journal of dental hygiene special supplement to access magazine dental … · 2014-06-09 ·...

Journalof Dental Hygiene

T H E A M E R I C A N D E N T A L H Y G I E N I S T S ’ A S S O C I A T I O N

2007Journal of

Dental Hygiene

Special Supplement to Access magazine

Incorporating Antimicrobial Mouthrinsesinto Oral Hygiene: Strategies for ManagingOral Biofilm and Gingivitis

• Changing Perspectives on the Use ofAntimicrobial Mouthrinses

• The Role of Dental Plaque Biofilm in Oral Health

• Safety and Efficacy of AntimicrobialMouthrinses in Clinical Practice

• Strategies for Incorporating AntimicrobialMouthrinses into Daily Oral Care

• Antimicrobial Mouthrinses in ContemporaryDental Hygiene Practice: The Take HomeMessage

This special issue of the Journal of Dental Hygiene as asupplement to Access was made possible through aneducational grant from Johnson & Johnson HealthcareProducts Division of McNEIL-PPC, Inc.

Guest Editor

■ MICHELE LEONARDI DARBY, RDH, MS, is the graduate program directorin dental hygiene at Old Dominion University in Norfolk, Virginia. Shelectures internationally, is the author of over 50 articles, has published 3books, and has served on several editorial advisory boards, currentlyserving as associate editor of the International Journal of Dental Hygieneand as an editorial review board member of the Journal of Dental Hygieneand Dimensions of Dental Hygiene. In 1981, she was a member of the firstdelegation of dental hygienists to visit the People’s Republic of China. Shehas received many awards, including the Warner Lambert–AmericanDental Hygienists’ Association Award for Excellence in Dental Hygiene andthe designation of Eminent Scholar by Old Dominion University.

Authors

■ JOANNA ASADOORIAN, RDH, MSc, is an associate professor in theSchool of Dental Hygiene at the University of Manitoba and worksprivately as a dental hygienist in periodontology. She has published andregularly lectures on her research interests, which include qualityassurance, maintaining competence in health care professionals, clinicaldecision making, and oral health care products for home use. Sheserves on the editorial review board for the Journal of Dental Hygiene.

■■ LOUIS G. DEPAOLA, DDS, MS, is a professor in the Department ofDiagnostic Sciences and Pathology at the University of Maryland DentalSchool and the director of dental training for the PA/Mid-Atlantic AIDSEducation and Training Center. He is an international lecturer; hasauthored and coauthored over 130 journal articles, book chapters, andabstracts; and has been awarded over 75 research and service grants,including ones for the study of antiplaque chemotherapeutic agents. Heserves as a consultant to many professional organizations and from2002 to 2005 served on the American Dental Association Council onScientific Affairs. He is a diplomate of the American Board of OralMedicine and the American College of Dentists.

■■ JOANN R. GURENLIAN, RDH, PhD, is a former chair of the Departmentof Dental Hygiene at Thomas Jefferson University in Philadelphia andpast president of the American Dental Hygienists’ Association. Shecontinues to consult and to offer continuing education services in thehealth care field. She has authored over 100 articles, is the coauthor ofThe Medical History: Clinical Implications and Emergency Prevention inDental Settings, and is the recipient of numerous awards, including theAmerican Dental Hygienists’ Association Distinguished Service Award.She is the vice president of the International Federation of DentalHygienists and chairs a work group for the National Diabetes EducationProgram.

■ ANN ESHENAUR SPOLARICH, RDH, PhD, holds several academicappointments and currently teaches at the Arizona School of Dentistryand Oral Health, University of Southern California School of Dentistry,and University of Maryland Dental School in addition to practicing dentalhygiene. An international lecturer, she has published over 60 articles and6 chapters in dental hygiene textbooks, has been active in research,serves on several editorial review boards, and is a consultant to theNational Center for Dental Hygiene Research. She is the current chair ofthe American Dental Hygienists’ Association Council on Research. Shehas received several awards, most recently, the University ofPennsylvania Dental Hygiene Alumni Achievement Award in 2002.

about the authorsThis special issue of the Journal of DentalHygiene was funded by an unrestrictededucational grant from Johnson & JohnsonHealthcare Products Division of McNEIL-PPC, Inc.

Continuing Education ProgramTo obtain 2 hours of continuing educationcredit, once you have thoroughly reviewed thissupplement, please complete the exam athttp://www.adha.org/CE_courses/course16/.

Open to all licensed U.S. dental hygienists,ADHA’s CE Program offers Journal ofDental Hygiene readers the opportunity toearn CE credit. Your exam will be graded bythe ADHA staff using questions reviewedand developed in cooperation with theUniversity of North Carolina School ofDentistry, a recognized provider of CEcredit.

Credit for this CE program expires one yearfrom the date of publication (both print andonline). Duplicate submissions will bedisregarded. Submit your exam only once.

Continuing education credits issued forparticipation in this CE activity may notapply toward license renewal in all licensingjurisdictions. It is the responsibility of eachparticipant to verify the licensingrequirements of his or her licensing orregulatory agency.

Any questions? Contact ADHACommunications Division: 312/440-8900.

Special supplement The Journal of Dental Hygiene 1

Journal of Dental Hygiene

3 Changing Perspectives on the Use of Antimicrobial Mouthrinses

Michele Leonardi Darby, RDH, MS

Incorporating Antimicrobial Mouthrinses into Oral Hygiene: Strategies for Managing Oral Biofilm and Gingivitis

4 The Role of Dental Plaque Biofilm in Oral HealthJoAnn R. Gurenlian, RDH, PhD

13 Safety and Efficacy of Antimicrobial Mouthrinses in Clinical PracticeLouis G. DePaola, DDS, MSAnn Eshenaur Spolarich, RDH, PhD

26 Strategies for Incorporating Antimicrobial Mouthrinses into Daily Oral CareJoanna Asadoorian, RDH, MSc

32 Antimicrobial Mouthrinses in Contemporary Dental Hygiene Practice: The Take Home MessageMichele Leonardi Darby, RDH, MS

Inside

Message

Supplement

2 The Journal of Dental Hygiene Special supplement

Journal of DentalHygiene

special supplement

■■ EDITORIAL REVIEW BOARD

Celeste M. Abraham, DDS, MSCynthia C. Amyot, BSDH, EdDJoanna Asadoorian, RDH, MScCaren M. Barnes, RDH, BS, MSPhyllis L. Beemsterboer, RDH, MS, EdDStephanie Bossenberger, RDH, MSKimberly S. Bray, RDH, MSLorraine Brockmann, RDH, MSPatricia Regener Campbell, RDH, MSDan Caplan, DDS, PhDBarbara H. Connolly, PT, EdD, FAPTAValerie J. Cooke, RDH, MS, EdDMaryAnn Cugini, RDH, MHPSusan J. Daniel, AAS, BS, MSMichele Leonardi Darby, RDH, MSCatherine Davis, RDH, PhD. FIDSAConnie Drisko, RDH, BS, DDSJacquelyn M. Dylla, DPT, PTDeborah E. Fleming, RDH, MSJane L. Forrest, BSDH, MS, EdDJacquelyn L. Fried, RDH, BA, MSMary George, RDH, BSDH, MEdEllen Grimes, RDH, MA, MPA, EdDJoAnn R. Gurenlian, RDH, PhDLinda L. Hanlon, RDH, BS, MEd, PhDKitty Harkleroad, RDH, MSHarold A. Henson, RDH, MEdLaura Jansen Howerton, RDH, MSLisa F. Harper Mallonee,BSDH,MPH,RD/LD

Heather L. Jared, RDH, BS, MSWendy Kerschbaum, RDH, MA, MPHSalme Lavigne, RDH, BA, MSDHJessica Y. Lee, DDS, MPH, PhDDeborah S. Manne,RDH,RN,MSN,OCNAnn L. McCann, RDH, BS, MSStacy McCauley, RDH, MSGayle McCombs, RDH, MSShannon Mitchell, RDH, MSTricia Moore, RDH, BSDH, MA, EdDChristine Nathe, RDH, MSKathleen J. Newell, RDH, MA, PhDJohanna Odrich, RDH, MS, DrPhPamela Overman, BSDH, MS, EdDVickie Overman, RDH, BS, MEdFotinos S. Panagakos, DMD, PhD, MEdM. Elaine Parker, RDH, MS, PhDCeib Phillips, MPH, PhDMarjorie Reveal, RDH, MS, MBAKip Rowland, RDH, MSJudith Skeleton, RDH, BS, MEd, PhDAnn Eshenaur Spolarich, RDH, PhDSheryl L. Ernest Syme, RDH, MSTerri Tilliss, RDH, BS, MS, MA, PhDNita Wallace, RDH, PhDKaren B. Williams, RDH, PhDCharlotte J. Wyche, RDH, MSPamela Zarkowski, BSDH, MPH, JD

■■ STATEMENT OF PURPOSE

The Journal of Dental Hygiene is the refereed, scientific publication of the American Dental Hygienists’ Association. It promotes the publication of original research related to the profession, the education, and the practice of dental hygiene. The journal supports the development and dissemination of a dental hygiene body of knowledge through scientific inquiry in basic, applied, and clinical research.

EXECUTIVE DIRECTORAnn Battrell, RDH, BS, [email protected]

DIRECTOR OF COMMUNICATIONSJeff [email protected]

EDITOR EMERITUSMary Alice Gaston, RDH, MS

EDITOR-IN-CHIEFRebecca S. Wilder, RDH, BS, [email protected]

STAFF EDITORKatie [email protected]

LAYOUT/DESIGNJean MajeskiPaul R. Palmer

■■ SUBSCRIPTIONS

The Journal of Dental Hygiene is published quarterly, online-only, by the AmericanDental Hygienists’ Association, 444 N. Michigan Avenue, Chicago, IL 60611. Copy-right 2007 by the American Dental Hygienists’ Association. Reproduction in whole orpart without written permission is prohibited. Subscription rates for nonmembers areone year, $45; two years, $65; three years, $90; prepaid.

■■ SUBMISSIONS

Please submit manuscripts for possible publication in the Journal of Dental Hygieneto Katie Barge at [email protected].


IntroductionIntroduction

s oral health care profes-sionals, we need to makeevidence-based recom-mendations to our patients.

Studies from which we derive our rec-ommendations need to have beenconducted with scientific rigor andneed to be confirmed with other well-designed studies. Given the numer-ous, long-term, peer-reviewed pub-lished studies on antimicrobialmouthrinses with consistent statisti-cally and clinically significant out-comes, it is time to change our pro-fessional thinking and practices.

When considering the oral envi-ronment, about 20% is occupied bytooth surfaces, that is, those areas tar-geted for toothbrushing and flossing.1

Dental plaque biofilm is not limited totooth surfaces. About 80% of theremaining surfaces include the oralmucosa and specialized mucosa of thetongue.1 Saliva, the tongue, and oralmucosa serve as reservoirs of patho-genic bacteria able to relocate and col-onize on the teeth and in sulci. Usingan antiseptic mouthrinse produces anantimicrobial effect throughout theentire mouth, including areas easilymissed during toothbrushing andinterdental cleaning. Therefore, it isnot surprising that in May 2007, theAmerican Dental Association Councilon Scientific Affairs issued newadvice highlighting the oral healthbenefits of ADA-Accepted antimi-crobial mouthrinses that help preventand reduce plaque and gingivitis.2

This special Supplement to theJournal of Dental Hygiene focuses onour changing beliefs about antimicro-bial mouthrinses and their value in

maintaining oral health. The paperswithin contain extensive informationabout dental plaque biofilms, the effec-tiveness of antimicrobial mouthrinses,and how to incorporate these agentsinto patients’oral self-care. Within thisSupplement, dental hygienists will findbest practices regarding antimicrobialmouthrinses so they can confidentlyrecommend their use to patients basedon the evidence. Patients look to den-tal hygienists for trustworthy informa-tion that can make a difference in theiroral and systemic health. In this Sup-plement, dental hygienists have evi-dence-based information about antimi-crobial mouthrinses from oral healthexperts.

Dr. Gurenlian provides a primer ondental plaque biofilm and the perpet-ual challenges facing its management.Drs. DePaola and Spolarich reviewthe safety and efficacy of the majormouthrinses on the market and pro-vide clear guidance on which prod-ucts can be confidently recommendedto yield predictable clinical healthoutcomes. New bodies of researchevidence encourage the replacementof old beliefs and practices with moreeffective therapies; but embracingchange is arduous, even with strongevidence to support the change.Joanna Asadoorian tackles the chal-lenge of promptly translating evi-dence-based information into prac-tice, particularly when it meanschange on the part of both the practi-tioner and the patient. From her paper,dental hygienists will better under-stand resistance to change, the processof change, and how to use change the-ory to help themselves and patients

incorporate health-promoting behav-iors such as twice-daily use of antimi-crobial mouthrinse. Asadoorian’sapproach is also useful in motivatingpatients to adopt other beneficial oralhygiene measures.

Clinically relevant and easilyapplied information can be foundwithin these pages. Through this newknowledge, dental hygienists will beequipped to better control plaque andgingivitis in patients who historicallymay have been excluded from antimi-crobial mouthrinse recommendations.I encourage you to read this issuefrom cover to cover because theknowledge within will make a differ-ence in the way you practice dentalhygiene. Share the issue with yourcolleagues, and keep an issue in yourreception area for patients to read.Patients will know that you are a valu-able source for oral health care rec-ommendations that improve and pro-mote their health status.

References

1. Mager DL, Ximenez-Fyvie LA, Haffa-jee AD, Socransky SS. Distribution ofselected bacterial species on intraoralsurfaces. J Clin Periodontol. 2003;30:644-654.

2. ADA affirms benefits of ADA-Acceptedantimicrobial mouth rinses and tooth-pastes, fluoride mouth rinses [newsrelease].Chicago, IL: American DentalAssociation; May 23, 2007. http://ada.org/public/media/releases/0705_release03.asp. Accessed July 27,2007.

Changing Perspectives on the Use ofAntimicrobial Mouthrinses

AMichele Leonardi Darby, RDH, MS


Introduction

In contrast to an accumulation ofindividual bacteria, a biofilm is acomplex, communal, 3-dimensionalarrangement of bacteria. Bacterialbiofilms are ubiquitous and are poten-tially found in a variety of sites withinthe human body. For example, theycan grow on indwelling catheters,ports, and implants; external surfacesof the eye; artificial heart valves;endotracheal tubes; and contaminatedprosthetic joints. A bacterial biofilm isoften the cause of persistent infec-tions and has been associated withosteomyelitis, pneumonia in patientswith cystic fibrosis, and prostatitis.1

In areas related to oral health care,bacterial biofilms are found in dentalunit water lines, on tooth surfaces anddental prosthetic appliances, and onoral mucous membranes. Biofilm inthe form of supragingival and sub-gingival plaque is the etiologic agentin dental caries and periodontal dis-eases (Figure 1).2-5 The pathogenicityof the dental plaque biofilm isenhanced by the fact that in biofilmform, the component bacteria haveincreased resistance to antibiotics andother chemotherapeutic agents andare less able to be phagocytized byhost inflammatory cells. Therefore,control of the dental plaque biofilm isa major objective of dental profes-sionals and critical to the maintenanceof optimal oral health. This articlereviews the characteristics of dentalbiofilm, its role in the etiology ofperiodontal diseases, and strategiesfor controlling the biofilm to promotehealth.

Changing Views ofDental Plaque

Over the past 50 years, the under-standing and characterization of dentalplaque have undergone significant evo-lution. Loesche6 proposed both a non-specific and a specific plaque hypoth-esis for periodontal disease initiationand progression.

The nonspecific plaque hypothesisproposed that the entire microbial com-munity of plaque that accumulated ontooth surfaces and in the gingivalcrevice contributed to the developmentof periodontal disease. Plaque bacteria

produced virulence factors and noxiousproducts that initiated inflammation,challenged the host defense system, andresulted in the destruction of periodon-tal tissues. Under this hypothesis, thequantity of plaque was considered tobe the critical factor in the developmentof periodontal disease. Thus, increasesin the amount of plaque (quantity), asopposed to specific pathogenicmicroorganisms (quality) found in theplaque, were viewed as being prima-rily responsible for inducing diseaseand disease progression.7,8

Studies on the microbial etiologyof various forms of periodontitis sup-

The Role of Dental Plaque Biofilm in Oral HealthJoAnn R. Gurenlian, RDH, PhD

SupplementSupplement

AbstractOverview. Microbial biofilms are complex communities of bacteria andare common in the human body and in the environment. In recent years,dental plaque has been identified as a biofilm, and the structure, microbi-ology, and pathophysiology of dental biofilms have been described. Thenature of the biofilm enhances the component bacteria’s resistance toboth the host’s defense system and antimicrobials. If not removed regularly,the biofilm undergoes maturation, and the resulting pathogenic bacterialcomplex can lead to dental caries, gingivitis, and periodontitis. In addition,dental biofilm, especially subgingival plaque in patients with periodontitis,has been associated with various systemic diseases and disorders, includ-ing cardiovascular disease, diabetes mellitus, respiratory disease, andadverse pregnancy outcomes.

