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

Home , Dental plaque, Oral hygiene, Periodontology

2007 Journal of Dental Hygiene Journal Special Supplement to Access magazine of Dental Hygiene

T HE A MERICAN D ENTAL H YGIENISTS’ASSOCIATION

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

• Changing Perspectives on the Use of Antimicrobial Mouthrinses • The Role of Dental Plaque Biofilm in Oral Health • Safety and Efficacy of Antimicrobial Mouthrinses in Clinical Practice • Strategies for Incorporating Antimicrobial Mouthrinses into Daily Oral Care • Antimicrobial Mouthrinses in Contemporary Dental Hygiene Practice: The Take Home Message

This special issue of the Journal of Dental Hygiene as a supplement to Access was made possible through an educational grant from Johnson & Johnson Healthcare Products Division of McNEIL-PPC, Inc. about the authors

Guest Editor This special issue of the Journal of Dental ■ MICHELE LEONARDI DARBY, RDH, MS, is the graduate program director Hygiene was funded by an unrestricted in dental hygiene at Old Dominion University in Norfolk, Virginia. She educational grant from Johnson & Johnson lectures internationally, is the author of over 50 articles, has published 3 Healthcare Products Division of McNEIL- books, and has served on several editorial advisory boards, currently PPC, Inc. serving as associate editor of the International Journal of Dental Hygiene and as an editorial review board member of the Journal of Dental Hygiene Continuing Education Program and Dimensions of Dental Hygiene. In 1981, she was a member of the first To obtain 2 hours of continuing education delegation of dental hygienists to visit the People’s Republic of China. She credit, once you have thoroughly reviewed this has received many awards, including the Warner Lambert–American supplement, please complete the exam at Dental Hygienists’ Association Award for Excellence in Dental Hygiene and http://www.adha.org/CE_courses/course16/. the designation of Eminent Scholar by Old Dominion University. Open to all licensed U.S. dental hygienists, Authors ADHA’s CE Program offers Journal of Dental Hygiene readers the opportunity to ■ JOANNA ASADOORIAN, RDH, MSc, is an associate professor in the earn CE credit. Your exam will be graded by School of Dental Hygiene at the University of Manitoba and works the ADHA staff using questions reviewed privately as a dental hygienist in periodontology. She has published and and developed in cooperation with the regularly lectures on her research interests, which include quality University of North Carolina School of assurance, maintaining competence in health care professionals, clinical Dentistry, a recognized provider of CE decision making, and oral health care products for home use. She credit. serves on the editorial review board for the Journal of Dental Hygiene. Credit for this CE program expires one year ■ LOUIS G. DEPAOLA, DDS, MS, is a professor in the Department of from the date of publication (both print and Diagnostic Sciences and Pathology at the University of Maryland Dental online). Duplicate submissions will be School and the director of dental training for the PA/Mid-Atlantic AIDS disregarded. Submit your exam only once. Education and Training Center. He is an international lecturer; has authored and coauthored over 130 journal articles, book chapters, and Continuing education credits issued for abstracts; and has been awarded over 75 research and service grants, participation in this CE activity may not including ones for the study of antiplaque chemotherapeutic agents. He apply toward license renewal in all licensing serves as a consultant to many professional organizations and from jurisdictions. It is the responsibility of each 2002 to 2005 served on the American Dental Association Council on participant to verify the licensing Scientific Affairs. He is a diplomate of the American Board of Oral requirements of his or her licensing or Medicine and the American College of Dentists. regulatory agency.

■ JOANN R. GURENLIAN, RDH, PhD, is a former chair of the Department Any questions? Contact ADHA of Dental Hygiene at Thomas Jefferson University in Philadelphia and Communications Division: 312/440-8900. past president of the American Dental Hygienists’ Association. She continues to consult and to offer continuing education services in the health care field. She has authored over 100 articles, is the coauthor of The Medical History: Clinical Implications and Emergency Prevention in Dental Settings, and is the recipient of numerous awards, including the American Dental Hygienists’ Association Distinguished Service Award. She is the vice president of the International Federation of Dental Hygienists and chairs a work group for the National Diabetes Education Program.

■ ANN ESHENAUR SPOLARICH, RDH, PhD, holds several academic appointments and currently teaches at the Arizona School of Dentistry and Oral Health, University of Southern California School of Dentistry, and University of Maryland Dental School in addition to practicing dental hygiene. An international lecturer, she has published over 60 articles and 6 chapters in dental hygiene textbooks, has been active in research, serves on several editorial review boards, and is a consultant to the National Center for Dental Hygiene Research. She is the current chair of the American Dental Hygienists’ Association Council on Research. She has received several awards, most recently, the University of Pennsylvania Dental Hygiene Alumni Achievement Award in 2002. Inside Journal of Dental Hygiene

Message

3 Changing Perspectives on the Use of Antimicrobial Mouthrinses Michele Leonardi Darby, RDH, MS

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

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

13 Safety and Efficacy of Antimicrobial Mouthrinses in Clinical Practice Louis G. DePaola, DDS, MS Ann Eshenaur Spolarich, RDH, PhD

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

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

Special supplement The Journal of Dental Hygiene 1 ■ STATEMENT OF PURPOSE The Journal of Dental Hygiene is the refereed, scientific publication of the American Dental Hygienists’ Association. It promotes the publication of Journal 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, of and clinical research. Dental ■ EDITORIAL REVIEW BOARD Hygiene Celeste M. Abraham, DDS, MS Heather L. Jared, RDH, BS, MS Cynthia C. Amyot, BSDH, EdD Wendy Kerschbaum, RDH, MA, MPH Joanna Asadoorian, RDH, MSc Salme Lavigne, RDH, BA, MSDH special supplement Caren M. Barnes, RDH, BS, MS Jessica Y. Lee, DDS, MPH, PhD Phyllis L. Beemsterboer, RDH, MS, EdD Deborah S. Manne,RDH,RN,MSN,OCN Stephanie Bossenberger, RDH, MS Ann L. McCann, RDH, BS, MS Kimberly S. Bray, RDH, MS Stacy McCauley, RDH, MS Lorraine Brockmann, RDH, MS Gayle McCombs, RDH, MS Patricia Regener Campbell, RDH, MS Shannon Mitchell, RDH, MS Dan Caplan, DDS, PhD Tricia Moore, RDH, BSDH, MA, EdD EXECUTIVE DIRECTOR Barbara H. Connolly, PT, EdD, FAPTA Christine Nathe, RDH, MS Ann Battrell, RDH, BS, MSDH Valerie J. Cooke, RDH, MS, EdD Kathleen J. Newell, RDH, MA, PhD [email protected] MaryAnn Cugini, RDH, MHP Johanna Odrich, RDH, MS, DrPh Susan J. Daniel, AAS, BS, MS Pamela Overman, BSDH, MS, EdD DIRECTOR OF COMMUNICATIONS Michele Leonardi Darby, RDH, MS Vickie Overman, RDH, BS, MEd Catherine Davis, RDH, PhD. FIDSA Fotinos S. Panagakos, DMD, PhD, MEd Jeff Mitchell Connie Drisko, RDH, BS, DDS M. Elaine Parker, RDH, MS, PhD [email protected] Jacquelyn M. Dylla, DPT, PT Ceib Phillips, MPH, PhD Deborah E. Fleming, RDH, MS Marjorie Reveal, RDH, MS, MBA EDITOR EMERITUS Jane L. Forrest, BSDH, MS, EdD Kip Rowland, RDH, MS Mary Alice Gaston, RDH, MS Jacquelyn L. Fried, RDH, BA, MS Judith Skeleton, RDH, BS, MEd, PhD Mary George, RDH, BSDH, MEd Ann Eshenaur Spolarich, RDH, PhD EDITOR-IN-CHIEF Ellen Grimes, RDH, MA, MPA, EdD Sheryl L. Ernest Syme, RDH, MS Rebecca S. Wilder, RDH, BS, MS JoAnn R. Gurenlian, RDH, PhD Terri Tilliss, RDH, BS, MS, MA, PhD [email protected] Linda L. Hanlon, RDH, BS, MEd, PhD Nita Wallace, RDH, PhD Kitty Harkleroad, RDH, MS Karen B. Williams, RDH, PhD Harold A. Henson, RDH, MEd Charlotte J. Wyche, RDH, MS STAFF EDITOR Laura Jansen Howerton, RDH, MS Pamela Zarkowski, BSDH, MPH, JD Katie Barge Lisa F. Harper Mallonee,BSDH,MPH,RD/LD [email protected]

LAYOUT/DESIGN Jean Majeski ■ SUBSCRIPTIONS Paul R. Palmer The Journal of Dental Hygiene is published quarterly, online-only, by the American Dental Hygienists’ Association, 444 N. Michigan Avenue, Chicago, IL 60611. Copy- right 2007 by the American Dental Hygienists’ Association. Reproduction in whole or part without written permission is prohibited. Subscription rates for nonmembers are one year, $45; two years, $65; three years, $90; prepaid.

■ SUBMISSIONS

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

2 The Journal of Dental Hygiene Special supplement Introduction

Changing Perspectives on the Use of Antimicrobial Mouthrinses

Michele Leonardi Darby, RDH, MS

s oral health care profes- maintaining oral health. The papers incorporate health-promoting behav- sionals, we need to make within contain extensive information iors such as twice-daily use of antimi- evidence-based recom- about dental plaque biofilms, the effec- crobial mouthrinse. Asadoorian’s A mendations to our patients. tiveness of antimicrobial mouthrinses, approach is also useful in motivating Studies from which we derive our rec- and how to incorporate these agents patients to adopt other beneficial oral ommendations need to have been into patients’oral self-care. Within this hygiene measures. conducted with scientific rigor and Supplement, dental hygienists will find Clinically relevant and easily need to be confirmed with other well- best practices regarding antimicrobial applied information can be found designed studies. Given the numer- mouthrinses so they can confidently within these pages. Through this new ous, long-term, peer-reviewed pub- recommend their use to patients based knowledge, dental hygienists will be lished studies on antimicrobial on the evidence. Patients look to den- equipped to better control plaque and mouthrinses with consistent statisti- tal hygienists for trustworthy informa- gingivitis in patients who historically cally and clinically significant out- tion that can make a difference in their may have been excluded from antimi- comes, it is time to change our pro- oral and systemic health. In this Sup- crobial mouthrinse recommendations. fessional thinking and practices. plement, dental hygienists have evi- I encourage you to read this issue When considering the oral envi- dence-based information about antimi- from cover to cover because the ronment, about 20% is occupied by crobial mouthrinses from oral health knowledge within will make a differ- tooth surfaces, that is, those areas tar- experts. ence in the way you practice dental geted for toothbrushing and flossing.1 Dr. Gurenlian provides a primer on hygiene. Share the issue with your Dental plaque biofilm is not limited to dental plaque biofilm and the perpet- colleagues, and keep an issue in your tooth surfaces. About 80% of the ual challenges facing its management. reception area for patients to read. remaining surfaces include the oral Drs. DePaola and Spolarich review Patients will know that you are a valu- mucosa and specialized mucosa of the the safety and efficacy of the major able source for oral health care rec- tongue.1 Saliva, the tongue, and oral mouthrinses on the market and pro- ommendations that improve and pro- mucosa serve as reservoirs of patho- vide clear guidance on which prod- mote their health status. genic bacteria able to relocate and col- ucts can be confidently recommended onize on the teeth and in sulci. Using to yield predictable clinical health an antiseptic mouthrinse produces an outcomes. New bodies of research antimicrobial effect throughout the evidence encourage the replacement References entire mouth, including areas easily of old beliefs and practices with more missed during toothbrushing and effective therapies; but embracing 1. Mager DL, Ximenez-Fyvie LA, Haffa- jee AD, Socransky SS. Distribution of interdental cleaning. Therefore, it is change is arduous, even with strong selected bacterial species on intraoral not surprising that in May 2007, the evidence to support the change. surfaces. J Clin Periodontol. 2003;30: American Dental Association Council Joanna Asadoorian tackles the chal- 644-654. on Scientific Affairs issued new lenge of promptly translating evi- 2. ADA affirms benefits of ADA-Accepted advice highlighting the oral health dence-based information into prac- antimicrobial mouth rinses and toothpastes, fluoride mouth rinses [news benefits of ADA-Accepted antimi- tice, particularly when it means release].Chicago, IL: American Dental crobial mouthrinses that help prevent change on the part of both the practi- Association; May 23, 2007. http:// and reduce plaque and gingivitis.2 tioner and the patient. From her paper, ada.org/public/media/releases/0705_ This special Supplement to the dental hygienists will better under- release03.asp. Accessed July 27, Journal of Dental Hygiene focuses on stand resistance to change, the process 2007. our changing beliefs about antimicro- of change, and how to use change the- bial mouthrinses and their value in ory to help themselves and patients

Special supplement The Journal of Dental Hygiene 3 Supplement

The Role of Dental Plaque Biofilm in Oral Health

JoAnn R. Gurenlian, RDH, PhD

Introduction Abstract In contrast to an accumulation of Overview. Microbial biofilms are complex communities of bacteria and individual bacteria, a biofilm is a are common in the human body and in the environment. In recent years, complex, communal, 3-dimensional dental plaque has been identified as a biofilm, and the structure, microbi- arrangement of bacteria. Bacterial ology, and pathophysiology of dental biofilms have been described. The biofilms are ubiquitous and are poten- nature of the biofilm enhances the component bacteria’s resistance to tially found in a variety of sites within both the host’s defense system and antimicrobials. If not removed regularly, the human body. For example, they the biofilm undergoes maturation, and the resulting pathogenic bacterial complex can lead to dental caries, gingivitis, and periodontitis. In addition, can grow on indwelling catheters, dental biofilm, especially subgingival plaque in patients with periodontitis, ports, and implants; external surfaces has been associated with various systemic diseases and disorders, includ- of the eye; artificial heart valves; ing cardiovascular disease, diabetes mellitus, respiratory disease, and endotracheal tubes; and contaminated adverse pregnancy outcomes. prosthetic joints. A bacterial biofilm is often the cause of persistent infec- Clinical Implications. An understanding of the nature and pathophysiology of the dental biofilm is important to implementing proper management tions and has been associated with strategies. Although dental biofilm cannot be eliminated, it can be reduced osteomyelitis, pneumonia in patients and controlled through daily oral care. A daily regimen of thorough mechan- 1 with cystic fibrosis, and prostatitis. ical oral hygiene procedures, including toothbrushing and interdental clean- In areas related to oral health care, ing, is key to controlling biofilm accumulation. Because teeth comprise bacterial biofilms are found in dental only 20% of the mouth’s surfaces, for optimal oral health, the use of an unit water lines, on tooth surfaces and antimicrobial mouthrinse helps to control biofilm not reached by brushing dental prosthetic appliances, and on and flossing as well as biofilm bacteria contained in oral mucosal reservoirs. oral mucous membranes. Biofilm in Key words: Antimicrobial mouthrinse, biofilm, dental plaque, oral health, the form of supragingival and sub- periodontal disease gingival plaque is the etiologic agent in dental caries and periodontal diseases (Figure 1).2-5 The pathogenicity of the dental plaque biofilm is Changing Views of produced virulence factors and noxious enhanced by the fact that in biofilm Dental Plaque products that initiated inflammation, form, the component bacteria have challenged the host defense system, and increased resistance to antibiotics and Over the past 50 years, the under- resulted in the destruction of periodon- other chemotherapeutic agents and standing and characterization of dental tal tissues. Under this hypothesis, the are less able to be phagocytized by plaque have undergone significant evo- quantity of plaque was considered to host inflammatory cells. Therefore, lution. Loesche6 proposed both a non- be the critical factor in the development control of the dental plaque biofilm is specific and a specific plaque hypoth- of periodontal disease. Thus, increases a major objective of dental profes- esis for periodontal disease initiation in the amount of plaque (quantity), as sionals and critical to the maintenance and progression. opposed to specific pathogenic of optimal oral health. This article The nonspecific plaque hypothesis microorganisms (quality) found in the reviews the characteristics of dental proposed that the entire microbial com- plaque, were viewed as being prima- biofilm, its role in the etiology of munity of plaque that accumulated on rily responsible for inducing disease periodontal diseases, and strategies tooth surfaces and in the gingival and disease progression.7,8 for controlling the biofilm to promote crevice contributed to the development Studies on the microbial etiology health. of periodontal disease. Plaque bacteria of various forms of periodontitis sup-

