride in a silica base. The additionof the copolymer to the dentifrice formulation allowed for greateruptake and retention of the triclosan to the enamel and buccalepithelial cells, providing long-lasting antimicrobial effects that arewell documented.1 Colgate® Total® is accepted as safe and effectiveby the American Dental Association and by dental associations inover 40 countries around the world.

Efficacy of Colgate® Total® ToothpasteReview of Clinical Benefits by an Independent OrganizationColgate® Total® Toothpaste was the subject of a recently published

review by the prestigious Cochrane Collaboration.2 They designeda meta-analysis that included 30 studies, published between 1990and 2012, involving 14,835 participants. The objective of the reviewwas to assess the effect of triclosan/copolymer-containing fluoridetoothpastes, compared with other fluoride toothpastes, for the long-term control of caries, plaque, and gingivitis in children and adults.The findings clearly support the beneficial oral health effects ofdaily use of Colgate® Total® Toothpaste on reduction of plaque,gingivitis, caries, and calculus. These effects were greater than thoseseen with non-triclosan-containing toothpaste use. Further, thereview found no indication of adverse effects associated with theuse of this dentifrice.

Plaque and GingivitisThe clinical efficacy and safety of triclosan/copolymer was

demonstrated in over 2,000 subjects who participated in 13 six-month, independent, double-blind clinical studies which followeda similar study design.3-15 The triclosan/copolymer dentifrice reducedplaque and gingivitis up to 58.9% and up to 41.9%, respectively, ascompared to a placebo dentifrice. These studies are summarizedin Table 1.

Oral MalodorClinical studies also demonstrate that a triclosan/copolymer/fluoride

dentifrice provides long-lasting fresh breath protection,16-18 andspecifically inhibits volatile sulfur compound (VSC)-producingbacteria.19 In addition, there were no significant local or systemicadverse effects observed following triclosan/copolymer/fluoridedentifrice use, including lack of development of bacterial resistance.This is not surprising since triclosan has a nearly four-decade historyof safe use in soaps and deodorants.20

PeriodontitisFour separate long-term clinical studies, one of which was five

years in duration, were conducted on over 1,200 subjects to assessthe effect of the daily use of a triclosan/copolymer/fluoride dentifriceon periodontitis.21-24 Results from these studies showed reductionsin attachment loss and pocket depth, and gains in clinical attachmentlevels. These data suggest that a triclosan/copolymer/fluoride dentifricemay be of benefit in stabilizing patients after periodontal therapy.

CalculusIn addition to benefits on periodontal health, four studies demonstrated

significant differences in supragingival calculus levels in patients who

Clinical Efficacy of a Triclosan/Copolymer DentifriceSebastian G. Ciancio, DDS

Colgate® Total® is accepted as safe and effective by the AmericanDental Association and by dental associations in over 40 countriesaround the world.

Table 1. Plaque and Gingivitis Efficacy of Triclosan/Copolymer Dentifrice Long-Term Clinical Studies

Investigators # Subjects Duration (Mo) Plaque Efficacy vs. Placebo Gingivitis Efficacy vs. Placebo% Plaque Reduction % Gingivitis Reduction

Mankodi, et al.11 294 6 -11.9 -19.7Bolden, et al.4 306 6 -17.9 -29.0Garcia-Godoy, et al.8 108 7 -58.9 -30.1Cubells, et al.5 108 6 -24.9 -19.7Deasy, et al.6 121 6 -32.3 -25.6Denepitiya, et al.7 145 6 -18.4 -31.5Palomo, et al.12 98 6 -12.7 -24.1Triratana, et al.15 120 6 -32.9 -18.8Lindhe, et al.10 110 6 -31.2 -26.6Renvert and Birkhed13 114 6 -25.0 -41.9Svatun, et al.14 220 7 – -25.0Hu, et al.9 183 6 -16.1 -24.3Allen, et al.3 110 6 -29.9 -33.2

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used the triclosan/copolymer/fluoride dentifrice as compared to a placebodentifrice (p < 0.01), with an average reduction of 34%.25-28

Anti-Inflammatory Effects of Colgate® Total® Toothpaste

Since excessive or chronic inflammation can cause tissue damageand has been associated with systemic diseases, control of inflammationis important for both gingival and general health. Research suggeststhat the anti-gingivitis effect of a triclosan/copolymer/fluoride dentifriceresults from its combined antimicrobial and anti-inflammatory properties. As early as 1993, it was suggested that triclosan could reduce

inflammation. Since then, a number of investigatorshave conductedstudies to assess the anti-inflammatory action of triclosan.29-33 Thesestudies demonstrated that triclosan inhibited the production of twoinflammatory cytokines — interleukin-1 beta (IL-1b) and tumor necrosisfactor alpha (TNF-a). These cytokines stimulate robust inflammatoryresponses that often result in both soft and hard tissue destruction. Inaddition, IL-1b and TNF-a can induce production of prostaglandin E2(PGE2), a potent inflammatory mediator, during the early stages ofinflammation. PGE2causes collagen breakdown and bone resorption,and exhibits a broad range of inflammatory effects. Importantly, triclosaninhibits both IL-1b and TNF-a-induced PGE2production for up to 24hours, likely due to the inhibition of PGE2biosynthesis. Finally, recent work indicates that triclosan can support the stability

of collagen by inhibiting matrix metalloproteinase (MMP) productionin fibroblasts and osteoblasts that were stimulated with inflammatorycytokines. This dual action is demonstrated in Figure 1.

Safety of Colgate TotalSafety of Long-Term Use of Colgate® Total® Toothpaste in HumansGovernment agencies and health officials around the world support

the use of triclosan where efficacy and safety has been demonstrated,

as is the case with Colgate® Total® Toothpaste.34-38 These agency reviewsinclude:• U.S. Food and Drug Administration;35

• U.S. Environmental Protection Agency, Cancer Assessment Review Committee (2005);34

• Health Canada;36

• Commission, Scientific Committee on Consumer Products (2009);39 and

• Australian Industrial Chemicals Notification and Assessment Scheme (2009).37

The reviews showed that no studies documented adverse humanhealth outcomes from the use of triclosan in toothpaste. The levels oftriclosan used in toothpaste and other consumer products have beendetermined by these regulatory agencies to be safe, efficacious for oralhealth, and not harmful to human health. Additionally, as part of a company’s approval under the U.S. Food

and Drug Administration (FDA) New Drug Application (NDA) process,if the company becomes aware of any serious adverse event, they arerequired to immediately report it to the FDA. All adverse events mustbe monitored for trends as part of a signal detection process. In thenearly 18 years that Colgate® Total® Toothpaste has been on the marketin the United States, there has been no signal of a safety issue fromadverse event reports. It is noteworthy that Colgate® Total® is the onlyFDA-approved toothpaste that has gone through the rigorous NDA process— the same process used to review the safety of prescription drugs.

Triclosan Does Not Induce Local or Systemic Bacterial ResistanceResistance of oral microorganisms to triclosan has not been

demonstrated clinically. It is hypothesized that microorganisms fail todevelop resistance because triclosan exerts its antibacterial propertiesthrough multiple, dose-dependent mechanisms. Further, severalpublications document the existence of multiple sites/modes of actionof triclosan.40 Its primary site of action is thought to be at the cytoplasmicmembrane, resulting in interference with uptake of amino acids, uracil,and other nutrients. At higher concentrations (more typical of thoseassociated with toothpaste use), membrane lesions and leakage of cellcontents are observed leading to cell death.41 Thus, triclosan exerts itseffects through multiple mechanisms, and this is thought to explainthe lack of microbial resistance observed.The development of microbial resistance in patients using a triclosan-

containing toothpaste has been carefully studied. Six long-term clinicalstudies (6–60 months) in approximately 1,000 patients concludedthat there was no significant adverse shift in flora comprising the normalplaque, nor the periodontopathogenic, cariogenic, or opportunisticmicrobes. Moreover, no resistant strains emerged over the experimentalperiod of 6–60 months after dentifrice usage. The results of these earlier studies are supported by findings from a

five-year clinical study in over 500 patients using Colgate® Total®

Toothpaste.21 This study evaluated both clinical and microbiologicendpoints in the active group compared to the controls. Results showed

Figure 1. Antibacterial and anti-inflammatory effects of triclosan.