Clinical Implications. An understanding of the nature and pathophysiol-ogy of the dental biofilm is important to implementing proper managementstrategies. Although dental biofilm cannot be eliminated, it can be reducedand controlled through daily oral care. A daily regimen of thorough mechan-ical oral hygiene procedures, including toothbrushing and interdental clean-ing, is key to controlling biofilm accumulation. Because teeth compriseonly 20% of the mouth’s surfaces, for optimal oral health, the use of anantimicrobial mouthrinse helps to control biofilm not reached by brushingand flossing as well as biofilm bacteria contained in oral mucosal reservoirs.

Key words: Antimicrobial mouthrinse, biofilm, dental plaque, oral health,periodontal disease


port the specific plaque hypothesis,which proposes that only certainmicroorganisms within the plaquecomplex are pathogenic. Despite thepresence of hundreds of species ofmicroorganisms in periodontal pock-ets, fewer than 20 are routinely foundin increased proportions at periodon-tally diseased sites. These specific vir-ulent bacterial species activate thehost’s immune and inflammatoryresponses that then cause bone and softtissue destruction.6,8,9

Socransky and colleagues4,10 recog-nized that early plaque consists pre-dominantly of gram-positive organ-isms and that if the plaque is leftundisturbed it undergoes a process ofmaturation resulting in a more com-plex and predominantly gram-nega-tive flora. These investigatorsassigned the organisms of the subgin-gival microbiota into groups, or com-plexes, based on their association withhealth and various disease severities(Figure 2).4,10 Color designations wereused to denote the association of par-ticular bacterial complexes with peri-

odontal infections. The blue,yellow, green, and purplecomplexes designate earlycolonizers of the subgingivalflora. Orange and red com-plexes reflect late colonizersassociated with mature sub-gingival plaque. Certain bac-terial complexes are associ-ated with health or disease.10,11

For example, the bacteria inthe red complex are morelikely to be associated withclinical indicators of peri-odontal disease such as peri-odontal pocketing and clini-cal attachment loss.

PlaqueRecognized as aBiofilm

Research over the pastdecade has led to the recogni-tion of dental plaque as abiofilm—a highly organized

Figure 1. Scanning electron micrograph of biofilm grown from thesubgingival plaque of a healthy subject for 10 days anaerobically onsaliva-coated hydroxyapatite discs. (Grown by Michael Sedlacek, PhD,and Clay Walker, PhD, at the University of Florida College of DentistryPeriodontal Disease Research Center. Image taken by the Universityof Florida Electron Microscopy Core Facility.)

Figure 2. Microbial complexes in subgingival biofilm.4,10 (Modified fromSocransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes insubgingival plaque. J Clin Periodontol 1998;25:134-144. Reprinted withpermission from Blackwell Publishing.)

A naeslundii 2 (A viscosus)

V parvulaA odontolyticus

P gingivalisT forsythensis

T denticola

P intermediaP nigrescens

P microsF nuc vincentii

F nuc nucleatumF nuc polymorphum

F periodonticum

S mitisS oralis

S sanguis

Streptococcus sp.S gordonii

S intermedius

E corrodensC gingivalisC sputigenaC ochraceaC concisusA actino. a

C gracilis C rectus

S constellatus E nodatum

C showaeS noxia

A actino b.


accumulation of microbial communi-ties attached to an environmental sur-face. Biofilms are organized to maxi-mize energy, spatial arrangements,communication, and continuity of thecommunity of microorganisms.

Biofilms protect bacteria livingwithin their structures and therebyprovide an advantage over free-float-ing (planktonic) bacteria. The slimyextracellular matrix produced bybiofilm bacteria encloses the micro-bial community and protects it fromthe surrounding environment, includ-ing attacks from chemotherapeuticagents. Chemotherapeutic agents havedifficulty penetrating the polysaccha-ride matrix to reach and affect themicroorganisms.1,11-13 Thus, the matrixhelps to protect bacteria deep withinthe biofilm from antibiotics and anti-septics, increasing the likelihood ofthe colonies’ survival. Furthermore,the extracellular matrix keeps the bac-teria banded together, so they are notflushed away by the action of salivaand gingival crevicular fluid. Mech-anical methods, including tooth-brushing, interdental cleaning, andprofessional scaling procedures, arerequired to regularly and effectivelydisrupt and remove the plaquebiofilm. Antiseptics, such asmouthrinses, can help to control thebiofilm but must be formulated so asto be able to penetrate the plaquematrix and gain access to the patho-genic bacteria.

Biofilms have a definite architec-tural structure. The bacteria are notuniformly distributed throughout thebiofilm; rather, there are aggregatesof microcolonies that vary in shapeand size. Channels between thecolonies allow for circulation of nutri-ents and by-products and provide asystem to eliminate wastes.14,15

Microorganisms on the outer surfaceof biofilms are not as stronglyattached within the matrix and tendto grow faster than those bacteriadeeper within the biofilm. Surfacemicroorganisms are more susceptibleto detachment, a characteristic thatfacilitates travel to form new biofilmcolonies on nearby oral structures andtissues.

Bacteria in biofilm communicatewith each other by a process calledquorum sensing. This dynamic,sophisticated communication systemenables bacteria to monitor eachother’s presence and to modulate theirgene expression in response to thenumber of bacteria in a given area ofthe biofilm.8 In addition, as a resultof quorum sensing, portions of thebiofilm can become detached in orderto maintain a cell density compatiblewith continued survival.

Stages of BiofilmFormation

The growth and development ofbiofilm are characterized by 4 stages:initial adherence, lag phase, rapidgrowth, and steady state. Biofilm for-mation begins with the adherence ofbacteria to a tooth surface, followedby a lag phase in which changes ingenetic expression (phenotypic shifts)occur. A period of rapid growth thenoccurs, and an exopolysaccharidematrix is produced. During the steadystate, the biofilm reaches growth equi-librium. Surface detachment andsloughing occur, and new bacteria areacquired.

Initial Adherence and Lag Phase

The first phase of supragingivalbiofilm formation is the deposition ofsalivary components, known asacquired pellicle, on tooth surfaces.This pellicle makes the surface recep-tive to colonization by specific bacte-ria. Salivary glands produce a varietyof proteins and peptides that furthercontribute to biofilm formation. For

example, salivary mucins, such asMUC5B and MUC7, contribute to theformation of acquired pellicle,16,17 andstatherin, a salivary acidic phospho-protein, and proline-rich proteins pro-mote bacterial adhesion to tooth sur-faces.18 Acquired pellicle formationbegins within minutes of a profes-sional prophylaxis; within 1 hour,microorganisms attach to the pellicle.Usually, gram-positive cocci are thefirst microorganisms to colonize theteeth. As bacteria shift from plank-

tonic to sessile life, a phenotypicchange in the bacteria occurs requir-ing significant genetic up-regulation(gene signaling that promotes thisshift). As genetic expression shifts,there is a lag in bacterial growth.

Rapid Growth

During the rapid growth stage,adherent bacteria secrete large amountsof water-insoluble extracellular poly-saccharides to form the biofilm matrix.The growth of microcolonies withinthe matrix occurs. With time, addi-tional varieties of bacteria adhere tothe early colonizers—a process knownas coaggregation—and the bacterialcomplexity of the biofilm increases.These processes involve unique, selec-tive molecular interactions leading tostructural stratification within thebiofilm. Coaggregation and subsequentcell division also increase the thicknessof biofilm.19-21

Steady State/Detachment

During the steady state phase, bac-teria in the interior of biofilms slowtheir growth or become static. Bacte-

Bacteria in biofilm communicate with each other bya process called quorum sensing. This dynamic,sophisticated communication system enablesbacteria to monitor each other’s presence and tomodulate their gene expression in response to thenumber of bacteria in a given area of the biofilm.

ria deep within the biofilm show signsof death with disrupted bacterial cellsand other cells devoid of cytoplasm;bacteria near the surface remain intact.During this phase, crystals can beobserved in the interbacterial matrixthat may represent initial calculusmineralization.22 As noted above, dur-ing the steady state stage, surfacedetachment and sloughing also occur,with some bacteria traveling to formnew biofilm colonies.

Biofilm and OralDisease

Biofilms can cover surfacesthroughout the oral cavity. Micro-colonies exist on oral mucosa, thetongue, biomaterials used for restora-tions and dental appliances, and toothsurfaces above and below the gingi-val margin (Figure 3). It is importantfor oral health professionals to com-municate to their patients that bothdental caries and periodontal diseaseare infectious diseases resulting fromdental plaque biofilm accumulation.Each of these diseases requires spe-cific strategies for prevention andtreatment.

With respect to periodontal disease,dental plaque biofilm demonstrates asuccession of microbial colonizationwith changes in bacterial floraobserved from health to disease.Researchers studied over 13,000plaque samples from 185 patients withconditions ranging from oral health toperiodontal disease.4,23 As notedabove, based on their findings, a num-ber of microbial complexes were iden-tified that were associated with vari-ous stages of disease initiation andprogression. Bacterial species con-tained in the yellow, green, and purplecomplexes appear to colonize the sub-gingival sulcus first and predominatein gingival health. In contrast, orangecomplex bacteria are associated withgingivitis and gingival bleeding. Inter-estingly, bacteria of the orange com-plex may also be associated with redcomplex microorganisms includingPorphyromonas gingivalis, Tannerellaforsythensis, and Treponema denti-

cola, organisms found in greater num-bers in diseased sites and in moreadvanced periodontal disease.10,24

Bacterial communities living in abiofilm possess resourceful survivalstrategies, including a broader habitatfor growth, nutrition, waste elimina-tion, and new colonization; environ-mental niches for safety; barriers tothwart antimicrobial drug therapy; pro-tection from the host’s defense systemincluding phagocytosis; and enhancedpathogenicity.1,8 These strategiesaccount for the ongoing challenge ofsuccessfully controlling periodontalinfection and disease progression.25

As the biofilm matures and prolif-erates, soluble compounds producedby pathogenic bacteria penetrate thesulcular epithelium. These com-pounds stimulate host cells to producechemical mediators associated withthe inflammatory process26 (see Figure4 on page 9).

• Interleukin-1 beta (IL-1β),prostaglandins, tumor necrosis fac-tor alpha (TNF-α), and matrixmetalloproteinases are mediatorsthat recruit neutrophils to the areavia chemotaxis and cause in-creased permeability of gingivalblood vessels, permitting plasma

proteins to migrate from within theblood vessels into the tissue.

• As the gingival inflammatoryprocess continues, additionalmediators are produced, and moreinflammatory cell types such asneutrophils, T cells, and mono-cytes are recruited to the area.

• Proinflammatory cytokines are pro-duced in the tissues as a response tothe chronic inflammatory process,and these proteins may further esca-late the local inflammatoryresponse and affect the initiationand progression of systemic inflam-mation and disease.

The result of this chronic inflam-mation is a breakdown of gingival col-lagen and accumulation of an inflam-matory infiltrate, leading to theclinical signs of gingivitis. In someindividuals, the inflammatory processwill also lead to the breakdown of col-lagen in the periodontal ligament andresorption of the supporting alveolarbone. It is at this point that the lesionprogresses from gingivitis to peri-odontitis, continuing the same chal-lenge from proinflammatory media-tors as with chronic gingivitis. Thus,controlling dental plaque biofilm isessential to preventing and reversing


Figure 3. Biofilm lodges in the crevices around the teeth both aboveand below the gingival margin. Accumulation of dental plaque biofilmcan result in dental caries and periodontal disease. (Figure copyright2006 Keith Kasnot, MA, CMI, FAMI.)


gingivitis as well as preventing andmanaging periodontitis.

Periodontal BiofilmInfection and SystemicHealth

In recent years, studies havedemonstrated an association betweenperiodontitis and various systemic dis-eases and conditions, including car-diovascular disease, diabetes mellitus,respiratory disease, adverse pregnancyoutcomes, obesity, pancreatic cancer,and Alzheimer’s disease.27-57 Whileseveral of these associations have notbeen definitively established, biolog-ical mechanisms explaining some ofthe more extensively studied relation-ships are emerging.

The association between periodon-tal disease and some systemic diseasesmay relate to the ability of subgingi-val plaque bacteria and/or their prod-ucts to gain access to the systemic cir-culation through the ulceratedepithelium of the periodontal pocket.For example, environmental nicheslike a subgingival pocket that containsanaerobic gram-negative microorgan-isms can potentially seed orange andred complex bacteria and/or theirproducts to distant sites through thecirculatory system. In this way, a den-tal biofilm infection can potentiallycontribute to both oral and systemicinflammation.25

Research on Periodontal Microor-ganisms

Atheromas. Direct evidence for therole of dental biofilm infection in sys-temic inflammation comes from find-

ings of periodontal microorganisms inhuman carotid atheromas. Studies ofatheromatous lesions in carotid arter-ies revealed that over 40% of athero-mas contain antigens from periodon-tal pathogens including P gingivalis, Tforsythensis, and Prevotella interme-dia.28,58 In addition, P gingivalis isknown to induce platelet aggregation,a component of atheroma and throm-bus formation,29 and invade endothe-lial cells in cell cultures.59 While suchfindings suggest a possible invasionof atheromas by oral pathogens aswell as possible contribution to theirdevelopment, it is important to notethat causality has yet to be established.

Preterm Birth. Research suggeststhat periodontal pathogens may travelvia the bloodstream from the oral cav-ity to the placenta initiating preterm

birth. In an animal model, Han andcoworkers60 found that periodontalbacteria, including Fusobacteriumnucleatum, entered the bloodstreamfrom ulcerated gingival sulci or peri-odontal pockets and negatively influ-enced the normal birth process.

Respiratory Disease. Likewise,biofilm in the oral cavity may serve asa reservoir of infection leading to res-piratory disease. Pseudomonas aerug-inosa, Staphylococcus aureus, andenteric bacteria have been shown tocolonize the teeth of patients admittedto hospitals and long-term care facil-ities. These bacteria may be releasedinto saliva and aspirated into the lowerairway causing respiratory infection.46-

49,61 Intubation is another vehicle bywhich bacteria from the oral biofilmcan be directly introduced into the res-piratory system. Intubation tubes sup-port biofilm growth contributing tonosocomial infection such as pneu-

monia. This is one reason why oralintubation raises the risk of nosoco-mial infection in intensive and criticalcare hospital populations.

Association With ChronicDiseases and Conditions

Research has also suggested thatthe association between oral inflam-mation and systemic inflammationmay be key to understanding andmanaging the significant, deleteriouseffects on the multiple organ systemsinvolved in some chronic diseases andconditions (Figure 4).26

Cardiovascular Disease. Cardio-vascular disease is characterized byinflammatory plaque accumulation inblood vessels that can cause throm-boses and lead to myocardial infarc-tion. Atherosclerosis represents achronic inflammatory process thatcauses endothelial dysfunction andinjury to the elastic and muscular arte-rial tissue. Early atherosclerotic lesionscontain neutrophils, monocytes, andlymphocytes. These leukocytes canaffect the vascular endothelial liningand cause oxidation of low-densitylipoproteins. As a result, monocytes,induced to become macrophages, takeup these oxidized lipoproteins andbecome lipid-laden foam cells. As thelesion progresses, the extracellularmatrix of the vessel wall is degraded byproteolytic enzymes and becomes sus-ceptible to rupture. Thromboses canocclude blood flow to the heart andbrain and eventually lead to infarction,heart attack, or stroke.26

Since atherosclerosis is inflamma-tory by nature, identifying inflamma-tory markers that correlate with diseasestate is important. One recognized andconsistent marker of systemic inflam-mation and poor cardiovascular prog-nosis is the acute-phase protein C-reac-tive protein (CRP), the level of whichrises with systemic inflammation.62,63

Animal model studies of the relation-ship between cardiovascular diseaseand periodontal disease demonstratethat clinically induced oral infectionwith P gingivalis will increase atheromasize and elevate CRP levels in theblood.30 Conversely, some studies have

In recent years, studies have demonstrated anassociation between periodontitis and varioussystemic diseases and conditions, includingcardiovascular disease, diabetes mellitus,respiratory disease, adverse pregnancy outcomes,obesity, pancreatic cancer, and Alzheimer’s disease.


shown that treatment of periodontitisdecreases CRP blood levels,64 thoughthis has not been a consistent finding.

Diabetes Mellitus. Diabetes mellitusis another chronic systemic diseaseassociated with periodontitis. In fact,periodontitis has been identified as oneof the major complications of dia-betes.65 Although diabetes increases thesusceptibility to periodontal dis-ease,38,39,65 periodontitis may alsoincrease the difficulty of maintainingsatisfactory glycemic control in peo-ple with diabetes as compared withthose with diabetes without periodon-titis.40 One biological mechanism pro-posed to explain the increased inci-dence and severity of periodontaldisease in individuals with diabetes isthe finding of elevated levels of inflam-

matory mediators in the gingivalcrevicular fluid from periodontal pock-ets of patients with diabetes with poorglycemic control as compared withthose with diabetes who are well con-trolled or those without diabetes. Thosewith poor glycemic control had con-siderable periodontal destruction withan equivalent bacterial challenge.39,66

Of note, the proinflammatory cytokineTNF-α plays a significant role in thisprocess. TNF-α has a major role ininsulin resistance, the primary cause oftype 2 diabetes, and is produced inlarge quantities by fat cells. Periodon-titis also has been associated withincreased levels of TNF-α. Elevatedlevels of TNF-α may lead to greaterbone loss by killing cells that repairdamaged connective tissue or bone.