4 The Journal of Dental Hygiene Special supplement port the specific plaque hypothesis, which proposes that only certain microorganisms within the plaque complex are pathogenic. Despite the presence of hundreds of species of microorganisms in periodontal pockets, fewer than 20 are routinely found in increased proportions at periodon- tally diseased sites. These specific vir- ulent bacterial species activate the host’s immune and inflammatory responses that then cause bone and soft tissue destruction.6,8,9 Socransky and colleagues4,10 recognized that early plaque consists predominantly of gram-positive organisms and that if the plaque is left undisturbed it undergoes a process of maturation resulting in a more complex and predominantly gram-negative flora. These investigators Figure 1. Scanning electron micrograph of biofilm grown from the assigned the organisms of the subgin- subgingival plaque of a healthy subject for 10 days anaerobically on gival microbiota into groups, or com- saliva-coated hydroxyapatite discs. (Grown by Michael Sedlacek, PhD, plexes, based on their association with and Clay Walker, PhD, at the University of Florida College of Dentistry health and various disease severities Periodontal Disease Research Center. Image taken by the University (Figure 2).4,10 Color designations were of Florida Electron Microscopy Core Facility.) used to denote the association of particular bacterial complexes with periodontal infections. The blue, yellow, green, and purple complexes designate early colonizers of the subgingival A naeslundii 2 (A viscosus) flora. Orange and red complexes reflect late colonizers V parvula associated with mature sub- A odontolyticus gingival plaque. Certain bacterial complexes are associ- S mitis 10,11 S oralis ated with health or disease. S sanguis For example, the bacteria in C gracilis C rectus the red complex are more Streptococcus sp. P intermedia likely to be associated with S gordonii P nigrescens clinical indicators of peri- S intermedius P micros P gingivalis odontal disease such as peri- S constellatus F nuc vincentii E nodatum F nuc nucleatum T forsythensis odontal pocketing and clini- F nuc polymorphum T denticola F periodonticum cal attachment loss. E corrodens C gingivalis C sputigena C showae Plaque C ochracea S noxia C concisus A actino b. Recognized as a A actino. a Biofilm

Figure 2. Microbial complexes in subgingival biofilm.4,10 (Modified from Research over the past Socransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes in decade has led to the recogni- subgingival plaque. J Clin Periodontol 1998;25:134-144. Reprinted with tion of dental plaque as a permission from Blackwell Publishing.) biofilm—a highly organized

Special supplement The Journal of Dental Hygiene 5 accumulation of microbial communi- Bacteria in biofilm communicate example, salivary mucins, such as ties attached to an environmental sur- with each other by a process called MUC5B and MUC7, contribute to the face. Biofilms are organized to maxi- quorum sensing. This dynamic, formation of acquired pellicle,16,17 and mize energy, spatial arrangements, sophisticated communication system statherin, a salivary acidic phospho- communication, and continuity of the enables bacteria to monitor each protein, and proline-rich proteins pro- community of microorganisms. other’s presence and to modulate their mote bacterial adhesion to tooth sur- Biofilms protect bacteria living gene expression in response to the faces.18 Acquired pellicle formation within their structures and thereby number of bacteria in a given area of begins within minutes of a profes- provide an advantage over free-float- the biofilm.8 In addition, as a result sional prophylaxis; within 1 hour, ing (planktonic) bacteria. The slimy of quorum sensing, portions of the microorganisms attach to the pellicle. extracellular matrix produced by biofilm can become detached in order Usually, gram-positive cocci are the biofilm bacteria encloses the micro- to maintain a cell density compatible first microorganisms to colonize the bial community and protects it from with continued survival. teeth. As bacteria shift from plank- the surrounding environment, including attacks from chemotherapeutic agents. Chemotherapeutic agents have Bacteria in biofilm communicate with each other by difficulty penetrating the polysaccha- a process called quorum sensing. This dynamic, ride matrix to reach and affect the microorganisms.1,11-13 Thus, the matrix sophisticated communication system enables helps to protect bacteria deep within bacteria to monitor each other’s presence and to the biofilm from antibiotics and antiseptics, increasing the likelihood of modulate their gene expression in response to the the colonies’ survival. Furthermore, number of bacteria in a given area of the biofilm. the extracellular matrix keeps the bacteria banded together, so they are not flushed away by the action of saliva and gingival crevicular fluid. Mech- tonic to sessile life, a phenotypic anical methods, including tooth- Stages of Biofilm change in the bacteria occurs requir- brushing, interdental cleaning, and Formation ing significant genetic up-regulation professional scaling procedures, are (gene signaling that promotes this required to regularly and effectively The growth and development of shift). As genetic expression shifts, disrupt and remove the plaque biofilm are characterized by 4 stages: there is a lag in bacterial growth. biofilm. Antiseptics, such as initial adherence, lag phase, rapid mouthrinses, can help to control the growth, and steady state. Biofilm for- Rapid Growth biofilm but must be formulated so as mation begins with the adherence of to be able to penetrate the plaque bacteria to a tooth surface, followed During the rapid growth stage, matrix and gain access to the patho- by a lag phase in which changes in adherent bacteria secrete large amounts genic bacteria. genetic expression (phenotypic shifts) of water-insoluble extracellular poly- Biofilms have a definite architec- occur. A period of rapid growth then saccharides to form the biofilm matrix. tural structure. The bacteria are not occurs, and an exopolysaccharide The growth of microcolonies within uniformly distributed throughout the matrix is produced. During the steady the matrix occurs. With time, addi- biofilm; rather, there are aggregates state, the biofilm reaches growth equi- tional varieties of bacteria adhere to of microcolonies that vary in shape librium. Surface detachment and the early colonizers—a process known and size. Channels between the sloughing occur, and new bacteria are as coaggregation—and the bacterial colonies allow for circulation of nutri- acquired. complexity of the biofilm increases. ents and by-products and provide a These processes involve unique, selec- system to eliminate wastes.14,15 Initial Adherence and Lag Phase tive molecular interactions leading to Microorganisms on the outer surface structural stratification within the of biofilms are not as strongly The first phase of supragingival biofilm. Coaggregation and subsequent attached within the matrix and tend biofilm formation is the deposition of cell division also increase the thickness to grow faster than those bacteria salivary components, known as of biofilm.19-21 deeper within the biofilm. Surface acquired pellicle, on tooth surfaces. microorganisms are more susceptible This pellicle makes the surface recep- Steady State/Detachment to detachment, a characteristic that tive to colonization by specific bacte- facilitates travel to form new biofilm ria. Salivary glands produce a variety During the steady state phase, bac- colonies on nearby oral structures and of proteins and peptides that further teria in the interior of biofilms slow tissues. contribute to biofilm formation. For their growth or become static. Bacte-

6 The Journal of Dental Hygiene Special supplement ria deep within the biofilm show signs of death with disrupted bacterial cells and other cells devoid of cytoplasm; bacteria near the surface remain intact. During this phase, crystals can be observed in the interbacterial matrix that may represent initial calculus mineralization.22 As noted above, during the steady state stage, surface detachment and sloughing also occur, with some bacteria traveling to form new biofilm colonies.

Biofilm and Oral Disease

Biofilms can cover surfaces throughout the oral cavity. Micro- colonies exist on oral mucosa, the Figure 3. Biofilm lodges in the crevices around the teeth both above tongue, biomaterials used for restora- and below the gingival margin. Accumulation of dental plaque biofilm tions and dental appliances, and tooth can result in dental caries and periodontal disease. (Figure copyright surfaces above and below the gingi- 2006 Keith Kasnot, MA, CMI, FAMI.) val margin (Figure 3). It is important for oral health professionals to com- cola, organisms found in greater num- proteins to migrate from within the municate to their patients that both bers in diseased sites and in more blood vessels into the tissue. dental caries and periodontal disease advanced periodontal disease.10,24 • As the gingival inflammatory are infectious diseases resulting from Bacterial communities living in a process continues, additional dental plaque biofilm accumulation. biofilm possess resourceful survival mediators are produced, and more Each of these diseases requires spe- strategies, including a broader habitat inflammatory cell types such as cific strategies for prevention and for growth, nutrition, waste elimina- neutrophils, T cells, and mono- treatment. tion, and new colonization; environ- cytes are recruited to the area. With respect to periodontal disease, mental niches for safety; barriers to • Proinflammatory cytokines are pro- dental plaque biofilm demonstrates a thwart antimicrobial drug therapy; produced in the tissues as a response to succession of microbial colonization tection from the host’s defense system the chronic inflammatory process, with changes in bacterial flora including phagocytosis; and enhanced and these proteins may further esca- observed from health to disease. pathogenicity.1,8 These strategies late the local inflammatory Researchers studied over 13,000 account for the ongoing challenge of response and affect the initiation plaque samples from 185 patients with successfully controlling periodontal and progression of systemic inflam- conditions ranging from oral health to infection and disease progression.25 mation and disease. periodontal disease.4,23 As noted As the biofilm matures and prolif- above, based on their findings, a num- erates, soluble compounds produced The result of this chronic inflam- ber of microbial complexes were iden- by pathogenic bacteria penetrate the mation is a breakdown of gingival col- tified that were associated with vari- sulcular epithelium. These com- lagen and accumulation of an inflam- ous stages of disease initiation and pounds stimulate host cells to produce matory infiltrate, leading to the progression. Bacterial species con- chemical mediators associated with clinical signs of gingivitis. In some tained in the yellow, green, and purple the inflammatory process26 (see Figure individuals, the inflammatory process complexes appear to colonize the sub- 4 on page 9). will also lead to the breakdown of col- gingival sulcus first and predominate lagen in the periodontal ligament and in gingival health. In contrast, orange • Interleukin-1 beta (IL-1β), resorption of the supporting alveolar complex bacteria are associated with prostaglandins, tumor necrosis fac- bone. It is at this point that the lesion gingivitis and gingival bleeding. Inter- tor alpha (TNF-α), and matrix progresses from gingivitis to peri- estingly, bacteria of the orange com- metalloproteinases are mediators odontitis, continuing the same chal- plex may also be associated with red that recruit neutrophils to the area lenge from proinflammatory media- complex microorganisms including via chemotaxis and cause in- tors as with chronic gingivitis. Thus, Porphyromonas gingivalis, Tannerella creased permeability of gingival controlling dental plaque biofilm is forsythensis, and Treponema denti- blood vessels, permitting plasma essential to preventing and reversing

Special supplement The Journal of Dental Hygiene 7 gingivitis as well as preventing and ings of periodontal microorganisms in monia. This is one reason why oral managing periodontitis. human carotid atheromas. Studies of intubation raises the risk of nosoco- atheromatous lesions in carotid arter- mial infection in intensive and critical ies revealed that over 40% of athero- care hospital populations. Periodontal Biofilm mas contain antigens from periodon- Infection and Systemic tal pathogens including P gingivalis, T Association With Chronic Health forsythensis, and Prevotella interme- Diseases and Conditions dia.28,58 In addition, P gingivalis is In recent years, studies have known to induce platelet aggregation, Research has also suggested that demonstrated an association between a component of atheroma and throm- the association between oral inflam- periodontitis and various systemic dis- bus formation,29 and invade endothe- mation and systemic inflammation eases and conditions, including car- lial cells in cell cultures.59 While such may be key to understanding and diovascular disease, diabetes mellitus, findings suggest a possible invasion managing the significant, deleterious respiratory disease, adverse pregnancy of atheromas by oral pathogens as effects on the multiple organ systems outcomes, obesity, pancreatic cancer, well as possible contribution to their involved in some chronic diseases and and Alzheimer’s disease.27-57 While development, it is important to note conditions (Figure 4).26 several of these associations have not that causality has yet to be established. Cardiovascular Disease. Cardio- been definitively established, biolog- Preterm Birth. Research suggests vascular disease is characterized by ical mechanisms explaining some of that periodontal pathogens may travel inflammatory plaque accumulation in the more extensively studied relation- via the bloodstream from the oral cav- blood vessels that can cause throm- ships are emerging. ity to the placenta initiating preterm boses and lead to myocardial infarction. Atherosclerosis represents a In recent years, studies have demonstrated an chronic inflammatory process that causes endothelial dysfunction and association between periodontitis and various injury to the elastic and muscular arte- systemic diseases and conditions, including rial tissue. Early atherosclerotic lesions contain neutrophils, monocytes, and cardiovascular disease, diabetes mellitus, lymphocytes. These leukocytes can respiratory disease, adverse pregnancy outcomes, affect the vascular endothelial lining and cause oxidation of low-density obesity, pancreatic cancer, and Alzheimer’s disease. lipoproteins. As a result, monocytes, induced to become macrophages, take up these oxidized lipoproteins and The association between periodon- birth. In an animal model, Han and become lipid-laden foam cells. As the tal disease and some systemic diseases coworkers60 found that periodontal lesion progresses, the extracellular may relate to the ability of subgingi- bacteria, including Fusobacterium matrix of the vessel wall is degraded by val plaque bacteria and/or their prod- nucleatum, entered the bloodstream proteolytic enzymes and becomes sus- ucts to gain access to the systemic cir- from ulcerated gingival sulci or peri- ceptible to rupture. Thromboses can culation through the ulcerated odontal pockets and negatively influ- occlude blood flow to the heart and epithelium of the periodontal pocket. enced the normal birth process. brain and eventually lead to infarction, For example, environmental niches Respiratory Disease. Likewise, heart attack, or stroke.26 like a subgingival pocket that contains biofilm in the oral cavity may serve as Since atherosclerosis is inflamma- anaerobic gram-negative microorgan- a reservoir of infection leading to res- tory by nature, identifying inflamma- isms can potentially seed orange and piratory disease. Pseudomonas aerug- tory markers that correlate with disease red complex bacteria and/or their inosa, Staphylococcus aureus, and state is important. One recognized and products to distant sites through the enteric bacteria have been shown to consistent marker of systemic inflam- circulatory system. In this way, a den- colonize the teeth of patients admitted mation and poor cardiovascular prog- tal biofilm infection can potentially to hospitals and long-term care facil- nosis is the acute-phase protein C-reac- contribute to both oral and systemic ities. These bacteria may be released tive protein (CRP), the level of which inflammation.25 into saliva and aspirated into the lower rises with systemic inflammation.62,63 airway causing respiratory infection.46- Animal model studies of the relation- Research on Periodontal Microor- 49,61 Intubation is another vehicle by ship between cardiovascular disease ganisms which bacteria from the oral biofilm and periodontal disease demonstrate can be directly introduced into the res- that clinically induced oral infection Atheromas. Direct evidence for the piratory system. Intubation tubes sup- with P gingivalis will increase atheroma role of dental biofilm infection in sys- port biofilm growth contributing to size and elevate CRP levels in the temic inflammation comes from find- nosocomial infection such as pneu- blood.30 Conversely, some studies have