It is noteworthy that Colgate® Total® is the only FDA-approvedtoothpaste that has gone through the rigorous NDA process — thesame process used to review the safety of prescription drugs.

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that clinical efficacy was maintained for the five-year period.Measurements of dental plaque bacteria (P. gingivalis, P. intermedia,and A. actinomycetemcomitans) showed results consistent with thelack of development of resistance by any of the organisms studied overthe five years. These studies are summarized in Table 2. Most recently, a 2014 study analyzed dental plaque samples collected

at eleven different times over 19 years from 58 adults using a 0.3%triclosan, 2.0% copolymer, and 0.243% sodium fluoride toothpaste.42

The study also included plaque samples from 97 adults using toothpastewithout triclosan. In addition, the susceptibility of supragingival dentalplaque collected from subjects who used the triclosan dentifrice for5–13 years was compared to subjects who used a dentifrice withouttriclosan. Each sample contained supragingival dental plaque collectedfrom the entire dentition. The samples were cultured in media alone,or in media with 7.5 or 25 �g/ml of triclosan. The concentrations oftriclosan used in this study were selected based on the MICs (MinimalInhibitory Concentration) for strains of oral bacteria.43

Results showed that the growth inhibition averaged 99.451%(91.209%–99.830%) on media containing 7.5 �g/ml triclosan and 99.989%(99.670%–100%) on media containing 25 �g/ml triclosan. There was nodiscernable change in microbial susceptibility to triclosan over timein plaque samples taken over 19 years, including samples from subjectsusing a triclosan-containing dentifrice for at least five years. For the susceptibility testing, supragingival plaque samples from

both groups demonstrated susceptibility to both concentrations oftriclosan. There was no significant difference in triclosan susceptibilitybetween those who regularly used triclosan dentifrice and those whodid not (p < 0.05). From this study the authors concluded that thecommunity-level assessment of microbial susceptibility to triclosan isconsistent with the long-term microbiologic safety of a 0.3% triclosan,2.0% copolymer, 0.243% sodium fluoride dentifrice. Thus, it is clearthat data generated from carefully controlled clinical trials of up tofive years in duration, a community-level assessment spanning 19 yearsof use, and over 25 years of daily use around the world fully supportthe microbiologic safety of Colgate® Total® Toothpaste.34-38

Lack of Relevance of Animal StudiesThere have been some questions raised by articles in the public

media relative to the safety of triclosan based on data from animalstudies. Studies in rats have suggested it causes an alteration of hormonesassociated with the thyroid gland and reproductive organs, as well ascarcinogenic effects in mice. However, it is important to note that animal

studies are used during drug development to establish the safety of aproduct and evaluate its pharmacological effects. To determine drugsafety, these experiments rely on high levels of triclosan; in some instancesinjected directly into the abdomen and at levels thousands of timesgreater than from exposure through the use of consumer products.Also, the safety evaluation of triclosan includes lifetime exposure studiesin laboratory animals such as rats, hamsters, and mice.44

In addition, the potential endocrine effect of triclosan in toothpastehas been assessed in two human clinical studies and neither studyshowed any adverse effect. In fact, not a single study has documentedadverse endocrine health outcomes from the use of triclosan in consumerproducts. A comprehensive, independent analysis of the scientificliterature regarding triclosan-containing toothpaste and endocrineeffects was conducted. It was published in the peer-reviewed journalCritical Reviews in Toxicology, and affirms the safety of Colgate® Total®

Toothpaste relative to endocrine function.45,46

Finally, there is no indication that lifetime exposure to triclosanresulted in an increase in tumor development in rats and hamsters.Tumors found in mice were due to a well-recognized mechanism specificto the species that is not relevant in humans. This non-relevance hasbeen affirmed by regulatory agencies.35,39 Every regulatory agency thathas reviewed the safety of triclosan, including its use in Colgate® Total®

Toothpaste, has concluded, based on evidence, that triclosan is notcarcinogenic in humans.

ConclusionTriclosan in a dentifrice formulation has been used since 1992, with

billions of doses applied by consumers. It is remarkable that with suchbroad use, adverse events reported have been minimal (less than1/100,000) and are the same as for non-triclosan-containing dentifrices.These users have also had no reports of clinical conditions suggestingthe development of opportunistic, pathogenic, or resistantmicroorganisms, or significant adverse effects on body organs and tissuesor oral tissues in studies ranging from six months to five years. It is noteworthy that 90 clinical studies over 20 years among 20,000

subjects support the safety and efficacy of Colgate®Total

®Toothpaste.

It comes as no surprise, therefore, that the American Dental Association,

Table 2. Summary of Microflora Studies with Triclosan/Copolymer Dentifrice

Investigator No. of Subjects Duration (Mo) Development of OrganismsOpportunistic Pathogenic Resistance

Zambon, et al.47 81 6 No No NoBonta, et al.48 74* 12 No No NoWalker, et al.49 136 6 No No NoZambon, et al.50 159 6 No No NoFine, et al.51 71 12** No No NoCullinan, et al.21 504 60 No No No*Continuation of subjects from study by Zambon, et al.47**Subjects followed for an additional 6 months following 6 months’ use of a triclosan/copolymer/fluoride dentifrice.

Every regulatory agency that has reviewed the safety of triclosan,including its use in Colgate® Total® Toothpaste, has concluded, basedon evidence, that triclosan is not carcinogenic in humans.

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on August 15, 2014, reaffirmed its acceptance of Colgate® Total®

Toothpaste for its Seal.

Acknowledgment: The author would like to thank Dr. Srinivas Rao Myneni forhis editorial and content assistance.

References

1. Gaffar A, Nabi N, Kashuba B, et al. Antiplaque effects of dentifrices containingtriclosan/copolymer/NaF system versus triclosan dentifrices without thecopolymer. Am J Dent 1990;3(Spec No):S7-14.

2. Riley P, Lamont T. Triclosan/copolymer containing toothpastes for oral health.The Cochrane Database Syst Rev 2013;12:CD010514.

3. Allen DR, Battista GW, Petrone DM, et al. The clinical efficacy of Colgate TotalPlus Whitening Toothpaste containing a special grade of silica and ColgateTotal Fresh Stripe Toothpaste in the control of plaque and gingivitis: a six-month clinical study. J Clin Dent 2002;13:59-64.

4. Bolden TE, Zambon JJ, Sowinski J, et al. The clinical effect of a dentifrice containingtriclosan and a copolymer in a sodium fluoride/silica base on plaque formationand gingivitis: a six-month clinical study. J Clin Dent 1992;3:125-31.

5. Cubells AB, Dalmau LB, Petrone ME, Chaknis P, Volpe AR. The effect of atriclosan/copolymer/fluoride dentifrice on plaque formation and gingivitis: a six-month clinical study. J Clin Dent 1991;2:63-9.

6. Deasy MJ, Singh SM, Rustogi KN, et al. Effect of a dentifrice containing triclosanand a copolymer on plaque formation and gingivitis. Clin Prev Dent 1991;13:12-9.

7. Denepitiya JL, Fine D, Singh S, DeVizio W, Volpe AR, Person P. Effect uponplaque formation and gingivitis of a triclosan/copolymer/fluoride dentifrice: a6-month clinical study. Am J Dent 1992;5:307-11.

8. Garcia-Godoy F, Garcia-Godoy F, DeVizio W, Volpe AR, Ferlauto RJ, Miller JM.Effect of a triclosan/copolymer/fluoride dentifrice on plaque formation andgingivitis: a 7-month clinical study. Am J Dent 1990;3(Spec No):S15-26.