Elevated TNF-α levels also may exac-erbate insulin resistance and worsenglycemic control.44,66,67

Adverse Pregnancy Outcomes.Studies also demonstrate that peri-odontal diseases are associated withthe risk of adverse pregnancy out-comes, especially preterm low-birth-weight infants.50-52 Chronic infection,such as that found with chronic peri-odontitis, can stimulate the inflamma-tory process throughout the body. Inthe placenta, this may lead to elevatedamniotic levels of prostaglandins,TNF-α, and IL-1 and IL-6, stimulat-ing premature rupture of membranes,preterm labor, and the birth of low-birth-weight infants. Intervention stud-ies are currently under way to investi-gate a cause and effect relationship

Figure 4. Subgingival plaque bacteria and/or their products may gain access to distant sites in the bodythrough the circulatory system and may potentially contribute to systemic inflammation; in this way, adental biofilm infection may potentially contribute to various systemic diseases and conditions.(Illustration owned by McNEIL-PPC, Inc. and provided for educational purposes only. May not bereproduced without the prior written permission of McNEIL-PPC, Inc.)

between advanced periodontitis andadverse pregnancy outcomes.

Strategies for ManagingDental Biofilm toPromote Health

Although dental biofilm cannot becompletely eliminated, its pathogenic-ity can be lessened through effectiveoral hygiene measures. Daily tooth-brushing, interdental cleaning, and theuse of topical antimicrobial chemother-apeutics are patient-based strategies toreduce the bacterial biofilm and to helpprevent periodontal diseases. Ameri-can Dental Association (ADA)–Accepted antimicrobial mouthrinseshave been shown to help prevent andreduce plaque and gingivitis whenadded to a daily oral hygiene regimenof mechanical plaque removal. Further,

bacteria from the biofilm on mucosaland tooth surfaces are shed constantlyinto saliva and transferred to otherareas of the mouth. Since oral mucosa,which represents about 80% of the oralcavity surface,68 can serve as a reservoirfor pathogenic bacteria that can betransferred to the tooth surface and sul-cus, supplementing mechanical plaquecontrol methods with topical antimi-crobials may also play an importantrole in reducing reservoirs ofpathogens that are unaffected by brush-ing and flossing directed at the toothsurface.

Using Evidence inPractice

Products recommended to patientsshould be those that have documentedefficacy and safety (see pages 13 to

25). Only 2 nationally branded anti-septic mouthrinses and their genericequivalents have received the ADACouncil on Scientific Affairs Seal ofAcceptance for control of supragingi-val plaque and gingivitis: Listerine®

(fixed combination of essential oils)and Peridex® (0.12% chlorhexidinegluconate). However, due to recentchanges in the ADA Seal Program,Peridex® and its generic equivalentsno longer carry the ADA Seal becausechlorhexidine gluconate is a prescrip-tion product (see also page 32 formore information on the ADA SealProgram). The fixed combination ofessential oils and cetylpyridiniumchloride have also been reviewed by aFood and Drug Administration (FDA)advisory committee and have receiveda Category I recommendation, mean-ing they have been found to be safeand effective for the control of


Active Ingredients Brands Indications Contraindications

0.12% Chlorhexidine Peridex®† (3M ESPE, Gingivitis, Those hypersensitive to gluconate (available St Paul, MN) supragingival plaque chlorhexidinegluconate or other by prescription) PerioGard®† (Colgate formula ingredients.

Oral Pharmaceuticals, Long-term use: can cause Inc., Canton, MA) moderate staining, increased

PerioRx®† (Discus calculus formation, and possible Dental, Culver City, CA) alteration of taste perceptionCanton, MA)

Various generics†

Four essential oils: Listerine® Antiseptic† Supragingival plaque, Children under 12 yearseucalyptol, menthol, (Johnson & Johnson gingivitis, oral malodormethyl salicylate, Healthcare Productsthymol Division of McNEIL-PPC,

Inc., Skillman, NJ)Various generics†

Cetylpyridinium Breath Rx® (Discus Dental, Supragingival plaque, Children under 6 yearschloride Culver City, CA) gingivitis, oral malodor

Colgate Viadent® (Colgate-Palmolive, New York, NY)

Crest® Pro-Health™ Rinse(Procter & Gamble,Cincinnati, OH)

Table I. Examples of Antiseptic Mouthrinses*

* For the mechanisms of actions of antiseptic mouthrinses, see pages19 and 20.

† Has received the ADA Seal of Acceptance; note that as the ADA Sealprogram has recently phased out prescription products, chlorhexidinegluconate products no longer carry the ADA Seal.

supragingival plaque and gingivitis.Peridex® and its generic equivalents,which are prescription products, havebeen approved for marketing by theFDA via the New Drug Applicationroute (or for generics, the AbbreviatedNew Drug Application process) (seealso pages 14 and 15). Examples ofeffective antimicrobial mouthrinsescurrently on the market appear inTable I.

Conclusion

Dental biofilm is a complex, organ-ized microbial community that is theprimary etiologic factor for the mostfrequently occurring oral diseases,dental caries and periodontal diseases.Although the dental biofilm cannot beeliminated, it can be controlled withcomprehensive mechanical andchemotherapeutic oral hygiene prac-

tices. Teaching patients to use dailybrushing, interdental cleaning, andantimicrobial mouthrinses that carrythe ADA Seal of Acceptance increasesthe likelihood of periodontal diseaseprevention and reduction. Althoughadditional research is needed, there isthe possibility that these cost-effec-tive, preventive strategies may mini-mize the effect of periodontal diseaseson specific systemic conditions.


References1. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms:

a common cause of persistent infections. Science.1999;284:1318-1322.

2. van Houte J. Role of micro-organisms in caries etiology. JDent Res. 1994;73:672-681.

3. Stenudd C, Nordlund A, Ryberg M, et al. The association ofbacterial adhesion with dental caries. J Dent Res.2001;80:2005-2010.

4. Socransky SS, Haffajee AD, Cugini MA, et al. Microbial com-plexes in subgingival plaque. J Clin Periodontol. 1998;25:134-144.

5. Haffajee AD, Socransky SS. Microbial etiological agents ofdestructive periodontal diseases. Periodontol 2000.1994;5:78-111.

6. Loesche WJ. Chemotherapy of dental plaque infections. OralSci Rev. 1976;9:65-107.

7. Theilade E. The non-specific theory in microbial etiology ofinflammatory periodontal disease. J Clin Periodontol.1986;13:905-911.

8. Thomas JG, Nakaishi LA. Managing the complexity of adynamic biofilm. J Am Dent Assoc. 2006;137(11 suppl):10S-15S.

9. Loesche WJ. DNA probe and enzyme analysis in periodon-tal diagnostics. J Periodontol. 1992;63:1102-1109.

10. Socransky SS, Haffajee AD. Periodontal microbial etiology.Periodontol 2000. 2005;38:135-187.

11. Socransky SS, Haffajee AD. Dental biofilms: difficult thera-peutic targets. Periodontol 2000. 2002;28:12-55.

12. Brown MR, Gilbert P. Sensitivity of biofilms to antimicrobialagents. J Appl Bacteriol. 1993;74(suppl):87S-97S.

13. Gilbert P, Das J, Foley I. Biofilm susceptibility to antimicro-bials. Adv Dent Res. 1997;11:160-167.

14. Costerton JW, Lewandowski Z, DeBeer D, et al. Biofilms,the customized microniche. J Bacteriol. 1994;176:2137-2142.

15. Wood SR, Kirkham J, Marsh PD, et al. Architecture of intactnatural human plaque biofilms studied by confocal laser scan-ning microscopy. J Dent Res. 2000; 79:21-27.

16. Levine MJ, Reddy MS, Tabak LA, et al. Structural aspects ofsalivary glycoproteins. J Dent Res. 1987;66:436-441.

17. Tabak LA, Levine MJ, Mandel ID, Ellison SA. Role of salivarymucins in the protection of the oral cavity. J Oral Pathol.1982;11:1-17.

18. Gibbons RJ, Hay DI. Human salivary acidic proline-rich pro-teins and statherin promote the attachment of Actinomycesviscosus LY7 to apatitic surfaces. Infect Immun. 1988;56:439-445.

19. Costerton JW, Cheng KJ, Geesey GG, et al. Bacterial biofilmsin nature and disease. Annu Rev Microbiol. 1987;41:435-464.

20. Gibbons RJ. Microbial ecology: adherent interactions whichmay affect microbial ecology in the mouth. J Dent Res.1984;63:378-385.

21. Whittaker CJ, Klier CM, Kolenbrander PE. Mechanisms ofadhesion by oral bacteria. Annu Rev Microbiol. 1996;50:513-552.

22. Wirthlin MR Jr, Armitage GC. Dental plaque and calculus:microbial biofilms and periodontal diseases. In: Rose LF,Mealey BL, Genco RJ, Cohen W, eds. Periodontics: Medi-cine, Surgery and Implants. St. Louis, MO: Elsevier Mosby;2004.

23. Socransky SS, Haffajee AD, Ximenez-Fyvie LA, et al. Eco-logical considerations in the treatment of Actinobacillus actin-omycetemcomitans and Porphyromonas gingivalis peri-odontal infections. Periodontol 2000. 1999;20:341-362.

24. Kojima T, Yasui S, Ishikawa I. Distribution of Porphyromonasgingivalis in adult periodontitis patients. J Periodontol.1993;64:1231-1237.

25. Grossi S, Mealey BL, Rose LF. Effects of periodontal infec-tion on the systemic condition. In: Rose LF, Mealey BL,Genco RJ, Cohen W, eds. Periodontics: Medicine, Surgeryand Implants. St. Louis, MO: Elsevier Mosby; 2004.

26. Gurenlian JR. Inflammation: the relationship between oralhealth and systemic disease. Access. 2006;20(4)(suppl):1-9.

27. Epstein SE. The multiple mechanisms by which infectionmay contribute to atherosclerosis development and course.Circ Res. 2002;90:2-4.

28. Haraszthy VI, Zambon JJ, Trevisan M, et al. Identification ofperiodontal pathogens in atheromatous plaques. J Peri-odontol. 2000;71:1554-1560.

29. Herzberg MC, Meyer MW. Effects of oral flora on platelets:possible consequences in cardiovascular disease. J Peri-odontol. 1996;67:1138-1142.

30. Paquette DW. The periodontal-cardiovascular link. CompendContin Educ Dent. 2004;25:681-692.

31. Desvarieux M, Demmer RT, Rundek T, et al. Periodontalmicrobiota and carotid intima-media thickness: the oral infec-tions and vascular disease epidemiology study (INVEST).Circulation. 2005;111:576-582.

32. Tiong AY, Brieger D. Inflammation and coronary artery dis-ease. Am Heart J. 2005;150:11-18.

33. Meurman JH, Sanz M, Janket SJ. Oral health, atherosclero-sis, and cardiovascular disease. Crit Rev Oral Biol Med.2004;15:403-413.

34. Chun YH, Chun KR, Olguin D, Wang HL. Biological founda-tion for periodontitis as a potential risk factor for atheroscle-rosis. J Periodontal Res. 2005;40:87-95.

35. Hung HC, Willett W, Merchant A, et al. Oral health and periph-eral arterial disease. Circulation. 2003;107:1152-1157.


36. Wu T, Trevisan M, Genco RJ, et al. Periodontal disease andrisk of cerebrovascular disease: the first national health andnutrition examination survey and its follow-up study. ArchIntern Med. 2000;160:2749-2755.

37. Joshipura KJ, Hung HC, Rimm EB, et al. Periodontal disease,tooth loss, and incidence of ischemic stroke. Stroke.2003;34:47-52.

38. Nishimura F, Takahashi K, Kurihara M, et al. Periodontal dis-ease as a complication of diabetes mellitus. Ann Periodon-tol. 1998;3:20-29.

39. Ryan ME, Carnu O, Kamer A. The influence of diabetes onthe periodontal tissues. J Am Dent Assoc. 2003;134:34S-40S.

40. Taylor GW, Burt BA, Becker MP, et al. Severe periodontitisand risk for poor glycemic control in patients with non-insulin-dependent diabetes mellitus. J Periodontol. 1996;67(suppl10):1085-1093.

41. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatment ofperiodontal disease in diabetics reduces glycated hemoglo-bin. J Periodontol. 1997;68:713-719.

42. Miller LS, Manwell MA, Newbold D, et al. The relationshipbetween reduction in periodontal inflammation and diabetescontrol: a report of 9 cases. J Periodontol. 1992;63:843-848.

43. Mealey BL, Rethman MP. Periodontal disease and diabetesmellitus: bidirectional relationship. Dent Today. 2003;22:107-113.

44. Grossi SG, Genco RJ. Periodontal disease and diabetesmellitus: a two-way relationship. Ann Periodontol. 1998;3:51-61.

45. Taylor GW. Bidirectional interrelationships between diabetesand periodontal diseases: an epidemiologic perspective. AnnPeriodontol. 2001;6:99-112.

46. Scannapieco FA. Role of oral bacteria in respiratory infection.J Periodontol. 1999;70:793-802.

47. Scannapieco FA, Bush RB, Paju S. Associations betweenperiodontal disease and risk for nosocomial bacterial pneu-monia and chronic obstructive pulmonary disease: a sys-tematic review. Ann Periodontol. 2003;8:54-69.

48. Hayes C, Sparrow D, Cohen M, et al. The associationbetween alveolar bone loss and pulmonary function: the VADental Longitudinal Study. Ann Periodontol. 1998;3:257-261.

49. Scannapieco FA, Ho AW. Potential associations betweenchronic respiratory disease and periodontal disease: analy-sis of National Health and Nutrition Examination Survey III.J Periodontol. 2001;72:50-56.

50. Offenbacher S, Katz V, Fertik G, et al. Periodontal infectionas a possible risk factor for preterm low birth weight. J Peri-odontol. 1996;67(suppl 10):1103-1113.

51. Jeffcoat MK, Geurs NC, Reddy MS, et al. Periodontal infec-tion and preterm birth: results of a prospective study. J AmDent Assoc. 2001;132:875-880.

52. Scannapieco FA, Bush RB, Paju S. Periodontal disease asa risk factor for adverse pregnancy outcomes: a systematicreview. Ann Periodontol. 2003;8:70-78.

53. Stein PS, Scheff S, Dawson DR III. Alzheimer’s disease andperiodontal disease: mechanisms underlying a potential bi-directional relationship. Grand Rounds Oral-Sys Med.2006;1:14-24D.

54. Michaud DS, Joshipura K, Giovannucci E, Fuchs CS. Aprospective study of periodontal disease and pancreatic can-cer in US male health professionals. J Natl Cancer Inst.2007;99:171-175.

55. Stolzenberg-Solomon RZ, Dodd KW, Blaser MJ, et al. Toothloss, pancreatic cancer, and Helicobacter pylori. Am J ClinNutr. 2003;78:176-181.

56. Al-Zahrani MS, Bissada NF, Borawskit EA. Obesity and peri-odontal disease in young, middle-aged, and older adults. JPeriodontol. 2003;74:610-615.

57. Reeves AF, Rees JM, Schiff M, Hujoel P. Total body weightand waist circumference associated with chronic periodonti-tis among adolescents in the United States. Arch PediatrAdolesc Med. 2006;160:894-899.

58. Chiu B. Multiple infections in carotid atherosclerotic plaques.Am Heart J. 1999;138:S534-S536.

59. Dorn BR, Burks JN, Seifert KN, Progulske-Fox A. Invasion ofendothelial and epithelial cells by strains of Porphyromonasgingivalis. FEMS Microbiol Lett. 2000;187:139-144.

60. Han YW, Redline RW, Li M, et al. Fusobacterium nucleatuminduces premature and term stillbirths in pregnant mice: impli-cation of oral bacteria in preterm birth. Infect Immun.2004;72:2272-2279.

61. Scannapieco FA. Periodontal inflammation: from gingivitisto systemic disease? Compend Contin Educ Dent.2004;25(suppl 1):16-25.

62. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactiveprotein and other markers of inflammation in the predictionof cardiovascular disease in women. N Engl J Med.2000;342:836-843.

63. Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognosticvalue of C-reactive protein and serum amyloid A protein insevere unstable angina. N Engl J Med. 1994;331:417-424.

64. D’Aiuto F, Parkar M, Andreou G, et al. Periodontitis and sys-temic inflammation: control of the local infection is associatedwith a reduction in serum inflammatory markers. J Dent Res.2004;83:156-160.

65. Löe H. Periodontal disease: the sixth complication of dia-betes mellitus. Diabetes Care. 1993;16:329-334.

66. Salvi GE, Yalda B, Collins JG, et al. Inflammatory mediatorresponse as a potential risk marker for periodontal diseasesin insulin-dependent diabetes mellitus patients. J Periodon-tol. 1997;68:127-135.

