Rationale for Comprehensive Nonsurgical Periodontal Therapy

Journalof Dental Hygiene

TH E AM E R I C A N DE N TA L HY G I E N I S T S’ AS S O C I AT I O N

2008Volume 83 Number 6Journal of

Dental Hygiene

Supplement to ADHA Access

Rationale for Comprehensive NonsurgicalPeriodontal Therapy: A Review of theClinical Evidence and Practice Protocol

• Microbes, Inflammation, Scaling andRoot Planing, and the PeriodontalCondition

• Locally Delivered Antimicrobials:Clinical Evidence and Relevance

• Periodontal Treatment Protocol (PTP)for the General Dental Practice

This supplement is sponsored by an educationalgrant from OraPharma, Inc.

■ Charles Cobb, DDS, PhD,graduated from the Univer-sity of Missouri-Kansas Citywith a dental degree, a Certi-ficate of Specialty in Perio-dontics, and a Master ofScience degree in Microbiol-ogy. He later earned a PhDin Anatomy from George-town University. He has heldacademic positions at Louisi-ana State University, the University of Alabama,and UMKC. In addition to teaching and research,Dr. Cobb has practiced periodontics full-time for15 years in a private dental practice. Dr. Cobbrecently retired from academics as ProfessorEmeritus at UMKC. He is a Diplomate of the Ameri-can Board of Periodontology, has published over165 peer-review articles, and presented over 120programs at regional, national, and internationalmeetings.

■ Larry Sweeting, DDS, gradu-ated from Emory UniversityDental School with a Doctorof Dental Surgery degreeand later earned a Certificatein Periodontics. Dr. Sweetingheld a clinical part-time facultyappointment in the Post-Doctoral Graduate Periodon-tics program at Emory Uni-versity Dental School from1986-1992 and is currently a clinical assistantprofessor at the Medical College of Georgia(MCG) in the Department of Periodontics. Hereceived the MCG “2007 Educator Award”presented by the American Academy of Perio-dontology in recognition of outstanding teachingand mentoring in Periodontics. For the past 20years, Dr. Sweeting has been the managingpartner and dental director for a 10-officemultispecialty group practice in Atlanta, Ga.

■ Karen Davis, RDH, BSDH,received her Bachelor ofScience in Dental Hygienefrom Midwestern State Uni-versity. She is the founder ofCutting Edge Concepts® anda trainer for RDH MastershipCertification courses fromThe JP Institute of SanDiego, Calif. In addition, Ms.Davis practices clinically inDallas, Tex. She speaks internationally and hasauthored numerous articles related to periodontaltherapy and practice management.

■ David W. Paquette, DMD, MPH, DMSc,is an associate professor, graduateprogram director in Periodontologyand assistant dean of graduate/advanced dental education at theUniversity of North Carolina atChapel Hill. He received his Doctorof Dental Medicine degree, Masterof Public Health, Doctor of MedicalSciences, and Certificate in Perio-dontics from Harvard University. Hiscurrent leadership roles include chairing the AmericanAcademy of Periodontology Subcommittee on ResearchSubmissions and serving on the editorial boards for 6journals. He also is a past president of the InternationalAssociation for Dental Research Periodontology ResearchGroup and is a past fellow with the American DentalEducation Association (ADEA) Leadership Institute. Hehas published 45 articles and 2 book chapters relating topossible links between periodontal and systemic healthand other issues related to periodontal disease. Dr.Paquette is an international speaker and consultant.

■ Maria Emanuel Ryan, DDS, PhD, a1989 Stony Brook School of DentalMedicine graduate, is a tenured fullprofessor in the Department of OralBiology and Pathology at the Schoolof Dental Medicine and a member ofthe Medical Staff at UniversityHospital at Stony Brook UniversityMedical Center. She also serves asdirector of clinical research. Dr. Ryanis actively involved in teaching,practice, and research at the School of Dental Medicine.Dr. Ryan serves on several scientific, dental, andmedical advisory boards. She is a nationally andinternationally known speaker and author and haspublished over 75 original scholarly works.

■ Rebecca Wilder, RDH, BS, MS, is anassociate professor and director ofthe Master of Science Degree pro-gram in Dental Hygiene Education atthe University of North Carolina atChapel Hill. She is also the directorof faculty development for the UNCSchool of Dentistry. Ms. Wilder is theeditor-in-chief of the Journal ofDental Hygiene and an author ofMosby’s Dental Hygiene: Cases, Concepts andCompetencies, published in 2008. She has publishedover 70 papers and 40 abstracts on oral health careissues. She is a consultant to the dental industry and isan international speaker in the areas of risk and practicemanagement and periodontics.

about the authors

Special supplement The Journal of Dental Hygiene 1

ver the last 30 years, we havelearned much about the etiol-

ogy, progression, and treatment ofperiodontal diseases. For example,we know that the accumulation ofdental biofilm can trigger resultantinflammatory and immune responses.Dental biofilm contains a vast diver-sity of microbial species, some ofwhich have been identified as etio-logic agents for systemic diseases.

Risk factors for periodontitis canbe grouped into categories such asmicrobial, systemic, behavioral, andlocal. Controlling risk factors isimportant to the management ofperiodontal diseases and is some-thing that should be an overall goalfor every dental hygienist. One riskfactor for disease that can be con-trolled in the majority of cases isdental biofilm. However, control ofdental biofilm is dependent on manyfactors including the knowledge ofthe dental hygienist regarding evi-dence-based strategies for diseaseprevention and treatment.

We have an extensive amount ofscientific evidence available to edu-cate every oral health care profes-sional about periodontal diseases.However, dental practice manage-ment experts report that many clini-cians are not adequately diagnosing,documenting, or monitoring diseasestatus or making treatment recom-

mendations to patients based on evi-dence-based strategies. Many ques-tions arise about the best treatmenttechniques, products, and recom-mendations for patients who havechronic periodontitis or are at risk forthe disease. The patient is dependenton the dental hygienist to be at theforefront of prevention. It is vital fordental hygienists to have up-to-date,accurate information so they can edu-cate and make appropriate recom-mendations for the individual patient.

This supplement of the Journal ofDental Hygiene includes articles thatwill educate every dental hygienistabout the evidence base for treat-ment of chronic periodontitis. Dr.Charles Cobb is an internationalexpert on dental biofilm and theeffect of nonsurgical methods forremoving biofilm and hard deposits(calculus) on the tooth and root sur-faces. He provides a comprehensive,evidence-based review of what den-tal hygienists can expect from non-surgical therapies. Drs. DavidPaquette and Maria Ryan, 2 world-renowned periodontists, and I pres-ent a comprehensive paper on theevidence base for the use of locallydelivered antimicrobials. Since theirinception 3 decades ago, oral healthcare professionals have been utiliz-ing locally delivered antimicro-bials/antibiotics to treat chronic peri-

odontitis. Still, questions arise abouttheir utility and ability to treat andcontrol this disease. This paper pres-ents the clinical evidence for use oflocally delivered antimicrobials inpatient care. Finally, Dr. LarrySweeting, Ms. Karen Davis, and Dr.Charles Cobb put the evidence intoan action plan for dental hygienists.Dr. Sweeting and Ms. Davis are den-tal clinicians as well as professionalspeakers and consultants. Theirpaper discusses the effectiveness ofusing a Periodontal Treatment Pro-tocol to assist in the early diagnosisand treatment of periodontal dis-eases. It also discusses insurancecoding, vital verbal skills to use withpatients, and considerations forimplementation of locally deliveredantimicrobials into a general clini-cal practice.

I want to extend sincere apprecia-tion to OraPharma, Inc. for their sup-port of this supplement. OraPharma,Inc. has been diligent in their goalof conducting evidence-based scien-tific investigations in order to helpall oral health care professionals bet-ter diagnose and treat periodontaldiseases.

Rebecca S. Wilder, RDH, BS, MSEditor-in-Chief, Journal of [email protected]

From the Editor-in-Chief of the Journal of Dental Hygiene

O

This special issue of the Journal of Dental Hygiene wassponsored by an educational grant from OraPharma, Inc.

This supplement can also be accessed online atwww.adha.org/CE_courses/

To obtain two hours of continuing education credit, complete thetest at www.adha.org/CE_courses/course20

■■ STATEMENT OF PURPOSE

The Journal of Dental Hygiene is the refereed, scientific publication of the AmericanDental Hygienists’ Association. It promotes the publication of original research relatedto the profession, the education, and the practice of dental hygiene. The journalsupports the development and dissemination of a dental hygiene body of knowledgethrough scientific inquiry in basic, applied, and clinical research.