9. Hu D, Zhang J, Wan H, Zhang Y, Volpe AR, Petrone ME. [Efficacy of atriclosan/copolymer dentifrice in the control of plaque and gingivitis: a six-month study in China]. Hua xi kou qiang yi xue za zhi = Huaxi kouqiangyixue zazhi = West China J Stomatol 1997;15:333-5.

10. Lindhe J, Rosling B, Socransky SS, Volpe AR. The effect of a triclosan-containingdentifrice on established plaque and gingivitis. J Clin Periodontol 1993;20:327-34.

11. Mankodi S, Walker C, Conforti N, DeVizio W, McCool JJ, Volpe AR. Clinicaleffect of a triclosan-containing dentifrice on plaque and gingivitis: a six-monthstudy. Clin Prev Dent 1992;14:4-10.

12. Palomo F WL, Sanchez A, et al. Plaque/gingivitis efficacy of triclosan dentrifices.J Dent Res 1993;72:334.

13. Renvert S, Birkhed D. Comparison between 3 triclosan dentifrices on plaque,gingivitis and salivary microflora. J Clin Periodontol 1995;22:63-70.

14. Svatun B, Sadxton CA, Huntington E, Cummins D. The effects of three silicadentifrices containing Triclosan on supragingival plaque and calculus formationand on gingivitis. Int Dent J 1993;43:441-52.

15. Triratana T, Kraivaphan P, Amornchat C, Rustogi K, Petrone MP, Volpe AR.Effect of a triclosan/copolymer pre-brush mouthrinse on established plaque

formation and gingivitis: a six-month clinical study in Thailand. J Clin Dent1995;6:142-7.

16. Niles HP, Vazquez J, Rustogi KN, Williams M, Gaffar A, Proskin HM. The clinicaleffectiveness of a dentifrice containing triclosan and a copolymer for providinglong-term control of breath odor measured chromatographically. J Clin Dent1999;10:135-8.

17. Sharma NC, Galustians HJ, Qaqish J, et al. The clinical efficacy of ColgateTotal Plus Whitening Toothpaste containing a special grade of silica and ColgateTotal Toothpaste for controlling breath odor twelve hours after toothbrushing:a single-use clinical study. J Clin Dent 2002;13:73-6.

18. Sreenivasan PK, Furgang D, Zhang Y, DeVizio W, Fine DH. Antimicrobial effectsof a new therapeutic liquid dentifrice formulation on oral bacteria includingodorigenic species. Clin Oral Invest 2005;9:38-45.

19. Gaffar A, Afflitto J, Nabi N, Herles S, Kruger I, Olsen S. Recent advances in plaque,gingivitis, tartar and caries prevention technology. Int Dent J 1994;44:63-70.

20. Regos J, Zak O, Solf R, Vischer WA, Weirich EG. Antimicrobial spectrum of triclosan,a broad-spectrum antimicrobial agent for topical application. II. Comparisonwith some other antimicrobial agents. Dermatologica 1979;158:72-9.

21. Cullinan MP, Westerman B, Hamlet SM, Palmer JE, Faddy MJ, Seymour GJ.The effect of a triclosan-containing dentifrice on the progression of periodontaldisease in an adult population. J Clin Periodontol 2003;30:414-9.

22. Ellwood RP, Worthington HV, Blinkhorn AS, Volpe AR, Davies RM. Effect of atriclosan/copolymer dentifrice on the incidence of periodontal attachmentloss in adolescents. J Clin Periodontol 1998;25:363-7.

23. Furuichi Y, Rosling B, Volpe AR, Lindhe J. The effect of a triclosan/copolymerdentifrice on healing after non-surgical treatment of recurrent periodontitis. JClin Periodontol 1999;26:63-6.

24. Rosling B, Wannfors B, Volpe AR, Furuichi Y, Ramberg P, Lindhe J. The use ofa triclosan/copolymer dentifrice may retard the progression of periodontitis. JClin Periodontol 1997;24:873-80.

25. Banoczy J, Sari K, Schiff T, Petrone M, Davies R. Anticalculus efficacy of threedentifrices. Am J Dent 1995;8:205-8.

26. Lobene RR, Battista GW, Petrone DM, Volpe AR, Petrone ME. Clinical efficacyof an anticalculus fluoride dentifrice containing triclosan and a copolymer: a6-month study. Am J Dent 1991;4:83-5.

27. Schiff T, Cohen S, Volpe AR, Petrone ME. Effects of two fluoride dentifricescontaining triclosan and a copolymer on calculus formation. Am J Dent1990;3(Spec No):S43-5.

28. Volpe AR, Schiff TJ, Cohen S, Petrone ME, Petrone D. Clinical comparison ofthe anticalculus efficacy of two triclosan-containing dentifrices. J Clin Dent1992;3:93-5.

29. Mustafa M, Bakhiet M, Wondimu B, Modeer T. Effect of triclosan on interferon-gamma production and major histocompatibility complex class II expressionin human gingival fibroblasts. J Clin Periodontol 2000;27:733-7.

30. Mustafa M, Wondimu B, Ibrahim M, Modeer T. Effect of triclosan on interleukin-1 beta production in human gingival fibroblasts challenged with tumor necrosisfactor alpha. Eur J Oral Sci 1998;106:637-43.

31. Mustafa M, Wondimu B, Yucel-Lindberg T, Kats-Hallstrom AT, Jonsson AS,Modeer T. Triclosan reduces microsomal prostaglandin E synthase-1 expressionin human gingival fibroblasts. J Clin Periodontol 2005;32:6-11.

32. Panagakos FS. Triclosan inhibition of cytokine-stimulated MMP production byosteoblast-like cells. J Dent Res 2003:2248.

33. Skold-Larsson K, Yucel-Lindberg T, Twetman S, Modeer T. Effect of a triclosan-containing dental gel on the levels of prostaglandin I2 and interleukin-1beta ingingival crevicular fluid from adolescents with fixed orthodontic appliances.Acta Odontol Scand 2003;61:193-6.

34. (www.epa.gov) USEPA.35. (www.fda.gov) USFaDA.36. (www.hc-sc.ca) HC.

Continued on pg. 10

Dr. Ciancio is Distinguished Service Professor,Chair in the Department of Periodontology, andDirector of the Center for Dental Studies at theState University of New York (SUNY) at Buffalo.He was recently named the 2014 recipient ofthe coveted Norton M. Ross Award for Excellencein Clinical Research.

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IntroductionAs dental professionals in the twenty-first century, we acknowledge

that one of the most essential components for optimal oral hygienecare is utilizing the toothbrush to effectively remove acquired pellicleand dental plaque biofilm, thus helping prevent dental caries, gingivitis,and periodontitis. This article will discuss the important role ergonomicsplays in tooth brushing, and how we as dental professionals need toselect the right toothbrush for our patients based upon their oral careneeds and level of manual dexterity, and encourage them throughprofessional recommendation and instruction to brush for at least atwo-minute period of time at least twice daily to effectively reach thegumline and tooth surfaces for improved oral health.

The Importance of ErgonomicsErgonomics refers to the application of scientific knowledge from

the fields of anatomy, physiology, mechanics, and psychology to utilizehuman energy most effectively. Examples of ergonomically developeditems include furniture that consumers use in their homes and at theworkplaces that are designed to fit a lifestyle by being comfortable andeasy to use; as well as toothbrushes that a person can grip and utilizeto effectively clean their teeth and gums. Ergonomics should provide asafe and non-threatening environment for continued use of these itemson both a daily and long-term basis.

When we look at the effect of ergonomics on tooth brushing with amanual or electric toothbrush, there is not an abundance of publishedresearch that offers insights in this area. Ergonomics plays a vital rolein assisting patients to comply with oral hygiene care at home afterthey have visited their dental professional for a six-month professionalcleaning and oral examination.