67. Lalla E, Lamster IB, Feit M, et al. Blockade of RAGE sup-presses periodontitis-associated bone loss in diabetic mice.J Clin Invest. 2000;105:1117-1124.

68. Mager DL, Ximenez-Fyvie LA, Haffajee AD, Socransky SS.Distribution of selected bacterial species on intraoral sur-faces. J Clin Periodontol. 2003;30:644-654.


Introduction

Mechanical plaque removal throughtoothbrushing and flossing has beenthe universally accepted “gold stan-dard” for maintaining oral health sincethe early 1960s. However, numerousstudies have shown that most patientsdo not effectively clean interdentallyto remove dental plaque daily.1-3 By theearly 1980s, chemotherapeutic agentswere marketed as adjuncts to brushingand flossing; however, no definitiveguidelines for the evaluation of theirsafety and efficacy were available.Both the American Dental Association(ADA) and the Food and Drug Admin-istration (FDA) have established stan-dards for assessing the safety and effi-cacy of over-the-counter (OTC) andprescription mouthrinses.

ADA Safety andEfficacy Guidelines forMouthrinses

Since 1931, the ADA, through itsvoluntary Seal of Acceptance Pro-gram, has promoted the use of oraland dental products that are both safeand effective. Published guidelinesdeveloped by the ADA list the accept-ance criteria for each type of agent,product, or device. In order to obtainthe Seal of Acceptance, a companymust provide evidence establishingthat a submitted agent, product, ordevice meets or exceeds the guide-lines for that particular usage and issafe and effective. Additionally, theproduct must have been approved formarketing in the United States by theFDA. In 1985, the ADA recognizedthe potential benefits of some chemo-therapeutic formulations, givingimpetus to the development of guide-

lines for the evaluation of antiplaqueand antigingivitis chemotherapeuticagents for inclusion in the Seal Pro-gram, which are still in use today.4 Inorder to be awarded the Seal, anantiplaque and antigingivitis chemo-therapeutic must5

• Be tested in populations of typicalproduct users in a randomized,parallel-group, or crossover clin-ical trial in which the test productis compared with a negative con-trol and, if appropriate, an activecontrol

• Be supported by data from atleast two 6-month studies con-ducted at independent sites, with

assessment of gingivitis andqualitative and quantitativeassessment of plaque performedat baseline, an intermediate point(usually 3 months), and 6months

• Document a statistically signifi-cant reduction of supragingivalplaque and gingivitis as com-pared with a negative control ineach of the 2 studies and demon-strate a statistically significantreduction of gingivitis for themouthrinse group of at least 15%for any one study and an aver-age reduction of 20% in the 2studies compared with the con-trol group

Safety and Efficacy of Antimicrobial Mouthrinsesin Clinical PracticeLouis G. DePaola, DDS, MS, and Ann Eshenaur Spolarich, RDH, PhD

AbstractEfficacy Overview. The use of an antimicrobial mouthrinse is an impor-tant adjunct to toothbrushing and interdental cleaning. To varying degrees,chlorhexidine gluconate (CHG), cetylpyridinium chloride (CPC), and essen-tial oils (EO) interrupt the integrity of the bacterial cell membrane, leadingto lysis and death. CHG binds to salivary mucins, tooth structure, dentalplaque, and oral soft tissues and is released slowly into the mouth, whereit inhibits adsorption of bacteria onto teeth. CHG is active against a widerange of gram-positive and gram-negative microorganisms. CPC binds toteeth and plaque to a lesser degree than CHG and is generally less effi-cacious than CHG. CHG and EO penetrate plaque biofilm and producechanges in microbial cell surface morphology that alter coaggregation,recolonization, and, thus, survival. CHG, CPC, and EO are active againsta wide variety of aerobic and anaerobic bacteria. An overview of the Foodand Drug Administration and American Dental Association rigorousapproval processes for efficacy and safety is provided.

Safety Overview. Long-term use of CHG or EO does not adversely affectthe ecology of oral microbial flora, including microbial overgrowth, oppor-tunistic infection, or development of microbial resistance. Long-term useof CHG, CPC, or EO does not contribute to soft tissue lesions or mucosalaberrations and has no serious adverse effect on salivary flow, taste, toothdeposits, or dental restoration. There is no evidence of a causal linkbetween alcohol-containing mouthrinses and the risk of oral and pharyn-geal cancer.

Key words: Antimicrobial mouthrinse, efficacy, gingivitis, mechanism ofaction, safety


• Establish product safety withrespect to soft tissues, teeth, tox-icology, and effects on the oralflora (eg, adverse shifts in micro-bial populations, the developmentof microbial resistance, and theemergence of opportunisticorganisms)

Data from the studies are then pre-sented to and reviewed by the ADACouncil on Scientific Affairs. If theproduct meets the established stan-dards, it is awarded the ADA Seal ofAcceptance.4,5

For the professional and consumer,the ADA Seal for antimicrobial mouth-rinses indicates that

• Product data have successfullyundergone an intensive, nonbiasedsafety and efficacy review

• Evidence supports the manufac-turer’s claim for effectivenessagainst supragingival dental plaqueand gingivitis

• The product is safe when used asdirected

FDA Regulation

The FDA regulates prescriptiondrugs as well as any OTC productsthat make therapeutic claims, such asthe reduction of gingivitis. The FDAhas accepted key elements for gin-givitis assessment used by the ADASeal Program as appropriate for itsreview. However, in contrast to theADA, which evaluates products, theFDA evaluates active ingredientswhile recognizing that the way inwhich an ingredient is formulated mayaffect its clinical activity. In 2003, therecommendations of the FDA’s Den-tal Plaque Subcommittee of the Non-

prescription Drugs Advisory Com-mittee were published, and theyincluded the conditions under whichOTC products for the reduction orprevention of dental plaque and gin-givitis would be recognized as safe,effective, and not misbranded.6,7 Inaddition to data supporting effective-ness, the following criteria are exam-ined by the FDA6:

• Incidence and risk of adversereactions and significant sideeffects when used according toadequate directions

• Margin of safety with normal use • Potential for harm from abuse or

misuse• Potential for inducing adverse

side effects (such as irritation,ulceration, inflammation, erosion,damage to teeth/restorations)

• Benefit-risk ratio

After assessing an OTC ingredient,the FDA assigns the ingredient to acategory of I, II, or III 6,7:

• Category I: The ingredient isboth safe and effective and is notmisbranded.

• Category II: The ingredient isnot generally recognized as safeand effective or is misbranded.

• Category III: There are insuffi-cient data to evaluate safetyand/or effectiveness.

The FDA may also approve prod-ucts, both prescription and OTC,through the New Drug Application(NDA) process. The NDA process isa more lengthy one that also requiresdocumentation of both the safety andefficacy of the product.

Mouthrinses That MeetADA and/or FDAGuidelines

Two antiseptic mouthrinses (andtheir generic equivalents) have beenawarded the ADA Seal for chemo-therapeutic control of supragingivalplaque and gingivitis: 0.12% chlor-hexidine gluconate (CHG) mouthrinse(Peridex®) and essential oils (EO)mouthrinse (Listerine®). Because of arecent change in the ADA Seal Pro-gram, Peridex® and its generic equiv-alents as prescription products nolonger carry the ADA Seal. However,no CPC formulation has yet to obtainthe ADA Seal. (See also page 32 formore information on the ADA SealProgram.)

The FDA’s Dental Plaque Sub-committee of the NonprescriptionDrugs Advisory Committee has clas-sified 2 OTC mouthrinse ingredientsas both safe and effective and not

KEY POINT:

The ADA and FDA have rigorous approval processes

The ADA grants its Seal of Acceptance to mouthrinses that havedocumented safety and efficacy through at least 2 longitudinal, controlledclinical trials. The FDA evaluates OTC ingredients making therapeuticclaims. It has adopted key elements for gingivitis assessment from theADA Seal of Acceptance criteria and assigns categories (I, II, or III)based on level of safety and efficacy. For certain prescriptionmouthrinses, the FDA evaluates safety and efficacy via the New DrugApplication (NDA) process.

Since 1931, the ADA, through its voluntary Seal of Acceptance Program,has promoted the use of oral and dental products that are both safeand effective.

misbranded (Category I): cetylpyri-dinium chloride (CPC; examples ofproducts include Colgate Viadent®

and Crest® Pro-Health™ Rinse) andEO.6,7 CHG was reviewed and foundto be safe and effective by the FDAby means of an NDA and is availablein the United States only by pre-scription.

Although many commercial mouth-rinse manufacturers claim antiplaqueand antigingivitis properties, most lackthe efficacy data required to earn theADA Seal. Stannous fluoride hasreceived Category I recommendationby the FDA’s advisory committee, andtriclosan has received NDA approval

by the FDA. However, these agents arenot found in mouthrinse formulationsin the United States. This article dis-cusses the safety and efficacy data ofmouthrinses that have been approvedby the FDA, recommended as Cate-gory I by the advisory committee, orawarded the ADA Seal.

AntimicrobialMouthrinse Safety

Two essential criteria for any productare safety and efficacy (see also pages 19to 22, Efficacy of Mouthrinses). Themost effective product would be use-

less if it were not safe; conversely, thesafest product would be inconsequen-tial if it did not work. Issues related tosafety in mouthrinses include the fol-lowing:

• Are there any adverse effects onthe oral microbial flora?

• Are there any oral soft tissueaberrations?

• Does routine use adversely affectdental restorative materials?

• Are there any contraindicationsfor the use of these products?

Each of these concerns merits care-ful consideration.


Mouthrinse Study Description Outcome References

0.12% Several studies of 6 months’ duration Routine use of CHG and EO did 8, 9,12Chlorhexidine or longer; dental plaque harvested at not cause adverse shifts in plaque gluconate (CGH) baseline, midpoint, and end. Minimum ecology, emergence of opportunisticand essential inhibitory concentration microbial pathogens, or development of oils (EO) samples taken resistant microbial strains

0.12% CHGand EO Candida species (C albicans, Both agents effective against test 13

C dubliniensis, C krusei, C glabrata, fungal species at commercially C tropicalis) grown in vitro and treated available concentrations with with 0.12% CHG or EO comparable inhibition between

CHG and EO

EO Randomized, crossover study with 29 Reduction in S mutans: Recover- 14 adults to determine whether regular able S mutans counts from the antimicrobial rinse use had the participants’ interproximal spacespotential for a selective increase of reduced by 75.4% with EO comparedStreptococcus mutans or an overgrowth with control. Total streptococci in inter-of fungal species. Participants rinsed proximal plaque declined by 69.9%.with EO or placebo for 14 days EO activity 37.1% greater against

S mutans than against other strepto-cocci. No increase in risk of caries

EO In vivo investigations in persons with Rinsing with EO twice daily was as 15,16denture stomatitis caused by an effective as nystatin oral suspensionovergrowth of C albicans and other in reducing clinical palatal inflammationfungal species in maxillary prostheses and candidiasis

Table I. Effect of CHG and EO on Normal Oral Flora


Do Mouthrinses Have AdverseEffects on Oral Microbiota?

Some dental professionals may fearthat antiseptic mouthrinses pose a riskin killing or inhibiting normal flora withsubsequent repopulation with oppor-tunistic and/or more pathogenic orresistant organisms. The microbial shiftwould manifest as an overgrowth ofopportunistic organisms, such as Can-dida. Fortunately, studies document noadverse effects on supragingival den-tal plaque microflora after 6 months ofcontinued use with either CHG or EO.8-

12 Table I describes the findings of sev-eral studies of the impact of EO andCHG on normal oral flora. Evidenceconfirms that daily, long-term use (6months or longer) of CHG or EO doesnot adversely affect oral microbial flora,including no microbial overgrowth,opportunistic infection, or developmentof microbial resistance.

Do Mouthrinses Cause OralMucosal or Other Soft TissueAberrations?

Concerns about potential adverseeffects on oral mucosa and other softtissue include the following:

• Does alcohol cause adverseeffects such as an increased riskof oral and pharyngeal cancer(OPC)?

• Are the active ingredients foundin CHG, CPC, and EO safe forlong-term use on the oral mucosa?

• Do mouthrinses affect salivaryflow?

• Are there adverse effects on tasteor tooth deposits?

Several studies have addressedthese issues and are discussed below.

Does alcohol cause adverseeffects such as an increased risk ofOPC? Many mouthrinses containpharmaceutical-grade alcohol to sol-ubilize active ingredients, make thembiologically active, or dissolve fla-voring agents. Typical alcohol levelsin mouthrinses include the follow-ing:

• CHG: generally 12.6% alcohol• CPC: 6% to 18% alcohol (tradi-

tional) and alcohol free, withhigh-bioavailability CPC, 0.07%17

• EO: 26.9% alcohol (original“gold” product) and 21.6% alco-hol (flavored products)

Oral care professionals may be reluc-tant to recommend an alcohol-con-taining mouthrinse (ACM) becauseof perceived risk for developingOPC. It is well known that tobaccousage and excessive alcoholic bev-erage consumption cause a substan-tial portion of the OPC.18-20 Sincemost mouthrinses contain alcohol, doACMs increase cancer risk as well?A number of studies have examineda cause-effect relationship betweenACMs and OPC with varyingresults.19,21-27 A critical review ofinvestigations that suggested a cause-effect relationship revealed a num-ber of deficiencies and study designflaws that necessitate rethinking theACM-cancer link28,29:

• Lack of a dose-response based onfrequency and/or duration of mouth-wash use

• Inconsistent findings among studies• Lack of a scientific or biological

basis to explain inconsistent find-ings between males and females

• Absence of correction for alcoholicbeverage ingestion and tobacco use

• Inclusion of pharyngeal cancer,an improper classification as mouth-rinses only contact the oral cavity

• Inclusion of other head and neckcarcinomas, lymphomas, and sar-comas as oral cancer, an improperclassification as mouthrinses onlycontact the oral cavity

A widely referenced study by theNational Cancer Institute erroneouslyconcluded that OPC risks were ele-vated 60% among female and 40%among male users of mouthwash(with >25% alcohol).27 This epi-demiologic retrospective investiga-tion consisted of interviews with 866patients with OPC, diagnosed Janu-ary 1984 through March 1985, and1249 controls from the general pop-ulation without OPC sampled from4 areas of the United States. Reanaly-sis of this report by independentreviewers concluded that manypatients in the OPC group (6.6% ofmen and 12.6% of women) hadtumors of nonmucosal histology thatcould not have been contacted by an

KEY POINT:

No link between ACMs and OPC

According to the FDA, National Cancer Institute, and ADA, there is noevidence of a causal relationship between ACMs and OPC.6,28 Mostmouthrinses accepted by the ADA as safe and effective contain alcohol.The ADA Seal documents a product’s safety and efficacy, and the ADArecommends that patients continue to use antiseptic mouthrinses asadvised by their dental hygienist and dentist.28,34

Evidence confirms that daily, long-term use of CHG or EO does not adversely affect oral microbial flora, including no microbialovergrowth, opportunistic infection, or development of microbial resistance.


ACM. Reanalysis of the data showedno relationship between ACMs andOPC.6,30,31 Additional investigatorscontinue to report that there is no evi-dence that ACM use increases OPCrisk.28,32,33

Data comparisons of topical alco-hol exposure of the oral mucosa fromACMs and alcoholic beverage con-sumption may be invalid. Two or even3 topical administrations of a 25%ACM, each lasting 30 seconds, seemunlikely to produce the same effect aslong-term, habitual alcoholic bever-age consumption. Pharmaceuticalalcohol is not a carcinogen.6,28 How-ever, chemicals and additives foundin alcoholic beverages can cause can-cer; for example, urethane, a knowncarcinogen, is commonly found inalcoholic beverages.6,19,28 Commercialmouthrinses contain pharmaceutical-grade denatured alcohol (pureethanol), which is free from contami-nating carcinogens.

Taking the following precautionsshould limit any potential problemswith ACMs:

• Advise patients to consult withtheir abuse sponsor (counselor)before using an ACM.

• EO is indicated for use in indi-viduals over the age of 12 years.The effectiveness and safety ofCHG have not been establishedin individuals under 18 years.35,36

• Use of an ACM in persons takingdisulfiram (Antabuse®) andmetronidazole (Flagyl®) is con-traindicated, because in combi-nation they may induce nausea,vomiting, and other unpleasantside effects.37,38

Do the active ingredients of CHG,CPC, and EO adversely affect theoral mucosa? Evidence supports thatlong-term use of CHG, CPC, or EOdoes not contribute to soft tissuelesions or mucosal aberrations. Long-term clinical trials (at least 6 months’duration) produced substantial evi-dence documenting the safety of theactive ingredients of CHG, CPC, andEO mouthrinses on the oral mucosaand periodontium.39-52 Complete oralsoft tissue examinations were per-formed at each data collection period(baseline, 3 months, and 6 months) inthese studies. Findings revealed nodifferences in the incidence or sever-ity of adverse events between theCHG, CPC, or EO groups and con-trol/placebo groups. With EO, usersreport an initial tingling/burning sen-sation that lessens rapidly with timeand is considerably reduced by theaddition of flavoring such as citrus.29,42

A burning sensation and occasionalmild desquamation have also beenreported with CPC use.53

Do mouthrinses affect salivaryflow? Xerostomia is a common sideeffect of many systemic diseases,radiation/chemotherapy, and numer-ous OTC and prescription medica-tions. A misconception is that the useof an ACM desiccates the oralmucosa, leading to xerostomia. How-ever, studies have shown that rinsingwith an EO mouthrinse does notinduce mucosal drying or aberra-tion.54,55 Table II summarizes thesestudy findings.