8 The Journal of Dental Hygiene Special supplement Figure 4. Subgingival plaque bacteria and/or their products may gain access to distant sites in the body through the circulatory system and may potentially contribute to systemic inflammation; in this way, a dental 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 be reproduced without the prior written permission of McNEIL-PPC, Inc.) shown that treatment of periodontitis matory mediators in the gingival Elevated TNF-α levels also may exac- decreases CRP blood levels,64 though crevicular fluid from periodontal pock- erbate insulin resistance and worsen this has not been a consistent finding. ets of patients with diabetes with poor glycemic control.44,66,67 Diabetes Mellitus. Diabetes mellitus glycemic control as compared with Adverse Pregnancy Outcomes. is another chronic systemic disease those with diabetes who are well con- Studies also demonstrate that peri- associated with periodontitis. In fact, trolled or those without diabetes. Those odontal diseases are associated with periodontitis has been identified as one with poor glycemic control had con- the risk of adverse pregnancy out- of the major complications of dia- siderable periodontal destruction with comes, especially preterm low-birth- betes.65 Although diabetes increases the an equivalent bacterial challenge.39,66 weight infants.50-52 Chronic infection, susceptibility to periodontal dis- Of note, the proinflammatory cytokine such as that found with chronic peri- ease,38,39,65 periodontitis may also TNF-α plays a significant role in this odontitis, can stimulate the inflamma- increase the difficulty of maintaining process. TNF-α has a major role in tory process throughout the body. In satisfactory glycemic control in peo- insulin resistance, the primary cause of the placenta, this may lead to elevated ple with diabetes as compared with type 2 diabetes, and is produced in amniotic levels of prostaglandins, those with diabetes without periodon- large quantities by fat cells. Periodon- TNF-α, and IL-1 and IL-6, stimulat- titis.40 One biological mechanism pro- titis also has been associated with ing premature rupture of membranes, posed to explain the increased inci- increased levels of TNF-α. Elevated preterm labor, and the birth of low- dence and severity of periodontal levels of TNF-α may lead to greater birth-weight infants. Intervention stud- disease in individuals with diabetes is bone loss by killing cells that repair ies are currently under way to investi- the finding of elevated levels of inflam- damaged connective tissue or bone. gate a cause and effect relationship

Special supplement The Journal of Dental Hygiene 9 Table I. Examples of Antiseptic Mouthrinses* 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 perception Canton, MA) Various generics†

Four essential oils: Listerine® Antiseptic† Supragingival plaque, Children under 12 years eucalyptol, menthol, (Johnson & Johnson gingivitis, oral malodor methyl salicylate, Healthcare Products thymol Division of McNEIL-PPC, Inc., Skillman, NJ) Various generics†

Cetylpyridinium Breath Rx® (Discus Dental, Supragingival plaque, Children under 6 years chloride Culver City, CA) gingivitis, oral malodor Colgate Viadent® (Colgate- Palmolive, New York, NY) Crest® Pro-Health™ Rinse (Procter & Gamble, Cincinnati, OH) * For the mechanisms of actions of antiseptic mouthrinses, see pages 19 and 20. † Has received the ADA Seal of Acceptance; note that as the ADA Seal program has recently phased out prescription products, chlorhexidine gluconate products no longer carry the ADA Seal.

between advanced periodontitis and bacteria from the biofilm on mucosal 25). Only 2 nationally branded anti- adverse pregnancy outcomes. and tooth surfaces are shed constantly septic mouthrinses and their generic into saliva and transferred to other equivalents have received the ADA areas of the mouth. Since oral mucosa, Council on Scientific Affairs Seal of Strategies for Managing which represents about 80% of the oral Acceptance for control of supragingi- Dental Biofilm to cavity surface,68 can serve as a reservoir val plaque and gingivitis: Listerine® Promote Health for pathogenic bacteria that can be (fixed combination of essential oils) transferred to the tooth surface and sul- and Peridex® (0.12% chlorhexidine Although dental biofilm cannot be cus, supplementing mechanical plaque gluconate). However, due to recent completely eliminated, its pathogenic- control methods with topical antimi- changes in the ADA Seal Program, ity can be lessened through effective crobials may also play an important Peridex® and its generic equivalents oral hygiene measures. Daily tooth- role in reducing reservoirs of no longer carry the ADA Seal because brushing, interdental cleaning, and the pathogens that are unaffected by brush- chlorhexidine gluconate is a prescrip- use of topical antimicrobial chemother- ing and flossing directed at the tooth tion product (see also page 32 for apeutics are patient-based strategies to surface. more information on the ADA Seal reduce the bacterial biofilm and to help Program). The fixed combination of prevent periodontal diseases. Ameri- essential oils and cetylpyridinium can Dental Association (ADA)– Using Evidence in chloride have also been reviewed by a Accepted antimicrobial mouthrinses Practice Food and Drug Administration (FDA) have been shown to help prevent and advisory committee and have received reduce plaque and gingivitis when Products recommended to patients a Category I recommendation, mean- added to a daily oral hygiene regimen should be those that have documented ing they have been found to be safe of mechanical plaque removal. Further, efficacy and safety (see pages 13 to and effective for the control of

10 The Journal of Dental Hygiene Special supplement supragingival plaque and gingivitis. Conclusion tices. Teaching patients to use daily Peridex® and its generic equivalents, brushing, interdental cleaning, and which are prescription products, have antimicrobial mouthrinses that carry Dental biofilm is a complex, organ- been approved for marketing by the the ADA Seal of Acceptance increases ized microbial community that is the FDA via the New Drug Application primary etiologic factor for the most the likelihood of periodontal disease route (or for generics, the Abbreviated frequently occurring oral diseases, prevention and reduction. Although New Drug Application process) (see dental caries and periodontal diseases. additional research is needed, there is also pages 14 and 15). Examples of Although the dental biofilm cannot be the possibility that these cost-effec- effective antimicrobial mouthrinses eliminated, it can be controlled with tive, preventive strategies may mini- currently on the market appear in comprehensive mechanical and mize the effect of periodontal diseases Table I. chemotherapeutic oral hygiene prac- on specific systemic conditions.

References 20. Gibbons RJ. Microbial ecology: adherent interactions which may affect microbial ecology in the mouth. J Dent Res. 1. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: 1984;63:378-385. a common cause of persistent infections. Science. 21. Whittaker CJ, Klier CM, Kolenbrander PE. Mechanisms of 1999;284:1318-1322. adhesion by oral bacteria. Annu Rev Microbiol. 1996;50:513- 2. van Houte J. Role of micro-organisms in caries etiology. J 552. Dent Res. 1994;73:672-681. 22. Wirthlin MR Jr, Armitage GC. Dental plaque and calculus: 3. Stenudd C, Nordlund A, Ryberg M, et al. The association of microbial biofilms and periodontal diseases. In: Rose LF, bacterial adhesion with dental caries. J Dent Res. Mealey BL, Genco RJ, Cohen W, eds. Periodontics: Medi- 2001;80:2005-2010. cine, Surgery and Implants. St. Louis, MO: Elsevier Mosby; 4. Socransky SS, Haffajee AD, Cugini MA, et al. Microbial com- 2004. plexes in subgingival plaque. J Clin Periodontol. 1998;25:134- 23. Socransky SS, Haffajee AD, Ximenez-Fyvie LA, et al. Eco- 144. logical considerations in the treatment of Actinobacillus actin- 5. Haffajee AD, Socransky SS. Microbial etiological agents of omycetemcomitans and Porphyromonas gingivalis peri- destructive periodontal diseases. Periodontol 2000. odontal infections. Periodontol 2000. 1999;20:341-362. 1994;5:78-111. 24. Kojima T, Yasui S, Ishikawa I. Distribution of Porphyromonas 6. Loesche WJ. Chemotherapy of dental plaque infections. Oral gingivalis in adult periodontitis patients. J Periodontol. Sci Rev. 1976;9:65-107. 1993;64:1231-1237. 7. Theilade E. The non-specific theory in microbial etiology of 25. Grossi S, Mealey BL, Rose LF. Effects of periodontal infec- inflammatory periodontal disease. J Clin Periodontol. tion on the systemic condition. In: Rose LF, Mealey BL, 1986;13:905-911. Genco RJ, Cohen W, eds. Periodontics: Medicine, Surgery 8. Thomas JG, Nakaishi LA. Managing the complexity of a and Implants. St. Louis, MO: Elsevier Mosby; 2004. dynamic biofilm. J Am Dent Assoc. 2006;137(11 suppl):10S- 26. Gurenlian JR. Inflammation: the relationship between oral 15S. health and systemic disease. Access. 2006;20(4)(suppl):1- 9. Loesche WJ. DNA probe and enzyme analysis in periodon- 9. tal diagnostics. J Periodontol. 1992;63:1102-1109. 27. Epstein SE. The multiple mechanisms by which infection 10. Socransky SS, Haffajee AD. Periodontal microbial etiology. may contribute to atherosclerosis development and course. Periodontol 2000. 2005;38:135-187. Circ Res. 2002;90:2-4. 11. Socransky SS, Haffajee AD. Dental biofilms: difficult thera- 28. Haraszthy VI, Zambon JJ, Trevisan M, et al. Identification of peutic targets. Periodontol 2000. 2002;28:12-55. periodontal pathogens in atheromatous plaques. J Peri- 12. Brown MR, Gilbert P. Sensitivity of biofilms to antimicrobial odontol. 2000;71:1554-1560. agents. J Appl Bacteriol. 1993;74(suppl):87S-97S. 29. Herzberg MC, Meyer MW. Effects of oral flora on platelets: 13. Gilbert P, Das J, Foley I. Biofilm susceptibility to antimicro- possible consequences in cardiovascular disease. J Peri- bials. Adv Dent Res. 1997;11:160-167. odontol. 1996;67:1138-1142. 14. Costerton JW, Lewandowski Z, DeBeer D, et al. Biofilms, 30. Paquette DW. The periodontal-cardiovascular link. Compend the customized microniche. J Bacteriol. 1994;176:2137-2142. Contin Educ Dent. 2004;25:681-692. 15. Wood SR, Kirkham J, Marsh PD, et al. Architecture of intact 31. Desvarieux M, Demmer RT, Rundek T, et al. Periodontal natural human plaque biofilms studied by confocal laser scan- microbiota and carotid intima-media thickness: the oral infec- ning microscopy. J Dent Res. 2000; 79:21-27. tions and vascular disease epidemiology study (INVEST). 16. Levine MJ, Reddy MS, Tabak LA, et al. Structural aspects of Circulation. 2005;111:576-582. salivary glycoproteins. J Dent Res. 1987;66:436-441. 32. Tiong AY, Brieger D. Inflammation and coronary artery dis- 17. Tabak LA, Levine MJ, Mandel ID, Ellison SA. Role of salivary ease. Am Heart J. 2005;150:11-18. mucins in the protection of the oral cavity. J Oral Pathol. 33. Meurman JH, Sanz M, Janket SJ. Oral health, atherosclero- 1982;11:1-17. sis, and cardiovascular disease. Crit Rev Oral Biol Med. 18. Gibbons RJ, Hay DI. Human salivary acidic proline-rich pro- 2004;15:403-413. teins and statherin promote the attachment of Actinomyces 34. Chun YH, Chun KR, Olguin D, Wang HL. Biological founda- viscosus LY7 to apatitic surfaces. Infect Immun. 1988;56:439- tion for periodontitis as a potential risk factor for atheroscle- 445. rosis. J Periodontal Res. 2005;40:87-95. 19. Costerton JW, Cheng KJ, Geesey GG, et al. Bacterial biofilms 35. Hung HC, Willett W, Merchant A, et al. Oral health and periph- in nature and disease. Annu Rev Microbiol. 1987;41:435-464. eral arterial disease. Circulation. 2003;107:1152-1157.

Special supplement The Journal of Dental Hygiene 11 36. Wu T, Trevisan M, Genco RJ, et al. Periodontal disease and 53. Stein PS, Scheff S, Dawson DR III. Alzheimer’s disease and risk of cerebrovascular disease: the first national health and periodontal disease: mechanisms underlying a potential bi- nutrition examination survey and its follow-up study. Arch directional relationship. Grand Rounds Oral-Sys Med. Intern Med. 2000;160:2749-2755. 2006;1:14-24D. 37. Joshipura KJ, Hung HC, Rimm EB, et al. Periodontal disease, 54. Michaud DS, Joshipura K, Giovannucci E, Fuchs CS. A tooth loss, and incidence of ischemic stroke. Stroke. prospective study of periodontal disease and pancreatic can- 2003;34:47-52. cer in US male health professionals. J Natl Cancer Inst. 38. Nishimura F, Takahashi K, Kurihara M, et al. Periodontal dis- 2007;99:171-175. ease as a complication of diabetes mellitus. Ann Periodon- 55. Stolzenberg-Solomon RZ, Dodd KW, Blaser MJ, et al. Tooth tol. 1998;3:20-29. loss, pancreatic cancer, and Helicobacter pylori. Am J Clin 39. Ryan ME, Carnu O, Kamer A. The influence of diabetes on Nutr. 2003;78:176-181. the periodontal tissues. J Am Dent Assoc. 2003;134:34S-40S. 56. Al-Zahrani MS, Bissada NF, Borawskit EA. Obesity and peri- 40. Taylor GW, Burt BA, Becker MP, et al. Severe periodontitis odontal disease in young, middle-aged, and older adults. J and risk for poor glycemic control in patients with non-insulin- Periodontol. 2003;74:610-615. dependent diabetes mellitus. J Periodontol. 1996;67(suppl 57. Reeves AF, Rees JM, Schiff M, Hujoel P. Total body weight 10):1085-1093. and waist circumference associated with chronic periodonti- 41. Grossi SG, Skrepcinski FB, DeCaro T, et al. Treatment of tis among adolescents in the United States. Arch Pediatr periodontal disease in diabetics reduces glycated hemoglo- Adolesc Med. 2006;160:894-899. bin. J Periodontol. 1997;68:713-719. 58. Chiu B. Multiple infections in carotid atherosclerotic plaques. 42. Miller LS, Manwell MA, Newbold D, et al. The relationship Am Heart J. 1999;138:S534-S536. between reduction in periodontal inflammation and diabetes 59. Dorn BR, Burks JN, Seifert KN, Progulske-Fox A. Invasion of control: a report of 9 cases. J Periodontol. 1992;63:843-848. endothelial and epithelial cells by strains of Porphyromonas 43. Mealey BL, Rethman MP. Periodontal disease and diabetes gingivalis. FEMS Microbiol Lett. 2000;187:139-144. mellitus: bidirectional relationship. Dent Today. 2003;22:107- 60. Han YW, Redline RW, Li M, et al. Fusobacterium nucleatum 113. induces premature and term stillbirths in pregnant mice: impli- 44. Grossi SG, Genco RJ. Periodontal disease and diabetes cation of oral bacteria in preterm birth. Infect Immun. mellitus: a two-way relationship. Ann Periodontol. 1998;3:51- 2004;72:2272-2279. 61. 61. Scannapieco FA. Periodontal inflammation: from gingivitis 45. Taylor GW. Bidirectional interrelationships between diabetes to systemic disease? Compend Contin Educ Dent. and periodontal diseases: an epidemiologic perspective. Ann 2004;25(suppl 1):16-25. Periodontol. 2001;6:99-112. 62. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive 46. Scannapieco FA. Role of oral bacteria in respiratory infection. protein and other markers of inflammation in the prediction J Periodontol. 1999;70:793-802. of cardiovascular disease in women. N Engl J Med. 47. Scannapieco FA, Bush RB, Paju S. Associations between 2000;342:836-843. periodontal disease and risk for nosocomial bacterial pneu- 63. Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic monia and chronic obstructive pulmonary disease: a sys- value of C-reactive protein and serum amyloid A protein in tematic review. Ann Periodontol. 2003;8:54-69. severe unstable angina. N Engl J Med. 1994;331:417-424. 48. Hayes C, Sparrow D, Cohen M, et al. The association 64. D’Aiuto F, Parkar M, Andreou G, et al. Periodontitis and sys- between alveolar bone loss and pulmonary function: the VA temic inflammation: control of the local infection is associated Dental Longitudinal Study. Ann Periodontol. 1998;3:257-261. with a reduction in serum inflammatory markers. J Dent Res. 49. Scannapieco FA, Ho AW. Potential associations between 2004;83:156-160. chronic respiratory disease and periodontal disease: analy- 65. Löe H. Periodontal disease: the sixth complication of dia- sis of National Health and Nutrition Examination Survey III. betes mellitus. Diabetes Care. 1993;16:329-334. J Periodontol. 2001;72:50-56. 66. Salvi GE, Yalda B, Collins JG, et al. Inflammatory mediator 50. Offenbacher S, Katz V, Fertik G, et al. Periodontal infection response as a potential risk marker for periodontal diseases as a possible risk factor for preterm low birth weight. J Peri- in insulin-dependent diabetes mellitus patients. J Periodon- odontol. 1996;67(suppl 10):1103-1113. tol. 1997;68:127-135. 51. Jeffcoat MK, Geurs NC, Reddy MS, et al. Periodontal infec- 67. Lalla E, Lamster IB, Feit M, et al. Blockade of RAGE sup- tion and preterm birth: results of a prospective study. J Am presses periodontitis-associated bone loss in diabetic mice. Dent Assoc. 2001;132:875-880. J Clin Invest. 2000;105:1117-1124. 52. Scannapieco FA, Bush RB, Paju S. Periodontal disease as 68. Mager DL, Ximenez-Fyvie LA, Haffajee AD, Socransky SS. a risk factor for adverse pregnancy outcomes: a systematic Distribution of selected bacterial species on intraoral sur- review. Ann Periodontol. 2003;8:70-78. faces. J Clin Periodontol. 2003;30:644-654.