Today’s ToothbrushesThe toothbrushes that are offered to consumers in both manual and

electric (which includes sonic) options today have evolved with regardto the shape of the toothbrush head, the length of the toothbrush handle,and the length of the bristles. Additionally, flat-trimmed brush headshave progressed to multi-leveled bristle configurations, bristleconfiguration has also advanced to include polishing cups, handle griphas improved for comfort during tooth brushing, timers have beenadded to electric toothbrushes to assist consumers in brushing quadrantslonger, and thousands of vibrating strokes provided per minute helpconsumers brush more thoroughly around teeth and the gingival marginto remove plaque biofilm.

Consumers’ Tooth Brushing TimesConsumer studies show that most people will brush their teeth for

less than a minute, versus the two minutes that the American Dental

Association advises.1,2 I would like to highlight two separate studiesthat review the length of consumer brushing time. The first study, whichincluded two global studies in Zurich conducted by Saxer, et al., reportedthat consumers’ estimated time they brushed was higher than the actualbrushing time; 134.1 to 148.1 seconds and 83.5 to 72.8 seconds,respectively.3 Gallagher, et al. reported that brushing for two minutesremoved 26 percent more plaque than brushing for 45 seconds, thusoral healthcare professionals should reinforce efforts to persuade patientsto brush for longer periods of time in order to provide clinically significantoral health benefits.4

Another study highlighted the use of powered toothbrushes vs. manualtoothbrushes in reducing plaque and calculus levels without formalinstruction. The use of powered toothbrushes equipped with timingdevices improved overall time spent tooth brushing as compared tousing a manual toothbrush. Dentino, et al. reported that 17 percent ofmanual toothbrush users met the two-minute brushing time as comparedto 66 percent of powered toothbrush users.5 The increased efficacy ofthe powered toothbrush is related to the small head design, as well asthe presence of the timing device to encourage longer brushing times.This study also showed that if subjects were instructed on proper oralhygiene there would be even greater oral care benefits.5

Manual and Electric ToothbrushesWhen ergonomics is explored in the manual toothbrush category,

we can consider the handle and grip design, angulation of the toothbrushhead, the design of the toothbrush head to reach posterior teeth, andtoothbrush bristles being able to reach the gumline and interproximalspaces to remove dental plaque biofilm and food debris.With electric toothbrushes, we observe these same elements as

mentioned above for manual toothbrushes. In addition, we need toconsider if the device is easy to turn on and off, what are the brushingspeeds offered to the user, if changes in brushing speeds provide feedback(audible or tactile), what these brushing speeds mean duringtoothbrushing, rechargeability of the toothbrush device, and the sizeof the toothbrush and holder, relative to storage and use in the bathroomat home.

The New Colgate® ProClinical™

A1500 Electric ToothbrushIn the fall of 2012, the Colgate-Palmolive Company launched its

first electric toothbrush, the Colgate® ProClinical™ A1500 ElectricToothbrush (Figure 1). This sonic toothbrush provides high frequencybrush strokes with an audibility range to the human ear as being roughly20Hz to 20kHz. Three brushing modes are offered (Auto, Optimum,and Deep Clean) and operate at a frequency range between 20,000 –32,500 strokes per minute.6

This engineered sonic-powered toothbrush provides the latesttechnology in the Auto mode, which allows the brush to adjust its audiblespeed while the user moves the handle in any direction in the oralcavity without having to change speed manually. This is a desirableoption; the toothbrush does the work of brushing for the user, allowing

Toothbrushing and ErgonomicsChristine A. Hovliaras, RDH, BS, MBA, CDE

Ergonomics plays a vital role in assisting patients to comply withoral hygiene care at home after they have visited their dentalprofessional for a six-month professional cleaning and oralexamination.

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the experience to be more pleasant and enjoyable. In low-speed, theColgate ProClinical A1500 toothbrush head will perform a back andforth sweeping motion to brush the buccal and lingual surfaces of theteeth.The Optimum mode operates at mid-speed at a frequency of 27,000

strokes per minute and moves in up-down and side-to-side strokes toclean the gumline at a 45° angle. This electric toothbrush utilizes anLED display that lights up on the handle when the consumer is brushingat a 45° angle along the gumline6 (Figure 2a).The Deep Clean mode operates at a frequency of 32,500 strokes per

minute, with up-down strokes that clean deep in between and behindteeth and the occlusal surfaces of teeth (Figure 2b).

This electric toothbrush contains accelerometers, which are electricsensors that adjust speed and motion to assist in measuring accelerationforces based upon the location of the toothbrush head in three dimensions.The accelerometer will adjust the speed and action of the toothbrushhead based upon its location in the mouth.

Ergonomic Evaluation of the Colgate ProClinical A1500 Electric ToothbrushThis is the first electric toothbrush to be evaluated by the Metaphase

Design Group, considered the ergonomic experts in the field. Two separatestudies evaluated the ergonomic elements of the Colgate ProClinicalA1500 electric toothbrush and consumer usability.7,8

The first study compared the Colgate ProClinical A1500 electric

toothbrush to the Sonicare FlexCare and Oral-B Smart Series electrictoothbrushes. Ergonomic experts evaluated the three brushes for oneweek and assessed the following ergonomic principles: grip design;handle length; use of controls; and sound audibility.8

The investigators concluded that each of the three electric toothbrusheshad adequate grip controls to properly handle the toothbrush, and providedeasy access to the on/off control button. The Colgate ProClinical A1500had the most distinct feature with the longitudinal shape of the handle,and that the handle angled downward from the top, which providedadditional control when gripping the toothbrush and improved ability tosee the brushing area in the mouth while the brush was in use (Figure3). The Colgate ProClinical A1500 provides ease of use with its changingspeeds when used while tooth brushing; brush movements and soundchange occur during changes in brushing speeds.8

The second study was a usability study with 14 participants, eachinstructed to use the Colgate ProClinical A1500 electric toothbrushtwice daily for 3 weeks. Four toothbrush trials were conducted andvideotaped during weekly visits to the study site. Participants alsovideotaped themselves brushing with their manual toothbrush at home,which was the baseline evaluation for this study.7

Participants who were included in this usability study for a 3-weekperiod did increase the length of the tooth brushing with the ColgateProClinical A1500 electric toothbrush, due largely to the sensing andcontrol technologies built into the product. When participants brushedwith their manual toothbrush in this study, they brushed for only 54seconds. When they brushed with the Colgate ProClinical A1500 electrictoothbrush, their brushing time averaged from 99 to 107 seconds duringTrials 1, 2, and 3. The users had a positive brushing experience beingable to manipulate this electric toothbrush in their mouths and brushingin the recommended angle. Participants commented that their teethwere cleaner after using the brush and the handle was lightweight andeasy to clean back teeth.7

Toothbrush Handle and Head Design, Interchangeable Heads,and PortabilityThe Colgate ProClinical electric toothbrush has a cylindrical-shaped

handle to allow the user to easily manipulate and rotate it in their hand.The handle angles downward at the top and provides a notch for the

Figure 1. The Colgate ProClinical A1500 electric toothbrush.

Figure 3. Shape and handle length of the three electric toothbrushes and brush heads:Colgate ProClinical A1500 at top, the Oral-B Smart Series in the middle, and the PhilipsSonicare FlexCare at the bottom. (From: J Clin Dent 2012;23(Spec Iss A):A26-30.Reprinted with permission.)

Figure 2a. Visual photograph of the Optimum Mode brush head movement operatingwith up-down and side-to-side strokes. b. Visual photograph of the Deep Clean Modebrush head movement operating with up-down strokes. (From: J Clin Dent 2012;23[SpecIss A]:A1-4. Reprinted with permission.)

a b

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index finger to hold the brushsecurely and keep the brushhead in line with the handle toposition and place thetoothbrush in the mouth. Theon-off button is easy to accesswith the thumb, and thebrushing modes are easy toobserve and operate (Figure 4).The toothbrush head is smallerthan other commerciallyavailable power toothbrushesand able to clean hard-to-reachareas in the posterior of themouth. The tapered outsidebristles clean deep along thegingival margin.6,9-10

The Colgate ProClinicalA1500 requires a 16-hour chargebefore it can be used the firsttime; after that it will not needto be recharged for 4 to 5 days.