Are there adverse effects on tasteand tooth deposits? Some patientsmay experience a bitter taste with EOuse.56 Taste alteration, as well as

Study Description Outcome References

Effect of EO versus placebo Under exaggerated conditions 54 on the salivary flow rate and (3 rinses/day instead of the oral mucosa of 19 volunteers recommended 2), no lesionswith documented xerostomia attributable to EO observedwho used 3 rinses daily for in the majority of patients.14 days followed by a cross- No statistically significant over after a 7-day washout differences detected betweenperiod. Pre- and postrinse pre- and postrinse salivarysalivary flow rates were flow rates for either the EO measured and oral soft or control grouptissues examined for evidence of irritation and inflammation

Effect on salivary flow or No significant effect on 55 symptoms of dry mouth salivary flow or dry mouthof an EO mouthrinse and between the 2 groupsa non–alcohol-containing mouthrinse

Table II. Effects of EO on Salivary Flow

A misconception is that the use of an ACM desiccates the oral mucosa, leading toxerostomia. However, studies have shown that rinsing with an EO mouthrinse does not induce mucosal drying or aberration.


increased supragingival calculus for-mation and brown staining of theteeth and tongue, is associated with

use of CHG and CPC.42,46,56-60 CHGstains teeth, esthetic restorations, andimplant abutments, and this staining

can be problematic in a society thatdesires cosmetic dentistry and whiterand brighter teeth.36,56

Does Routine Use of MouthrinsesAdversely Affect DentalRestorative Materials?

A number of studies have ad-dressed the concern raised about theeffect of antimicrobial mouthrinseson dental materials. Other than thepotential for staining with CHG andCPC, there are no documentedadverse effects on dental materials.Table III summarizes the findings ofthese studies.

Mouthrinse Study Description Outcome References

Seven mouthrinses In vitro study of resin specimens placed No statistical difference 61(5 alcohol-containing in 1 of 7 mouthrinses and vibrated for among the testedmouthrinses [ACMs], 30 seconds or 1 minute twice daily (to solutions. ACMs caused1 alcohol free, simulate actual use exposure times) no increased reduction inand 1 plain water) for 180 days composite resin hardness

Essential oils In vitro study measured effect of EO No differences in SBS 62(EO) on resin bond strength on human found between the EO

teeth embedded in dental stone. and control groups at allTooth surfaces etched and rinsed for dilutions. EO had no 30 seconds with distilled water or effect on resin bond various EO dilutions. Each tooth was strengththen dried, a film of adhesive resinapplied followed by composite resin,and shear bond strength (SBS) recorded

EO Direct effect of EO use on dental No significant differences 63materials. Specimens of amalgam, between the EO and glass ionomer, and composite subjected control groups detectedto EO or distilled water for a continuous in vitro or in vivo. EO use10-day period. For each material, com- had no adverse effect onpressive strength and water fluid restorative materials absorption were compared; surface testedporosity was evaluated with scanning electron micrographs (SEM). Also, 10 subjects wore appliances with implantedstudy materials and rinsed twice daily for 30 seconds with EO or placebo. After 10 days, dental materials examined by SEM

Table III. Effects of Antimicrobial Mouthrinses on Dental Materials

KEY POINT:

CHG, CPC, and EO cause no serious adverse effects in agenerally healthy population when used according todirections

This includes effects on salivary flow, taste, tooth deposits, and dentalrestorations. Some users may experience minor taste alteration, staining,and supragingival calculus formation with some CHG and CPCformulations.

Efficacy of Mouthrinses

How Antimicrobial MouthrinsesWork

Antiseptics are chemical agentsused to eliminate oral microorganismsin a variety of ways:

• By producing cell death• By inhibiting microbial repro-

duction• By inhibiting cellular metabolism

Most antiseptic agents are bacteri-cidal, although some are bacteriosta-tic. The effectiveness of these agentsvaries widely and is dependent uponproduct formulation, concentration ofthe active agent, dose, substantivity,compliance, and interactions with otherchemicals present in the oral cavity atthe time of use. Different antimicro-bial mouthrinses have demonstratedefficacy against bacteria, fungi, viruses,and spores. Some products produce awide spectrum of activity, while othersare effective against selected microor-ganisms only.56 Notably, most studies,including longitudinal trials, testing theefficacy of CHG used the commercialproduct Peridex®, and Listerine® wasthe EO commercial product used forall studies cited in this paper. CPCcommercial preparations used inresearch studies vary by product con-centration and brand.

Mechanism of action of CHG.CHG (0.12%) is a bactericidal bis-biguanide antiseptic, with demon-strated efficacy against the followingorganisms:

• A wide range of gram-positiveand gram-negative organisms64

• Aerobes and anaerobes, many ofwhich are associated with plaqueand gingivitis, including Fuso-bacterium and Prevotella inter-media65

• Herpes simplex virus 1 and 2,human immunodeficiency virus1, cytomegalovirus, influenza A,parainfluenza, and hepatitisB.12,66,67 CHG is not approved forthe prevention and treatment ofviral infections

• Seven species of Candida andother yeasts13,68,69 (often used aloneor in combination with other anti-fungal medications to reduceopportunistic infections in at-riskpopulations, such as those under-going treatment for leukemia orbone marrow transplantation70,71)

Exposure to CHG causes ruptur-ing of the bacterial cell membrane,which allows for leakage of the cyto-plasmic contents, resulting in celldeath.72,73 CHG binds to salivarymucins, reducing pellicle formationand inhibiting colonization of plaquebacteria.64,74 It also binds to bacteria,which inhibits their adsorption ontothe teeth.64 CHG has been shown topenetrate the dental plaque biofilm,which enables CHG to access andkill pathogens embedded within thebiofilm.72

CHG binds tightly to tooth struc-ture, dental plaque, and oral soft tis-sues. It is released slowly into themouth, which allows antimicrobialeffects to be sustained for up to 12hours, thus its high degree of sub-stantivity.64,75 A 30-minute interval isoptimal between toothbrushing andrinsing with CHG to avoid an inter-action between the positively chargeddetergents found in dentifrices (eg,sodium lauryl sulfate) and thecationic CHG rinse. This interaction,and possible inactivation of CHG,can also occur with the anionic fluo-ride ion found in stannous fluorideand in some toothpastes andmouthrinses.73,76

Mechanism of action of CPC.CPC, a quaternary ammonium com-pound, demonstrates bactericidalactivity. Its mechanism of action issimilar to CHG in that it ruptures the

bacterial cell wall membrane, result-ing in leakage of the intracellular con-tents and eventual cell death. CPC isalso thought to alter bacterial metab-olism and inhibit cell growth.73, 77

CPC binds to tooth structure anddental plaque biofilm; however, thedegree of binding is not as strong aswith CHG. Further, CPC is rapidlyreleased from binding sites, whichexplains why it is generally less effi-cacious than CHG.73 Like CHG, thiscationic rinse may adversely interactwith other charged ions found in den-tifrices and mouthrinses, possibly lim-iting its biological activity.

Published data regarding the effi-cacy of CPC-containing mouthrinsesare limited. In the United States, CPCis available in 2 concentrations:0.05% found in cosmetic mouth-rinses (Cepacol® and Scope®) and0.07% found in therapeutic mouth-rinses (BreathRx® and Crest® Pro-Health™ Rinse). It has been suggestedthat the unique vehicle found in Crest®

Pro-Health™ Rinse is purported toincrease the product’s oral bioavail-ability when compared with otherCPC-containing mouthrinses.78

In vitro studies have documentedthat CPC can be effective against thefollowing organisms:

• Actinomyces viscosus, Porphy-romonas gingivalis, Campylobac-ter rectus, Streptococcus sanguis,Eikenella corrodens, Salmonellatyphimurium, Fusobacteriumnucleatum, Haemophilus actino-mycetemcomitans, Lactobacilluscasei, and P intermedia78

• Several species of Candida68,69,79-81

CPC, like CHG, has been suggestedas a possible agent for the prevention


Different antimicrobial mouthrinses havedemonstrated efficacy against bacteria, fungi,viruses, and spores. Some products produce a wide spectrum of activity, while others are effective against selected microorganisms only.

and treatment of fungal infections.However, CPC mouthrinses mayadversely affect systemic azole drugtreatment of oropharyngeal candidiasisin immunocompromised persons. Thisnegative outcome may be attributed toeither a cross-resistance to the azoledrugs against CPC-resistant organismsor drug antagonism between CPC andazole antifungal medications whenthey are used in combination.82 Two of5 fluconazole-resistant C albicansstrains have also exhibited reducedsusceptibility to CPC.82

Mechanism of action of EO. EOantiseptic mouthrinse is a bacterici-dal combination of phenolic essen-tial oils, including eucalyptol, men-thol, methyl salicylate, and thymol.Phenolic compounds exert theirantimicrobial effects by the followingmechanisms77, 83-87:

• Cause protein denaturation• Alter the cell membrane, resulting

in leakage of the intracellular con-tents and eventual cell death

• Alter bacterial enzyme activity• Exhibit anti-inflammatory prop-

erties by inhibiting prosta-glandin synthetase, an enzymeinvolved in the formation ofprostaglandins, which are pri-mary inflammatory mediators.Note that the anti-inflammatoryeffect of phenolic compoundsoccurs at concentrations lowerthan those needed for antibac-terial activity

• Cause perforation of the cellmembrane and rapid efflux ofintracellular contents (especiallythymol)

• Alter neutrophil function by sup-pressing the formation of andscavenging existing free radicalsgenerated in neutrophils and byaltering neutrophil chemotaxis(especially thymol)

A 30-second exposure time to EOproduces morphologic cell surfacealterations in a variety of oralpathogens that suggest the loss of cellmembrane integrity.88 Cell surfacechanges may also alter bacterial coag-gregation and recolonization that

could potentially affect the growthand metabolism of these organisms.Microscopic evidence of cell surfaceroughening was obtained for the fol-lowing microorganisms:

• C albicans• F nucleatum• A viscosus • Actinobacillus actinomycetem-

comitans• S sanguis

Cell surface changes that resultfrom a short exposure time to EOmay adversely affect bacterial andfungal survival.88 Exposure to levelsof EO sublethal to microorganismsalso reduces bacterial coaggregationwith gram-positive pioneer species,an essential step in plaque matura-tion and the development of thecomplex pathogenic flora found ingingival disease. Decreased bacterialcoaggregation reduces the rate ofplaque maturation, which in turnmay result in a decreased plaquemass, as is observed clinically withEO use.89 EO also has been shownto extract endotoxins from gram-negative bacteria.90 Endotoxins playan important role in pathogenesis;thus, reduction in endotoxin levelshould manifest as a decrease in gin-gival inflammation.

Unlike other OTC mouthrinses,EO has been shown to penetrate thedental plaque biofilm and is activeagainst bacteria embedded within thebiofilm.72,91-93 EO kills a wide varietyof aerobic and anaerobic bacteriaassociated with plaque biofilm andgingivitis, including the following94

• A actinomycetemcomitans• A viscosus• S mutans• S sanguis• Bacteroides species

Efficacy against gram-positive andgram-negative organisms occurs evenat concentrations that are less than fullstrength.94,95 A single 30-second rinsereaches and exerts an antibacterialeffect interproximally, an importantconsideration given that gingival dis-

ease starts between the teeth and thatindividuals often cannot access inter-proximal areas with mechanicalplaque removal techniques such astoothbrushing and flossing. Totalrecovered bacteria from proximaltooth surfaces was 43.8% lower fol-lowing a single 30-second rinse of EOcompared with a control (P=.001).96

Rinsing twice daily with EO as anadjunct to brushing for 11 daysreduced total recoverable streptococciin interproximal plaque by 69.9%(P<.001), with EO producing a 37.1%greater activity against S mutans thanother streptococci. A significantreduction of 75.4% in total recover-able S mutans count was observed(P<.001).14 Studies also have demon-strated significant suppression of theoral flora for several hours after rins-ing, documenting that the antimicro-bial activity of EO extends beyond therinsing period.97-99

In vitro studies have shown that EOis also active against viruses, includ-ing herpes simplex virus 1 and 2, hep-atitis B, human immunodeficiencyvirus 1, and influenza A virus, as wellas against 7 species of Candida.13,67,100

Like CHG, EO is not approved for theprevention and treatment of viralinfections.

Unlike CHG and CPC, EO has aneutral electrical charge and does notinteract negatively with othercharged ions found in dentifrices andmouthrinses.73 Moreover, its actionis not inhibited by proteins in bloodserum that inactivate many antimi-crobial agents, including CHG.94,95

Efficacy of Mouthrinses onPlaque Biofilm and Gingivitis

The primary indication for antimi-crobial mouthrinse use is the reduc-tion of supragingival plaque biofilmand gingivitis in patients. A recentmeta-analysis of 6-month clinical tri-als to evaluate the efficacy of a vari-ety of antiplaque and antigingivitisproducts revealed that the largestbody of studies supported the effi-cacy of EO.101 A smaller body of stud-ies supported the antiplaque andantigingivitis efficacy of 0.12%



CHG. Results regarding the efficacyof CPC varied and were dependentupon product formulation.101 Efficacystudies of CHG, CPC, and EO aresummarized in Tables IV, V, and VI,respectively.

The following observations can bemade from these study results:

• CHG generally reduces moreplaque than either CPC or EO, apredictable outcome given itsgreater substantivity; the longeran antimicrobial agent stays in

contact with plaque bacteria, thegreater its effect.

• CHG and EO are comparable inreducing gingivitis.39-41,43-45,48-50,102-104

• In head-to-head comparisonstudies that evaluated both CHGand EO in the same participants,antiplaque effects were greaterfor CHG, but antigingivitiseffects were similar for bothagents.42,46,47

• Both CHG and EO demonstrategreater reductions in supragingi-val plaque and gingivitis as com-

pared with CPC (see Tables IV-VI).

Perhaps one EO study best sum-marizes the effectiveness of mouthrinsesas an aid to reducing supragingivalplaque and controlling gingivitis. In alarge, randomized, controlled clinicaltrial involving 237 participants, thosewho added twice-daily rinsing withEO to their homecare routine of reg-ular brushing and flossing demon-strated a 51.9% greater reduction inplaque and a 21.0% greater reduction

Trial Concentration Plaque GingivitisLength No. of of CHG Decrease Decrease

Investigator (months) Subjects (%) (%) (%)

Löe et al, 197649 24 120 0.20 45 27

Lang et al, 198250 6 158 0.10 16.2 66.6

0.20 19.4 80.4

Segreto et al, 1986102 3 600 0.12 36 37

0.20 28 28

Grossman et al, 198648 6 430 0.12 61 39

Grossman et al, 198947 6 481 0.12 49 31

Brightman et al, 1991103 3 34 0.12 64.9 60.0

Overholser et al, 199042 6 124 0.12 50.3 30.5

Eaton et al, 1997104 3 121 0.12 28 25

Charles et al, 200446 6 108 0.12 21.6 18.2

Table IV. Effects of CHG on Supragingival Plaque and Gingivitis

Trial Concentration Plaque GingivitisLength No. of of CHG Decrease Decrease

Investigator (months) Subjects (%) (%) (%)

Allen et al, 1998105 6 111 0.05 28.2 24.0

Mankodi et al, 200551 6 139 0.07 15.8 15.4

Stookey et al, 200552* 6 366 0.075 17 23

0.10 19 20

* The mouthrinse formulations in this study were experimental.

Table V. Effects of CPC on Supragingival Plaque and Gingivitis


in gingivitis, as compared with thosewho brushed and flossed only.45 Thisstudy demonstrates the benefit ofadding an EO mouthrinse to regularmechanical plaque removal andshows that mouthrinses are able toreach bacteria in areas that are diffi-cult to access and where mechanicalmethods often leave residual plaquebehind.

Approved Mouthrinses Are Effica-cious Throughout the EntireMouth

Using an antiseptic mouthrinse pro-duces an antimicrobial effect through-out the entire mouth, including areaseasily missed during toothbrushing andinterdental cleaning. Studies havedemonstrated that antiseptics kill bac-teria in saliva and on the soft tissues ofthe mouth, including the tongue andoral mucosa, which are reservoirs ofpathogenic bacteria that are able totransfer and colonize onto the teeth.98,105-

108 These collective research findings,with consideration given to the respec-tive adverse events profiles of antisep-tic agents, reinforce the value of usingCHG, CPC, and EO in addition tomechanical plaque control for long-term maintenance of gingival health.