12 The Journal of Dental Hygiene Special supplement Safety and Efficacy of Antimicrobial Mouthrinses in Clinical Practice

Louis G. DePaola, DDS, MS, and Ann Eshenaur Spolarich, RDH, PhD

Introduction Abstract Mechanical plaque removal through Efficacy Overview. The use of an antimicrobial mouthrinse is an impor- toothbrushing and flossing has been tant adjunct to toothbrushing and interdental cleaning. To varying degrees, the universally accepted “gold stan- chlorhexidine gluconate (CHG), cetylpyridinium chloride (CPC), and essen- dard” for maintaining oral health since tial oils (EO) interrupt the integrity of the bacterial cell membrane, leading the early 1960s. However, numerous to lysis and death. CHG binds to salivary mucins, tooth structure, dental studies have shown that most patients plaque, and oral soft tissues and is released slowly into the mouth, where do not effectively clean interdentally it inhibits adsorption of bacteria onto teeth. CHG is active against a wide 1-3 range of gram-positive and gram-negative microorganisms. CPC binds to to remove dental plaque daily. By the teeth and plaque to a lesser degree than CHG and is generally less effi- early 1980s, chemotherapeutic agents cacious than CHG. CHG and EO penetrate plaque biofilm and produce were marketed as adjuncts to brushing changes in microbial cell surface morphology that alter coaggregation, and flossing; however, no definitive recolonization, and, thus, survival. CHG, CPC, and EO are active against guidelines for the evaluation of their a wide variety of aerobic and anaerobic bacteria. An overview of the Food safety and efficacy were available. and Drug Administration and American Dental Association rigorous Both the American Dental Association approval processes for efficacy and safety is provided. (ADA) and the Food and Drug Admin- Safety Overview. Long-term use of CHG or EO does not adversely affect istration (FDA) have established stan- the ecology of oral microbial flora, including microbial overgrowth, oppor- dards for assessing the safety and effi- tunistic infection, or development of microbial resistance. Long-term use cacy of over-the-counter (OTC) and of CHG, CPC, or EO does not contribute to soft tissue lesions or mucosal prescription mouthrinses. aberrations and has no serious adverse effect on salivary flow, taste, tooth deposits, or dental restoration. There is no evidence of a causal link between alcohol-containing mouthrinses and the risk of oral and pharyn- ADA Safety and geal cancer. Efficacy Guidelines for Key words: Antimicrobial mouthrinse, efficacy, gingivitis, mechanism of Mouthrinses action, safety

Since 1931, the ADA, through its voluntary Seal of Acceptance Pro- gram, has promoted the use of oral lines for the evaluation of antiplaque assessment of gingivitis and and dental products that are both safe and antigingivitis chemotherapeutic qualitative and quantitative and effective. Published guidelines agents for inclusion in the Seal Pro- assessment of plaque performed developed by the ADA list the accept- gram, which are still in use today.4 In at baseline, an intermediate point ance criteria for each type of agent, order to be awarded the Seal, an (usually 3 months), and 6 product, or device. In order to obtain antiplaque and antigingivitis chemo- months the Seal of Acceptance, a company therapeutic must5 • Document a statistically signifi- must provide evidence establishing cant reduction of supragingival that a submitted agent, product, or • Be tested in populations of typical plaque and gingivitis as com- device meets or exceeds the guide- product users in a randomized, pared with a negative control in lines for that particular usage and is parallel-group, or crossover clin- each of the 2 studies and demon- safe and effective. Additionally, the ical trial in which the test product strate a statistically significant product must have been approved for is compared with a negative con- reduction of gingivitis for the marketing in the United States by the trol and, if appropriate, an active mouthrinse group of at least 15% FDA. In 1985, the ADA recognized control for any one study and an aver- the potential benefits of some chemo- • Be supported by data from at age reduction of 20% in the 2 therapeutic formulations, giving least two 6-month studies con- studies compared with the con- impetus to the development of guide- ducted at independent sites, with trol group

Special supplement The Journal of Dental Hygiene 13 Since 1931, the ADA, through its • Category II: The ingredient is not generally recognized as safe voluntary Seal of Acceptance Program, and effective or is misbranded. has promoted the use of oral and • Category III: There are insufficient data to evaluate safety dental products that are both safe and/or effectiveness. and effective. The FDA may also approve products, both prescription and OTC, through the New Drug Application • Establish product safety with prescription Drugs Advisory Com- (NDA) process. The NDA process is respect to soft tissues, teeth, tox- mittee were published, and they a more lengthy one that also requires icology, and effects on the oral included the conditions under which documentation of both the safety and flora (eg, adverse shifts in micro- OTC products for the reduction or efficacy of the product. bial populations, the development prevention of dental plaque and gin- of microbial resistance, and the givitis would be recognized as safe, emergence of opportunistic effective, and not misbranded.6,7 In Mouthrinses That Meet organisms) addition to data supporting effective- ADA and/or FDA ness, the following criteria are exam- Guidelines Data from the studies are then pre- ined by the FDA6: sented to and reviewed by the ADA Two antiseptic mouthrinses (and Council on Scientific Affairs. If the • Incidence and risk of adverse their generic equivalents) have been product meets the established stan- reactions and significant side awarded the ADA Seal for chemo- dards, it is awarded the ADA Seal of effects when used according to therapeutic control of supragingival Acceptance.4,5 adequate directions plaque and gingivitis: 0.12% chlor- For the professional and consumer, • Margin of safety with normal use hexidine gluconate (CHG) mouthrinse the ADA Seal for antimicrobial mouth- • Potential for harm from abuse or (Peridex®) and essential oils (EO) rinses indicates that misuse mouthrinse (Listerine®). Because of a • Potential for inducing adverse recent change in the ADA Seal Pro- • Product data have successfully side effects (such as irritation, gram, Peridex® and its generic equiv- undergone an intensive, nonbiased ulceration, inflammation, erosion, alents as prescription products no safety and efficacy review damage to teeth/restorations) longer carry the ADA Seal. However, • Evidence supports the manufac- • Benefit-risk ratio no CPC formulation has yet to obtain turer’s claim for effectiveness the ADA Seal. (See also page 32 for against supragingival dental plaque After assessing an OTC ingredient, more information on the ADA Seal and gingivitis the FDA assigns the ingredient to a Program.) • The product is safe when used as category of I, II, or III 6,7: The FDA’s Dental Plaque Sub- directed committee of the Nonprescription • Category I: The ingredient is Drugs Advisory Committee has clas- both safe and effective and is not sified 2 OTC mouthrinse ingredients FDA Regulation misbranded. as both safe and effective and not

The FDA regulates prescription drugs as well as any OTC products that make therapeutic claims, such as KEY POINT: the reduction of gingivitis. The FDA has accepted key elements for gin- The ADA and FDA have rigorous approval processes givitis assessment used by the ADA Seal Program as appropriate for its The ADA grants its Seal of Acceptance to mouthrinses that have documented safety and efficacy through at least 2 longitudinal, controlled review. However, in contrast to the clinical trials. The FDA evaluates OTC ingredients making therapeutic ADA, which evaluates products, the claims. It has adopted key elements for gingivitis assessment from the FDA evaluates active ingredients ADA Seal of Acceptance criteria and assigns categories (I, II, or III) while recognizing that the way in based on level of safety and efficacy. For certain prescription which an ingredient is formulated may mouthrinses, the FDA evaluates safety and efficacy via the New Drug affect its clinical activity. In 2003, the Application (NDA) process. recommendations of the FDA’s Den- tal Plaque Subcommittee of the Non-

14 The Journal of Dental Hygiene Special supplement Table I. Effect of CHG and EO on Normal Oral Flora Mouthrinse Study Description Outcome References

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

0.12% CHG and 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 spaces potential for a selective increase of reduced by 75.4% with EO compared Streptococcus 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 streptococci. No increase in risk of caries

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

misbranded (Category I): cetylpyri- by the FDA. However, these agents are less if it were not safe; conversely, the dinium chloride (CPC; examples of not found in mouthrinse formulations safest product would be inconsequen- products include Colgate Viadent® in the United States. This article dis- tial if it did not work. Issues related to and Crest® Pro-Health™ Rinse) and cusses the safety and efficacy data of safety in mouthrinses include the fol- EO.6,7 CHG was reviewed and found mouthrinses that have been approved lowing: to be safe and effective by the FDA by the FDA, recommended as Cate- by means of an NDA and is available gory I by the advisory committee, or • Are there any adverse effects on in the United States only by pre- awarded the ADA Seal. the oral microbial flora? scription. • Are there any oral soft tissue Although many commercial mouth- aberrations? rinse manufacturers claim antiplaque Antimicrobial • Does routine use adversely affect and antigingivitis properties, most lack Mouthrinse Safety dental restorative materials? the efficacy data required to earn the • Are there any contraindications ADA Seal. Stannous fluoride has Two essential criteria for any product for the use of these products? received Category I recommendation are safety and efficacy (see also pages 19 by the FDA’s advisory committee, and to 22, Efficacy of Mouthrinses). The Each of these concerns merits care- triclosan has received NDA approval most effective product would be useful consideration.

Special supplement The Journal of Dental Hygiene 15 Evidence confirms that daily, long-term use Oral care professionals may be reluctant to recommend an alcohol-con- of CHG or EO does not adversely affect taining mouthrinse (ACM) because oral microbial flora, including no microbial of perceived risk for developing OPC. It is well known that tobacco overgrowth, opportunistic infection, or usage and excessive alcoholic bev- development of microbial resistance. erage consumption cause a substantial portion of the OPC.18-20 Since most mouthrinses contain alcohol, do ACMs increase cancer risk as well? A number of studies have examined a cause-effect relationship between Do Mouthrinses Have Adverse • Does alcohol cause adverse ACMs and OPC with varying Effects on Oral Microbiota? effects such as an increased risk results.19,21-27 A critical review of of oral and pharyngeal cancer investigations that suggested a cause- Some dental professionals may fear (OPC)? effect relationship revealed a num- that antiseptic mouthrinses pose a risk • Are the active ingredients found ber of deficiencies and study design in killing or inhibiting normal flora with in CHG, CPC, and EO safe for flaws that necessitate rethinking the subsequent repopulation with oppor- long-term use on the oral mucosa? ACM-cancer link28,29: tunistic and/or more pathogenic or • Do mouthrinses affect salivary resistant organisms. The microbial shift flow? • Lack of a dose-response based on would manifest as an overgrowth of • Are there adverse effects on taste frequency and/or duration of mouth- opportunistic organisms, such as Can- or tooth deposits? wash use dida. Fortunately, studies document no • Inconsistent findings among studies adverse effects on supragingival den- Several studies have addressed • Lack of a scientific or biological tal plaque microflora after 6 months of these issues and are discussed below. basis to explain inconsistent find- continued use with either CHG or EO.8- ings between males and females 12 Table I describes the findings of sev- Does alcohol cause adverse • Absence of correction for alcoholic eral studies of the impact of EO and effects such as an increased risk of beverage ingestion and tobacco use CHG on normal oral flora. Evidence OPC? Many mouthrinses contain • Inclusion of pharyngeal cancer, confirms that daily, long-term use (6 pharmaceutical-grade alcohol to sol- an improper classification as mouth- months or longer) of CHG or EO does ubilize active ingredients, make them rinses only contact the oral cavity not adversely affect oral microbial flora, biologically active, or dissolve fla- • Inclusion of other head and neck including no microbial overgrowth, voring agents. Typical alcohol levels carcinomas, lymphomas, and sar- opportunistic infection, or development in mouthrinses include the follow- comas as oral cancer, an improper of microbial resistance. ing: classification as mouthrinses only contact the oral cavity Do Mouthrinses Cause Oral • CHG: generally 12.6% alcohol Mucosal or Other Soft Tissue • CPC: 6% to 18% alcohol (tradi- A widely referenced study by the Aberrations? tional) and alcohol free, with National Cancer Institute erroneously high-bioavailability CPC, 0.07%17 concluded that OPC risks were ele- Concerns about potential adverse • EO: 26.9% alcohol (original vated 60% among female and 40% effects on oral mucosa and other soft “gold” product) and 21.6% alco- among male users of mouthwash tissue include the following: hol (flavored products) (with >25% alcohol).27 This epidemiologic retrospective investiga- tion consisted of interviews with 866 KEY POINT: patients with OPC, diagnosed Janu- ary 1984 through March 1985, and No link between ACMs and OPC 1249 controls from the general population without OPC sampled from According to the FDA, National Cancer Institute, and ADA, there is no 4 areas of the United States. Reanaly- evidence of a causal relationship between ACMs and OPC.6,28 Most sis of this report by independent mouthrinses accepted by the ADA as safe and effective contain alcohol. reviewers concluded that many The ADA Seal documents a product’s safety and efficacy, and the ADA patients in the OPC group (6.6% of recommends that patients continue to use antiseptic mouthrinses as men and 12.6% of women) had advised by their dental hygienist and dentist.28,34 tumors of nonmucosal histology that could not have been contacted by an