ConclusionErgonomics plays a vital role in the development of manual and electric

toothbrushes to assist patients in complying with the oral healthrecommendations of dental professionals. The Colgate ProClinical A1500provides the important ergonomic features, such as grip design, handlelength to reach posterior teeth, ease of use, and differentiating soundsto identify the angle of toothbrush. The brush guides the user to thearea and angle they should be brushing, and reach a 45° angle to brushthe gumline as well as interproximal and occlusal surfaces to effectivelyclean the teeth. Study participants have brushed longer with the ColgateProClinical A1500 electric toothbrush and have had cleaner teeth anda positive tooth brushing experience for improved patient complianceand optimal oral health.

Figure 4. Colgate ProClinical A1500 ElectricToothbrush controls and user interface. (From:J Clin Dent 2012;23[Spec Iss A]:A26-30.)

Christine Hovliaras is President of Professional Savvy,LLC, an oral care consulting, professional marketingand continuing education company in New Jersey.She is a dental hygienist with over 30 years of clinical,educational, and industry positions during her career.She is adjunct faculty at New York UniversityDepartment of Dental Hygiene and works as a part-time dental hygienist in a prosthodontic practice inMorristown, New Jersey.

References

1. Toothbrushes. American Dental Association. Available at: http://www.ada.org/1321.aspx. Accessed October 3, 2014.

2. Brushing your teeth. American Dental Association Mouth Healthy site. Availableat: http://www.mouthhealthy.org/en/az-topics/b/brushing-your-teeth. AccessedOctober 3, 2014.

3. Saxer UP, Barbakow J, Yankell SL. New studies on actual and estimated toothbrushingtimes and dentifrice use. J Clin Dent 1998;9:49-51.

4. Gallagher A, Sowinski J, Bowman J, et al. The effect of brushing time and dentifriceon dental plaque removal in vivo. J Dent Hyg 2009;83:111-6.

5. Dentino AR, Derderian G, Wolf MA, et al. Six month comparison of powered vs.manual tooth brushing for safety and efficacy in the absence of professional instructionin mechanical plaque control. J Periodontol 2002;3:770-8.

6. Gatzemeyer J, Panagakos F. Intelligent technology for superior cleaning of teethand gums. J Clin Dent 2012;23(Spec Iss A):A1-4.

7. Hunter G, Burns L, Bone B, Mintel T, Jimenez E. Usability research study of a speciallyengineered sonic powered toothbrush with unique sensing and control technologies.J Clin Dent 2012;23(Spec Iss A):A31-4.

8. Hunter G, Burns L, Bone B, Mintel T, Jimenez E. Ergonomic audit of a speciallyengineered sonic powered toothbrush with unique sensing and control technologies,the sonicare flexcare and the Oral-B smart series 5000. J Clin Dent 2012;23(SpecIss A):A26-30.

9. Nathoo S, Mankodi S, Mateo LR, Chaknis P, Panagakos F. A clinical study comparingthe supragingival plaque and gingivitis efficacy of a specially engineered sonic poweredtoothbrush with unique sensing and control technologies to a commercially availablemanual flat-trim toothbrush. J Clin Dent 2012;23(Spec Iss A):A11-6.

10. Take two minutes to brush. American Dental Association. Available at:http://www.ada.org/news/7484.aspx. Accessed September 19, 2013.

37. (www.nicnas.gov.au) AICNaAS.38. Commission SCoCSotE. (http://ec.europa.eu).39. European Commission SCoCPheeehscieh.40. Suller MT, Russell AD. Triclosan and antibiotic resistance in Staphylococcus

aureus. J Antimicrob Chemother 2000;46:11-18.41. Mencke BE KR, Lynch DL. Effect of Irqasan on bacterial growth and its absorption

into the cell wall. Microbiology 1980;28:133-47.42. Haraszthy VI, Sreenivasan PK, Zambon JJ. Community-level assessment of

dental plaque bacteria susceptibility to triclosan over 19 years. BMC OralHealth 2014;14:61.

43. Webster J, Faoagali JL, Cartwright D. Elimination of methicillin-resistantStaphylococcus aureus from a neonatal intensive care unit after hand washingwith triclosan. J Paediatr Child Health 1994;30:59-64.

44. Rodricks JV, Swenberg JA, Borzelleca JF, Maronpot RR, Shipp AM. Triclosan:a critical review of the experimental data and development of margins of safetyfor consumer products. Crit Rev Toxicol 2010;40:422-84.

45. Witorsch RJ. Critical analysis of endocrine disruptive activity of triclosan and

its relevance to human exposure through the use of personal care products.Crit Rev Toxicol 2014;44:535-55.

46. Cullinan MP, Palmer JE, Carle AD, West MJ, Seymour GJ. Long term use oftriclosan toothpaste and thyroid function. Sci Total Environ 2012;416:75-9.

47. Zambon JJ, Reynolds HS, Dunford RG, Bonta CY. Effect of atriclosan/copolymer/fluoride dentifrice on the oral microflora. Am J Dent1990;3(Spec No):S27-34.

48. Bonta Y, Reynolds H, Dunford R, Zambon J. Long term effect of atriclosan/copolymer dentrifice on oral microflora. J Dent Res 1992;71:577.

49. Walker C, Borden LC, Zambon JJ, Bonta CY, DeVizio W, Volpe AR. The effectsof a 0.3% triclosan-containing dentifrice on the microbial composition ofsupragingival plaque. J Clin Periodontol 1994;21:334-41.

50. Zambon JJ, Reynolds HS, Dunford RG, et al. Microbial alterations in supragingivaldental plaque in response to a triclosan-containing dentifrice. Oral MicrobiolImmunol 1995;10:247-55.

51. Fine DH, Furgang D, Bonta Y, et al. Efficacy of a triclosan/NaF dentifrice in thecontrol of plaque and gingivitis and concurrent oral microflora monitoring.Am J Dent 1998;11:259-70.

Continued from pg. 7

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The dental community recognizes that oral health means muchmore than a dazzling set of white teeth. To us, oral health includes thestability of hard tissues, the strength of the chewing muscles, theproductivity of the salivary glands, and the health of the oral soft tissuesand lips. Maintaining the condition of the entire oral cavity is vital formaintaining the strength of the dentition. Without any of the key pieces,the health of the oral cavity is incomplete. Unfortunately, many patientsdo not understand this concept, so we must bridge this disconnect ona worldwide scale and help establish a healthy preventive knowledgebase. By assisting patients in finding an effective home care regimen,we will improve the health of the oral cavity. In this article, we willdiscuss the importance of including an oral rinse as an integral part ofa daily care regimen to build a foundation for gingival health.The burden of oral disease is a global concern. As the percentage

of older adults continues to grow worldwide, chronic disease is amajor concern, and these chronic oral conditions include gingivalinflammation and periodontal disease. Poor oral health is not onlyfound in this mature category of people, but across all age groups.The incidence of oral inflammation must be addressed as theseconditions continue to be associated to other chronic diseases affectinginternational populations. The challenge of educating populationson the topic of gingival inflammation and periodontitis lies inestablishing programs and products that will address these concernsinto the future. During this time of emerging research, science isavailable to identify products that are effective and to recommendthem to those who will benefit from their use.1