Conclusion

Antimicrobial mouthrinses that areapproved by the FDA and carry theADA Seal of Acceptance are safe andeffective for the reduction of supragin-gival plaque and gingivitis. Productsthat have not been evaluated in long-term clinical trials have no scientificevidence documenting safety or effi-

cacy and should be used with caution.Antimicrobial mouthrinses with estab-lished safety and efficacy are animportant and effective addition tomechanical plaque control methods toestablish a healthy mouth. Mostpatients will benefit by adding anADA-Accepted antimicrobial mouth-rinse to their self-care daily regimenof brushing and interdental cleaning.

Using an antiseptic mouthrinse produces an antimicrobial effectthroughout the entire mouth, including areas easily missed duringtoothbrushing and interdental cleaning.

Trial Plaque GingivitisLength No. of Rinsing Decrease Decrease

Investigator (months) Subjects Supervision (%) (%)

Lamster et al, 198340 6 145 Supervised 22 28

Gordon et al, 198539 9 85 Supervised 19.5 23.9

DePaola et al, 198941 6 107 Supervised 34 34

Overholser et al, 199042 6 124 Supervised 36.1 35.9

Charles et al, 200143 6 316 Unsupervised 56.1 22.9

Bauroth et al, 200344 6 326 Unsupervised 21 12

Sharma et al, 200445 6 237 Unsupervised 51.9 21.0

Charles et al, 200446 6 108 Unsupervised 18.8 14.0

Table VI. Effects of EO (Listerine®) on Supragingival Plaque and Gingivitis


References1. Beals D, Ngo T, Feng Y, et al. Development and labora-

tory evaluation of a new toothbrush with a novel brushhead design. Am J Dent. 2000;13:5A-14A.

2. Bader HI. Floss or die: implications for dental profession-als. Dent Today. 1998;17:76-82.

3. Oliver RC, Brown LJ, Löe H. Periodontal diseases in theUnited States population. J Periodontol. 1998;69:269-278.

4. Council on Dental Therapeutics. Guidelines for accept-ance of chemotherapeutic products for the control ofsupragingival dental plaque and gingivitis. J Am DentAssoc. 1986;112:529-532.

5. American Dental Association Council on Scientific Affairs.Acceptance Program Guidelines: Chemotherapeutic Prod-ucts for Control of Gingivitis. Available at: http://www.ada.org/ada/seal/standards/guide_chemo_ging.pdf. Pub-lished July 1997. Accessed May 1, 2007.

6. Food and Drug Administration. Oral health care drug prod-ucts for over-the-counter human use; antigingivitis/antiplaque drug products; establishment of a monograph;proposed rules. Fed Regist. May 29, 2003;68:32232-32287.

7. Wu CD, Savitt ED. Evaluation of the safety and efficacy ofover-the-counter oral hygiene products for the control ofplaque and gingivitis. Periodontol 2000. 2002;28:91-105.

8. Minah GE, DePaola LG, Overholser CD, et al. Effects of6 months use of an antiseptic mouthrinse on supragingi-val dental plaque microflora. J Clin Periodontol.1989;16:347-352.

9. Walker C, Clark W, Tyler K, et al. Evaluation of microbialshifts following long-term use of an oral antisepticmouthrinse [abstract]. J Dent Res. 1989;68:412. Abstract1845.

10. Emilson CG, Fornell J. Effect of toothbrushing withchlorhexidine gel on salivary microflora, oral hygiene, andcaries. Scand J Dent Res. 1976;84:308-319.

11. Schiott CR, Briner WW, Loe H. Two year oral use ofchlorhexidine in man. II. The effect on the salivary bacte-rial flora. J Periodontal Res. 1976;11:145-152.

12. Briner WW, Grossman E, Buckner RY, et al. Effect ofchlorhexidine gluconate mouthrinse on plaque bacteria. JPeriodontal Res. 1986;21(suppl):44-52.

13. Meiller TF, Kelley JI, Jabra-Rizk MA, et al. In vitro studiesof the efficacy of antimicrobials against fungi. Oral SurgOral Med Oral Pathol Oral Radiol Endod. 2001;91:663-670.

14. Fine DH, Furgang D, Barnett ML, et al. Effect of an essen-tial oil-containing antiseptic mouthrinse on plaque andsalivary Streptococcus mutans levels. J Clin Periodontol.2000;27:157-161.

15. DePaola LG, Minah GE, Elias SA, et al. Clinical and micro-bial evaluation of treatment regimens to reduce denturestomatitis. Int J Prosthodont. 1990;3:369-374.

16. DePaola LG, Minah GE, Leupold RL, et al. The effect ofantiseptic mouthrinses on oral microbial flora and den-ture stomatitis. Clin Prev Dent. 1986;8:3-8.

17. White DJ. An alcohol-free therapeutic mouthrinse withcetylpyridinium chloride (CPC)—the latest advance in pre-ventive care: Crest Pro-Health Rinse. Am J Dent.2005;18:3A-8A.

18. Parkin DM, Pisani P, Lopez AD, Masuyer E. At least onein seven cases of cancer is caused by smoking: globalestimates for 1985. Int J Cancer. 1994;59:494-504.

19. Blot WJ, McLaughlin JK, Winn DM, et al. Smoking anddrinking in relation to oral and pharyngeal cancer. CancerRes. 1988;48:3282-3287.

20. Negri E, La Vecchia C, Franceschi S, Tavani A. Attributablerisk for oral cancer in northern Italy. Cancer EpidemiolBiomarkers Prev. 1993;2:189-193.

21. Garro AJ, Leiber CS. Alcohol and cancer. Annu Rev Phar-macol Toxicol. 1990;30:219-249.

22. Weaver A, Fleming SM, Smith DB. Mouthwash use andoral cancer: carcinogen or coincidence? J Oral Surg.1979;37:250-253.

23. Mashberg A, Barsa P, Grossman ML. A study of the rela-tionship between mouthwash use and oral and pharyngealcancer. J Am Dent Assoc. 1985;110:731-734.

24. Kabat GC, Herbert JR, Wynder EL. Risk factors for oralcancer in women. Cancer Res. 1989;49:2803-2806.

25. Young TB, Ford CN, Brandenburg JH. An epidemiologicstudy of oral cancer in a statewide network. Am J Oto-laryngol. 1986;7:200-208.

26. Wynder EL, Kabat G, Rosenberg S, Levenstein M. Oralcancer and mouthwash use. J Natl Cancer Inst.1983;70:255-260.

27. Winn DM, Blot WJ, McLaughlin JK, et al. Mouthwash andoral conditions in the risk of oral and pharyngeal cancer.Cancer Res. 1991;51:3044-3047.

28. Ciancio SG. Alcohol in mouthrinse: lack of associationwith cancer. Biol Ther Dent. 1993;9:1-2.

29. Silverman S, Wilder R. Antimicrobial mouthrinse as part ofa comprehensive oral care regimen: safety and compli-ance factors. J Am Dent Assoc. 2006;137:22S-26S.

30. Cole P et al. Alcohol-containing mouthwash and oropha-ryngeal cancer: an epidemiologic prospective. Unpub-lished study in OTC 2001;Vol 210476.

31. FDC Reports. Alcohol-containing mouthwash concern“alleviated” by existing data. The Tan Sheet. June 10,1996;4(24):1-5.

32. Cole P, Rodu B, Mathisen A. Alcohol-containing mouth-wash and oropharyngeal cancer: a review of the epi-demiology. J Am Dent Assoc. 2003;134:1079-1087.

33. Elmore JG, Horwitz RI. Oral cancer and mouthwash use:evaluation of the epidemiologic evidence. OtolaryngolHead Neck Surg. 1995;113:253-261.

34. American Dental Association Council on Dental Thera-peutics. Mouthrinse use and the risk of oral and pharyn-geal cancer (position statement) Sept. 29, 1991.

35. Listerine® Antiseptic [package insert]. Skillman, NJ: John-son & Johnson Healthcare Products Division of McNEIL-PPC, Inc.; 2007.

36. Peridex® (chlorhexidine gluconate 0.12% ) Oral Rinse[package insert]. West Palm Beach FL: 3M ESPE; 2007.

37. Antabuse® (disulfiram) [package insert]. East Hanover,NJ: Odyssey Pharmaceuticals, Inc.; 2001.

38. Gage TW, Pickett FA. Mosby’s Dental Drug Reference. 6thed. St Louis, MO. Mosby/Elsevier; 2003.

39. Gordon JM, Lamster IB, Seiger MC. Efficacy of Listerineantiseptic in inhibiting the development of plaque and gin-givitis. J Clin Periodontol. 1985;12:697-704.

40. Lamster IB, Alfano MC, Seiger MC, et al. The effect of Lis-terine antiseptic on the reduction of existing plaque andgingivitis. Clin Prev Dent. 1983;5:12-16.

41. DePaola LG, Overholser CD, Meiller TF, et al. Chemother-apeutic inhibition of supragingival dental plaque and gin-givitis development. J Clin Periodontol. 1989;16:311-315.

42. Overholser CD, Meiller TF, DePaola LG, et al. Compara-tive effects of 2 chemotherapeutic mouthrinses on thedevelopment of supragingival dental plaque and gingivi-tis. J Clin Periodontol. 1990;17:575-579.

43. Charles CH, Sharma NC, Galustians HJ, et al. Compara-tive efficacy of an antiseptic mouthrinse and anantiplaque/antigingivitis dentifrice: a six-month clinical trial.J Am Dent Assoc. 2001;132:670-675.


44. Bauroth K, Charles CH, Mankodi SM, et al. The efficacyof an essential oil antiseptic mouthrinse vs. dental floss incontrolling interproximal gingivitis: a comparative study. JAm Dent Assoc. 2003;134:359-365.

45. Sharma N, Charles CH, Lynch MC, et al. Adjunctive ben-efit of an essential oil-containing mouthrinse in reducingplaque and gingivitis in patients who brush and floss reg-ularly: a six-month study. J Am Dent Assoc. 2004;135:496-504.

46. Charles CH, Mostler KM, Bartels LL, Mankodi SM. Com-parative antiplaque and antigingivitis effectiveness of achlorhexidine and an essential oil mouthrinse: 6-monthclinical trial. J Clin Periodontol. 2004;31:878-884.

47. Grossman E, Meckel AH, Issacs RL, et al. A clinical com-parison of antibacterial mouthrinses: effects of chlorhex-idine, phenolics and sanguinarine on dental plaque andgingivitis. J Periodontol. 1989;60:435-440.

48. Grossman E, Reiter G, Sturzenberger OP, et al. Six-monthstudy of the effects of a chlorhexidine mouthrinse on gin-givitis in adults. J Periodontal Res. 1986;21(suppl 16):33-43.

49. Löe H, Schiött CR, Glavind L, Karring G. Two years oraluse of chlorhexidine in man. I. General design and clini-cal effects. J Periodontal Res. 1976;11:135-144.

50. Lang NP, Hotz P, Graf H, et al. Effects of supervisedchlorhexidine mouthrinses in children. A longitudinal clin-ical trial. J Periodontal Res. 1982;17:101-111.

51. Mankodi S, Bauroth K, Witt JJ, et al. A 6-month clinical trialto study the effects of a cetylpyridinium chloride mouthrinseon gingivitis and plaque. Am J Dent. 2005;18:9A-14A.

52. Stookey GK, Beiswanger B, Mau M, et al. A 6-month clin-ical study assessing the safety and efficacy of two cetylpyri-dinium chloride mouthrinses. Am J Dent. 2005;18:24A-28A.

53. Ashley FP, Skinner A, Jackson P, et al. The effect of a0.1% cetylpyridinium chloride mouthrinse on plaque andgingivitis in adult subjects. Br Dent J. 1984;157:191-196.

54. Fischman SL, Aguirre A, Charles CH. Use of essential oil-containing mouthrinses by xerostomic individuals: deter-mination of potential for oral mucosal irritation. Am J Dent.2004;17:23-26.

55. Kerr AR, Katz RW, Ship JA. A comparison of the effects oftwo commercially available non-prescription mouthrinseson salivary flow rates and xerostomia: a pilot study. Quin-tessence Int. In press.

56. Ciancio SG. Antiseptics and antibiotics as chemothera-peutic agents for periodontitis management. CompendContin Educ Dent. 2000;21:59-78.

57. Mandel ID. Chemotherapeutic agents for controlling plaqueand gingivitis. J Clin Periodontol. 1988;15:488-498.

58. Kerr AR, Ship JA. Tooth discoloration. Available at:http://www.emedicine.com/derm/topic646.htm. AccessedApril 8, 2007.

59. Sheen S, Addy M. An in vitro evaluation of the availabilityof cetylpyridinium chloride and chlorhexidine in some com-mercially available mouthrinse products. Br Dent J.2003;194:207-210.

60. Bascones A, Morante S, Mateos L, et al. Influence of addi-tional active ingredients on the effectiveness of non-alco-holic chlorhexidine mouthwashes: a randomized controlledtrial. J Periodontol. 2005;76:1469-1475.

61. Norman R. Surface hardness effects of variousmouthrinses on a composite resin [abstract]. J Dent Res.1997;76:325. Abstract 2490.

62. Von Fraunhofer JA, Kelley JJ, DePaola LG, Meiller TF. Theeffect of a dental unit waterline treatment solution on com-posite-dentin shear bond strengths. J Clin Dent.2004;15:28-32.

63. Von Fraunhofer J, Kelley JI, DePaola LG, Meiller TF. Theeffect of a mouthrinse containing essential oils on dentalrestorative materials. Gen Dent. 2006;54:403-407.

64. Wolff LF. Chemotherapeutic agents in the prevention andtreatment of periodontal disease. Northwest Dent.1985;64:15-24.

65. De Boever EH, Loesche WJ. Assessing the contribution ofanaerobic microflora of the tongue to oral malodor. J AmDent Assoc. 1995;126:1384-1393.

66. Bernstein D, Schiff G, Echler G, et al. In vitro virucidaleffectiveness of a 0.12% chlorhexidine gluconatemouthrinse. J Dent Res. 1990;69:874-876.

67. Baqui AA, Kelley JI, Jabra-Rizk MA, et al. In vitro effect oforal antiseptics on human immunodeficiency virus-1 andherpes simplex virus type 1. J Clin Periodontol.2001;28:610-616.

68. Giuliana G, Pizzo G, Milici ME, et al. In vitro antifungalproperties of mouthrinses containing antimicrobial agents.J Periodontol. 1997;68:729-733.

69. Giuliana G, Pizzo G, Milici ME, Giangreco R. In vitro activ-ities of antimicrobial agents against Candida species. OralSurg Oral Med Oral Pathol Oral Radiol Endod.1999;87:44-49.

70. Sharon A, Berdicevsky I, Ben-Aryeh H, Gutman D. Theeffect of chlorhexidine mouth rinses on oral Candida in agroup of leukemic patients. Oral Surg Oral Med OralPathol. 1977;44:201-205.

71. Epstein JB, Vickars L, Spinelli J, Reece D. Efficacy ofchlorhexidine and nystatin rinses in prevention of oralcomplications in leukemia and bone marrow transplanta-tion. Oral Surg Oral Med Oral Pathol. 1992;73:682-689.

72. Foster JS, Pan PC, Kolenbrander PE. Effects of antimi-crobial agents on oral biofilms in a saliva-conditioned flow-cell. Biofilms. 2004;1:5-12.

73. Ciancio SG. Chemical agents: plaque control, calculusreduction and treatment of dentinal hypersensitivity. Peri-odontol 2000. 1995;8:75-86.

74. Fine DH. Mouthrinses as adjuncts for plaque and gingivi-tis management: a status report for the American Journalof Dentistry. Am J Dent. 1988;1:259-263.

75. Weeks C, Briner W, Rebitski G, et al. Immediate and pro-longed effect of 0.12% chlorhexidine on salivary bacteria[abstract]. J Dent Res. 1988;67:326. Abstract 1711.

76. Barkvoll P, Rølla G, Svendsen AK. Interaction betweenchlorhexidine digluconate and sodium lauryl sulfate invivo. J Clin Periodontol. 1989;16:593-595.

77. Scheie AA. Modes of action of currently known chemicalantiplaque agents other than chlorhexidine. J Dent Res.1989;68:1609-1616.

78. Witt J, Ramji N, Gibb R, et al. Antibacterial and antiplaqueeffects of a novel, alcohol-free oral rinse with cetylpyri-dinium chloride. J Contemp Dent Pract. 2005;6:1-9.

79. Meier S, Collier C, Scaletta MG, et al. An in vitro investi-gation of the efficacy of CPC for use in toothbrush decon-tamination. J Dent Hyg. 1996;70:161-165.

80. Nakamoto K, Tamamoto M, Hamada T. In vitro effective-ness of mouthrinses against Candida albicans. Int JProsthodont. 1995;8:486-489.

81. Phillips BJ, Kaplan W. Effect of cetylpyridinium chloride onpathogenic fungi and Nocardia asteroides in sputum. JClin Microbiol. 1976;3:272-276.

82. Edlind MP, Smith WL, Edlind TD. Effects of cetylpyridiniumchloride resistance and treatment on fluconazole activityversus Candida albicans. Antimicrob Agents Chemother.2005;49:843-845.

83. Goodson JM. Response. In: Loe H, Kleinman DV, eds.Dental Plaque Control Measures and Oral Hygiene Prac-tices. Oxford, England: IRL Press; 1986:143-146.