16 The Journal of Dental Hygiene Special supplement Effects of EO on Salivary Flow Do the active ingredients of CHG, Table II. CPC, and EO adversely affect the Study Description Outcome References oral mucosa? Evidence supports that long-term use of CHG, CPC, or EO Effect of EO versus placebo Under exaggerated conditions 54 does not contribute to soft tissue on the salivary flow rate and (3 rinses/day instead of the lesions or mucosal aberrations. Long- oral mucosa of 19 volunteers recommended 2), no lesions term clinical trials (at least 6 months’ duration) produced substantial evi- with documented xerostomia attributable to EO observed dence documenting the safety of the who used 3 rinses daily for in the majority of patients. active ingredients of CHG, CPC, and 14 days followed by a cross- No statistically significant EO mouthrinses on the oral mucosa over after a 7-day washout differences detected between and periodontium.39-52 Complete oral period. Pre- and postrinse pre- and postrinse salivary soft tissue examinations were per- salivary flow rates were flow rates for either the EO formed at each data collection period measured and oral soft or control group (baseline, 3 months, and 6 months) in tissues examined for these studies. Findings revealed no evidence of irritation and differences in the incidence or sever- inflammation ity of adverse events between the CHG, CPC, or EO groups and con- Effect on salivary flow or No significant effect on 55 trol/placebo groups. With EO, users report an initial tingling/burning sen- symptoms of dry mouth salivary flow or dry mouth sation that lessens rapidly with time of an EO mouthrinse and between the 2 groups and is considerably reduced by the a non–alcohol-containing addition of flavoring such as citrus.29,42 mouthrinse A burning sensation and occasional mild desquamation have also been reported with CPC use.53 Do mouthrinses affect salivary flow? Xerostomia is a common side ACM. Reanalysis of the data showed • Advise patients to consult with effect of many systemic diseases, no relationship between ACMs and their abuse sponsor (counselor) radiation/chemotherapy, and numer- OPC.6,30,31 Additional investigators before using an ACM. ous OTC and prescription medica- continue to report that there is no evi- • EO is indicated for use in indi- tions. A misconception is that the use dence that ACM use increases OPC viduals over the age of 12 years. of an ACM desiccates the oral risk.28,32,33 The effectiveness and safety of mucosa, leading to xerostomia. How- Data comparisons of topical alco- CHG have not been established ever, studies have shown that rinsing hol exposure of the oral mucosa from in individuals under 18 years.35,36 with an EO mouthrinse does not ACMs and alcoholic beverage con- • Use of an ACM in persons taking induce mucosal drying or aberra- sumption may be invalid. Two or even disulfiram (Antabuse®) and tion.54,55 Table II summarizes these 3 topical administrations of a 25% metronidazole (Flagyl®) is con- study findings. ACM, each lasting 30 seconds, seem traindicated, because in combi- Are there adverse effects on taste unlikely to produce the same effect as nation they may induce nausea, and tooth deposits? Some patients long-term, habitual alcoholic bever- vomiting, and other unpleasant may experience a bitter taste with EO age consumption. Pharmaceutical side effects.37,38 use.56 Taste alteration, as well as alcohol is not a carcinogen.6,28 How- ever, chemicals and additives found in alcoholic beverages can cause cancer; for example, urethane, a known A misconception is that the use of an carcinogen, is commonly found in alcoholic beverages.6,19,28 Commercial ACM desiccates the oral mucosa, leading to mouthrinses contain pharmaceutical- xerostomia. However, studies have shown grade denatured alcohol (pure ethanol), which is free from contami- that rinsing with an EO mouthrinse does not nating carcinogens. induce mucosal drying or aberration. Taking the following precautions should limit any potential problems with ACMs:

Special supplement The Journal of Dental Hygiene 17 Table III. Effects of Antimicrobial Mouthrinses on Dental Materials 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 tested mouthrinses [ACMs], 30 seconds or 1 minute twice daily (to solutions. ACMs caused 1 alcohol free, simulate actual use exposure times) no increased reduction in and 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 all Tooth 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 strength then dried, a film of adhesive resin applied followed by composite resin, and shear bond strength (SBS) recorded

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

increased supragingival calculus for- use of CHG and CPC.42,46,56-60 CHG can be problematic in a society that mation and brown staining of the stains teeth, esthetic restorations, and desires cosmetic dentistry and whiter teeth and tongue, is associated with implant abutments, and this staining and brighter teeth.36,56

Does Routine Use of Mouthrinses KEY POINT: Adversely Affect Dental Restorative Materials? CHG, CPC, and EO cause no serious adverse effects in a generally healthy population when used according to A number of studies have ad- directions dressed the concern raised about the effect of antimicrobial mouthrinses This includes effects on salivary flow, taste, tooth deposits, and dental on dental materials. Other than the restorations. Some users may experience minor taste alteration, staining, potential for staining with CHG and and supragingival calculus formation with some CHG and CPC CPC, there are no documented formulations. adverse effects on dental materials. Table III summarizes the findings of these studies.

18 The Journal of Dental Hygiene Special supplement Efficacy of Mouthrinses Different antimicrobial mouthrinses have demonstrated efficacy against bacteria, fungi, How Antimicrobial Mouthrinses Work viruses, and spores. Some products produce a Antiseptics are chemical agents wide spectrum of activity, while others are used to eliminate oral microorganisms effective against selected microorganisms only. in a variety of ways:

• By producing cell death • By inhibiting microbial reproduction • Seven species of Candida and bacterial cell wall membrane, result- • By inhibiting cellular metabolism other yeasts13,68,69 (often used alone ing in leakage of the intracellular con- or in combination with other anti- tents and eventual cell death. CPC is Most antiseptic agents are bacteri- fungal medications to reduce also thought to alter bacterial metab- cidal, although some are bacteriosta- opportunistic infections in at-risk olism and inhibit cell growth.73, 77 tic. The effectiveness of these agents populations, such as those under- CPC binds to tooth structure and varies widely and is dependent upon going treatment for leukemia or dental plaque biofilm; however, the product formulation, concentration of bone marrow transplantation70,71) degree of binding is not as strong as the active agent, dose, substantivity, with CHG. Further, CPC is rapidly compliance, and interactions with other Exposure to CHG causes ruptur- released from binding sites, which chemicals present in the oral cavity at ing of the bacterial cell membrane, explains why it is generally less effi- the time of use. Different antimicro- which allows for leakage of the cyto- cacious than CHG.73 Like CHG, this bial mouthrinses have demonstrated plasmic contents, resulting in cell cationic rinse may adversely interact efficacy against bacteria, fungi, viruses, death.72,73 CHG binds to salivary with other charged ions found in den- and spores. Some products produce a mucins, reducing pellicle formation tifrices and mouthrinses, possibly lim- wide spectrum of activity, while others and inhibiting colonization of plaque iting its biological activity. are effective against selected microor- bacteria.64,74 It also binds to bacteria, Published data regarding the effi- ganisms only.56 Notably, most studies, which inhibits their adsorption onto cacy of CPC-containing mouthrinses including longitudinal trials, testing the the teeth.64 CHG has been shown to are limited. In the United States, CPC efficacy of CHG used the commercial penetrate the dental plaque biofilm, is available in 2 concentrations: product Peridex®, and Listerine® was which enables CHG to access and 0.05% found in cosmetic mouth- the EO commercial product used for kill pathogens embedded within the rinses (Cepacol® and Scope®) and all studies cited in this paper. CPC biofilm.72 0.07% found in therapeutic mouth- commercial preparations used in CHG binds tightly to tooth struc- rinses (BreathRx® and Crest® Pro- research studies vary by product con- ture, dental plaque, and oral soft tis- Health™ Rinse). It has been suggested centration and brand. sues. It is released slowly into the that the unique vehicle found in Crest® Mechanism of action of CHG. mouth, which allows antimicrobial Pro-Health™ Rinse is purported to CHG (0.12%) is a bactericidal bis- effects to be sustained for up to 12 increase the product’s oral bioavail- biguanide antiseptic, with demon- hours, thus its high degree of sub- ability when compared with other strated efficacy against the following stantivity.64,75 A 30-minute interval is CPC-containing mouthrinses.78 organisms: optimal between toothbrushing and In vitro studies have documented rinsing with CHG to avoid an inter- that CPC can be effective against the • A wide range of gram-positive action between the positively charged following organisms: and gram-negative organisms64 detergents found in dentifrices (eg, • Aerobes and anaerobes, many of sodium lauryl sulfate) and the • Actinomyces viscosus, Porphy- which are associated with plaque cationic CHG rinse. This interaction, romonas gingivalis, Campylobac- and gingivitis, including Fuso- and possible inactivation of CHG, ter rectus, Streptococcus sanguis, bacterium and Prevotella inter- can also occur with the anionic fluo- Eikenella corrodens, Salmonella media65 ride ion found in stannous fluoride typhimurium, Fusobacterium • Herpes simplex virus 1 and 2, and in some toothpastes and nucleatum, Haemophilus actino- human immunodeficiency virus mouthrinses.73,76 mycetemcomitans, Lactobacillus 1, cytomegalovirus, influenza A, Mechanism of action of CPC. casei, and P intermedia78 parainfluenza, and hepatitis CPC, a quaternary ammonium com- • Several species of Candida68,69,79-81 B.12,66,67 CHG is not approved for pound, demonstrates bactericidal the prevention and treatment of activity. Its mechanism of action is CPC, like CHG, has been suggested viral infections similar to CHG in that it ruptures the as a possible agent for the prevention

Special supplement The Journal of Dental Hygiene 19 and treatment of fungal infections. could potentially affect the growth ease starts between the teeth and that However, CPC mouthrinses may and metabolism of these organisms. individuals often cannot access inter- adversely affect systemic azole drug Microscopic evidence of cell surface proximal areas with mechanical treatment of oropharyngeal candidiasis roughening was obtained for the fol- plaque removal techniques such as in immunocompromised persons. This lowing microorganisms: toothbrushing and flossing. Total negative outcome may be attributed to recovered bacteria from proximal either a cross-resistance to the azole • C albicans tooth surfaces was 43.8% lower fol- drugs against CPC-resistant organisms • F nucleatum lowing a single 30-second rinse of EO or drug antagonism between CPC and • A viscosus compared with a control (P=.001).96 azole antifungal medications when • Actinobacillus actinomycetem- Rinsing twice daily with EO as an they are used in combination.82 Two of comitans adjunct to brushing for 11 days 5 fluconazole-resistant C albicans • S sanguis reduced total recoverable streptococci strains have also exhibited reduced in interproximal plaque by 69.9% susceptibility to CPC.82 Cell surface changes that result (P<.001), with EO producing a 37.1% Mechanism of action of EO. EO from a short exposure time to EO greater activity against S mutans than antiseptic mouthrinse is a bacterici- may adversely affect bacterial and other streptococci. A significant dal combination of phenolic essen- fungal survival.88 Exposure to levels reduction of 75.4% in total recover- tial oils, including eucalyptol, men- of EO sublethal to microorganisms able S mutans count was observed thol, methyl salicylate, and thymol. also reduces bacterial coaggregation (P<.001).14 Studies also have demon- Phenolic compounds exert their with gram-positive pioneer species, strated significant suppression of the antimicrobial effects by the following an essential step in plaque matura- oral flora for several hours after rins- mechanisms77, 83-87: tion and the development of the ing, documenting that the antimicro- complex pathogenic flora found in bial activity of EO extends beyond the • Cause protein denaturation gingival disease. Decreased bacterial rinsing period.97-99 • Alter the cell membrane, resulting coaggregation reduces the rate of In vitro studies have shown that EO in leakage of the intracellular con- plaque maturation, which in turn is also active against viruses, includ- tents and eventual cell death may result in a decreased plaque ing herpes simplex virus 1 and 2, hep- • Alter bacterial enzyme activity mass, as is observed clinically with atitis B, human immunodeficiency • Exhibit anti-inflammatory prop- EO use.89 EO also has been shown virus 1, and influenza A virus, as well erties by inhibiting prosta- to extract endotoxins from gram- as against 7 species of Candida.13,67,100 glandin synthetase, an enzyme negative bacteria.90 Endotoxins play Like CHG, EO is not approved for the involved in the formation of an important role in pathogenesis; prevention and treatment of viral prostaglandins, which are pri- thus, reduction in endotoxin level infections. mary inflammatory mediators. should manifest as a decrease in gin- Unlike CHG and CPC, EO has a Note that the anti-inflammatory gival inflammation. neutral electrical charge and does not effect of phenolic compounds Unlike other OTC mouthrinses, interact negatively with other occurs at concentrations lower EO has been shown to penetrate the charged ions found in dentifrices and than those needed for antibac- dental plaque biofilm and is active mouthrinses.73 Moreover, its action terial activity against bacteria embedded within the is not inhibited by proteins in blood • Cause perforation of the cell biofilm.72,91-93 EO kills a wide variety serum that inactivate many antimi- membrane and rapid efflux of of aerobic and anaerobic bacteria crobial agents, including CHG.94,95 intracellular contents (especially associated with plaque biofilm and thymol) gingivitis, including the following94 Efficacy of Mouthrinses on • Alter neutrophil function by sup- Plaque Biofilm and Gingivitis pressing the formation of and • A actinomycetemcomitans scavenging existing free radicals • A viscosus The primary indication for antimi- generated in neutrophils and by • S mutans crobial mouthrinse use is the reduc- altering neutrophil chemotaxis • S sanguis tion of supragingival plaque biofilm (especially thymol) • Bacteroides species and gingivitis in patients. A recent meta-analysis of 6-month clinical tri- A 30-second exposure time to EO Efficacy against gram-positive and als to evaluate the efficacy of a vari- produces morphologic cell surface gram-negative organisms occurs even ety of antiplaque and antigingivitis alterations in a variety of oral at concentrations that are less than full products revealed that the largest pathogens that suggest the loss of cell strength.94,95 A single 30-second rinse body of studies supported the effi- membrane integrity.88 Cell surface reaches and exerts an antibacterial cacy of EO.101 A smaller body of stud- changes may also alter bacterial coag- effect interproximally, an important ies supported the antiplaque and gregation and recolonization that consideration given that gingival dis- antigingivitis efficacy of 0.12%

20 The Journal of Dental Hygiene Special supplement Table IV. Effects of CHG on Supragingival Plaque and Gingivitis Trial Concentration Plaque Gingivitis Length 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 V. Effects of CPC on Supragingival Plaque and Gingivitis Trial Concentration Plaque Gingivitis Length 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.

CHG. Results regarding the efficacy contact with plaque bacteria, the pared with CPC (see Tables IV- of CPC varied and were dependent greater its effect. VI). upon product formulation.101 Efficacy • CHG and EO are comparable in studies of CHG, CPC, and EO are reducing gingivitis.39-41,43-45,48-50,102-104 Perhaps one EO study best sum- summarized in Tables IV, V, and VI, • In head-to-head comparison marizes the effectiveness of mouthrinses respectively. studies that evaluated both CHG as an aid to reducing supragingival The following observations can be and EO in the same participants, plaque and controlling gingivitis. In a made from these study results: antiplaque effects were greater large, randomized, controlled clinical for CHG, but antigingivitis trial involving 237 participants, those • CHG generally reduces more effects were similar for both who added twice-daily rinsing with plaque than either CPC or EO, a agents.42,46,47 EO to their homecare routine of reg- predictable outcome given its • Both CHG and EO demonstrate ular brushing and flossing demon- greater substantivity; the longer greater reductions in supragingi- strated a 51.9% greater reduction in an antimicrobial agent stays in val plaque and gingivitis as com- plaque and a 21.0% greater reduction

Special supplement The Journal of Dental Hygiene 21 Table VI. Effects of EO (Listerine®) on Supragingival Plaque and Gingivitis Trial Plaque Gingivitis Length 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

in gingivitis, as compared with those Conclusion cacy and should be used with caution. who brushed and flossed only.45 This Antimicrobial mouthrinses with estab- study demonstrates the benefit of Antimicrobial mouthrinses that are lished safety and efficacy are an adding an EO mouthrinse to regular approved by the FDA and carry the important and effective addition to mechanical plaque removal and ADA Seal of Acceptance are safe and mechanical plaque control methods to shows that mouthrinses are able to effective for the reduction of supragin- establish a healthy mouth. Most reach bacteria in areas that are diffi- gival plaque and gingivitis. Products patients will benefit by adding an cult to access and where mechanical that have not been evaluated in long- ADA-Accepted antimicrobial mouth- methods often leave residual plaque term clinical trials have no scientific rinse to their self-care daily regimen behind. evidence documenting safety or effi- of brushing and interdental cleaning.

Approved Mouthrinses Are Effica- cious Throughout the Entire Mouth

Using an antiseptic mouthrinse produces an antimicrobial effect throughout the entire mouth, including areas easily missed during toothbrushing and interdental cleaning. Studies have Using an antiseptic mouthrinse demonstrated that antiseptics kill bacteria in saliva and on the soft tissues of produces an antimicrobial effect the mouth, including the tongue and throughout the entire mouth, oral mucosa, which are reservoirs of pathogenic bacteria that are able to including areas easily missed during transfer and colonize onto the teeth.98,105- toothbrushing and interdental cleaning. 108 These collective research findings, with consideration given to the respec- tive adverse events profiles of antiseptic agents, reinforce the value of using CHG, CPC, and EO in addition to mechanical plaque control for long- term maintenance of gingival health.