2 The Journal of Dental Hygiene Special supplement

Journal of DentalHygiene

special supplement

■■ EDITORIAL REVIEW BOARD

Celeste M. Abraham, DDS, MSCynthia C. Amyot, BSDH, EdDJoanna Asadoorian, AAS, BScD, MScCaren M. Barnes, RDH, BS, MSPhyllis L. Beemsterboer, RDH, MS, EdDStephanie Bossenberger, RDH, MSLinda D. Boyd, RDH, RD, LS, EdDKimberly S. Bray, RDH, MSLorraine Brockmann, RDH, MSPatricia Regener Campbell, RDH, MSDan Caplan, DDS, PhDMarie Collins, RDH, EdDBarbara H. Connolly, PT, EdD, FAPTAValerie J. Cooke, RDH, MS, EdDMaryAnn Cugini, RDH, MHPSusan J. Daniel, AAS, BS, MSMichele Darby, BSDH, MSCatherine Davis, RDH, PhD. FIDSASusan Duley, BS, MS, EdS, EdD, LPC, CEDSJacquelyn M. Dylla, DPT, PTKathy Eklund, RDH, BS, MHPDeborah E. Fleming, RDH, MSJane L. Forrest, BSDH, MS, EdDJacquelyn L. Fried, RDH, BA, MSMary George, RDH, BSDH, MEdKathy Geurink, RDH, BS, MAMaria Perno Goldie, RDH, BA, MSEllen Grimes, RDH, MA, MPA, EdDJoAnn R. Gurenlian, RDH, PhDLinda L. Hanlon, RDH, BS, MEd, PhDKitty Harkleroad, RDH, MSLisa F. Harper Mallonee,BSDH,MPH,RD/LDHarold A. Henson, RDH, MEdLaura Jansen Howerton, RDH, MS

Olga A.C. Ibsen, RDH, MSHeather L. Jared, RDH, BS, MSWendy Kerschbaum, RDH, MA, MPHSalme Lavigne, RDH, BA, MSDHJessica Y. Lee, DDS, MPH, PhDMadeleine Lloyd, MS, FNP-BC, MHNP-BCDeborah Lyle, RDH, BS, MSDeborah S. Manne,RDH,RN,MSN,OCNAnn L. McCann, RDH, BS, MS, PhDStacy McCauley, RDH, MSGayle McCombs, RDH, MSTricia Moore, RDH, BSDH, MA, EdDChristine Nathe, RDH, MSKathleen J. Newell, RDH, MA, PhDJohanna Odrich, RDH, MS, DrPhPamela Overman, BSDH, MS, EdDVickie Overman, RDH, BS, MEdFotinos S. Panagakos, DMD, PhD, MEdM. Elaine Parker, RDH, MS, PhDCeib Phillips, MPH, PhDMarjorie Reveal, RDH, MS, MBAPamela D. Ritzline, PT, EdDJudith Skeleton, RDH, BS, MEd, PhDAnn Eshenaur Spolarich, RDH, PhDSheryl L. Ernest Syme, RDH, MSTerri Tilliss, RDH, BS, MS, MA, PhDLynn Tolle, BSDH, MSMargaret Walsh, RDH, MS, MA, EdDDonna Warren-Morris, RDH, MS, MEdCheryl Westphal, RDH, MSKaren B. Williams, RDH, PhDCharlotte J. Wyche, RDH, MSPamela Zarkowski, BSDH, MPH, JD

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

DIRECTOR OF COMMUNICATIONSJeff [email protected]

EDITOR EMERITUSMary Alice Gaston, RDH, MS

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

STAFF EDITORKatie [email protected]

LAYOUT/DESIGNJean MajeskiPaul R. Palmer

■■ BOOK REVIEW BOARD

Sandra Boucher-Bessent, RDH, BSJacqueline R. Carpenter, RDHMary Cooper, RDH, MSEdHeidi Emmerling, RDH, PhDMargaret J. Fehrenbach, RDH, MSCathryn L. Frere, BSDH, MSEdPatricia A. Frese, RDH, BS, MEdJoan Gibson-Howell, RDH, MSEd, EdDAnne Gwozdek,RDH, BA, MA

Cassandra Holder-Ballard, RDH, MPALynne Carol Hunt, RDH, MSShannon Mitchell, RDH, MSKip Rowland, RDH, MSLisa K. Shaw, RDH, MSMargaret Six, RDH, BS, MSDHRuth Fearing Tornwall, RDH, BS, MSSandra Tuttle, RDH, BSDHJean Tyner, RDH, BS

■■ SUBSCRIPTIONS

The Journal of Dental Hygiene is published quarterly, online-only, by the AmericanDental Hygienists’ Association, 444 N. Michigan Avenue, Chicago, IL 60611. Copy-right 2008 by the American Dental Hygienists’ Association. Reproduction in whole orpart without written permission is prohibited. Subscription rates for nonmembers areone year, $45; two years, $65; three years, $90; prepaid.

■■ SUBMISSIONS

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


Journal of Dental Hygiene

1 From the Editor-in-Chief of the Journal of Dental HygieneRebecca S. Wilder, RDH, BS, MS

4 Microbes, Inflammation, Scaling and Root Planing, and the Periodontal ConditionCharles M. Cobb, DDS, MS, PhD

10 Locally Delivered Antimicrobials: Clinical Evidence and RelevanceDavid W. Paquette, DMD, MPH, DMSc; Maria Emanuel Ryan, DDS, PhD; Rebecca S. Wilder, RDH, BS, MS

16 Periodontal Treatment Protocol (PTP) for the General Dental PracticeLarry A. Sweeting, DDS; Karen Davis, RDH, BSDH; Charles M. Cobb, DDS, PhD

Inside

Message

Supplement


Introduction

Typically, the term “periodontal dis-ease” refers to gingivitis and periodonti-tis, both common inflammatory diseasesthat involve a variety of pathogenic bac-terial species and an innate host responseto those bacteria.1 Gingivitis, the mostfamiliar form of inflammatory perio-dontal disease, has a high prevalencerate, affecting 50%-90% of adultsworldwide.2,3 By definition, gingivitis islimited to an inflammation that involvesonly the gingival soft tissues, ie, gingi-val epithelium and subjacent fibrousconnective tissues. In spite of its highprevalence rate and worldwide distribu-tion, biofilm (plaque)- induced gingivitisis preventable and rather easily reversedby routine oral hygiene measures.

Inflammation that extends into thedeeper tissues to involve bone, resultingin resorption of tooth supporting bone, istermed periodontitis. Concomitant withthe loss of bone is the formation of adeepened space between the root of thetooth and the gingiva, a periodontalpocket. Periodontitis can present as achronic and slowly progressing disease(most common form) or as an aggres-sive disease causing loss of bone over arelatively short period of time. Peri-odontitis of advanced severity can resultin tooth mobility, occasional pain anddiscomfort (generally associated withabscess formation), impaired ability tomasticate food, and eventual tooth loss.

Although more common to adults,epidemiologic data indicate that peri-odontitis can also be found in childrenand adolescents.4,5 In the United States,chronic periodontitis is more prevalentin men than women, and in AfricanAmericans, Native Americans, andMexican Americans than Caucasians.2,6,7

Various epidemiology studies, when

considered in aggregate, suggest a pro-gressive decrease in the prevalence ofperiodontitis between the years 1988-2004.7-11 The more recent of these stud-ies indicate a prevalence rate for mod-erate to advanced periodontitis rangingfrom approximately 5% to 15% for indi-viduals > 18 years of age.9-11 Given thecurrent US Department of Census pro-jections, a 5% to 15% prevalence ratetranslates to 11 to 33 million US adultsthat may exhibit periodontitis of moder-ate to advanced severity.12 If oneincludes slight severity, the prevalencerate for periodontitis increases toapproximately 30% of the US adult pop-

ulation, or roughly 65 million individu-als.9-12 However, all epidemiology stud-ies that have reported on the prevalenceof chronic periodontitis have utilizedpartial-mouth examinations, which tendto underestimate prevalence, extent, andseverity of disease.13-15

Microbes and Biofilm

A biofilm is a complex community ofmicroorganisms characterized by theexcretion of an adhesive and protectiveextracellular matrix, microbe-to-microbeattachment, structural heterogeneity,

SupplementSupplement

Abstract

Biofilms are a complex community of microorganisms characterized bythe excretion of an adhesive and protective extracellular matrix, microbe-to-microbe attachment, structural heterogeneity, genetic diversity, andcomplex community interactions. Bacteria growing in dental biofilmsdisplay an increased tolerance to antibiotics and antimicrobial agents,including those used in dentifrices and mouthrinses.

The microbial challenge associated with the inflammatory periodontaldiseases induces an immediate inflammatory and immune response inthe host. The nature and magnitude of the response has an impact onthe severity and rate of progression of the periodontal disease. It is thishost inflammatory-immune response that ultimately leads to the clinicalsigns and symptoms of gingivitis and chronic periodontitis. The traditionaltreatment modality of scaling and root planing (SRP) remains the “goldstandard” for the non-surgical management of chronic periodontitis.Even clinically successful treatment has a high probability of pocket re-infection. Re-infection of periodontal pockets results from residualbiofilms, increased tolerance of microbes within a dense, mature biofilmto antibiotics, reservoirs of bacteria in calculus, and reservoirs of bac-teria within the dentinal tubules of infected root surfaces. Thus, for max-imum effect, a combination of scaling and root planing and locally deliv-ered antimicrobials should be considered if non-surgical therapy is thetreatment of choice.