Compliance with effective techniques such as c-wrap flossing, sulculartooth brushing, and the use of interproximal dental aides can presenta challenge to patients. Using a mouthrinse can assist patients in theremoval of food particles, plaque, and plaque acids. Choosing an effectiveoral rinse can be challenging, as the combinations of oral microfloravary from patient to patient. In addition, each patient presents withextenuating medical conditions that might also vary their level ofsaliva, immunocompromisation level, and susceptibility to bacterialadherence. Multiple antiseptic mouthrinses are on the market today,both over-the-counter and by prescription. These oral rinse formulasare used for both their therapeutic and prophylactic qualities, andclinicians must educate themselves on both oral rinse compositionand indications for use.In addition to basic ingredients such as cleansers, water, flavors,

colors, and alcohol, manufacturers often use scientific research to addmedicaments for patient benefit. Fluoride is often added forremineralization and antimicrobial benefits, depending on which typeof fluoride is chosen. Manufacturers add antimicrobial agents to targetbacteria that contribute to gingival inflammation, and to assist in thereduction of dental caries, periodontitis, and halitosis. Herbal formulationsand cultural oil rinsing techniques are also emerging with a high levelof patient popularity. These formulations, however, have limited scientificresearch or support. The formulation for each individual rinse determines

the health value of the rinse to the patient. Since there are many healthrequests made by patients, there are numerous rinses on the markettoday, generally falling into one of three categories: cosmetic, toothdecay prevention, and periodontal inflammation reducing. While tooth decay is certainly one of the most predominant oral

diseases affecting the human population worldwide,1 inflammatoryperiodontal disease is the focus of this discussion. Despite large stridesmade in the field of oral disease prevention, the incidence of gingivalinflammation continues to grow.2 As clinicians, it is imperative thatwe have a clear understanding of various medicaments available toassist our patients in using these agents as an adjunct to the treatmentreceived in-office. Rinses vary in composition, with the most effectivepower to reduce biofilm-induced gingival inflammation found in oneof three categories: chlorhexidine gluconate, cetylpyridinium chloride,or essential oil compounds. Each of these compounds can effectivelyreduce the growth of various species of plaque bacteria.3-7

Essential oil (EO) compound rinses have been available over thecounter in the United States for over 100 years. EO rinses effectivelyreduce aerobic bacteria with a low incidence of staining.

Chlorhexidine gluconate(CHX) oral rinse (0.12%) continues to beconsidered the “gold standard” in antimicrobial rinses, and is availableby prescription only in the United States.8 Colgate® PerioGard® Rinseis a brand name of CHX rinse, and has been shown, in a five-week study,to reduce both anaerobic and aerobic bacteria without changes inbacterial resistance, causing overgrowth of potentially opportunisticbacteria or adverse changes in oral microflora.3 CHX is generally usedbetween professional visits as part of a periodontal maintenance programfor treating gingival inflammation and swelling, often measured bybleeding upon periodontal probing. CHX has been linked to an increasedamount of supragingival calculus and staining,9 but for those who arebattling chronic periodontitis, CHX can be an effective medicament ina rinse solution.Cetylpyridinium chloride (0.05 to 0.075%) is a compound with

powerful antiseptic properties that can be found over the counter globallyin rinses with and without alcohol. Cetylpyridinium chloride rinse(CPC) inhibits aerobic and anaerobic micro-organisms associated withdental caries, gingival inflammation, periodontitis, and halitosis.4,6 Someformulations of CPC may cause brown staining of the teeth and tonguedue to the method of action of the medicament, yet the over-the-countereffectiveness in the reduction of gingival inflammation offsets the presenceof stain in terms of overall oral health.10 Colgate-produced rinses whichcontain 0.075% CPC are sold under the Colgate® Total® Rinse brand inthe United States, the United Kingdom, and Canada, and under theColgate® Plax Rinse brand outside the United States.

The Benefits of Incorporating a Therapeutic Rinse for Gingival Health

Emily Boge, RDH, BS, MPAc

Cetylpyridinium chloride rinse (CPC) inhibits aerobic and anaerobicmicro-organisms associated with dental caries, gingivalinflammation, periodontitis, and halitosis.

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The challenge faced by dental professionals is the acceptance andcompliance by patients with the inclusion of a daily therapeutic rinseduring oral hygiene. It is well known that patients do not brush for therecommended amount of time, and most do not floss, so asking themto add another step is very demanding. However, as professionals wemust advise our patients regarding the beneficial effects that adding atherapeutic rinse can have, both in treating existing disease andpreventing future disease. Balancing the normal oral flora whileeliminating pathogenic bacteria is a challenging act for patients andtheir clinicians. Yet the addition of an oral rinse to the daily homecareroutine can help a patient reduce the chances of gingival inflammation.The addition of a rinse, such as Colgate Total or Colgate Plax, to a twice-daily regimen of tooth brushing, can improve the control of plaqueand the diseases it causes. It is an easy step that will have both therapeutic,as well as cosmetic benefits.

References

1. Petersen PE, Bourgeois D, Ogawa H, Estupinan-Day S, Ndiaye C. The global burdenof oral diseases and risks to oral health. Bull World Health Organ 2005;83(9): 661-9.

2. Mdala I, Olsen I, Haffajee AD, Socransky SS, Thoresen M, Blasio BF. Comparingclinical attachment level and pocket depth for predicting periodontal diseaseprogression in healthy sites of patients with chronic periodontitis using multi-stateMarkov models. J Clin Periodontol 2014;41(9):837-45.

3. Yates R, Shearer BH, Huntington E, Addy M. A method to compare four mouthrinses.J Clin Periodontol 2002;29(6):519-23.

4. Sreenivasan P, Haraszthy V, Zambon J. Antimicrobial efficacy of 0·05% cetylpyridiniumchloride mouthrinses. Lett Appl Microbiol 2013;56(1):14-20.

5. Albert-Kiszely A, Pjetursson BE, Salvi GE, Witt J, Hamilton A, Persson GR, LangNP. Comparison of the effects of cetylpyridinium chloride with an essential oilmouth rinse on dental plaque and gingivitis – a six-month randomized controlledclinical trial. J Clin Periodontol 2007;34(8):658-67.

6. Asadoorian J, Williams KB. Cetylpyridinium chloride mouth rinse on gingivitis andplaque. J Dent Hyg 2008:82(5):42.

7. Axelsson P, Lindhe J. Efficacy of mouthrinses in inhibiting dental plaque and gingivitisin man. J Clin Periodontol 1987;14(4):205-12.

8. Brownstein CN, Briggs SD, Schweitzer KL, Briner WW, Kornman KS. Irrigationwith chlorhexidine to resolve naturally occurring gingivitis. J Clin Periodontol1990;17(8):588-93.

9. Van Strydonck DC, Slot DE, Van der Velden U, Van der Weijden F. Effect of achlorhexidine mouthrinse on plaque, gingival inflammation and staining in gingivitispatients: a systematic review. J Clin Periodontol 2012;39(11):1042-55.

10. Quirynen M, Soers C, Desnyder M, Dekeyser C, Pauwels M, Steenberghe D. A 0.05%cetylpyridinium chloride/0.05% chlorhexidine mouth rinse during maintenancephase after initial periodontal therapy. J Clin Periodontol 2005;32(4):390-400.

Emily Boge, RDH, BS, MPAc is currently ahealth sciences public administrationmaster’s degree candidate at Upper IowaUniversity. She has practiced dental hygienesince 2003 in Manchester, Iowa, USA. Emilyis also the owner of Think Big Dental, aconsulting and writing firm specializing ineducating professionals on the role of a dentalhygienist.

2010;119:551-8. doi:10.1007/s10549-009-0333-1.4. Bos PD, Zhang XH, Nadal C, Shu W, Gomis RR, Nguyen DX, Minn AJ,

van de Vijver MJ, Gerald WL, Foekens JA, Massague J. Genes that mediatebreast cancer metastasis to the brain. Nature 2009;459:1005-9.doi:10.1038/ nature08021.