22 The Journal of Dental Hygiene Special supplement References 20. Negri E, La Vecchia C, Franceschi S, Tavani A. Attributable risk for oral cancer in northern Italy. Cancer Epidemiol 1. Beals D, Ngo T, Feng Y, et al. Development and labora- Biomarkers Prev. 1993;2:189-193. tory evaluation of a new toothbrush with a novel brush 21. Garro AJ, Leiber CS. Alcohol and cancer. Annu Rev Phar- head design. Am J Dent. 2000;13:5A-14A. macol Toxicol. 1990;30:219-249. 2. Bader HI. Floss or die: implications for dental profession- 22. Weaver A, Fleming SM, Smith DB. Mouthwash use and als. Dent Today. 1998;17:76-82. oral cancer: carcinogen or coincidence? J Oral Surg. 3. Oliver RC, Brown LJ, Löe H. Periodontal diseases in the 1979;37:250-253. United States population. J Periodontol. 1998;69:269-278. 23. Mashberg A, Barsa P, Grossman ML. A study of the relationship between mouthwash use and oral and pharyngeal 4. Council on Dental Therapeutics. Guidelines for accept- cancer. J Am Dent Assoc. 1985;110:731-734. ance of chemotherapeutic products for the control of 24. Kabat GC, Herbert JR, Wynder EL. Risk factors for oral supragingival dental plaque and gingivitis. J Am Dent cancer in women. Cancer Res. 1989;49:2803-2806. Assoc. 1986;112:529-532. 25. Young TB, Ford CN, Brandenburg JH. An epidemiologic 5. American Dental Association Council on Scientific Affairs. study of oral cancer in a statewide network. Am J Oto- Acceptance Program Guidelines: Chemotherapeutic Prod- laryngol. 1986;7:200-208. ucts for Control of Gingivitis. Available at: http://www. 26. Wynder EL, Kabat G, Rosenberg S, Levenstein M. Oral ada.org/ada/seal/standards/guide_chemo_ging.pdf. Pub- cancer and mouthwash use. J Natl Cancer Inst. lished July 1997. Accessed May 1, 2007. 1983;70:255-260. 6. Food and Drug Administration. Oral health care drug prod- 27. Winn DM, Blot WJ, McLaughlin JK, et al. Mouthwash and ucts for over-the-counter human use; antigingivitis/ oral conditions in the risk of oral and pharyngeal cancer. antiplaque drug products; establishment of a monograph; Cancer Res. 1991;51:3044-3047. proposed rules. Fed Regist. May 29, 2003;68:32232- 28. Ciancio SG. Alcohol in mouthrinse: lack of association 32287. with cancer. Biol Ther Dent. 1993;9:1-2. 7. Wu CD, Savitt ED. Evaluation of the safety and efficacy of 29. Silverman S, Wilder R. Antimicrobial mouthrinse as part of over-the-counter oral hygiene products for the control of a comprehensive oral care regimen: safety and compli- plaque and gingivitis. Periodontol 2000. 2002;28:91-105. ance factors. J Am Dent Assoc. 2006;137:22S-26S. 8. Minah GE, DePaola LG, Overholser CD, et al. Effects of 30. Cole P et al. Alcohol-containing mouthwash and oropha- 6 months use of an antiseptic mouthrinse on supragingi- ryngeal cancer: an epidemiologic prospective. Unpub- val dental plaque microflora. J Clin Periodontol. lished study in OTC 2001;Vol 210476. 1989;16:347-352. 31. FDC Reports. Alcohol-containing mouthwash concern 9. Walker C, Clark W, Tyler K, et al. Evaluation of microbial “alleviated” by existing data. The Tan Sheet. June 10, shifts following long-term use of an oral antiseptic 1996;4(24):1-5. mouthrinse [abstract]. J Dent Res. 1989;68:412. Abstract 32. Cole P, Rodu B, Mathisen A. Alcohol-containing mouth- 1845. wash and oropharyngeal cancer: a review of the epi- 10. Emilson CG, Fornell J. Effect of toothbrushing with demiology. J Am Dent Assoc. 2003;134:1079-1087. chlorhexidine gel on salivary microflora, oral hygiene, and 33. Elmore JG, Horwitz RI. Oral cancer and mouthwash use: caries. Scand J Dent Res. 1976;84:308-319. evaluation of the epidemiologic evidence. Otolaryngol 11. Schiott CR, Briner WW, Loe H. Two year oral use of Head Neck Surg. 1995;113:253-261. chlorhexidine in man. II. The effect on the salivary bacte- 34. American Dental Association Council on Dental Thera- rial flora. J Periodontal Res. 1976;11:145-152. peutics. Mouthrinse use and the risk of oral and pharyn- 12. Briner WW, Grossman E, Buckner RY, et al. Effect of geal cancer (position statement) Sept. 29, 1991. chlorhexidine gluconate mouthrinse on plaque bacteria. J 35. Listerine® Antiseptic [package insert]. Skillman, NJ: John- Periodontal Res. 1986;21(suppl):44-52. son & Johnson Healthcare Products Division of McNEIL- 13. Meiller TF, Kelley JI, Jabra-Rizk MA, et al. In vitro studies PPC, Inc.; 2007. of the efficacy of antimicrobials against fungi. Oral Surg 36. Peridex® (chlorhexidine gluconate 0.12% ) Oral Rinse Oral Med Oral Pathol Oral Radiol Endod. 2001;91:663- [package insert]. West Palm Beach FL: 3M ESPE; 2007. 670. 37. Antabuse® (disulfiram) [package insert]. East Hanover, 14. Fine DH, Furgang D, Barnett ML, et al. Effect of an essen- NJ: Odyssey Pharmaceuticals, Inc.; 2001. tial oil-containing antiseptic mouthrinse on plaque and 38. Gage TW, Pickett FA. Mosby’s Dental Drug Reference. 6th salivary Streptococcus mutans levels. J Clin Periodontol. ed. St Louis, MO. Mosby/Elsevier; 2003. 2000;27:157-161. 39. Gordon JM, Lamster IB, Seiger MC. Efficacy of Listerine 15. DePaola LG, Minah GE, Elias SA, et al. Clinical and micro- antiseptic in inhibiting the development of plaque and gin- bial evaluation of treatment regimens to reduce denture givitis. J Clin Periodontol. 1985;12:697-704. stomatitis. Int J Prosthodont. 1990;3:369-374. 40. Lamster IB, Alfano MC, Seiger MC, et al. The effect of Lis- 16. DePaola LG, Minah GE, Leupold RL, et al. The effect of terine antiseptic on the reduction of existing plaque and antiseptic mouthrinses on oral microbial flora and den- gingivitis. Clin Prev Dent. 1983;5:12-16. ture stomatitis. Clin Prev Dent. 1986;8:3-8. 41. DePaola LG, Overholser CD, Meiller TF, et al. Chemother- 17. White DJ. An alcohol-free therapeutic mouthrinse with apeutic inhibition of supragingival dental plaque and gin- cetylpyridinium chloride (CPC)—the latest advance in pre- givitis development. J Clin Periodontol. 1989;16:311-315. ventive care: Crest Pro-Health Rinse. Am J Dent. 42. Overholser CD, Meiller TF, DePaola LG, et al. Compara- 2005;18:3A-8A. tive effects of 2 chemotherapeutic mouthrinses on the 18. Parkin DM, Pisani P, Lopez AD, Masuyer E. At least one development of supragingival dental plaque and gingivi- in seven cases of cancer is caused by smoking: global tis. J Clin Periodontol. 1990;17:575-579. estimates for 1985. Int J Cancer. 1994;59:494-504. 43. Charles CH, Sharma NC, Galustians HJ, et al. Compara- 19. Blot WJ, McLaughlin JK, Winn DM, et al. Smoking and tive efficacy of an antiseptic mouthrinse and an drinking in relation to oral and pharyngeal cancer. Cancer antiplaque/antigingivitis dentifrice: a six-month clinical trial. Res. 1988;48:3282-3287. J Am Dent Assoc. 2001;132:670-675.

Special supplement The Journal of Dental Hygiene 23 44. Bauroth K, Charles CH, Mankodi SM, et al. The efficacy 63. Von Fraunhofer J, Kelley JI, DePaola LG, Meiller TF. The of an essential oil antiseptic mouthrinse vs. dental floss in effect of a mouthrinse containing essential oils on dental controlling interproximal gingivitis: a comparative study. J restorative materials. Gen Dent. 2006;54:403-407. Am Dent Assoc. 2003;134:359-365. 64. Wolff LF. Chemotherapeutic agents in the prevention and 45. Sharma N, Charles CH, Lynch MC, et al. Adjunctive ben- treatment of periodontal disease. Northwest Dent. efit of an essential oil-containing mouthrinse in reducing 1985;64:15-24. plaque and gingivitis in patients who brush and floss reg- 65. De Boever EH, Loesche WJ. Assessing the contribution of ularly: a six-month study. J Am Dent Assoc. 2004;135:496- anaerobic microflora of the tongue to oral malodor. J Am 504. Dent Assoc. 1995;126:1384-1393. 46. Charles CH, Mostler KM, Bartels LL, Mankodi SM. Com- 66. Bernstein D, Schiff G, Echler G, et al. In vitro virucidal parative antiplaque and antigingivitis effectiveness of a effectiveness of a 0.12% chlorhexidine gluconate chlorhexidine and an essential oil mouthrinse: 6-month mouthrinse. J Dent Res. 1990;69:874-876. clinical trial. J Clin Periodontol. 2004;31:878-884. 67. Baqui AA, Kelley JI, Jabra-Rizk MA, et al. In vitro effect of 47. Grossman E, Meckel AH, Issacs RL, et al. A clinical com- oral antiseptics on human immunodeficiency virus-1 and parison of antibacterial mouthrinses: effects of chlorhex- herpes simplex virus type 1. J Clin Periodontol. idine, phenolics and sanguinarine on dental plaque and 2001;28:610-616. gingivitis. J Periodontol. 1989;60:435-440. 68. Giuliana G, Pizzo G, Milici ME, et al. In vitro antifungal 48. Grossman E, Reiter G, Sturzenberger OP, et al. Six-month properties of mouthrinses containing antimicrobial agents. study of the effects of a chlorhexidine mouthrinse on gin- J Periodontol. 1997;68:729-733. givitis in adults. J Periodontal Res. 1986;21(suppl 16):33- 69. Giuliana G, Pizzo G, Milici ME, Giangreco R. In vitro activ- 43. ities of antimicrobial agents against Candida species. Oral 49. Löe H, Schiött CR, Glavind L, Karring G. Two years oral Surg Oral Med Oral Pathol Oral Radiol Endod. use of chlorhexidine in man. I. General design and clini- 1999;87:44-49. cal effects. J Periodontal Res. 1976;11:135-144. 70. Sharon A, Berdicevsky I, Ben-Aryeh H, Gutman D. The 50. Lang NP, Hotz P, Graf H, et al. Effects of supervised effect of chlorhexidine mouth rinses on oral Candida in a chlorhexidine mouthrinses in children. A longitudinal clin- group of leukemic patients. Oral Surg Oral Med Oral ical trial. J Periodontal Res. 1982;17:101-111. Pathol. 1977;44:201-205. 51. Mankodi S, Bauroth K, Witt JJ, et al. A 6-month clinical trial 71. Epstein JB, Vickars L, Spinelli J, Reece D. Efficacy of to study the effects of a cetylpyridinium chloride mouthrinse chlorhexidine and nystatin rinses in prevention of oral on gingivitis and plaque. Am J Dent. 2005;18:9A-14A. complications in leukemia and bone marrow transplanta- 52. Stookey GK, Beiswanger B, Mau M, et al. A 6-month clin- tion. Oral Surg Oral Med Oral Pathol. 1992;73:682-689. ical study assessing the safety and efficacy of two cetylpyri- 72. Foster JS, Pan PC, Kolenbrander PE. Effects of antimi- dinium chloride mouthrinses. Am J Dent. 2005;18:24A- crobial agents on oral biofilms in a saliva-conditioned flow- 28A. cell. Biofilms. 2004;1:5-12. 53. Ashley FP, Skinner A, Jackson P, et al. The effect of a 73. Ciancio SG. Chemical agents: plaque control, calculus 0.1% cetylpyridinium chloride mouthrinse on plaque and reduction and treatment of dentinal hypersensitivity. Peri- gingivitis in adult subjects. Br Dent J. 1984;157:191-196. odontol 2000. 1995;8:75-86. 54. Fischman SL, Aguirre A, Charles CH. Use of essential oil- 74. Fine DH. Mouthrinses as adjuncts for plaque and gingivi- containing mouthrinses by xerostomic individuals: deter- tis management: a status report for the American Journal mination of potential for oral mucosal irritation. Am J Dent. of Dentistry. Am J Dent. 1988;1:259-263. 2004;17:23-26. 75. Weeks C, Briner W, Rebitski G, et al. Immediate and pro- 55. Kerr AR, Katz RW, Ship JA. A comparison of the effects of longed effect of 0.12% chlorhexidine on salivary bacteria two commercially available non-prescription mouthrinses [abstract]. J Dent Res. 1988;67:326. Abstract 1711. on salivary flow rates and xerostomia: a pilot study. Quin- 76. Barkvoll P, Rølla G, Svendsen AK. Interaction between tessence Int. In press. chlorhexidine digluconate and sodium lauryl sulfate in 56. Ciancio SG. Antiseptics and antibiotics as chemothera- vivo. J Clin Periodontol. 1989;16:593-595. peutic agents for periodontitis management. Compend 77. Scheie AA. Modes of action of currently known chemical Contin Educ Dent. 2000;21:59-78. antiplaque agents other than chlorhexidine. J Dent Res. 57. Mandel ID. Chemotherapeutic agents for controlling plaque 1989;68:1609-1616. and gingivitis. J Clin Periodontol. 1988;15:488-498. 78. Witt J, Ramji N, Gibb R, et al. Antibacterial and antiplaque 58. Kerr AR, Ship JA. Tooth discoloration. Available at: effects of a novel, alcohol-free oral rinse with cetylpyri- http://www.emedicine.com/derm/topic646.htm. Accessed dinium chloride. J Contemp Dent Pract. 2005;6:1-9. April 8, 2007. 79. Meier S, Collier C, Scaletta MG, et al. An in vitro investi- 59. Sheen S, Addy M. An in vitro evaluation of the availability gation of the efficacy of CPC for use in toothbrush decon- of cetylpyridinium chloride and chlorhexidine in some com- tamination. J Dent Hyg. 1996;70:161-165. mercially available mouthrinse products. Br Dent J. 80. Nakamoto K, Tamamoto M, Hamada T. In vitro effective- 2003;194:207-210. ness of mouthrinses against Candida albicans. Int J 60. Bascones A, Morante S, Mateos L, et al. Influence of addi- Prosthodont. 1995;8:486-489. tional active ingredients on the effectiveness of non-alco- 81. Phillips BJ, Kaplan W. Effect of cetylpyridinium chloride on holic chlorhexidine mouthwashes: a randomized controlled pathogenic fungi and Nocardia asteroides in sputum. J trial. J Periodontol. 2005;76:1469-1475. Clin Microbiol. 1976;3:272-276. 61. Norman R. Surface hardness effects of various 82. Edlind MP, Smith WL, Edlind TD. Effects of cetylpyridinium mouthrinses on a composite resin [abstract]. J Dent Res. chloride resistance and treatment on fluconazole activity 1997;76:325. Abstract 2490. versus Candida albicans. Antimicrob Agents Chemother. 62. Von Fraunhofer JA, Kelley JJ, DePaola LG, Meiller TF. The 2005;49:843-845. effect of a dental unit waterline treatment solution on com- 83. Goodson JM. Response. In: Loe H, Kleinman DV, eds. posite-dentin shear bond strengths. J Clin Dent. Dental Plaque Control Measures and Oral Hygiene Prac- 2004;15:28-32. tices. Oxford, England: IRL Press; 1986:143-146.