84. Walker CB. Microbiological effects of mouthrinses con-taining antimicrobials. J Clin Periodontol. 1988;15:499-505.

85. Shapiro S, Meier A, Guggenheim B. The antimicrobialactivity of essential oils and essential oil componentstowards oral bacteria. Oral Microbiol Immunol.1994;9:202-208.

86. Kuehl FA Jr, Humes JL, Egar RW, et al. Role ofprostaglandin endoperoxide PGG2 in inflammatoryprocesses. Nature. 1977;265:170-172.

87. Azuma Y, Ozaza N, Ueda Y, Takagi N. Pharmacologicalstudies on the anti-inflammatory action of phenolic com-pounds. J Dent Res. 1986;65:53-56.

88. Kubert D, Rubin M, Barnett ML, Vincent JW. Antisepticmouthrinse-induced microbial cell surface alterations. AmJ Dent. 1993;6:277-279.

89. Fine DH, Furgang D, Lieb R, et al. Effects of sublethalexposure to an antiseptic mouthrinse on representativeplaque bacteria. J Clin Periodontol. 1996;23:444-451.

90. Fine DH, Letizia J, Mandel ID. The effect of rinsing withListerine antiseptic on the properties of developing dentalplaque. J Clin Periodontol. 1985;12:660-666.

91. Pan P, Barnett ML, Coelho J, et al. Determination of thein situ bactericidal activity of an essential oil mouthrinseusing a vital stain method. J Clin Periodontol. 2000;27:256-261.

92. Fine DH, Furgang D, Barnett ML. Comparative antimi-crobial activities of antiseptic mouthrinses against iso-genic planktonic and biofilm forms of Actinobacillus actin-omycetemcomitans. J Clin Periodontol. 2001;28:697-700.

93. Ouhayoun JP. Penetrating the plaque biofilm: impact ofessential oil mouthrinse. J Clin Periodontol. 2003;30(suppl5):10-12.

94. Ross NM, Charles CH, Dills SS. Long-term effects of Lis-terine antiseptic on dental plaque and gingivitis. J ClinDent. 1989;1:92-95.

95. Whitaker EJ, Pham K, Feik D, et al. Effect of an essentialoil-containing antiseptic mouthrinse on induction of plateletaggregation by oral bacteria in vitro. J Clin Periodontol.2000;27:370-373.

96. Charles CH, Pan PC, Sturdivant L, Vincent JW. In vivoantimicrobial activity of an essential oil-containingmouthrinse on interproximal plaque bacteria. J Clin Dent.2000;11:94-97.

97. Pitts G, Brogdon C, Hu L, et al. Mechanism of action of an anti-septic, anti-odor mouthwash. J Dent Res. 1983;62:738-742.

98. DePaola LG, Minah GE, Overholser CD, et al. Effect of anantiseptic mouthrinse on salivary microbiotia. Am J Dent.1996;9:93-95.

99. Furgang K, Sinatra K, Schreiner H, et al. In vitro antimi-crobial activity of an essential oil mouthrinse. J Dent Res.2002;81(special issue A). Abstract 2854.

100. Dennison DK, Meredith GM, Shillitoe EJ, Caffesse RG.The antiviral spectrum of Listerine antiseptic. Oral SurgOral Med Oral Pathol Oral Radiol Endod. 1995;79:442-448.

101. Gunsolley JC. A meta-analysis of six-month studies ofantiplaque and antigingivitis agents. J Am Dent Assoc.2006;137:1649-1657.

102. Segreto VA, Collins EM, Beiswanger BB, et al. A com-parison of mouthrinses containing two concentrations ofchlorhexidine. J Periodontal Res. 1986;21(suppl):23-32.

103. Brightman LJ, Terezhalmy GT, Greenwell H, et al. Theeffects of a 0.12% chlorhexidine gluconate mouthrinse onorthodontic patients aged 11 through 17 with establishedgingivitis. Am J Orthod Dentofacial Orthop. 1991;100:324-329.

104. Eaton KA, Rimini FM, Zak E, et al. The effects of a 0.12%chlorhexidine–digluconate-containing mouthrinse versusa placebo on plaque and gingival inflammation over a 3-month period. A multicentre study carried out in generaldental practices. J Clin Periodontol. 1997;24:189-197.

105. Allen DR, Davies R, Bradshaw B, et al. Efficacy of amouthrinse containing 0.05% cetylpyridinium chloride forthe control of plaque and gingivitis: a 6-month clinicalstudy in adults. Compend Contin Educ Dent. 1998;19(2suppl):20-26.

106. Dahlen G. Effect of antimicrobial mouthrinses on salivarymicroflora in healthy subjects. Scand J Dent Res.1984;92:38-42.

107. Jenkins S, Addy M, Wade W, Newcombe RG. The mag-nitude and duration of the effects of some mouthrinseproducts on salivary bacterial counts. J Clin Periodontol.1994;21:397-401.

108. Pitts G, Pianotti R, Feary TW, et al. The in vivo effects ofan antiseptic mouthwash on odor-producing microorgan-isms. J Dent Res. 1981;60:1891-1896.

109. Fine DH, Furgang D, Sinatra K, et al. In vivo antimicrobialeffectiveness of an essential oil-containing mouth rinse12 h after a single use and 14 days’ use. J Clin Peri-odontol. 2005;32:335-340.


Introduction

The merits of oral hygiene to healthhave long been valued by oral healthcare providers. However, publicawareness of the importance of oralhealth and the links between oral andsystemic health and disease hasincreased in recent years, particularlysince the publication of Oral Health inAmerica: A Report of the SurgeonGeneral in 2000 and the subsequentrelease and implementation of theNational Call to Action to PromoteOral Health, a public-private partner-ship under the leadership of the Officeof the Surgeon General.1,2 Dentalhygienists now have an importantwindow of opportunity to counselpatients on behaviors that promoteoral health. Health care providers,including dental hygienists, can act ascatalysts for change by teachingpatients about oral health, modelinghealth behaviors, and helping patientsadopt healthy behaviors.3

It has been noted that “the mostcost-effective opportunity to improvepatient outcomes over the next quar-ter century will likely come not fromdiscovering new therapies but fromdiscovering how to deliver therapiesthat are known to be effective.”4 Theaim of this article is to enable dentalhygienists to put evidence-basedinformation about antimicrobialmouthrinses into practice by effec-tively communicating research find-ings with patients and promotingincorporation of healthy behaviorsinto their self-care regimens. Thisreview will focus on practical meth-ods for promoting positive change andsuggest ways to involve patients inoptimizing their oral health. By pro-moting optimal oral care, dentalhygienists can make a significant dif-

ference in the health and well-being oftheir patients.

Initiating BehavioralChange

While encouraging patients toadopt new, healthful behaviors issomething dental hygienists fre-quently do, they may find it difficultto recommend new behaviors, such asuse of antimicrobial mouthrinses. Bar-riers to change are varied and include:

• Habit: Dental hygienists may rec-ommend traditional oral hygienemethods most often (such asbrushing and flossing), despiteresearch demonstrating the effec-tiveness of other oral hygiene aidsand techniques.5

• Lack of confidence6: Dentalhygienists may lack the confi-dence to use motivational inter-viewing techniques (please seePractical Strategies for Change)

• Lowered expectations: Hygienistsmay feel that patients are unlikelyto change their behaviors despitecounseling. Patients that dentalhygienists have the lowest expec-tation of—those with high plaquelevels—may receive less genuineverbal interaction and not receivethe more intensive instructionthey need.7 These more challeng-ing patients may be ideal candi-dates for dental hygienists tobegin targeting for incorporatingantimicrobial oral rinsing intodaily home care.

• Not enough time: Lack of interestand resistance from the patient

Strategies for Incorporating Antimicrobial Mouthrinsesinto Daily Oral CareJoanna Asadoorian, RDH, MSc

AbstractOverview. A cost-effective way of improving patient outcomes is adoptingpreventive practices known to be effective. As “front-line” providers of den-tal health services and information, dental hygienists are an important cat-alyst for the implementation of evidence-based preventive practices—such as the twice-daily use of antimicrobial mouthrinses—in the self-careroutines of patients. However, encouraging patients to adopt new behav-iors can present a challenge: providers may be uncomfortable with rec-ommending new behaviors and patients may be resistant to learning newskills. As expert clinicians, educators, and counselors, dental hygienists arein an excellent position to help patients make changes and learn newbehaviors.

Clinical Implications. This article discusses practical methods for pro-moting change. Targeting interventions to individual patient values, stage ofreadiness to change, and skill set encourages patient incorporation of newbehaviors. Time should be allotted for supervised practice of new skills, andpatients should be supported in planning for effective and lasting behaviorchange. Through effective communication, skills teaching, and use of fol-low-up, dental hygienists can help patients adopt healthy behaviors.

Key words: Antimicrobial mouthrinse, compliance, dental hygiene, oralhealth, patient education


The patient is the center of any successful change effort.Promoting change starts with listening to the patient andproviding suggestions and skills teaching that are alignedwith the patient’s values. Dental hygienists need to be com-fortable with actively questioning and interviewing patientsto elicit the patient’s beliefs and values about oral hygiene,health, and disease and be prepared for responses that donot conform with ideals.28 Effective questioning minimizespatient defensiveness, allowing patients to consider change.The following are strategies that can promote effective dia-logue and support adoption of healthy behaviors.

• Ask patient about current oral health practicesBegin with determining the patient’s current level of self-care. Example: “What do you do each day to take careof your teeth and gums?” You may want to ask thepatient questions that elicit felt needs, such as, “If youcould change anything about your oral health, whatwould you change?” Avoid a confrontational approach,and be sure to support healthy activities the patient isalready performing.

• Assess patient readiness to changeDetermine the patient’s readiness to incorporate newself-care behaviors.23 The initial question may be “Wouldyou be willing to try using an antimicrobial mouthrinsetwice daily?” If the patient responds positively, move topractical support. If the patient responds with disinter-est, determine any obstacles to change. “Have you triedthem in the past? Did you find one you liked? Why not?Why don’t you think it would be helpful?” Be sure tomaintain a nonconfrontational attitude. It may help towrite down patient objections, and continue to listen toobjections until the patient is finished. Active listeningmay diffuse patient resistance. If the patient is unwillingto consider change, providing interventions over multi-ple visits can encourage the patient to rethink his or herdecision. Always work within the patient’s stage of readi-ness to change.

• Supervise new skills / behaviorsIf the patient is ready to attempt new behaviors, super-vised practice will enhance patient self-efficacy.3 Encour-age the patient to practice using mouthrinse, and showthe patient what to look for on the label. This will increasethe patient’s comfort level and success with the newbehavior. Remind the patient that if a product was shownvia research to be effective with twice daily use, using theproduct once daily may not yield the desired outcomes.

• Structure a plan for successful adoption of the newbehaviorIf the patient is ready to change, it is also important to helpwith the plan for success. Unlike other negative behav-iors such as overeating or smoking, patients do not derivepositive satisfaction when neglecting oral self-care. Theprimary obstacle is apathy. Work with the patient todevelop a brief change plan that incorporates environ-

mental support. Encourage the patient to be specific.These planning steps maximize the likelihood of suc-cessful change. Example: “I’m glad you’re ready to makea positive change. I’ve seen many patients significantlyimprove the health of their gums by adding an antimi-crobial mouthrinse to their daily routine. Do you have anantimicrobial mouthrinse? Do you know where to look tofind out if your rinse is ADA-Accepted? When do youplan to use your rinse? Will your use of the rinse matchthe manufacturer’s recommendations for daily care?”

• Anticipate obstaclesStressful life experiences can disrupt the formation ofpositive habits.18 Encourage the patient to incorporateexternal memory triggers (eg, notes to self) to allow himor her to maintain or resume positive oral health prac-tices during disruptive or stressful periods. If the patientdoes not discuss obstacles, you may want to engage inself-disclosure or share examples from your experiencewith other patients. Example: “It can be hard sometimesto remember new healthy habits when we’re busy, sick,traveling, or stressed out. I’m a dental hygienist, andsome days I’m so busy I barely have time to brush myteeth. What are some ways that help you remember todo things when life is stressful? What are some obsta-cles that may keep you from using an antimicrobialmouthrinse twice daily?”

• Follow up with the patientAsk the patient about whether he or she has success-fully incorporated the behavior and any obstacles thatwere encountered: “Were you able to find a productyou really liked? Could you easily access the product?Was it hard to be consistent? What was your biggestchallenge?” Praise any progress toward the desiredbehavior, and revise the patient’s action plan accord-ingly: “Even though you weren’t able to use the rinseevery day twice daily, I’m glad that you were able touse it before bed most nights. You have made a greatstart! Do you think you can use it more often? When doyou think you can incorporate a second rinse into yourday?” Specific follow-up demonstrates care for thepatient and is appreciated. Follow-up is also central tomaintaining change.26,27

While it takes time to change behaviors, the above inter-ventions are brief and can be incorporated into a preven-tive, therapeutic, or periodontal maintenance visit. Throughuse of effective questioning and encouraging patients toshare their health values and behaviors, dental hygienistscan offer targeted advice and be perceived as caring andsupportive while fulfilling their responsibility to educatepatients. Nonconfrontational questioning minimizes patientdefensiveness and ensures they will be as receptive aspossible to receiving information on their oral health.Repeated interventions can assist patients as they adoptpositive behaviors that will improve oral health and qual-ity of life.

Practical Strategies for Change


and poor financial incentives fororal hygiene instruction may con-tribute to limiting the time spenton education.8,9

For all of these reasons, dentalhygienists may tend to continue torecommend the traditional therapiesof brushing and flossing alone. How-ever, compliance with daily flossinghas been reported to be generally low,ranging from only 10% to 30%,5 sopatients may benefit from informationabout new and adjunctive methods forthorough plaque removal.

But changing dental hygienistbehavior is difficult due to the com-plexity of the process, and differentbarriers likely respond to differentapproaches to change.10,11 Simpleexposure to new knowledge may beinsufficient to overcome most barriersto change practices,11,12 but dissemina-tion of information can be more effec-tive in changing behavior when com-bined with other methods such asinteractive educational activities,enabling tools, and reminders.13 Inaddition, comparing one’s currentpractice behaviors to sources of evi-dence, such as guidelines and externalfeedback, has been shown to motivatechange.12,14 Reading journal articlesthat summarize the evidence base in asubject area, like the ones published inthis journal supplement, and compar-ing the findings to one’s current prac-tice may stimulate a need that encour-ages practitioners to change theirprofessional behaviors.

Recently, two professional dentalorganizations have officially acknowl-edged evidence about the adjunctiveuse of daily antimicrobial rinsing. TheAmerican Dental Association (ADA)

released a statement in support of theuse of ADA–Accepted antimicrobialmouthrinses in addition to traditionalbrushing and interdental cleaning.15

The Canadian Dental Hygienists’Association (CDHA) published a posi-tion statement supporting the incorpo-ration of antimicrobial rinsing inpatient home care routines.16 Both ofthese documents provide support forthe dental hygienist as he or she rec-ommends that patients incorporate oralrinsing into their daily routine.

EncouragingCompliance / Adherence

Once a dental hygienist decides toassist patients in improving their oralhealth status through the implementa-tion of an evidence-based product, (eg,an antimicrobial mouthrinse), the den-tal hygienist must motivate the patientto change his or her daily oral care rou-tine. Research confirms what dentalhygienists know intuitively, that

patients are reluctant to change theirhome care routines and, overall, maynot display interest in oral hygieneinstruction.9,17

Despite the value people place onoral health, patients are increasingly

strained with meeting the demands ofdaily life.18 Stressful life events havealso been shown to interfere with self-care.18 In a study examining the impactof oral hygiene education, patientswith poor oral hygiene subsequent toinstructions and education reportedhaving difficulty taking care of theirteeth and had more factors that inter-fered with self-care than the more suc-cessful study participants.19 Moreover,because incorporating complex behav-iors—such as traditional oral self-carebehaviors—may be met with lesscompliance than simpler strategies,19

oral rinsing interventions may produceimproved adherence (see Adherenceversus Compliance below).

Further complicating the issue ofcompliance, research evidence demon-strates that even persons with highplaque levels believe they are doing agood job with their oral home care.19

The fact that patients have an inabilityto evaluate their oral hygiene effec-tiveness and monitor their oral healthstatus has been raised as a weakness

undermining dental hygiene instruc-tion.8 Finally, compliance in behaviorspreventing conditions perceived to benon–life threatening, such as peri-odontal disease and dental caries, mayhave a lower priority for patients.18,20

Dental hygienists can encouragepatients to adopt healthy behaviors,such as the twice-daily use of anADA-Accepted antimicrobial mouth-rinse, by a variety of methods. Den-tal hygienists can listen to patientfeelings and values and emphasizethe value and relevance of oralhygiene care before providing oralhygiene education.21 This allowspatients to link improved healthbehaviors to these values, enhancing

Adherence versus Compliance

Compliance is a common term used in oral health care literature to describea patient’s willingness to follow a practitioner’s instructions.20,28 The term hasbeen criticized because it implies that the patient assumes a passive role andacquiesces to professional recommendations he or she may not under-stand or agree with.17,20,28 Some authors use the term adherence instead ofcompliance, as it implies that the patient takes a more active role in decisionmaking and thereby improves behavior change.20

Despite the value people place on oral health,patients are increasingly strained with meeting the demands of daily life.Stressful life events have also been shown tointerfere with self-care.

their readiness to make positivechanges.21

In addition, change efforts shouldbe tailored to the patient’s expressedreadiness to change. According to theTranstheoretical Model of Change,patients are in one of several stagesof readiness to incorporate newbehaviors,20, 22-23 and interventions

should be targeted accordingly. TableI shows stages of change and appro-priate interventions based on thepatient’s stages of readiness.