Keywords: periodontal disease, periodontal infection, chronic peri-odontitis, scaling and root planing, dental biofilm

Microbes, Inflammation, Scaling and Root Planing,and the Periodontal ConditionCharles M. Cobb, DDS, MS, PhD


genetic diversity, and complex commu-nity interactions. Dental plaque is amicrobial biofilm (Figure 1). As withany biofilm, the constituent microbesare tightly adherent to each other andto an oral substrate by means of anextracellular matrix, ie, slime layer orglycocalix, into which they are embed-ded.16,17 The microbial populations inbiofilm have 2 strategies that enablethem to successfully survive withintheir community. The first is a high rateof reproduction for continued survival,and the second is physiologic adapta-tion to the available environmentalresources or life-supporting capacity ofthe environment.18

Biofilms inherently dictate profoundchanges in the behavior of individualmicrobes, their relationship to the host,and their response to environmentalconditions.19 Indeed, oral biofilms, asdistinct entities, are the causative agentsof biological processes such as dentalcaries, periodontal disease, and peri-implantitis, rather than any singlemicrobe evading the host defense andcausing disease.20 Biofilms exhibit char-acteristics that impact the clinical man-agement of inflammatory periodontaldisease. For example, both altered pat-terns of microbial gene expression andthe composition and density of the

extracellular matrix reduce the suscep-tibility of microbes to antimicrobialagents.21-23 Bacteria growing in dentalbiofilms display an increased toleranceto antimicrobial agents, including thoseused in dentifrices and mouthrinses.24-27

In addition, confocal microscopy of insitu established natural biofilms showedthat chlorhexidine only affected theouter layers of cells in 24 and 48 hourplaque biofilms, suggesting eitherquenching of the agent at the biofilmsurface or a lack of penetration.28 Fur-ther, biofilms of oral bacteria are alsomore tolerant of antibiotics (eg, amoxy-cillin, doxycycline, minocycline, andmetronidazole) than planktonic cells.29-31

In this regard, biofilms of Porphy-romonas gingivalis have been shown totolerate 160 times the minimuminhibitory concentration (MIC) ofmetronidazole that was determined forplanktonic cells.32

Over 700 species of aerobic andanaerobic bacteria have been identifiedin the human oral cavity.33,34 Themicrobes grow as complex, mixed,interdependent colonies in biofilms, andmay achieve considerable thickness,achieving a thickness of 1 mm within96 hours, if left undisturbed.16,17 Oralbiofilms, like all microbial biofilms,exhibit a successional colonization with

gram-positive aerobic Streptococcispecies (spp.) being the initial coloniz-ers, followed in sequence by Actino-myces spp., Corynebacterium spp., Veil-lonella spp., and then in more maturebiofilm, a variety of gram-negativeanaerobic microbes such as Treponemaspp., Fusobacterium spp., Porphy-romonas spp., Prevotella spp., and Tan-nerella spp.17,35,36

As the biofilm is allowed to maturewith concomitant increases in thick-ness, the percentage of Gram-negativeanaerobic microbes increases. Specificcomplexes of such microbes com-monly cohabit subgingival sites andare consistently associated withinflammatory periodontal diseases.35

These putative microbial pathogensinclude Porphyromonas gingivalis,Tannerella forsythia, and Treponemadenticola.35

In the human host, the transition fromgingivitis to periodontitis does not occurautomatically, either in every patient orevery site, but depends on 3 factors: 1)degree of host susceptibility, 2) presenceand numbers of pathogenic bacteria, and3) presence and numbers of protectivebacteria.36 Pathogenic bacteria exhibitvirulence features that decrease theeffectiveness of the host response byinducing tissue degradation and retard-ing attempts at healing.

Host defense mechanisms are im-paired through a variety of mecha-nisms. As one example, consider thatAggregatibacter (formally Actinobacil-lus) actinomycetemcomitans produces aleukotoxin that alters the cell mem-branes of neutrophils and monocytesand thereby alters chemotactic andphagocytic responses.36 Infection withGram-negative anaerobes is accompa-nied by the release of epitheliotoxins,endotoxins, leukotoxins, collagenase,gellatinase, elastase, fibrinolysins, andother proteolytic enzymes.37 These bac-terial toxins and enzymes are tissue irri-tants and/or cytotoxic and viewed bythe host immune system as foreign pro-teins (Figure 2). The aggregate cellu-lar/tissue insult activates the hostimmune system locally and is gener-ally visualized at a clinical level asinflammation with all the inherent gin-gival changes, eg, vasculitis, edema andswelling, change in tissue color fromwhite-pink to red or red-purple, andspontaneous gingival bleeding or bleed-ing on provocation.38

Figure 1. Scanning electron microscopic photograph of root associ-ated dental biofilm (plaque). Bar = 10 micron at an original magnifi-cation of 2840x.


Role of the HostImmune Response

Bacteria are necessary but not suffi-cient by themselves to produce adestructive periodontal disease. Diseaseinitiation and progression requires asusceptible host.38 The microbial chal-lenge induces an immediate inflamma-tory and immune response in the host.The nature and magnitude of theresponse have an impact on the sever-ity and rate of progression of the peri-odontal disease.39 Locally, bacteria andtheir metabolic byproducts stimulate acellular immune response within theaffected gingiva represented by a denseinfiltration of neutrophils, macro-phages, and lymphoid cells. These cellsand host connective tissue cells withinthe developing inflammatory lesion arestimulated to synthesize and releaseproinflammatory cytokines, prosta-noids, and proteolytic enzymes, eg,interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necro-sis factor-alpha (TNF-α), prostaglandinE2 (PGE2), matrix metalloproteinases.38

It is this host inflammatory-immuneresponse that ultimately leads to theclinical signs of gingivitis and chronicperiodontitis and their characteristicfeatures of fibrous connective tissuedegradation, resorption of tooth sup-porting alveolar bone, and periodontalpocket formation.

In contrast to the epidermis of skin,the epithelial lining of the soft tissuewall of a periodontal pocket lacks a stra-tum corneum and stratum granulosum.Consequently, the pocket epithelium iseasily ulcerated and breached by inva-sive subgingival pathogenic bacteria.40

In addition, endotoxins and other micro-bial antigens may gain access to theunderlying connective tissues and gin-gival vasculature, leading to bacteremiaand endotoxemia. There is considerableevidence that the locally produced pro-inflammatory cytokines and prostanoidsgain access to the circulatory system andmay, in turn, induce the production ofliver-derived markers of a systemicinflammatory reaction, such as C-reac-tive protein, fibrinogen, serum amyloid-A, and haptoglobin.41-45 Elevations inboth the locally generated inflammatorymediators and systemic markers ofinflammation have been associated withvarious systemic diseases such as ath-

erosclerosis,46 cardiovascular disease,47

ischemic stroke,48 pre-eclampsia,49 andpoor glycemic control 50 in diabeticpatients.

Risk FactorsAssociated WithDevelopment ofChronic Periodontitis

In addition to the accepted associa-tions of pathogenic microbes to thepathogenesis of inflammatory peri-odontal diseases, several genetic andenvironmental risk factors have beenidentified that affect the host response. Itis well established that the prevalenceand severity of chronic periodontitisincreases with advancing age, poor oralhygiene, marginally or poorly controlledtype I and II diabetes, and use oftobacco.51,52 In addition, data from twinstudies indicate that about 50% of thepopulation variance in periodontitis canbe attributed to genetic factors.53,54 Sev-eral studies indicate that genetic poly-morphisms (variations) in a cluster of atleast 3 genes on chromosome 2q13,

which control the production of proin-flammatory cytokines, may affect thesystemic inflammatory response in asignificant percentage of people withchronic periodontitis.55,56

Scaling and RootPlaning in the Controlof Chronic Periodontitis

Periodontitis is a chronic and pro-gressive inflammatory disease forwhich there is no known cure. It is nowwell-established that periodontitis isnot associated with a single microor-ganism but rather the initiation andprogression of periodontitis is theresult of the host’s immune responseto a consortium of bacteria. For peri-odontopathic bacteria to initiate peri-odontitis, it is essential that they areable to colonize subgingival pocketsand produce virulence factors thatdirectly damage host tissue. Thus, amajor goal of nonsurgical periodontaltherapy is to suppress, to the extentpossible, the subgingival pathogenicmicrobial flora and thereby signifi-

Figure 2.Transmission electron microscopic photograph of a nega-tively stained Phorphyromonas gingivalis featuring fimbriae andnumerous surface blebs that likely contain endotoxin. Both fimbriaeand endotoxin are potent antigens that solicit a host immuneresponse. Original magnification of 35 000x.

cantly reduce or eliminate the associ-ated inflammatory lesion.

Dental calculus was the original eti-ologic agent associated with develop-ment of chronic periodontitis. In the1960s and 1970s it was established thatthe rough, irregular surface of dental cal-culus was always covered with a non-mineralized microbial biofilm (Figure3).57-59 In addition to the surface biofilm,at least one recent study has identifiedthe presence of several viable periodon-tal pathogens within the mass of dentalcalculus, ie, Aggregatibacter actino-mycetemcomitans, Treponema denticolaand Porphyromonas gingivalis.60 Inter-estingly, the persistence of Porphy-romonas gingivalis in the subgingivalenvironment following periodontal ther-apy has been associated with progres-sive alveolar bone loss.61 In support ofthis observation, Offenbacher et al62

recently reported a significant associa-tion between serum immuneoglobulinG (IgG) titers against Porphyromonasgingivalis in patients that exhibit deepPDs (> 4 mm) and moderate (> 10% to< 50%) and severe (> 50%) bleeding onprobing.

In spite of the fact that calculus canserve as a reservoir for pathogenicmicrobes, the role of subgingival cal-culus, as an etiologic agent in chronicperiodontitis, was relegated to second-ary status once microbial biofilm wasdeclared the primary, extrinsic etiologicfactor. Thus, the need for completeremoval of subgingival calculusbecame a subject for debate.63 How-ever, the traditional treatment modal-ity of scaling and root planing (SRP)remains the “gold standard” for thenonsurgical management of periodon-titis.64

The periodontal literature is repletewith studies showing that treatment ofperiodontitis by SRP results in reduc-tions in probing depth (eg, a meanreduction of 1.29 mm for 4-6 mm pock-ets and a mean of 2.16 mm for pocketsof > 7 mm) and subgingival bacterialloads and gains in clinical attachment.65-

67 Probing depth (PD) reduction is gen-erally greater at sites with deeper ini-tial probing depths. The decrease in PDis the result of 2 phenomena: shrinkageof the pocket soft tissue wall manifestedas recession of the gingival marginwhich results from a decrease in softtissue inflammation and the inherentedema; and gain in clinical attachment.