5. Alizadeh AA, Eisen MB, Davis RE, Ma C, Lossos IS, Rosenwald A, BoldrickJC, Sabet H, Tran T, Yu X, Powell JI, Yang L, Marti GE, Moore T, HudsonJ Jr, Lu L, Lewis DB, Tibshirani R, Sherlock G, Chan WC, Greiner TC,Weisenburger DD, Armitage JO, Warnke R, Levy R, Wilson W, GreverMR, Byrd JC, Botstein D, Brown PO, Staudt LM. Distinct types of diffuselarge B-cell lymphoma identified by gene expression profiling. Nature2000;403:503-11.

6. Perou CM, Sorlie T, Eisen MB, van de Rijn M, Jeffrey SS, Rees CA, PollackJR, Ross DT, Johnsen H, Akslen LA, Fluge O, Pergamenschikov A,Williams C, Zhu SX, Lonning PE, Borresen-Dale AL, Brown PO, BotsteinD. Molecular portraits of human breast tumours. Nature 2000;406:747-52.

7. Colangelo V, Schurr J, Ball MJ, Pelaez RP, Bazan NG, Lukiw WJ. Geneexpression profiling of 12633 genes in Alzheimer hippocampal CA1:transcription and neurotrophic factor down-regulation and up-regulationof apoptotic and pro-inflammatory signaling. J Neurosci Res 2002;70:462-73.

8. Thornton S, Sowders D, Aronow B, Witte DP, Brunner HI, Giannini EH,Hirsch R. DNA microarray analysis reveals novel gene expression profilesin collagen-induced arthritis. Clin Immunol 2002;105:155-68.

9. Burke W. Genomics as a probe for disease biology. N Engl J Med2003;349:969-74.

10. Demmer RT, Behle JH, Wolf DL, Handfield M, Kebschull M, Celenti R,Pavlidis P, Papapanou PN. Transcriptomes in healthy and diseasedgingival tissues. J Periodontol 2008;79:2112-24. doi:10.1902/jop.2008.080139.

11. Papapanou PN, Behle JH, Kebschull M, Celenti R, Wolf DL, HandfieldM, Pavlidis P, Demmer RT. Subgingival bacterial colonization profilescorrelate with gingival tissue gene expression. BMC Microbiol2009;9:221.doi:10.1186/1471-2180-9-221.

12. Kebschull M, Guarnieri P, Demmer RT, Boulesteix AL, Pavlidis P,Papapanou PN. Molecular differences between chronic and aggressiveperiodontitis. J Dent Res 2013;92:1081-8. doi:10.1177/0022034513506011.

13. Kebschull M, Demmer RT, Grun B, Guarnieri P, Pavlidis P, PapapanouPN. Gingival tissue transcriptomes identify distinct periodontitisphenotypes. J Dent Res 2014;93:459-68. doi:10.1177/0022034514527288.

14. Picolos DK, Lerche-Sehm J, Abron A, Fine JB, Papapanou PN. Infectionpatterns in chronic and aggressive periodontitis. J Clin Periodontol2005;32:1055-61.

15. Jönsson D, Ramberg P, Demmer RT, Kebschull M, Dahlen G, PapapanouPN. Gingival tissue transcriptomes in experimental gingivitis. J ClinPeriodontol 2011;38:599-611. doi:10.1111/j.1600-051X.2011.01719.x.

16. Bostanci, N., Ramberg, P., Wahlander, A., Grossman, J., Jonsson, D.,Barnes, V. M. & Papapanou, P. N. (2013) Label-free quantitativeproteomics reveals differentially regulated proteins in experimentalgingivitis. J Proteome Res 12, 657-78. doi:10.1021/pr300761e.

Continued from pg. 3

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IntroductionAyurveda is a holistic system of medicine that evolved in India some

3000–5000 years ago. It is a system of traditional medicine native to theIndian subcontinent, now practiced in other parts of the world as a formof consequent medicine. Ayurvedic medicine is one of the world’s oldestwhole body remedial systems. The concept of healing is based on theassociation of the body with mind and spirit. The best analogy is that ofa tree whose roots are nourished so that it becomes strong and able tofight off stress and disease.1 Today, health is becoming more of an articleof trade to be purchased, whereas in Ayurveda it is held that health is away of life, to be inculcated as a culture.The earliest inscription on Indian medical systems appeared during

the Vedic period in India; the Su�ruta Samhit� and the Charaka Samhit�are its earliest trustworthy texts. Over the centuries, Ayurvedic practitionersformulated an extensive array of medicinal compounds for the treatmentof various ailments and diseases. In recent years, harmonizing andunconventional medicine are gaining popularity over conventional allopathicmedicine as the products and practices used are natural and safe.2 Thereis a provision of self treatment with an added advantage of cost effectiveness.

Oil PullingOil pulling is a powerful detoxifying Ayurvedic technique that has

gained statuary rank as a complementary and alternative remedy.3 Oilworks wonders as a natural cleaner for oral health. The therapy ispreventive and, at the same time, curative. With its use, surgery andits possible complications can be prevented for a number of chronicillnesses. The vitalizing aspect of this healing method lies in its simplicity. Oil pulling is a procedure that involves swishing oil in the mouth for

oral and systemic health benefits. It has its mention in the Ayurvedictext Charaka Samhita where it was called Kavala or Gandusha, and isclaimed to alleviate about 30 systemic diseases ranging from headacheand migraine to diabetes and asthma. Oil pulling has been usedextensively as a traditional Indian folk remedy for many years to preventoral malodor, bleeding gums, dryness of throat, and cracked lips, andfor strengthening teeth, gums, and the jaw, as well as preventing toothdecay.4 However, there are very few clinical trials evaluating the effectof oil pulling therapy on oral health.

Oil Pulling TherapyOil pulling therapy can be done using oils like sunflower oil or sesame

oil. The Sesamum indicum of the Pedaliaceae family has been considereda gift of nature to mankind for its nutritional qualities and desirablehealth effects. Sesame oil is considered to be the king of oil due to itsbeneficial effects.5 A tablespoon of sesame seed oil is taken in the mouth,sipped, sucked, and swished between the teeth for 10 to 15 minutesuntil the oil loses its thickness and becomes milky white in color. Thenit is expectorated and the mouth is rinsed thoroughly with water severaltimes. It is preferably practiced during early morning on an emptystomach and can be done for a maximum of three times in a day incase of acute diseases.6 There is no contraindication for the practice ofoil pulling except for use in children below the age of 5 years, as they

find difficulty in swishing and there is a chance of aspiration andswallowing.

Oil pulling is simple to practice, cost effective, and does not causeany staining of teeth, persistent taste, or known allergic reactions. Oilpulling is an interesting theory without any stated negative effects.Since the world has become so widely dispersed in ethnicity, thelikelihood of encountering a patient who practices oil pulling is verypossible.7

How Does It Work?How can swishing oil provide these therapeutic benefits? Two schools

of thought have been put forth to explain the mechanism.Some researchers claim that swishing of oil in the mouth activates

enzymes and draws toxins out of the blood. Sesame seed oil has a highconcentration of polyunsaturated fatty acids and is a good source ofvitamins.8 The antioxidants present in sesame seed oil include sesamin,sesamolin, and sesaminol. These lignans act as detoxificants, antioxidants,are able to potentiate the action of vitamin E, and prevent lipidperoxidation; its antibiotic effect helps in the control of microorganisms.Sesamin has been found to inhibit the absorption of cholesterol aswell as its production in the liver, reduce lipogenesis, and exhibit anantihypertensive action. However, the exact mechanism of the actionof oil pulling therapy is still not fully understood.The second hypothesis is based on simple biology. Most of the

microorganisms that are part of oral ecology in the mouth consist of asingle cell with a fatty membrane making up the outer wall of the cell.When the oil pulling is done, these fatty membranes are attracted tothe oil while the oil is pulled or swished. During swishing of the oilaround teeth and gums, bacteria hiding in the crevicular space of thegingival tissue and exposed tubules within the teeth are sucked out oftheir “hiding places” and become a part of the thick foam that is formedduring oil pulling. This is the reason one needs to pull oil in the mouthfor a sufficient duration of time to pull all the microbes from the mouth.9

The saliva and oil together can attract and pull all the food particles,and cleans and frees an individual’s mouth from harmful substancesand maintains overall health and the body’s capacity to self heal. However,as with the first hypothesis regarding mechanism of action, there islittle research to support the second hypothesis.Oil pulling appears to work by removing all types of microorganisms

and reducing the number of potentially harmful ones. But clinical researchneeds to be carried out to prove its effectiveness on positively alteringthe bacterial load in the mouth, as well its effects on the soft tissue.Researchers have tried various ways to alter the bacterialmicropopulations in people’s mouths. These populations can be alteredby mechanically cleaning the teeth, using antiseptic toothpastes ormouthwashes, and even taking antibiotics. However, the ordinary

Since the world has become so widely dispersed in ethnicity, thelikelihood of encountering a patient who practices oil pulling isvery possible.