24 The Journal of Dental Hygiene Special supplement 84. Walker CB. Microbiological effects of mouthrinses con- 98. DePaola LG, Minah GE, Overholser CD, et al. Effect of an taining antimicrobials. J Clin Periodontol. 1988;15:499-505. antiseptic mouthrinse on salivary microbiotia. Am J Dent. 85. Shapiro S, Meier A, Guggenheim B. The antimicrobial 1996;9:93-95. activity of essential oils and essential oil components 99. Furgang K, Sinatra K, Schreiner H, et al. In vitro antimi- towards oral bacteria. Oral Microbiol Immunol. crobial activity of an essential oil mouthrinse. J Dent Res. 1994;9:202-208. 2002;81(special issue A). Abstract 2854. 86. Kuehl FA Jr, Humes JL, Egar RW, et al. Role of 100. Dennison DK, Meredith GM, Shillitoe EJ, Caffesse RG. prostaglandin endoperoxide PGG2 in inflammatory The antiviral spectrum of Listerine antiseptic. Oral Surg processes. Nature. 1977;265:170-172. Oral Med Oral Pathol Oral Radiol Endod. 1995;79:442- 87. Azuma Y, Ozaza N, Ueda Y, Takagi N. Pharmacological 448. studies on the anti-inflammatory action of phenolic com- 101. Gunsolley JC. A meta-analysis of six-month studies of pounds. J Dent Res. 1986;65:53-56. antiplaque and antigingivitis agents. J Am Dent Assoc. 88. Kubert D, Rubin M, Barnett ML, Vincent JW. Antiseptic 2006;137:1649-1657. mouthrinse-induced microbial cell surface alterations. Am 102. Segreto VA, Collins EM, Beiswanger BB, et al. A com- J Dent. 1993;6:277-279. parison of mouthrinses containing two concentrations of 89. Fine DH, Furgang D, Lieb R, et al. Effects of sublethal chlorhexidine. J Periodontal Res. 1986;21(suppl):23-32. exposure to an antiseptic mouthrinse on representative 103. Brightman LJ, Terezhalmy GT, Greenwell H, et al. The plaque bacteria. J Clin Periodontol. 1996;23:444-451. effects of a 0.12% chlorhexidine gluconate mouthrinse on 90. Fine DH, Letizia J, Mandel ID. The effect of rinsing with orthodontic patients aged 11 through 17 with established Listerine antiseptic on the properties of developing dental gingivitis. Am J Orthod Dentofacial Orthop. 1991;100:324- plaque. J Clin Periodontol. 1985;12:660-666. 329. 91. Pan P, Barnett ML, Coelho J, et al. Determination of the 104. Eaton KA, Rimini FM, Zak E, et al. The effects of a 0.12% in situ bactericidal activity of an essential oil mouthrinse chlorhexidine–digluconate-containing mouthrinse versus using a vital stain method. J Clin Periodontol. 2000;27: a placebo on plaque and gingival inflammation over a 3- 256-261. month period. A multicentre study carried out in general 92. Fine DH, Furgang D, Barnett ML. Comparative antimi- dental practices. J Clin Periodontol. 1997;24:189-197. crobial activities of antiseptic mouthrinses against iso- 105. Allen DR, Davies R, Bradshaw B, et al. Efficacy of a genic planktonic and biofilm forms of Actinobacillus actin- mouthrinse containing 0.05% cetylpyridinium chloride for omycetemcomitans. J Clin Periodontol. 2001;28:697-700. the control of plaque and gingivitis: a 6-month clinical 93. Ouhayoun JP. Penetrating the plaque biofilm: impact of study in adults. Compend Contin Educ Dent. 1998;19(2 essential oil mouthrinse. J Clin Periodontol. 2003;30(suppl suppl):20-26. 5):10-12. 106. Dahlen G. Effect of antimicrobial mouthrinses on salivary 94. Ross NM, Charles CH, Dills SS. Long-term effects of Lis- microflora in healthy subjects. Scand J Dent Res. terine antiseptic on dental plaque and gingivitis. J Clin 1984;92:38-42. Dent. 1989;1:92-95. 107. Jenkins S, Addy M, Wade W, Newcombe RG. The mag- 95. Whitaker EJ, Pham K, Feik D, et al. Effect of an essential nitude and duration of the effects of some mouthrinse oil-containing antiseptic mouthrinse on induction of platelet products on salivary bacterial counts. J Clin Periodontol. aggregation by oral bacteria in vitro. J Clin Periodontol. 1994;21:397-401. 2000;27:370-373. 108. Pitts G, Pianotti R, Feary TW, et al. The in vivo effects of 96. Charles CH, Pan PC, Sturdivant L, Vincent JW. In vivo an antiseptic mouthwash on odor-producing microorgan- antimicrobial activity of an essential oil-containing isms. J Dent Res. 1981;60:1891-1896. mouthrinse on interproximal plaque bacteria. J Clin Dent. 109. Fine DH, Furgang D, Sinatra K, et al. In vivo antimicrobial 2000;11:94-97. effectiveness of an essential oil-containing mouth rinse 97. Pitts G, Brogdon C, Hu L, et al. Mechanism of action of an anti- 12 h after a single use and 14 days’ use. J Clin Peri- septic, anti-odor mouthwash. J Dent Res. 1983;62:738-742. odontol. 2005;32:335-340.

Special supplement The Journal of Dental Hygiene 25 Strategies for Incorporating Antimicrobial Mouthrinses into Daily Oral Care Joanna Asadoorian, RDH, MSc

Introduction Abstract The merits of oral hygiene to health Overview. A cost-effective way of improving patient outcomes is adopting have long been valued by oral health preventive practices known to be effective. As “front-line” providers of den- care providers. However, public tal health services and information, dental hygienists are an important cat- awareness of the importance of oral alyst for the implementation of evidence-based preventive practices— health and the links between oral and such as the twice-daily use of antimicrobial mouthrinses—in the self-care systemic health and disease has routines of patients. However, encouraging patients to adopt new behav- increased in recent years, particularly iors can present a challenge: providers may be uncomfortable with rec- ommending new behaviors and patients may be resistant to learning new since the publication of Oral Health in skills. As expert clinicians, educators, and counselors, dental hygienists are America: A Report of the Surgeon in an excellent position to help patients make changes and learn new General in 2000 and the subsequent behaviors. release and implementation of the National Call to Action to Promote Clinical Implications. This article discusses practical methods for pro- Oral Health moting change. Targeting interventions to individual patient values, stage of , a public-private partner- readiness to change, and skill set encourages patient incorporation of new ship under the leadership of the Office behaviors. Time should be allotted for supervised practice of new skills, and 1,2 of the Surgeon General. Dental patients should be supported in planning for effective and lasting behavior hygienists now have an important change. Through effective communication, skills teaching, and use of fol- window of opportunity to counsel low-up, dental hygienists can help patients adopt healthy behaviors. patients on behaviors that promote Key words: Antimicrobial mouthrinse, compliance, dental hygiene, oral oral health. Health care providers, health, patient education including dental hygienists, can act as catalysts for change by teaching patients about oral health, modeling health behaviors, and helping patients adopt healthy behaviors.3 ference in the health and well-being of • Lack of confidence6: Dental It has been noted that “the most their patients. hygienists may lack the confi- cost-effective opportunity to improve dence to use motivational inter- patient outcomes over the next quar- viewing techniques (please see ter century will likely come not from Initiating Behavioral Practical Strategies for Change) discovering new therapies but from Change • Lowered expectations: Hygienists discovering how to deliver therapies may feel that patients are unlikely that are known to be effective.”4 The While encouraging patients to to change their behaviors despite aim of this article is to enable dental adopt new, healthful behaviors is counseling. Patients that dental hygienists to put evidence-based something dental hygienists fre- hygienists have the lowest expec- information about antimicrobial quently do, they may find it difficult tation of—those with high plaque mouthrinses into practice by effec- to recommend new behaviors, such as levels—may receive less genuine tively communicating research find- use of antimicrobial mouthrinses. Bar- verbal interaction and not receive ings with patients and promoting riers to change are varied and include: the more intensive instruction incorporation of healthy behaviors they need.7 These more challeng- into their self-care regimens. This • Habit: Dental hygienists may rec- ing patients may be ideal candi- review will focus on practical meth- ommend traditional oral hygiene dates for dental hygienists to ods for promoting positive change and methods most often (such as begin targeting for incorporating suggest ways to involve patients in brushing and flossing), despite antimicrobial oral rinsing into optimizing their oral health. By pro- research demonstrating the effec- daily home care. moting optimal oral care, dental tiveness of other oral hygiene aids • Not enough time: Lack of interest hygienists can make a significant dif- and techniques.5 and resistance from the patient

26 The Journal of Dental Hygiene Special supplement Practical Strategies for Change The patient is the center of any successful change effort. mental support. Encourage the patient to be specific. Promoting change starts with listening to the patient and These planning steps maximize the likelihood of suc- providing suggestions and skills teaching that are aligned cessful change. Example: “I’m glad you’re ready to make with the patient’s values. Dental hygienists need to be com- a positive change. I’ve seen many patients significantly fortable with actively questioning and interviewing patients improve the health of their gums by adding an antimi- to elicit the patient’s beliefs and values about oral hygiene, crobial mouthrinse to their daily routine. Do you have an health, and disease and be prepared for responses that do antimicrobial mouthrinse? Do you know where to look to not conform with ideals.28 Effective questioning minimizes find out if your rinse is ADA-Accepted? When do you patient defensiveness, allowing patients to consider change. plan to use your rinse? Will your use of the rinse match The following are strategies that can promote effective dia- the manufacturer’s recommendations for daily care?” logue and support adoption of healthy behaviors. • Anticipate obstacles Stressful life experiences can disrupt the formation of • Ask patient about current oral health practices positive habits.18 Encourage the patient to incorporate Begin with determining the patient’s current level of self- external memory triggers (eg, notes to self) to allow him care. Example: “What do you do each day to take care or her to maintain or resume positive oral health prac- of your teeth and gums?” You may want to ask the tices during disruptive or stressful periods. If the patient patient questions that elicit felt needs, such as, “If you does not discuss obstacles, you may want to engage in could change anything about your oral health, what self-disclosure or share examples from your experience would you change?” Avoid a confrontational approach, with other patients. Example: “It can be hard sometimes and be sure to support healthy activities the patient is to remember new healthy habits when we’re busy, sick, already performing. traveling, or stressed out. I’m a dental hygienist, and some days I’m so busy I barely have time to brush my • Assess patient readiness to change teeth. What are some ways that help you remember to Determine the patient’s readiness to incorporate new do things when life is stressful? What are some obsta- self-care behaviors.23 The initial question may be “Would cles that may keep you from using an antimicrobial you be willing to try using an antimicrobial mouthrinse mouthrinse twice daily?” twice daily?” If the patient responds positively, move to practical support. If the patient responds with disinter- • Follow up with the patient est, determine any obstacles to change. “Have you tried Ask the patient about whether he or she has success- them in the past? Did you find one you liked? Why not? fully incorporated the behavior and any obstacles that Why don’t you think it would be helpful?” Be sure to were encountered: “Were you able to find a product maintain a nonconfrontational attitude. It may help to you really liked? Could you easily access the product? write down patient objections, and continue to listen to Was it hard to be consistent? What was your biggest objections until the patient is finished. Active listening challenge?” Praise any progress toward the desired may diffuse patient resistance. If the patient is unwilling behavior, and revise the patient’s action plan accord- to consider change, providing interventions over multi- ingly: “Even though you weren’t able to use the rinse ple visits can encourage the patient to rethink his or her every day twice daily, I’m glad that you were able to decision. Always work within the patient’s stage of readi- use it before bed most nights. You have made a great ness to change. start! Do you think you can use it more often? When do you think you can incorporate a second rinse into your • Supervise new skills / behaviors day?” Specific follow-up demonstrates care for the If the patient is ready to attempt new behaviors, super- patient and is appreciated. Follow-up is also central to vised practice will enhance patient self-efficacy.3 Encour- maintaining change.26,27 age the patient to practice using mouthrinse, and show the patient what to look for on the label. This will increase the patient’s comfort level and success with the new While it takes time to change behaviors, the above inter- behavior. Remind the patient that if a product was shown ventions are brief and can be incorporated into a preven- via research to be effective with twice daily use, using the tive, therapeutic, or periodontal maintenance visit. Through product once daily may not yield the desired outcomes. use of effective questioning and encouraging patients to share their health values and behaviors, dental hygienists • Structure a plan for successful adoption of the new can offer targeted advice and be perceived as caring and behavior supportive while fulfilling their responsibility to educate If the patient is ready to change, it is also important to help patients. Nonconfrontational questioning minimizes patient with the plan for success. Unlike other negative behav- defensiveness and ensures they will be as receptive as iors such as overeating or smoking, patients do not derive possible to receiving information on their oral health. positive satisfaction when neglecting oral self-care. The Repeated interventions can assist patients as they adopt primary obstacle is apathy. Work with the patient to positive behaviors that will improve oral health and qual- develop a brief change plan that incorporates environ- ity of life.

Special supplement The Journal of Dental Hygiene 27 and poor financial incentives for released a statement in support of the strained with meeting the demands of oral hygiene instruction may con- use of ADA–Accepted antimicrobial daily life.18 Stressful life events have tribute to limiting the time spent mouthrinses in addition to traditional also been shown to interfere with self- on education.8,9 brushing and interdental cleaning.15 care.18 In a study examining the impact The Canadian Dental Hygienists’ of oral hygiene education, patients For all of these reasons, dental Association (CDHA) published a posi- with poor oral hygiene subsequent to hygienists may tend to continue to tion statement supporting the incorpo- instructions and education reported recommend the traditional therapies ration of antimicrobial rinsing in having difficulty taking care of their of brushing and flossing alone. How- patient home care routines.16 Both of teeth and had more factors that inter- ever, compliance with daily flossing these documents provide support for fered with self-care than the more suc- has been reported to be generally low, the dental hygienist as he or she rec- cessful study participants.19 Moreover, ranging from only 10% to 30%,5 so ommends that patients incorporate oral because incorporating complex behav- patients may benefit from information rinsing into their daily routine. iors—such as traditional oral self-care about new and adjunctive methods for behaviors—may be met with less thorough plaque removal. compliance than simpler strategies,19 But changing dental hygienist Encouraging oral rinsing interventions may produce behavior is difficult due to the com- Compliance / Adherence improved adherence (see Adherence plexity of the process, and different versus Compliance below). barriers likely respond to different Once a dental hygienist decides to Further complicating the issue of approaches to change.10,11 Simple assist patients in improving their oral compliance, research evidence demon- exposure to new knowledge may be health status through the implementa- strates that even persons with high insufficient to overcome most barriers tion of an evidence-based product, (eg, plaque levels believe they are doing a to change practices,11,12 but dissemina- an antimicrobial mouthrinse), the den- good job with their oral home care.19 tion of information can be more effec- tal hygienist must motivate the patient The fact that patients have an inability tive in changing behavior when com- to change his or her daily oral care rou- to evaluate their oral hygiene effec- bined with other methods such as tine. Research confirms what dental tiveness and monitor their oral health interactive educational activities, hygienists know intuitively, that status has been raised as a weakness enabling tools, and reminders.13 In addition, comparing one’s current practice behaviors to sources of evi- Adherence versus Compliance dence, such as guidelines and external Compliance is a common term used in oral health care literature to describe feedback, has been shown to motivate a patient’s willingness to follow a practitioner’s instructions.20,28 The term has 12,14 change. Reading journal articles been criticized because it implies that the patient assumes a passive role and that summarize the evidence base in a acquiesces to professional recommendations he or she may not under- subject area, like the ones published in stand or agree with.17,20,28 Some authors use the term adherence instead of this journal supplement, and compar- compliance, as it implies that the patient takes a more active role in decision ing the findings to one’s current prac- making and thereby improves behavior change.20 tice may stimulate a need that encourages practitioners to change their professional behaviors. patients are reluctant to change their undermining dental hygiene instruc- Recently, two professional dental home care routines and, overall, may tion.8 Finally, compliance in behaviors organizations have officially acknowl- not display interest in oral hygiene preventing conditions perceived to be edged evidence about the adjunctive instruction.9,17 non–life threatening, such as peri- use of daily antimicrobial rinsing. The Despite the value people place on odontal disease and dental caries, may American Dental Association (ADA) oral health, patients are increasingly have a lower priority for patients.18,20 Dental hygienists can encourage patients to adopt healthy behaviors, such as the twice-daily use of an Despite the value people place on oral health, ADA-Accepted antimicrobial mouth- patients are increasingly strained with rinse, by a variety of methods. Den- tal hygienists can listen to patient meeting the demands of daily life. feelings and values and emphasize Stressful life events have also been shown to the value and relevance of oral hygiene care before providing oral interfere with self-care. hygiene education.21 This allows patients to link improved health behaviors to these values, enhancing

28 The Journal of Dental Hygiene Special supplement Table I. Transtheoretical Stages of Change and Suggested Interventions20, 22-23 Stage Characteristics Suggested Intervention

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

“I won’t change” “Are you aware of the health benefits of using an antimicrobial 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 changes in your oral self-care. That’s great! What would you say is holding you back from taking that step?”