The latter usually accounts for roughlyone-half of the probing depth reduc-tion.65-67 In general, clinicians shouldevaluate post-SRP healing at 4 to 6weeks following treatment. After 6weeks, most of the healing has takenplace but repair and collagen matura-tion may continue for an additional 9months.67,68

Three relevant observations must beconsidered when deciding to use non-surgical therapy as the primary modal-ity for treatment of early to moderatechronic periodontitis. First, regardingSRP, clinicians must be careful wheninterpreting data from published clini-cal trials as they may not accuratelyreflect the private practice setting interms of time, skill level, severity ofdisease, and diversity of patient popu-lation.65 For example, university-con-ducted clinical trials often use highlyskilled clinicians, select patients forlevel of disease, and report spending 10minutes per tooth when performingSRP.66,67 Ten minutes per tooth equatesto about 70 minutes per quadrant. It isthe experience of this author that in pri-vate practice a quadrant of SRP may becompleted in approximately 60 minutes,regardless of the level of disease, and

this allows approximately 10 minutesfor setting of the patient and adminis-tration of anesthetic. Greenstein67 hasrightfully noted that decreased timedevoted to SRP in more recent studiesprobably accounts for the diminishedresults reported when to the more clas-sic clinical trials. Second, one mustremember that microbes embedded ina mature, undisturbed subgingivalbiofilm may exhibit an increased toler-ance to antimicrobial agents.28-32 Third,even when chronic periodontitis istreated successfully, the reduction insubgingival pathogenic microbes istransitory. SRP of diseased root sur-faces can open dentinal tubules, allow-ing invasion by periodontal pathogensinto the exposed tubules, and possiblythen serve as a reservoir for re-infec-tion of the pocket.69,70 Thus, the need forfollow-up treatment, usually consistingof supra- and subgingival debridementat 3 to 4 month intervals, is necessary tomaintain the initially gained beneficialeffects.71,72 Collectively considered, thedistinct probability of less than idealresults from SRP and pocket re-infec-tion by residual microbes is a forcefulargument for the use of adjunctivetreatment modalities in addition to SRP.


Figure 3. Scanning electron microscopic photograph of dental cal-culus characterized by a superficial layer of microbial biofilm. Bar =10 micron at an original magnification of 1,770x.


Clinical Implications

1. The prevalence rate for chronicperiodontitis (slight, moderate,and advanced severity) is approx-imately 30% of the US adult pop-ulation or roughly 65 million indi-viduals.

2. Bacteria growing in undisturbeddental biofilms exhibit a signifi-cant increased tolerance to antimi-crobial agents and antibiotics.

3. The transition from gingivitis toperiodontitis does not occur auto-

matically, either in every patientor every site, but depends on 3factors: 1) degree of host suscep-tibility, 2) presence and numbersof pathogenic bacteria, and 3)presence and numbers of protec-tive bacteria.

4. Even when chronic periodontitisis treated successfully, the reduc-tion in subgingival pathogenicmicrobes is transitory. Thus, theneed for follow-up treatment, usu-ally consisting of supra- and sub-gingival debridement at 3 to 4month intervals, is necessary to

maintain the initially gained ben-eficial effects.

5. Due to limitations of SRP and re-infection of the periodontalpocket, adjunctive treatmentmodalities may increase the like-lihood of improvement in the peri-odontal condition.

Disclosure

Dr. Cobb has served as a scientificadvisor and consultant for OraPharma,Inc.

References

1. Armitage GC. Development of a classification system forperiodontal diseases and conditions. Ann Periodontol.1999;4:1-6.

2. Albandar JM, Kingman A. Gingival recession, gingivalbleeding, and dental calculus in adults 30 years of ageand older in the United States, 1988-1994. J Periodontol.1999; 70:30-43.

3. Albandar JM, Rams TE. Global epidemiology of perio-dontal diseases: an overview. Periodontol 2000. 2002;29:7-10.

4. Löe H, Brown LJ. Early-onset periodontitis in the UnitedStates of America. J Periodontol. 1991;62:608-616.

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6. Douglass CW, Fox CH. Cross-sectional studies in peri-odontal disease: current status and implications for dentalpractice. Adv Dent Res. 1993;7:25-31.

7. Albandar JM, Brunelle JA, Kingman A. Destructive peri-odontal disease in adults 30 years of age and older in theUnited States, 1988-1994. J Periodontol. 1999;70:13-29.

8. Brown LJ, Oliver RC, Löe H. Evaluating periodontal statusof US employed adults. J Am Dent Assoc. 1990;121: 226-232.

9. Borrell LN, Burt BA, Taylor GW. Prevalence and trends inperiodontitis in the USA: The NHANES, 1988 to 2000. JDent Res. 2005;84:924-930.

10. Page RC, Eke PI. Case definition for use in population-based surveillance of periodontitis. J Periodontol. 2007; 78:1387-1399.

11. Borrell LN, Crawford ND. Social disparities in periodonti-tis among United States adults 1999-2004. CommunityDent Oral Epidemiol 2008;36:In Press. Published articleonline: 18-Oct-2007, www.Blackwell-Synergy.com

12. Cobb CM, Williams KB, Gerkovitch M. Is The Prevalenceof Periodontitis in the United States in Decline? Periodon-tol 2000. 2008; In Press.

13. Kingman A, Morrison E, Löe H. Systematic errors in esti-mating prevalence and severity of periodontal disease. JPeriodontol. 1988;59:707-713.

14. Hunt R, Fann S. Effect of examining half teeth in a partialperiodontal recording of older adults. J Dent Res.1991;70:1380-1385.

15. Eaton KA, Duffy S, Griffiths GS, Gilthorpe MS, JohnsonNW. The influence of partial and full-mouth recordings on

estimates of prevalence and extent of lifetime cumulativeattachment loss: A study in a population of young malemilitary recruits. J Periodontol. 2001;72:140-145.

16. Listgarten MA. Structure of the microbial flora associatedwith periodontal health and diseases in man. J Periodon-tol. 1976;47:1-18.

17. Cobb CM, Killoy WJ. Microbial colonization in human peri-odontal disease: an illustrated tutorial on selected ultra-structural and ecologic considerations. Scan Microsc.1990;4:675-691.

18. Nishihara T, Koseki T. Microbial etiology of periodontitis.Periodontol 2000. 2004;36:14-26.

19. Marsh PD. Dental plaque as a microbial biofilm. CariesRes. 2004;38:204-221.

20. Caldwell DE, Atuku E, Wilkie DC, et al. Germ theory vs.community theory in understanding and controlling theproliferation of biofilms. Adv Dent Res. 1997;11:4-13.

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22. Gilbert P, Maira-Litran T, McBain AJ, Rickard AH, WhyteFW. The physiology and collective recalcitrance of micro-bial biofilm communities. Adv Microbial Physiol. 2002;46:203–255.

23. Stewart PS, Costerton JW. Antibiotic resistance of bacte-ria in biofilms. Lancet. 2001;358:135-138.

24. Marsh PD, Bradshaw DJ. Microbiological effects of newagents in dentifrices for plaque control. Inter Dent J.1993;43:399-406.

25. Kinniment SL, Wimpenny JWT, Adams D, Marsh PD. Theeffect of chlorhexidine on defined, mixed culture oralbiofilms grown in a novel model system. J Appl Bacteriol.1996;81:120-125.

26. Wilson M. Susceptibility of oral bacterial biofilms to antimi-crobial agents. J Med Microbiol. 1996;44:79-87.

27. Pratten J, Wilson M. Antimicrobial susceptibility and com-position of microcosm dental plaques supplemented withsucrose. Antimicrob Agents Chemother. 1999;43:1595-1599.

28. Zaura-Arite E, van Marle J, ten Cate JM. Confocalmicroscopy study of undisturbed and chlorhexidine-treateddental biofilm. J Dent Res. 2001;80:1436-1440.

29. Larsen T. Susceptibility of Porphyromonas gingivalis inbiofilms to amoxicillin, doxycycline and metronidazole. OralMicrobiol Immunol. 2002;17:267-271.

30. Socransky SS, Haffajee AD. Dental biofilms: difficult ther-apeutic targets. Periodontol 2000. 2002;28:12–55.

31. Noiri Y, Okami Y, Narimatsu M, Takahashi Y, Kawahara T,Ebisu S. Effects of chlorhexidine, minocycline, and metron-

idazole on Porphyromonas gingivalis strain 381 in biofilms.J Periodontol. 2003;74:1647-1651.

32. Wright TL, Ellen RP, Lacroix JM, Sinnadurai S, MittelmanMW. Effects of metronidazole on Porphyromonas gingi-valis biofilms. J Periodont Res. 1997;32:473-477.

33. Aas JA, Paster BJ, Stokes LN, Olsen I, Dewhirst FE. Defin-ing the normal bacterial flora of the oral cavity. J Clin Micro-biol. 2005;43:5721-5732.