Oil Pulling and Oral Health: A Myth or a Reality?S.G. Damle, PhD, MDS, FDS, RCS, FAMS

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inhabitants and their relative proportions reestablish, on their own, indue course of time. Killing oral bacteria helps to reduce their numbers,but it does not change the types of organisms that thrive in mouth.So-called “friendly organisms” can inhibit or even kill the moretroublesome ones. Oil pulling is very unlikely to cause any such damagewith routine use.10 Some researchers have suggested that after oil pullingin the mouth, the mouth should be swished with warm water to removethe biofilm, whereas another school of thought recommends the useof salt water which will act as an antimicrobial and reduce tissueinflammation. Amith, et al.11 reported significant improvement in plaquescores, while Asokan, et al.12 demonstrated its effectiveness in inhibitingmicroorganisms.

A 2009 study was conducted by Asokan, et al.10 to evaluate the effectof oil pulling with sesame oil on plaque-induced gingivitis, and to compareits efficacy with chlorhexidine mouthwash. A total of 20 age-matchedadolescent boys with plaque-induced gingivitis were selected randomlyinto the study to be in the oil pulling group, a control group, or achlorhexidine group. Plaque index and modified gingival scores wererecorded and baseline plaque samples collected. At the conclusion ofthe study, there was a statistically significant reduction of the pre- andpost-values of the plaque and modified gingival index scores in boththe study and control groups. Oil pulling therapy showed a reductionin the plaque index, modified gingival scores, and total colony countof aerobic microorganisms in the plaque of adolescents with plaque-induced gingivitis.Thaweboon, et al,13 in 2011, conducted a study to investigate the

effect of oil pulling using coconut oil, corn oil, rice bran oil, palm oil,sesame oil, sunflower oil, and soy bean oil on biofilm models formedby Streptococcus mutans KPSK2, Lactobacillus casei ATCC 6363,and Candida albicansATCC 13803 on salivary-coated microtiter plates.Saline solution and 0.2% chlorhexidine gluconate solution were usedas negative and positive controls, respectively. The investigators foundthat coconut oil exhibited antimicrobial activity against S. mutansand C. albicans. Sesame oil had antibacterial activity against S. mutans,whereas sunflower oil had antifungal activity against C. albicans. However,L. caseiwas found to be resistant to all tested oils. Thus, they concludedthat oil pulling therapy could probably be used as a preventive hometherapy to maintain oral hygiene against dental caries, especially indeveloping countries.

ConclusionsAyurveda is the science of healing and rejuvenation based upon

universal principles. Oil pulling is a form of Ayurveda. It should be

noted that sufficient scientific research has not been carried out toevaluate the effect of oil pulling therapy on oral health, and this needsto be addressed. In the very near future, it is possible that oil pulling will open new

avenues in oral healthcare, but the current evidence-based data isinadequate and unconvincing. Nonetheless, it might be considered ofsome value when used as an adjunct to preventive home therapy indeveloping countries.

References

1. Dwivedi G, Dwivedi S. History of medicine: Sushruta – the clinician –teacher par excellence. Indian J Chest Dis Allied Sci 2007;49:243–4.

2. Bethesda M. A Closer Look at Ayurvedic Medicine. Focus onComplementary and Alternative Medicine. National Center forComplementary and Alternative Medicine. US National Institutes ofHealth, 2006;XII(4).

3. Amrutesh S. Dentistry and Ayurveda - An evidence-based approach. Int JClin Dent Sci 2010;2:3-9.

4. Shirley T, Naveen K, Balkrishna A. Use of Ayurveda in promoting dentalhealth and preventing dental caries. Indian J Dent Res 2009;20:246.

5. Namiki M. The chemistry and physiological functions of sesame. FoodRev Int 2002;11:281-329.

6. Asokan S. Oil pulling therapy. Indian J Dent Res 2008;19:169.7. Hebbar A, Keluskar V, Shetti A. Oil pulling – Unraveling the path to mystic

cure. J Int Oral Health 2010;2:11-4.8. Madianos PN, Bobetsis YA, Kinane DF. Generation of inflammatory stimuli:

how bacteria set up inflammatory responses in the gingiva. J Clin Periodontol2005;32(S6):57-71.

9. Botelho MA, Bezerra-Filho JG, Correa LL, Heukelbach J. Effect of a novelessential oil mouthrinse without alcohol on gingivitis: a double-blindedrandomized controlled trial. J Appl Oral Sci 2007;15:175-80.

10. Asokan S, Emmadi P, Chamundeswari R. Effect of oil pulling on plaqueinduced gingivitis: A randomized, controlled, triple-blind study. Ind JDent Res 2009;20(1):47-51.

11. Amith HV, Ankola AV, Nagesh L. Effect of oil pulling on plaque and gingivitis.J Oral Health Comm Dent 2007;1:12-8.

12. Asokan S, Rathinasamy TK, Inbamani N, Menon T, Kumar SS, Emmadi P,et al. Mechanism of oil- pulling therapy - In vitro study. Indian J Dent Res2011;22:34-7.

13. Thaweboon S, Nakaparksin J, Thaweboon B. Effect of oil-pulling on oralmicroorganisms in biofilm models. Asia J Public Health 2011;2(2):62-6.

14. Hammer KA, Carson CF, Riley TV. Antimicrobial activity of essential oilsand other plant extracts. J Applied Microbiol 1999;86:985-90.

Professor Damle is Vice Chancellor, MaharishiMarkandeshwar University, Mullana (Ambala)Haryana (India), and Professor of Pediatricand Preventive Dentistry in MaharishiMarkandeshwar College of Dental Sciences &Research, Mullana.

In the very near future, it is possible that oil pulling will open newavenues in oral healthcare.

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December 2014 marked the release of the Second Edition ofthe Colgate-sponsored textbook Periodontal Disease and OverallHealth: A Clinician’s Guide. The first edition of the populartextbook was published in 2010.The newly expanded 370-page edition contains updated

findings in the study of the relationship between oral and systemichealth. Chapter authors include 32 scientists from dentistryand medicine, each on the cutting edge of global research inthis growing field. It is a must read for medical and dentalpractitioners.In the words of Editors Robert J. Genco and Ray C. Williams,

“The integration of medicine and dentistry grows daily, and acommon resource such as this textbook can serve as aconstructive tool to help the two disciplines work collaboratively.We are hopeful that this textbook will find broad readershipand will be useful to the dental and medical communities and—most important—that it will result in better general health aswell as oral health.”The complete textbook will be freely accessible at

www.colgateprofessional.com, as well as on the Colgate OralHealth Network (http://www.colgateoralhealthnetwork.com).An e-book version is planned and hard copies will be availableon a limited basis.

Periodontal Disease and Overall Health: A Clinician’s Guide

Second Edition

Copyright © 2015 The Colgate-Palmolive CompanyProduced for Colgate by Professional Audience Communications, Inc., Yardley, PA, USA

Forward all comments to: [email protected]

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