Preparation Patient is ready to take Verify patient’s state of readiness positive 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 you need to take? (eg, suggest purchasing a mouthrinse known to reduce plaque and gingivitis)

Action Patient is making initial Verify patient’s state of readiness steps 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 readiness behavior 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 hygiene visit. Let me show you how to monitor yourself at home.”

their readiness to make positive should be targeted accordingly. Table questioning, imparting knowledge, changes.21 I shows stages of change and appro- and teaching skills, the dental hygien- In addition, change efforts should priate interventions based on the ist can influence the key dimensions of be tailored to the patient’s expressed patient’s stages of readiness. patient behavior including acquiring readiness to change. According to the In addition to matching educational knowledge, changing attitudes, height- Transtheoretical Model of Change, interventions to patient readiness for ening perceived needs, and improving patients are in one of several stages change, it is important to tailor infor- motivation.19,24 While the actual inter- of readiness to incorporate new mation to each individual patient. ventions recommended may be the behaviors,20, 22-23 and interventions Through the skillful use of listening, same across a variety of patients—for

Special supplement The Journal of Dental Hygiene 29 Table II. Dental Hygienist Actions for Supporting Patient Behavior Change General for All Patients Individualized to Specific Patient

Target high-risk patients Provide sufficient contact time Clarify patient values Ensure mastery of one skill at a time Determine the patient’s state of readiness for change Provide meaningful praise Inquire about current behaviors Include intraoral demonstrations Tailor approach—ensure relevance Include supervised practice Convince patient of effectiveness of intervention Encourage a partnership incorporating two-way communication Highlight the pleasurable sensations and social benefits of oral hygiene and health Ensure patient can self-monitor improvements (eg, decreased redness, swelling, and bleeding) Maintain a positive environment Provide patient specific written educational materials to Display warmth and genuineness supplement interventions Provide ongoing reminders Assist patient in managing when home care will occur, Be prepared for relapse incorporating contingency plans

Key elements to maximize that patients maintain that patients maintain their new behaviors include the use of positive their new behaviors include the use of feedback, patient reminders (such as positive feedback, patient reminders phone calls and postcards), and adapting dental hygiene instructions (such as phone calls and postcards), to the needs of the patient.20 In a and adapting dental hygiene instructions series of 3 studies evaluating the maintenance of self-care behavior to the needs of the patient programs, adherence was improved when reminders were used, seem- example, twice daily use of an antimi- plaque and gingivitis scores can help ingly for as long as the reminders crobial rinse—the individual tailoring patients see the relevance of instruc- were provided.26 Therefore, mainte- of educational sessions to these behav- tion to their oral health.7 nance of behavioral change is an ioral dimensions are critical for moti- Table II summarizes important fea- ongoing and deliberate process.27 vating change.19,25 As new products are tures of successful dental hygiene introduced to the market, the dental interventions designed to motivate hygienists’ role becomes crucial in patients into changing their home care Conclusions helping patients understand the per- behaviors. These factors combined sonal health care implications of the with the patient’s belief that he or she As preventive oral health experts, research literature.25 has control over his or her oral dental hygienists must continually eval- The provision of information about hygiene and health will increase the uate methods of enhancing oral health safe and effective antimicrobial likelihood for positive behavior and recommend those techniques and mouthrinses is important, but infor- change.3 products with evidence-based effec- mation alone will not change patient The fact that research-supported, tiveness to their patients. This article behavior.8,9 The teaching of new skills oral health–promoting behaviors has examined strategies for promoting is a necessary component of an effec- (such as the twice-daily use of a safe behavioral change in the context of tive intervention. Skills acquisition is and effective antimicrobial mouth- adoption of twice-daily use of antimi- facilitated by introducing skills one at rinse) need to be carried out over crobial mouthrinses, which have been a time, allowing time for supervised one’s lifetime contributes to the chal- shown to effectively reduce plaque and practice. This approach increases the lenge.17 Studies consistently show promote oral health when used as part chance for successful transfer of that modest gains achieved initially of a daily self-care regimen. These prin- knowledge from the office to the in changing patient behavior dimin- ciples can also be applied when teach- home setting.7 Using quantitative ish with time and minimize initial ing patients about other health care hygiene assessment tools such as gains.19 Key elements to maximize products and behaviors.

30 The Journal of Dental Hygiene Special supplement References 14. Mead P. Clinical guidelines: promoting clinical effectiveness or a professional minefield? J Adv Nurs. 2000;31:110-116. 15. ADA affirms benefits of ADA-Accepted antimicrobial mouth 1. US Department of Health and Human Services. Oral Health rinses and toothpastes, fluoride mouth rinses [news in America: A Report of the Surgeon General. Rockville, release].Chicago, IL: American Dental Association; May 23, MD: US Department of Health and Human Services, 2007. http://ada.org/public/media/releases/0705_release03. National Institute of Dental and Craniofacial Research, asp. Accessed July 27, 2007. National Institutes of Health; 2000. http://www2.nidcr. 16. Asadoorian J. Oral rinsing: Canadian Dental Hygienists Asso- nih.gov/sgr/sgrohweb/welcome.htm. ciation Position Statement. CDHA position paper on com- 2. US Department of Health and Human Services. National mercially available over-the-counter oral rinsing products. Call to Action to Promote Oral Health. Rockville, MD: US CJDH. 2006;40:168-183. Department of Health and Human Services, Public Health 17. Blinkhorn AS. Factors affecting the compliance of patients with Service, National Institutes of Health, National Institute of preventive dental regimens. Int Dent J.1993;43,294-298. Dental and Craniofacial Research; 2003. NIH Publication 18. Ower P. The role of self-administered plaque control in the No. 03-5303. http://www.surgeongeneral.gov/topics/oralhealth/ management of periodontal diseases: 2. Motivation, tech- nationalcalltoaction.htm. niques and assessment. Dent Update. 2003;30:110-116. 3. Koelen MA, Lindstrom B. Making healthy choices easy 19. Weinstein P, Milgrom P, Melnick S, et al. How effective is choices: the role of empowerment. Eur J Clin Nutr. 2005; oral hygiene instruction? Results after 6 and 24 weeks. J 59(suppl 1):S10-S16. Public Health Dent. 1989;49:32-38. 4. Berenholz S, Pronovost PJ. Barriers to translating evidence 20. Silverman S, Wilder R. Antimicrobial mouthrinse as part of a into practice. Curr Opin Crit Care. 2003;9:321-325. comprehensive oral care regimen: safety and compliance 5. Asadoorian J. Flossing: Canadian Dental Hygienists Asso- factors. J Am Dental Assoc. 2006;137(11 suppl ):22S-26S. ciation Position Statement: CDHA Position Paper. CJDH. 21. Horowitz LG, Dillenberg J, Rattray J. Self-care motivation: a 2006;40:112-144 model for primary preventive oral health behavior change. J 6. Cabana MD, Rand CS, Powe NR, et al. Why don’t physi- Sch Health. 1987;57:114-118 cians follow clinical practice guidelines? A framework for 22. Prochaska JO, Norcross JC, DiClemente CC. Changing for improvement. JAMA. 1999;282:1458-1465. Good: The Revolutionary Program That Explains the Six 7. Milgrom P, Weinstein P, Melnick S, et al. Oral hygiene Stages of Change and Teaches You How to Free Yourself Instruction and health risk assessment in dental practice. J From Bad Habits. New York: William Morrow; 1994. Public Health Dent. 1989:49:24-31. 23. Astroth, DB, Cross-Poline GN, Stach DJ, et al. The trans- 8. McConaughy FL, Lukken KM. Toevs SE. Health promotion theoretical model: an approach to behavioral change. J Dent behaviors of private practice dental hygienists. J Dent Hyg. 2002;76:286-295. Hyg.1991:54: 222-230. 24. Uitenbroek DG, Schaub RMH, Tromp JA, Kant JH. Dental 9. Basson WJ. Oral health education provided by oral hygien- hygienists’ influence on the patients’ knowledge, motivation, ists in private practice. SADJ. 1999;54: 53-57. self-care, and perception of change. Community Dent Oral 10. Bosse G, Breuer JP, Spies C. The resistance to changing Epidemiol. 1989;17:87-90. guidelines—what are the challenges and how to meet them. 25. Gluch-Scranton J. Motivational strategies in dental hygiene Best Pract Res Clin Anaesthesiol. 2006;20:379-395. care. Semin Dent Hyg. 1991;3:1-4, 6-8. 11. Bain KT. Barriers and strategies to influencing physician 26. McCaul KD, Glasgow RE, O’Neill HK. The problem of creat- behavior. Am J Med Qual. 2007;22, 5-7. ing habits: establishing health-protective dental behaviors. 12. Bloom BS. Effects of continuing medical education on improv- Health Psychol. 1992;11:101-110. ing physician clinical care and patient health: A review of 27. Cifuentes M, Fernald DH, Green LA, et al. Prescription for systematic reviews. Int J Technol Assess Health Care. 2005; health: changing primary care practice to foster healthy 21:380-385. behaviors. Ann Fam Med. 2005;3:S4-S12. 13. Gray J. Changing physician prescribing behaviour. Can J 28. Chu R, Craig B. Understanding the determinants of preven- Clin Pharmacol. 2006;13:e81-e84. tive oral health behaviours. Probe. 1996; 30:12-18.

Special supplement The Journal of Dental Hygiene 31 Conclusion

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

Introduction birth. Most patients will improve their oral health by adding an ADA- The primary indication for antimi- Accepted antimicrobial mouthrinse to crobial mouthrinse use is to achieve a their self-care daily regimen of brush- reduction in supragingival plaque and ing and interdental cleaning. There- gingivitis. Evidence shows that an fore, the incorporation of an ADA- American Dental Association (ADA)– Accepted mouthrinse into the daily Accepted antimicrobial mouthrinse regimen of brushing and cleaning can result in a greater reduction in interdentally is important to achieve plaque and gingivitis than brushing optimal oral health outcomes. and flossing alone.1 Therefore, even the most diligent brusher and flosser Figure 1. The American can benefit from the addition of an The ADA Seal of Dental Association Seal ADA-Accepted antimicrobial mouth- Acceptance Program of Acceptance. (Cour- rinse to the daily homecare regimen. tesy of the American Antimicrobial mouthrinses reduce More than 100 companies volun- Dental Association.) the bacterial count and inhibit the tarily participate in the ADA Seal of pathogenic bacterial activity in den- Acceptance Program and more than tal biofilm that can cause gingivitis, a 400 oral care products marketed the importance of oral and systemic precursor to periodontitis. Brushing directly to consumers carry the ADA health, and product safety and effi- and flossing alone may not always be Seal (Figure 1).2 Oral health care pro- cacy, this list is likely to expand and enough to control the pathogenicity fessionals and consumers can visit should be reviewed regularly. of dental biofilm. Untreated, gingivi- http://www.ada.org/ada/seal/adaseal_ The safety and efficacy data for the tis can advance to periodontitis and consumer_shopping.pdf to identify twice-daily use of an antiplaque and tooth loss and may be associated with products that have earned the ADA antigingivitis antimicrobial mouth- other chronic diseases and conditions Seal of Acceptance to guide their rec- rinse is unequivocal. Products that such as diabetes mellitus, cardiovas- ommendations and purchases of over- have been found effective against cular disease, obesity, and pre-term the-counter (OTC) products. Given plaque and gingivitis and that have earned the ADA Seal are those that contain 0.12% chlorhexidine gluconate (CHG) or a fixed combination More than 100 companies voluntarily of essential oils (EO). Listerine®— a participate in the ADA Seal of fixed combination of EO—and its generic equivalents carry the ADA Acceptance Program and more than Seal; however, because of recent 400 oral care products marketed directly to changes in the ADA Seal program, prescription products such as Peridex® consumers carry the ADA Seal. (0.12% CHG), even if they have pre-

32 The Journal of Dental Hygiene Special supplement viously earned the ADA Seal, are no subject areas are also available from an ADA-Accepted antimicrobial longer included in the ADA Seal pro- the Cochrane Library including the mouthrinse to help prevent and reduce gram, as the granting of the ADA Seal Cochrane Database of Systematic plaque and gingivitis and speak with for prescription product has been Reviews at www.cochrane.org. This their dental hygienist or dentist for phased out. site is an essential resource for busy additional guidance. Understanding dental hygienists who strive to main- the process of change and matching tain an evidence-based practice. professional oral care recommenda- Evidence-Based In general, possessing a basic tions to patient’s specific needs, goals, Literature knowledge of what constitutes appro- values, and levels of readiness to priate research methods and the abil- change may lead to patient adherence In addition to the ADA Seal, well- ity to read the professional literature and attainment of desired clinical out- prepared, published systematic increases the dental hygienist’s com- comes over the long term. Regardless reviews and meta-analyses that syn- petence as a critical consumer of of the level of adherence to profes- thesize a large number of rigorous research, enabling the dental hygien- sional recommendations, patients need studies on a focused topic and that ist to translate important research find- regular instruction and encouragement arrive at clear conclusions can be ings into practice in a timely manner. from a dental hygienist they trust. extremely valuable in guiding clinical decisions regarding products, devices, treatments, and interventions. Conclusions References 1. Sharma N, Charles CH, Lynch MC, et Many such studies and reviews in al. Adjunctive benefit of an essential addition to original research papers In conclusion, most patients will oil-containing mouthrinse in reducing are cited throughout this supplement, improve their oral health by adding an plaque and gingivitis in patients who and these references can provide fur- ADA-Accepted antimicrobial brush and floss regularly: a six-month ther background and information on mouthrinse to their self-care daily reg- study. J Am Dent Assoc. 2004;135: 496-504. the benefits of using an antimicrobial imen of toothbrushing and interdental 2. About the ADA Seal of Acceptance. mouthrinse as part of a daily regimen. cleaning. Within the context of clinical American Dental Association Web One good example cited within practice and current research evidence, site. http://www.ada.org/ada/seal/ these pages is a recent meta-analysis dental hygienists should recommend index.asp. Accessed July 30, 2007. 3. Gunsolley JC. A meta-analysis of six- of 6-month studies of antiplaque and that patients practice a three-step daily month studies of antiplaque and 3 antigingivitis agents. Moreover, sys- oral hygiene regimen of brushing, antigingivitis agents. J Am Dent Assoc. tematic reviews on a variety of dental interdental cleaning, and rinsing with 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® Antiseptic may 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 and other health problems. To learn more, visit www.listerine.com, or ask your dentist, dental hygienist or physician about the mouth-body connection.*

DO IT FOR DO IT FOR

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 the gumline, when used as directed.”