34. Paster BJ, Olsen I, Aas JA, Dewhirst FE. The breadth ofbacterial diversity in the human periodontal pocket andother oral sites. Periodontol 2000. 2006;42:80-87.

35. Socransky SS, Haffajee AD, Cugini MA, Smith C, KentRL, Jr. Microbial complexes in subgingival plaque. J ClinPeriodontol. 1998;25:134-144.

36. Sbordone L, Bortolaia C. Oral microbial biofilms andplaque-related diseases: Microbial communities and theirrole in the shift from oral health to disease. Clin Oral Invest.2003;7:181-188.

37. Zambon JJ. Periodontal diseases: Microbial factors. AnnPeriodontol. 1996;1:879-925.

38. Offenbacher S. Periodontal diseases: pathogenesis. AnnPeriodontol. 1996;1:821-878.

39. Page RC, Kornman KS. The pathogenesis of human peri-odontitis: an introduction. Periodontol 2000. 1997:14:9-11.

40. Hujoel PP, White BA, Garcia RI, Listgarten MA. The den-togingival epithelial surface area revisited. J PeriodontRes. 2001;36:48-55.

41. Ebersole JL, Machen RL, Steffen MJ, Willmann DE. Sys-temic acute-phase reactants, C-reactive protein and hap-toglobin in adult periodontitis. Clin Exper Immunol.1997;107:347-352.

42. Noack B, Genco RJ, Trevisan M, Grossi S, Zambon JJ, DeNardin E. Periodontal infections contribute to elevated sys-temic C-reactive protein level. J Periodontol. 2001;72:1221-1227.

43. Amar S, Gokce N, Morgan S, Loukideli M, Van Dyke TE,Vita JA. Periodontal disease is associated with brachialartery endothelial dysfunction and systemic inflammation.Arterioscler Thromb Vasc Biol. 2003;23:1245-1249.

44. Slade GD, Ghezzi EM, Heiss G, Beck JD, Riche E, Offen-bacher S. Relationship between periodontal disease andC-reactive protein among adults in the AtherosclerosisRisk in Communities study. Arch Intern Med.2003;163:1172-1179.

45. Leivadaros E, van der Velden U, Bizzaro S, et al. A pilotstudy into measurements of markers of atherosclerosis inperiodontitis. J Periodontol. 2005;76:121-128.

46. Tonetti MS, D’Aiuto F, Nibali L, et al. Treatment of peri-odontitis and endothelial function. N Eng J Med.2007;356:911-920.

47. Kinane DF, Lowe GD. How periodontal disease may con-tribute to cardiovascular disease. Periodontol 2000.2000;23:121-126.

48. Grau AJ, Becher H, Ziegler CM, et al. Periodontal diseaseas a risk factor for ischemic stroke. Stroke. 2004;35:496-501.

49. Siqueira FM, Cota LOM, Costa JE, Haddad JPA, LanaAMQ, Costa FO. Maternal periodontitis as a potential riskvariable for preeclampsia: A case-control study. J Peri-odontol. 2008;79:207-215.

50. Hein C, Cobb CM, Iacopino A. Report of an independentpanel of experts of the Scottsdale Project. The independ-ent study initiative for collaboration in diabetes, cardio-vascular disease and periodontal disease intervention.Grand Rounds in Oral-Sys Med. 2007;2(Suppl):2-27.

51. Abdellatif HM, Burt BA. An epidemiological investigationinto the relative importance of age and oral hygiene status

as determinants of periodontitis. J Dent Res. 1987;66: 13-18.

52. American Academy of Periodontology. Position paper: Epi-demiology of periodontal disease. J Periodontol.1996;67:935-945.

53. Michalowicz BS, Aeppli D, Virag JG, et al. Periodontal find-ings in adult twins. J Periodontol. 1991;62:293-299.

54. Michalowicz BS, Diehl SR, Gunsolley JC, et al. Evidenceof a substantial genetic basis for risk of adult periodontitis.J Periodontol. 2000;71:1699-1707.

55. Kornman KS, Crane A, Wang HY, et al. The interleukin-1genotype as a severity factor in adult periodontal disease.J Clin Periodontol. 1997;24:72-77.

56. D’Aiuto F, Parkar M, Brett PM, Ready D, Tonetti MS. Genepolymorphisms in proinflammatory cytokines are associ-ated with systemic inflammation in patients with severeperiodontal infections. Cytokine. 2004;28:29-34.

57. Baumhammers A, Conway JC, Saltzberg D, Matta RK.Scanning electron microscopy of supragingival calculus. JPeriodontol. 1973;44:92-94.

58. Muhleman HR, Schroeder HE. Dynamics of supragingivalcalculus formation. Adv Oral Biol. 1964;1:175-203.

59. Mandel ID. Dental plaque: Nature, formation and effects.J Periodontol. 1966;37:357-367.

60. Calabrese N, Galgut P, Mordan N. Identification of Acti-nobacillus actinomycetemcomitans, Treponema denticolaand Porphyromonas gingivalis within human dental cal-culus: A pilot investigation. J Inter Acad Periodontol.2007;9:118-128.

61. Chaves ES, Jeffcoat MK, Ryerson CC, Snyder B. Persis-tent bacterial colonization of Porphyromonas gingivalis,Prevotella intermedia, and Actinobacillus actinomycetem-comitans in periodontitis and its association with alveolarbone loss after 6 months of therapy. J Clin Periodontol.2000;27:897-903.

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Introduction

Periodontal disease is a common,mixed oral infection affecting the sup-porting structures around the teeth.While 75% of the adult population has atleast mild periodontal disease (gingivi-tis), 20%-30% exhibits the severedestructive form (chronic periodontitis).1

Characteristically, the disease is silentuntil the advanced stage when patientsmay report symptoms like swelling(abscess), discomfort, shifting of thedentition, or tooth mobility. The clini-cal signs of periodontitis emanate frominflammatory and destructive changesin the gingiva, connective tissues, alve-olar bone, periodontal ligament, and rootcementum. These signs include the for-mation of periodontal pockets, loss ofclinical attachment, and resorption ofalveolar bone.2

Accordingly, periodontitis beginswith a pathogenic shift in the bacterialflora around teeth. Gram-negativeorganisms, such as Porphyromonas gin-givalis, Tannerella forsythia, Treponemadenticola and Aggregatibacter (formallyActinobacillus) actinomycetemcomi-tans, predominate in the subgingivalspace and organize as a biofilm.3 Severalof the gram-negative bacteria in thebiofilm are particularly importantbecause they have been identified asred-complex bacteria (T. forsythia, P.gingivalis, and T. denticola) and havebeen linked with important parametersof periodontal diagnosis, such as pocketdepth and bleeding on probing.3 Thisbacterial biofilm is in direct contact withhost tissues along an ulcerated epithe-lial interface called a periodontal pocket.Locally, bacteria and their products (eg,lipopolysaccharide entotoxin) penetratehost periodontal tissues and stimulatehost expression of inflammatory medi-ators like arachidonic acid metabolites(prostaglandin E2) and cytokines (inter-leukin-1).4 These mediators in turn trig-ger local inflammatory and destructivechanges in the tissues.

Longitudinal population studies indi-cate that these destructive changes (dis-ease progression) are not continuousover time but appear restricted to “ran-dom bursts” of activity confined to shortintervals (6 months or less).5 Risk fac-tors associated with progressive peri-odontitis include smoking, diabetes,obesity, poor plaque control, and certaingenetic polymorphisms.6-10 In addition,residual or persistent deep probingdepths are associated with periodontitisprogression.11 Paulander and coworkersrecently demonstrated that periodontitissubjects with moderate (4-5 mm) anddeep (> 6 mm) probing depths were 2 to3 times more likely to exhibit alveolarbone loss over 10 years.12 Similarly fortooth loss, the odds ratio for moderatepockets was 2.9 (95% CI, 1.9-4.2), andthe odds for deep pockets was 4.2 (95%CI, 2.4-7.3). These data imply pocketdepth reduction (or resolution) is a clin-ically important treatment goal toensure stability and maintenance inpatients.

ComplementaryMedical-MechanicalTreatment Model withAdjunctiveAntimicrobials

Strategies for treating periodontitisprincipally focus on addressing the etio-logic bacteria or biofilm.13,14 According tothe mechanical model, the bacterial bio-film is disrupted and removed via scalingand root planing (SRP) procedures. Thesedebridement procedures can be accom-plished nonsurgically or surgically, andboth approaches result in pocket depth(PD) reductions in patients.15,16 In addi-tion, a number of adjunctive chemothera-peutic approaches have been developed,tested and approved for use in patientswith chronic periodontitis (Table 1). These“locally delivered antimicrobials” followa complementary medical-mechanicaltreatment model since they are used incombination with SRP for enhanced effi-cacy. These formulations typically cou-

Abstract

Periodontitis is a common oral infection and inflammatory condition.Following treatment, residual or persistent periodontal inflammation isassociated with disease progression and tooth loss. Cumulative evi-dence from clinical trials and meta-analyses support a complementarymedical-mechanical model that combines locally delivered antimicrobialswith scaling and root planing for the treatment of chronic periodontitis.Accordingly, greater pocket depth reductions and/or attachment levelgains occur in patients treated with adjunctive locally administeredantimicrobials (eg, tetracycline, chlorhexidine, doxycycline, and minocy-cline). These responses are clinically relevant because they are accom-panied by a higher probability of patient maintenance or pocket resolu-tion. Recent trials also indicate that locally administered antimicrobialsmay enhance the effects of periodontal surgical therapy and may reducethe signs of peri-implantitis. The consistency of these findings supportsthe use of locally administered antimicrobials for managing dentalpatients with chronic periodontitis.