In addition to matching educationalinterventions to patient readiness forchange, it is important to tailor infor-mation to each individual patient.Through the skillful use of listening,

questioning, imparting knowledge,and teaching skills, the dental hygien-ist can influence the key dimensions ofpatient behavior including acquiringknowledge, changing attitudes, height-ening perceived needs, and improvingmotivation.19,24 While the actual inter-ventions recommended may be thesame across a variety of patients—for


Stage Characteristics Suggested Intervention

Precontemplation Patient is unaware of the Verify patient’s state of readinessneed for behavior change or resistant to change Raise patient awareness

“I won’t change” “Are you aware of the health benefits of using anantimicrobial mouthrinse twice daily?”

Contemplation Patient has considered Verify patient’s state of readiness changing behavior but is not currently taking action Compliment patient on thinking about making a change

“I might change” “Sounds like you’ve been thinking about making changesin your oral self-care. That’s great! What would you sayis holding you back from taking that step?”

Preparation Patient is ready to take Verify patient’s state of readinesspositive action

Provide actionable information“I will change”

I’m glad you’re ready to make a healthy change. If you wanted to use mouthrinse tonight, what steps would youneed to take? (eg, suggest purchasing a mouthrinse known to reduce plaque and gingivitis)

Action Patient is making initial Verify patient’s state of readinesssteps toward behavior change Support change

“I am making a change” “I’m glad you decided to give mouthrinse a try. Have you thought about ways to make it easier to continue your new habit?” (eg, suggest placing it on the counters in all the bathrooms, placing a reminder note on the bathroom mirror, or including it in an oral care kit at work)

Maintenance Patient has incorporated Verify patient’s state of readinessbehavior change successfully,although some relapse Support behavior maintenance, explore potential may have occurred obstacles, make contingency plans

“I have been making “That’s wonderful to hear you’re using mouthrinse! I can changes” see the improvement in your plaque and gingival bleeding

scores. It takes time to change lifetime habits.We will keep monitoring your oral health status at each dental hygienevisit. Let me show you how to monitor yourself at home.”

Table I. Transtheoretical Stages of Change and Suggested Interventions20, 22-23


example, twice daily use of an antimi-crobial rinse—the individual tailoringof educational sessions to these behav-ioral dimensions are critical for moti-vating change.19,25 As new products areintroduced to the market, the dentalhygienists’ role becomes crucial inhelping patients understand the per-sonal health care implications of theresearch literature.25

The provision of information aboutsafe and effective antimicrobialmouthrinses is important, but infor-mation alone will not change patientbehavior.8,9 The teaching of new skillsis a necessary component of an effec-tive intervention. Skills acquisition isfacilitated by introducing skills one ata time, allowing time for supervisedpractice. This approach increases thechance for successful transfer ofknowledge from the office to thehome setting.7 Using quantitativehygiene assessment tools such as

plaque and gingivitis scores can helppatients see the relevance of instruc-tion to their oral health.7

Table II summarizes important fea-tures of successful dental hygieneinterventions designed to motivatepatients into changing their home carebehaviors. These factors combinedwith the patient’s belief that he or shehas control over his or her oralhygiene and health will increase thelikelihood for positive behaviorchange.3

The fact that research-supported,oral health–promoting behaviors(such as the twice-daily use of a safeand effective antimicrobial mouth-rinse) need to be carried out overone’s lifetime contributes to the chal-lenge.17 Studies consistently showthat modest gains achieved initiallyin changing patient behavior dimin-ish with time and minimize initialgains.19 Key elements to maximize

that patients maintain their newbehaviors include the use of positivefeedback, patient reminders (such asphone calls and postcards), andadapting dental hygiene instructionsto the needs of the patient.20 In aseries of 3 studies evaluating themaintenance of self-care behaviorprograms, adherence was improvedwhen reminders were used, seem-ingly for as long as the reminderswere provided.26 Therefore, mainte-nance of behavioral change is anongoing and deliberate process.27

Conclusions

As preventive oral health experts,dental hygienists must continually eval-uate methods of enhancing oral healthand recommend those techniques andproducts with evidence-based effec-tiveness to their patients. This articlehas examined strategies for promotingbehavioral change in the context ofadoption of twice-daily use of antimi-crobial mouthrinses, which have beenshown to effectively reduce plaque andpromote oral health when used as partof a daily self-care regimen. These prin-ciples can also be applied when teach-ing patients about other health careproducts and behaviors.

General for All Patients Individualized to Specific Patient

Table II. Dental Hygienist Actions for Supporting Patient Behavior Change

Target high-risk patients

Clarify patient values

Determine the patient’s state of readiness for change

Inquire about current behaviors

Tailor approach—ensure relevance

Convince patient of effectiveness of intervention

Highlight the pleasurable sensations and social benefits of oral hygiene and health

Maintain a positive environment

Display warmth and genuineness

Provide ongoing reminders

Be prepared for relapse

Provide sufficient contact time

Ensure mastery of one skill at a time

Provide meaningful praise

Include intraoral demonstrations

Include supervised practice

Encourage a partnership incorporating two-way communication

Ensure patient can self-monitor improvements (eg,decreased redness, swelling, and bleeding)

Provide patient specific written educational materials tosupplement interventions

Assist patient in managing when home care will occur,incorporating contingency plans

Key elements to maximize that patients maintaintheir new behaviors include the use of positive feedback, patient reminders (such as phone calls and postcards), and adapting dental hygiene instructions to the needs of the patient


References

1. US Department of Health and Human Services. Oral Healthin America: A Report of the Surgeon General. Rockville,MD: US Department of Health and Human Services,National Institute of Dental and Craniofacial Research,National Institutes of Health; 2000. http://www2.nidcr.nih.gov/sgr/sgrohweb/welcome.htm.

2. US Department of Health and Human Services. NationalCall to Action to Promote Oral Health. Rockville, MD: USDepartment of Health and Human Services, Public HealthService, National Institutes of Health, National Institute ofDental and Craniofacial Research; 2003. NIH PublicationNo. 03-5303. http://www.surgeongeneral.gov/topics/oralhealth/nationalcalltoaction.htm.

3. Koelen MA, Lindstrom B. Making healthy choices easychoices: the role of empowerment. Eur J Clin Nutr. 2005;59(suppl 1):S10-S16.

4. Berenholz S, Pronovost PJ. Barriers to translating evidenceinto practice. Curr Opin Crit Care. 2003;9:321-325.

5. Asadoorian J. Flossing: Canadian Dental Hygienists Asso-ciation Position Statement: CDHA Position Paper. CJDH.2006;40:112-144

6. Cabana MD, Rand CS, Powe NR, et al. Why don’t physi-cians follow clinical practice guidelines? A framework forimprovement. JAMA. 1999;282:1458-1465.

7. Milgrom P, Weinstein P, Melnick S, et al. Oral hygieneInstruction and health risk assessment in dental practice. JPublic Health Dent. 1989:49:24-31.

8. McConaughy FL, Lukken KM. Toevs SE. Health promotionbehaviors of private practice dental hygienists. J DentHyg.1991:54: 222-230.

9. Basson WJ. Oral health education provided by oral hygien-ists in private practice. SADJ. 1999;54: 53-57.

10. Bosse G, Breuer JP, Spies C. The resistance to changingguidelines—what are the challenges and how to meet them.Best Pract Res Clin Anaesthesiol. 2006;20:379-395.

11. Bain KT. Barriers and strategies to influencing physicianbehavior. Am J Med Qual. 2007;22, 5-7.

12. Bloom BS. Effects of continuing medical education on improv-ing physician clinical care and patient health: A review ofsystematic reviews. Int J Technol Assess Health Care. 2005;21:380-385.

13. Gray J. Changing physician prescribing behaviour. Can JClin Pharmacol. 2006;13:e81-e84.

14. Mead P. Clinical guidelines: promoting clinical effectivenessor a professional minefield? J Adv Nurs. 2000;31:110-116.

15. ADA affirms benefits of ADA-Accepted antimicrobial mouthrinses and toothpastes, fluoride mouth rinses [newsrelease].Chicago, IL: American Dental Association; May 23,2007. http://ada.org/public/media/releases/0705_release03.asp. Accessed July 27, 2007.

16. Asadoorian J. Oral rinsing: Canadian Dental Hygienists Asso-ciation Position Statement. CDHA position paper on com-mercially available over-the-counter oral rinsing products.CJDH. 2006;40:168-183.

17. Blinkhorn AS. Factors affecting the compliance of patients withpreventive dental regimens. Int Dent J.1993;43,294-298.

18. Ower P. The role of self-administered plaque control in themanagement of periodontal diseases: 2. Motivation, tech-niques and assessment. Dent Update. 2003;30:110-116.

19. Weinstein P, Milgrom P, Melnick S, et al. How effective isoral hygiene instruction? Results after 6 and 24 weeks. JPublic Health Dent. 1989;49:32-38.

20. Silverman S, Wilder R. Antimicrobial mouthrinse as part of acomprehensive oral care regimen: safety and compliancefactors. J Am Dental Assoc. 2006;137(11 suppl ):22S-26S.

21. Horowitz LG, Dillenberg J, Rattray J. Self-care motivation: amodel for primary preventive oral health behavior change. JSch Health. 1987;57:114-118

22. Prochaska JO, Norcross JC, DiClemente CC. Changing forGood: The Revolutionary Program That Explains the SixStages of Change and Teaches You How to Free YourselfFrom Bad Habits. New York: William Morrow; 1994.

23. Astroth, DB, Cross-Poline GN, Stach DJ, et al. The trans-theoretical model: an approach to behavioral change. J DentHyg. 2002;76:286-295.

24. Uitenbroek DG, Schaub RMH, Tromp JA, Kant JH. Dentalhygienists’ influence on the patients’ knowledge, motivation,self-care, and perception of change. Community Dent OralEpidemiol. 1989;17:87-90.

25. Gluch-Scranton J. Motivational strategies in dental hygienecare. Semin Dent Hyg. 1991;3:1-4, 6-8.

26. McCaul KD, Glasgow RE, O’Neill HK. The problem of creat-ing habits: establishing health-protective dental behaviors.Health Psychol. 1992;11:101-110.

27. Cifuentes M, Fernald DH, Green LA, et al. Prescription forhealth: changing primary care practice to foster healthybehaviors. Ann Fam Med. 2005;3:S4-S12.

28. Chu R, Craig B. Understanding the determinants of preven-tive oral health behaviours. Probe. 1996; 30:12-18.

ConclusionConclusion


Introduction

The primary indication for antimi-crobial mouthrinse use is to achieve areduction in supragingival plaque andgingivitis. Evidence shows that anAmerican Dental Association (ADA)–Accepted antimicrobial mouthrinsecan result in a greater reduction inplaque and gingivitis than brushingand flossing alone.1 Therefore, eventhe most diligent brusher and flossercan benefit from the addition of anADA-Accepted antimicrobial mouth-rinse to the daily homecare regimen.

Antimicrobial mouthrinses reducethe bacterial count and inhibit thepathogenic bacterial activity in den-tal biofilm that can cause gingivitis, aprecursor to periodontitis. Brushingand flossing alone may not always beenough to control the pathogenicityof dental biofilm. Untreated, gingivi-tis can advance to periodontitis andtooth loss and may be associated withother chronic diseases and conditionssuch as diabetes mellitus, cardiovas-cular disease, obesity, and pre-term

birth. Most patients will improve theiroral health by adding an ADA-Accepted antimicrobial mouthrinse totheir self-care daily regimen of brush-ing and interdental cleaning. There-fore, the incorporation of an ADA-Accepted mouthrinse into the dailyregimen of brushing and cleaninginterdentally is important to achieveoptimal oral health outcomes.

The ADA Seal ofAcceptance Program

More than 100 companies volun-tarily participate in the ADA Seal ofAcceptance Program and more than400 oral care products marketeddirectly to consumers carry the ADASeal (Figure 1).2 Oral health care pro-fessionals and consumers can visithttp://www.ada.org/ada/seal/adaseal_consumer_shopping.pdf to identifyproducts that have earned the ADASeal of Acceptance to guide their rec-ommendations and purchases of over-the-counter (OTC) products. Given

the importance of oral and systemichealth, and product safety and effi-cacy, this list is likely to expand andshould be reviewed regularly.

The safety and efficacy data for thetwice-daily use of an antiplaque andantigingivitis antimicrobial mouth-rinse is unequivocal. Products thathave been found effective againstplaque and gingivitis and that haveearned the ADA Seal are those thatcontain 0.12% chlorhexidine glu-conate (CHG) or a fixed combinationof essential oils (EO). Listerine®— afixed combination of EO—and itsgeneric equivalents carry the ADASeal; however, because of recentchanges in the ADA Seal program,prescription products such as Peridex®

(0.12% CHG), even if they have pre-

Antimicrobial Mouthrinses in Contemporary DentalHygiene Practice: The Take Home MessageMichele Leonardi Darby, RDH, MS

More than 100 companies voluntarily participate in the ADA Seal of Acceptance Program and more than 400 oral care products marketed directly toconsumers carry the ADA Seal.

Figure 1.The AmericanDental Association Sealof Acceptance. (Cour-tesy of the AmericanDental Association.)

viously earned the ADA Seal, are nolonger included in the ADA Seal pro-gram, as the granting of the ADA Sealfor prescription product has beenphased out.

Evidence-BasedLiterature

In addition to the ADA Seal, well-prepared, published systematicreviews and meta-analyses that syn-thesize a large number of rigorousstudies on a focused topic and thatarrive at clear conclusions can beextremely valuable in guiding clini-cal decisions regarding products,devices, treatments, and interventions.Many such studies and reviews inaddition to original research papersare cited throughout this supplement,and these references can provide fur-ther background and information onthe benefits of using an antimicrobialmouthrinse as part of a daily regimen.

One good example cited withinthese pages is a recent meta-analysisof 6-month studies of antiplaque andantigingivitis agents.3 Moreover, sys-tematic reviews on a variety of dental

subject areas are also available fromthe Cochrane Library including theCochrane Database of SystematicReviews at www.cochrane.org. Thissite is an essential resource for busydental hygienists who strive to main-tain an evidence-based practice.

In general, possessing a basicknowledge of what constitutes appro-priate research methods and the abil-ity to read the professional literatureincreases the dental hygienist’s com-petence as a critical consumer ofresearch, enabling the dental hygien-ist to translate important research find-ings into practice in a timely manner.

Conclusions

In conclusion, most patients willimprove their oral health by adding anADA-Accepted antimicrobialmouthrinse to their self-care daily reg-imen of toothbrushing and interdentalcleaning. Within the context of clinicalpractice and current research evidence,dental hygienists should recommendthat patients practice a three-step dailyoral hygiene regimen of brushing,interdental cleaning, and rinsing with

an ADA-Accepted antimicrobialmouthrinse to help prevent and reduceplaque and gingivitis and speak withtheir dental hygienist or dentist foradditional guidance. Understandingthe process of change and matchingprofessional oral care recommenda-tions to patient’s specific needs, goals,values, and levels of readiness tochange may lead to patient adherenceand attainment of desired clinical out-comes over the long term. Regardlessof the level of adherence to profes-sional recommendations, patients needregular instruction and encouragementfrom a dental hygienist they trust.

References1. Sharma N, Charles CH, Lynch MC, et

al. Adjunctive benefit of an essentialoil-containing mouthrinse in reducingplaque and gingivitis in patients whobrush and floss regularly: a six-monthstudy. J Am Dent Assoc. 2004;135:496-504.

2. About the ADA Seal of Acceptance.American Dental Association Website. http://www.ada.org/ada/seal/index.asp. Accessed July 30, 2007.

3. Gunsolley JC. A meta-analysis of six-month studies of antiplaque andantigingivitis agents. J Am Dent Assoc.2006;137:1649-1657.


Rinse twice a day and call me in the morning.Taking care of your mouth may be important to your overall health. Rinsing with LISTERINE® Antisepticmay help. It kills germs that cause gingivitis. That’s important because, if left untreated, gingivitis could

progress to advanced gum disease, which emerging science associates with heart disease, diabetes andother health problems. To learn more, visit www.listerine.com, or ask your dentist, dental hygienist

or physician about the mouth-body connection.*

The Seal on the product means: *If brushing and flossing aren’t enough, use as directed as part of your regular oral care routine to help prevent and reduce plaque and gingivitis.“The ADA Council on Scientific Affairs’ Acceptance of Listerine is based on its finding that the product is effective in helping to prevent or reduce gingivitis and plaque above thegumline, when used as directed.”

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