Keywords: periodontitis, antibiotics, antimicrobials, local delivery, peri-implantitis, scaling and root planing

Locally Delivered Antimicrobials:Clinical Evidence and RelevanceDavid W. Paquette, DMD, MPH, DMSc; Maria Emanuel Ryan, DDS, PhD;Rebecca S. Wilder, RDH, BS, MS


ple an antimicrobial or antibiotic with adrug polymer that extends drug releasewithin the periodontal pocket (controlled-release delivery).17

A recent systematic review and meta-analysis conducted by Hanes andcoworkers demonstrated that adjunctivelocally administered antimicrobialsimproved PD over SRP alone in chronicperiodontitis patients.18 This group ofinvestigators searched electronic data-bases and relevant dental journals andidentified 32 clinical studies fitting selec-tion criteria. The studies (28 randomizedcontrolled clinical trials, 2 cohort, and 2case-control studies) represented a vari-ety of locally administered antimicro-bials (eg, minocycline, doxycycline,tetracycline, metronidazole, and chlor-hexidine formulations). The resultingmeta-analysis indicated an overall sig-nificant reduction in PD with adjunctivelocal antimicrobials versus SRP alone.These findings strongly support the useof locally administered antimicrobials incombination with SRP in patients withchronic periodontitis, especially those atrisk for disease progression.

The first local delivery systemapproved for use by the US Food andDrug Administration (FDA) was calledActisite® (ALZA Corporation, Palo Alto,Calif, USA) and was developed by Dr.Max Goodson in 1983.19 This productconsisted of a nonresorbable polymerfiber of ethyl vinyl acetate containingtetracycline hydrochloride (25% or 12.7mg). Each fiber (23 cm) was placed sub-gingivally similar to retraction cord.Since that time, clinicians have been

introduced to second generation locallydelivered antimicrobials that are easierto utilize and produce greater clinicallysignificant results. Following is a dis-cussion about the 3 products currentlyavailable in the United States.

ChlorhexidineGluconate Chip

The PerioChip® (Dexcel Technolo-gies Limited, Jerusalem, Israel) is abiodegradable gelatin-based polymersystem containing the active antimicro-bial, chlorhexidine gluconate (2.5 mg).Each chlorhexidine (CHX)-gelatinwafer or chip is placed subgingivallywith cotton pliers. While pharmacoki-netic studies indicate that chlorhexidineis released from the system for 7-10days in periodontal pockets, microbialstudies have shown suppression of thepocket flora for up to 11 weeks follow-ing CHX chip treatment.20,21 In the phase3 clinical trials, CHX chip treatmentplus SRP significantly reduced PD andmaintained CAL at 9 months comparedwith SRP controls.22 Importantly, SRPwas limited in these trials to one hour ofultrasonic scaling. In addition, retreat-ment with CHX chip occurred at 3 and6 months at sites with residual pockets(> 5 mm). Nevertheless, after 9 monthsof adjunctive CHX chip treatment, nosites exhibited bone loss, and 25% ofthe sites exhibited bone gain as meas-ured with subtraction radiography.23 Incontrast, 15% of periodontal sites treatedwith SRP alone exhibited bone loss.

Chlorhexidine gluconate chip has a doc-umented safety profile, and unlikechlorhexidine mouthrinse, does notcause any visible staining of teeth.

DoxycyclineBioresorbable Gel

Atridox® (Atrix Laboratories, FortCollins, Colo, USA) is a 10% formula-tion of doxycycline (50 mg) in a biore-sorbable gel system (poly DL-lactide andN-methyl-2-pyrrolidone mixture). Thesystem is supplied as 2 pre-filled syringesthat are mixed chair-side and applied sub-gingivally to the base periodontal pock-ets using a syringe. The “flowable” poly-mer gel fills and conforms to pocketmorphology, then solidifies to a wax-likeconsistency upon contact with gingivalcrevicular fluid. Doxycycline is releasedat effective concentrations over 7 days,and significant reductions (60%) inanaerobic pathogens are sustained for upto 6 months posttreatment.24,25 In subjectswith chronic periodontitis, the applica-tion of doxycycline gel (at baseline and 4months later) reduced PD (1.3 mm) andimproved CAL (0.8 mm) comparable toSRP alone at 9 months following treat-ment.26While current and former smokerswithin the trials did not respond as well toSRP alone, smoking status did not dimin-ish the clinical improvements observedwith doxycycline gel.27 While these stud-ies demonstrated equivalency of doxy-cycline gel (monotherapy) with SRP andsupported regulatory approval, this sys-tem like other locally delivered antimi-

Locally Pivotal NumberAdministered Active Trial of ExperimentalAntimicrobial Agent Polymer Reference Subjects Treatment Controls Results

Periochip® Chlorhexidine Cross-linked 25 447 Periochip® plus Placebo chip Periochip® plus SRP significantlygluconnate hydrolyzed SRP (adjunct) plus SRP reduced PD and increased CAL at(2.5 mg) gelatin SRP alone 9 months compared to SRP alone.

Atridox® Doxycycline poly DL- 29 411 Atridox® alone Placebo gel, Treatment with Atridox® alone(10% or lactide (monotherapy) SRP alone, produced improvements in PD and50 mg) no treatment CAL at 9 months that were equiv-

lent to SRP alone.

Arestin® Minocycline Polyglycolide- 33 748 Arestin® plus Placebo Subjects treated with Arestin® plus(1 mg) co-dl-lactide SRP (adjunct) microspheres SRP exhibited significantly greater

plus SRP, PD reductions at 1, 3, 6, and 9SRP alone months versus SRP alone.

Table 1. Summary of FDA-approved locally administered antimicrobials andclinical evidence from pivotal trials.

crobials is conventionally used as an adjunct to SRP inclinical practice.

One phase 4 or postmarketing trial investigated theuse of doxycycline gel as an adjunct to SRP and demon-strated incremental benefits when the system was usedin combination with SRP.28 Accordingly, one arm of theadjunctive use trial involved initiating treatment withultrasonic scaling plus doxycycline gel at baseline, andthen isolated SRP at 3 months for those sites with resid-ual pocketing (PD > 5 mm). The second arm of the studyinvolved SRP alone at baseline, and then isolated ultra-sonic scaling and doxycycline gel at those sites withresidual pocketing. While both treatment strategies wereequally effective at improving probing depths and clin-ical attachment levels over 6 months, responses weregreater on average for the adjunctive doxycycline geltreatment at 3 months compared to SRP alone.

Minocycline MicrospheresArestin® (OraPharma, Inc.,

Warminster, Pa, USA) is anapproved local delivery systemfeaturing 1mg of minocyclinehydrochloride microencapsu-lated in resorbable polymermicrospheres (polyglycolide-co-dl-lactide). The delivery sys-tem (cartridge and syringe) isdesigned for quick and easyadministration of one unit doseof Arestin subgingivally inperiodontal pockets measuring> 5 mm with bleeding on probing (BOP) (Figure 1).With this system, minocycline hydrochloride is main-tained within pockets for 21 days at concentrations effec-tive against periodontal pathogens. The agent may alsoblock collagenases that are implicated in host tissuebreakdown.29

The pivotal clinical trials of minocycline microspheresinvolved approximately 750 subjects with generalizedmoderate to advanced chronic periodontitis recruited at 18centers.30 Periodontitis subjects meeting inclusion criteriaat baseline were randomized to 1 of 3 treatments: 1) scal-ing and root planing (SRP) alone (positive control); 2)SRP plus polymer vehicle (placebo control); or 3) SRPplus minocycline microspheres. Full mouth probingexams were performed at baseline (prior to treatment) andat 1, 3, 6, and 9 months. Figure 2 graphs mean probingdepth reductions observed in the 9-month trial for all sub-jects (intent-to-treat population) in the primary analysis.Analyses of covariance adjusting for centers indicatedsignificant-inter-group differences in probing depth reduc-tions at all time points (p < 0.001). In particular, subjectstreated with adjunctive minocycline microspheres exhib-ited significantly greater probing depth reductions as com-pared to control subjects treated with SRP alone. Whensmokers (Figure 3) or those with advanced periodontitis(mean baseline PD > 6 mm) (Figure 4), were consideredin secondary analyses, again ANCOVA indicated signif-icant probing depth reductions with adjunctive minocy-

Figure 2. Mean probing-depth reductions over ninemonths for periodontitis subjects treated with adjunctiveminocycline microspheres, adjunctive vehicle, or SRPalone. Adapted from Williams et al.30

Figure 1. Syringehandle and pre-measured car-tridges for dispens-ing minocyclinemicrospheres.

Figure 3. Mean probing-depth reductions over ninemonths for periodontitis subjects who smoke and weretreated with minocycline, adjunctive vehicle, or SRPalone. Adapted from Paquette et al.31

Figure 4. Mean probing-depth reductions over ninemonths for advanced periodontitis subjects (mean base-line probing depth > 6 mm) treated with minocycline,adjunctive vehicle, or SRP alone. Adapted from Williamset al.30



cline microspheres over control treat-ments.31 Indeed, inter-group differencesin PD reduction were greater amongadvanced periodontitis subjects versusthe overall population.

A priori, a shift in subject mean prob-ing depth < 5 mm with treatment wasconsidered a clinically relevant and“maintainable” response. When regres-sion analyses were performed compar-ing response odds with adjunctiveminocycline microspheres treatmentversus SRP alone, the odds ratios forsubjects who smoked or who hadadvanced periodontitis were 2.06 (95%CI 1.10, 3.85) and 2.86 (95% CI 1.45,5.66), respectively.32 These data indicatethat patients with advanced periodonti-tis or smokers are 2 to 3 times morelikely to respond, and that this increasein odds is clinically relevant. Site analy-ses on pocket resolution (posttreatmentPD < 5 mm) were also designated asmeaningful. Again, a significantly andconsistently higher percent of pocketswere “resolved” with adjunctiveminocycline microspheres versus SRPalone for all subjects and smokers,respectively (Table 2).33

A large, phase 4 (postmarketing) trialinvolving 2805 patients and 895 dentists

was conducted to evaluate the use ofminocycline microspheres in privatepractices throughout the United States.34

Accordingly, 1095 patients received 2applications of minocycline micros-pheres (at baseline and 3 months) perprotocol, and 1710 patients receivedonly one minocycline microsphereapplication (at baseline). Mean 6-monthpocket depth reductions were 1.82 and1.94 mm for the patients receiving oneand 2 minocycline microspheres treat-ments, respectively. Similar results wereobtained in smokers, diabetic patients,and cardiovascular disease patients.After one minocycline microspherestreatment, 62% of sites had decreasedto less than 5 mm, and after 2 treatmentsthe corresponding proportion increasedto 67%. This large private practice studydemonstrated that minocycline micros-pheres plus SRP is effective in reducingpocket depth and that efficacy increasedwith retreatment (dose-response).

One recently published trial indicatesthat the effects of flap surgery may beenhanced with adjunctive minocyclinemicrospheres treatment. Hellström andcoworkers recruited 60 periodontitispatients and randomized them to eitherflap surgery plus minocycline micros-

pheres therapy (baseline and weeks 2,3, and 5) or surgery alone.35 At week 25,the mean PD reduction from baselinewas 2.51 mm in the surgery plusminocycline microspheres (test) groupversus 2.18 mm in the control group.Smokers in the test group had a signifi-cantly greater probing depth reduction(2.30 mm) as compared to smokers inthe control group (2.05 mm). In addi-tion, the number of sites with probingdepth reductions of 2 mm or more wassignificantly higher in the test groupthan in the control group. Hence,minocycline microspheres may beadjuncts to both nonsurgical and surgi-cal therapies for patients with moderateto severe, chronic periodontitis.

These efficacy findings for minocy-cline microspheres have been extendedto peri-implantitis, an inflammatoryprocess around one or more osseointe-grated implants in function, resulting in aloss of supporting bone and associatedwith a similar pathogenic flora. Renvertand coworkers conducted a clinical trial inwhich 32 subjects with peri-implantitis(one implant with PD > 4 mm, bleedingand/or exudate on probing and the pres-ence of putative pathogens) randomlyreceived debridement plus minocycline

Baseline PD

TreatmentAll Subjects

Month 1

Month 3

Month 9

Treatment Smokers

Month 1

Month 3

Month 9

5mm

Mino SRPMicro Alone

76 69p<0.0001

78 71p<0.0001

75 66p<0.0001

Mino SRPMicro Alone

73 66p<0.0001

74 66p<0.001

70 61p<0.0001

6mm

Mino SRPMicro Alone

47 39p<0.001

52 48p=0.01

54 49p=0.0005

Mino SRPMicro Alone

40 34p=0.003

44 41p=0.17

45 39p=0.006

7mm

Mino SRPMicro Alone

22 20p=0.31

28 23p=0.01

34 27p=0.001

Mino SRPMicro Alone

17 15p=0.53

22 15p=0.04

27 20p=0.04

>8mm

Mino SRPMicro Alone

10 8p=0.24

19 14p=0.02

22 16p=0.01

Mino SRPMicro Alone

6 3p=0.09

16 5p=0.003

20 12p=0.04

Table 2. Percentage of periodontal pockets resolving with adjunctiveminocycline microspheres versus SRP. Adapted from Paquette et al.33


microspheres or debridement pluschlorhexidine gel (0.2%) at baseline, 1month, and 3 months.36 While both treat-ments reduced putative pathogens,adjunctive minocycline microsphere treat-ment resulted in significant improvementsin PD compared to chlorhexidine gel at 1month, 3 months, and 6 months. Signifi-cant reductions in bleeding on probingwere also noted for up to 12 months. Thisinvestigative group published the resultsfrom a second trial with 30 peri-implanti-tis subjects. Again, adjunctive minocy-cline microspheres improved PD andbleeding scores, whereas the adjunctiveuse of chlorhexidine gel had limitedeffects on bleeding scores.37 Anotherinvestigative team, Salvi and coworkers,also noted consistent efficacy withminocycline microspheres for treatingperi-implantitis.38 Here, the investigatorsapplied minocycline microspheres toimplant sites exhibiting bone loss and PD> 5 mm following a 3-week debridementand hygiene interval. While 6 of 31implants were either rescued or exitedfrom the trial because of persistent peri-implantitis, all other implants (80.6%)showed significant reduction in both PDand BOP over 12 months with minocy-cline microspheres therapy. The investi-gators also examined peri-implantmicroflora using DNA-DNA checker-board hybridization techniques andobserved significant reductions in A.actinomycetemcomitans at 12 months andreductions in “red complex” bacteria (T.forsythia, P. gingivalis, and T. denticola)for 6 months.39 Binary regression analysisshowed that the clinical parameters andsmoking history could not discriminatebetween successfully treated and res-cued/exited implants at any observationtime point. In addition, failures in treat-ment could not be associated with thepresence of specific pathogens or by thetotal bacterial load at baseline. Collec-tively, these new data indicate improve-ments in the clinical signs of peri-implan-titis over 12 months with adjunctivelocally administered minocycline.

Goodson and coworkers conducted aclinical trial utilizing 124 subjects with

moderate to advanced chronic peri-odontitis. Subjects were randomlyassigned to either SRP alone or minocy-cline microspheres and SRP. All patientsreceived full-mouth SRP at baseline, fol-lowed by treatment with minocyclinemicrospheres if assigned to the SRP andminocycline microspheres group. Theexaminer was blinded to the patient’streatment. Clinical assessments weremade and plaque samples were collectedat baseline and at Day 30. The resultsdemonstrated that adjunctive minocy-cline microspheres significantly reducedred-complex periodontal pathogens ascompared to SRP alone by one month.40

Another investigation conducted byOringer et al41 investigated the effect ofminocycline microspheres on gingivalcrevicular fluid (GCF) levels pyridino-line cross-linked carboxy-terminaltelopeptide of type I collagen (ICTP)and interleukin 1-beta (IL-1). ICTP is abone-specific degradation product andIL-1 is a potent bone-resorptive cyto-kine. Forty eight periodontitis patientswere randomized to receive SRP fol-lowed by minocycline microspheres orvehicle. Eight healthy individuals servedas a control group. Results found apotent short term reduction of ICTP andIL-1 in the SRP plus minocyclinemicrospheres group.

Summary andConclusions

Residual or persistent periodontalinflammation is associated with insta-bility of dental tissues (periodontal dis-ease progression and tooth loss). Cumu-lative data from clinical trials andmeta-analyses support a complementarymedical-mechanical model using locallydelivered antimicrobials for treatingchronic periodontitis. Overall, the clini-cal evidence accrued to date consistentlyshows that when locally administeredantimicrobials are used adjunctively, sig-nificantly greater PD reductions and/orattachment level gains occur in patients.These responses are clinically relevant

because they are accompanied by agreater likelihood for patient mainte-nance or pocket resolution. Recent trialsalso indicate that locally administeredantimicrobials may enhance the effectsof periodontal surgical therapy and mayreduce the signs of peri-implantitis. Theconsistency of these findings supportsthe use of locally administered antimi-crobials for managing dental patientswith chronic periodontitis.

Clinical Implications

• Recent clinical trials indicate thatlocally administered antimicrobialsmay enhance the effects of periodon-tal surgical therapy and may reducethe signs of peri-implantitis.

• Patients with periodontitis exhibitingmoderate (4-5mm) and deep (> 6mm) probing depths were 2 to 3 timesmore likely to exhibit alveolar boneloss over 10 years.

• A systematic review and meta-analy-sis demonstrated that adjunctivelocally administered antimicrobialsimproved PD over SRP alone inchronic periodontitis patients.

• Patients with advanced periodontitisor smokers are 2 to 3 times more likelyto respond to SRP + minocyclinemicrospheres than to SRP alone.

• Use of minocycline microspheres hasbeen shown to be advantageous whenused as an adjunctive therapy to bothnonsurgical and surgical therapies inpatients with moderate to severe,chronic periodontitis.

• Adjunctive use of minocyclinemicrospheres has shown a reductionin red-complex periodontal pathogensas compared to SRP alone.

Disclosure

Dr. Paquette has served as a scien-tific consultant and investigator forOraPharma, Inc. Dr. Ryan and Ms.Wilder are scientific consultants forOrapharma, Inc.

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odontal disease in adults 30 years of age and older in theUnited States, 1988-1994. J Periodontol 1999;70:13-29.

2. Flemmig TF. Periodontitis. Ann Periodontol 1999;4:32-38.

3. Socransky SS, Haffajee AD. Periodontal microbial ecol-ogy. Periodontol 2000 2005;38:135-187.

4. Offenbacher S. Periodontal diseases: pathogenesis. AnnPeriodontol 1996;1:821-878.

5. Socransky SS, Haffajee AD, Goodson JM, Lindhe J. Newconcepts of destructive periodontal disease. J Clin Peri-


odontol 1984; 11:21-32.6. American Academy of Periodontology Research, Science

and Therapy Committee. Tobacco use and the periodon-tal patient. J Periodontol 1999;70: 1419-1427.

7. Grossi SG, Genco RJ. Periodontal disease and diabetesmellitus: a two-way relationship. Ann Periodontol1998;3:51-61.

8. Saito T, Shimazaki Y, Sakamoto M. Obesity and peri-odontitis. N Eng J Med. 1998;482-483.

9. Ramfjord SP, Morrison EC, Burgett FG, Nissle RR, ShickRA, Zann GJ, Knowles JW. Oral hygiene and maintenanceof periodontal support. J Periodontol 1982;53:26-30.

10. Kornman KS, Crane A, Wang HY, di Giovine FS, NewmanMG, Pirk FW, Wilson TG Jr et al. The interleukin-1 geno-type as a severity factor in adult periodontal disease. JClin Periodontol 1997;24:72-77.

11. Halazonetis TD, Haffajee AD, Socransky SS. Relationshipof clinical parameters to attachment loss in subsets of sub-jects with destructive periodontal diseases. J Clin Peri-odontol 1989;16:563-568.

12. Paulander J, Axelsson P, Lindhe J, Wennstrom J. Intra-oralpattern of tooth and periodontal bone loss between theage of 50 and 60 years. A longitudinal prospective study.Acta Odontol Scand 2004;62:214-222.

13. American Academy of Periodontology. Parameter onchronic periodontitis with slight to moderate loss of peri-odontal support. J Periodontol 2000;71:853-855.

14. American Academy of Periodontology. Parameter onchronic periodontitis with advanced loss of periodontalsupport. J Periodontol 2000;71:856-858.

15. Cobb CM. Non-surgical pocket therapy: Mechanical. AnnPeriodontol 1996;1:450-490.

16. Palcanis KG. Surgical pocket therapy. Ann Periodontol1996;1:589-606.

17. Drisko CH. Nonsurgical pocket therapy: Pharmacothera-peutics. Ann Periodontol 1996;1:491-566.

18. Hanes PJ, Purvis JP, Gunsolley JC. Local anti-infectivetherapy: pharmacological agents. A systematic review. AnnPeriodontol 2003;8:79-98.

19. Goodson JM, Holborow D, Dunn RL, Hogan P, Dunham S.Monolithic tetracycline-containing fibers for controlled deliv-ery to periodontal pockets. J Periodontol 1983; 54:575-579.

20. Soskolne WA, Chajek T, Flashner M, Landau I, StabholtzA, Kolatch B, Lerner EI. An in vivo study of the chlorhexi-dine release profile of the PerioChip in the gingival crevic-ular fluid, plasma and urine. J Clin Periodontol1998;25:1017-1021.

21. Stabholz A, Sela MN, Friedman M, Golomb G, SoskolneA. Clinical and microbiological effects of sustained releasechlorhexidine in periodontal pockets. J Clin Periodontol1986;13:783-788.

22. Jeffcoat MK, Bray KS, Ciancio SG, Dentino AR, Fine DH,Gordon JM et al. Adjunctive use of a subgingival con-trolled-release chlorhexidine chip reduces probing depthand improves attachment level compared with scaling androot planing alone. J Periodontol 1998;69:989-997.

23. Jeffcoat MK, Palcanis KG, Weatherford TW, Reese M,Geurs NC, Flashner M. Use of a biodegradable chlorhex-idine chip in the treatment of adult periodontitis: clinicaland radiographic findings. J Periodontol 2000;71:256-262.

24. Stoller NH, Johnson LR, Trapnell S, Harrold CQ, Garrett S.The pharmacokinetic profile of a biodegradable controlled-release delivery system containing doxycycline comparedto systemically delivered doxycycline in gingival crevicularfluid, saliva, and serum. J Periodontol 1998;69:1085-91.

25. Walker CB, Godowski KC, Borden L, Lennon J, Nango S,Stone C et al. The effects of sustained release doxycycline on

the anaerobic flora and antibiotic-resistant patterns in sub-gingival plaque and saliva. J Periodontol 2000;71:768-774.

26. Garrett S, Johnson L, Drisko CH, Adams DF, Bandt C,Beiswanger B et al. Two multi-center studies evaluatinglocally delivered doxycycline hyclate, placebo control, oralhygiene, and scaling and root planing in the treatment ofperiodontitis. J Periodontol 1999;70:490-503.

27. Ryder MI, Pons B, Adams D, Beiswanger B, Blanco V,Bogle G et al. Effects of smoking on local delivery of con-trolled-release doxycycline as compared to scaling androot planing. J Clin Periodontol 1999;26:683-691.

28. Wennstrom JL, Newman HN, MacNeill SR, Killoy WJ, Grif-fiths GS, Gillam DG et al. Utilisation of locally delivereddoxycycline in non-surgical treatment of chronic peri-odontitis. A comparative multi-centre trial of 2 treatmentapproaches. J Clin Periodontol 2001;28:753-761.

29. Oringer RJ, Al-Shammari KF, Aldredge WA, Iacono VJ,Eber RM, Wang HL, Berwald B et al. Effects of locallydelivered minocycline microspheres on markers of boneresorption. J Periodontol 2002;73:835-842.

30. Williams R, Paquette D, Offenbacher S, Adams D,Armitage G, Bray K et al, Treatment of periodontitis bylocal administration of minocycline microspheres: a con-trolled trial. J Periodontol 2001;72:1535-1544.

31. Paquette DW, Oringer R, Lessem J, Offenbacher S, GencoR, Persson GR, Williams R. Locally delivered minocyclinemicrospheres for the treatment of periodontitis in smokers.J Clin Periodontol 2003;30:787-794.

32. Paquette DW. Pocket depth reduction as an outcome measureof inflammation and soft tissue changes in Periodontitis trials.J Int Acad Periodontol 2005;7/4 (Supplement):147-156.

33. Paquette DW, Williams RC, Hanlon A, Lessem J. Clinicalrelevance of adjunctive minocycline microspheres inpatients with chronic periodontitis: secondary analysis of aphase 3 trial. J Periodontol 2004;75:531-536.

34. Lessem J, Hanlon A. A post-marketing study of 2805patients treated for periodontal disease with Arestin. J IntAcad Periodontol 2004;6:150-153.

35. Hellström MK, McClain PK, Schallhorn RG, Bellis L, Han-lon AL, Ramberg P. Local minocycline as an adjunct tosurgical therapy in moderate to severe, chronic periodon-titis. J Clin Periodontol 2008;35:525-31.

36. Renvert S, Lessem J, Dahlén G, Lindahl C, Svensson M.Topical minocycline microspheres versus topical chlorhex-idine gel as an adjunct to mechanical debridement of incip-ient peri-implant infections: a randomized clinical trial. JClin Periodontol 2006;33:362-9.

37. Renvert S, Lessem J, Dahlén G, Renvert H, Lindahl C.Mechanical and repeated antimicrobial therapy using a localdrug delivery system in the treatment of peri-implantitis: arandomized clinical trial. J Periodontol 2008;79:836-44.

38. Salvi GE, Persson GR, Heitz-Mayfield LJ, Frei M, Lang NP.Adjunctive local antibiotic therapy in the treatment of peri-implantitis II: clinical and radiographic outcomes. Clin OralImplants Res 2007;18:281-5.

39. Persson GR, Salvi GE, Heitz-Mayfield LJ, Lang NP. Antimi-crobial therapy using a local drug delivery system (Arestin)in the treatment of peri-implantitis. I: Microbiological out-comes. Clin Oral Implants Res 2006;17:386-93.

40. Goodson JM, Gunsolley JC, Grossi SG, Bland PS, Otomo-Corgel J, Doherty F, Comiskey J. Minocycline HCl micros-pheres reduce red-complex bacteria in periodontal dis-ease therapy.J Periodontol. 2007;78:1568-79.

41. Oringer RJ, Al-Shammari KF, Aldredge WA, Iacono VJ,Eber RM, Wang HL et al. Effects of locally deliveredminocycline microspheres on markers of bone resorption.J Periodontol. 2002; 73:835-842.


Introduction

Hujoel et al1 estimated a 31%decrease in the prevalence of periodon-titis between the years 1955 and 2000.Further, these authors estimate an addi-tional 8% decrease by the year 2020. Inspite of the decreased use of smokingtobacco,2 better understanding of thepathogenesis of periodontal diseases,and more refined and goal directed ther-apies, there remains evidence that den-tistry is not consistently achieving atimely diagnosis and appropriate andtimely treatment of existing periodonti-tis.3,4 Although the evidence is limited,there is a strong suggestion that use of aperiodontal probe for diagnosis andrecording of periodontal status in treat-ment records in general dental practiceshas yet to achieve the level of a routineand consistent habit.5-9 Indeed, McFallet al8 determined that except for radi-ographs, most private practice patientrecords were so deficient in diagnosticinformation that periodontal status couldnot be established. It should be self-evi-dent that treatment requires a definitivediagnosis, ie, a disease cannot be ade-quately treated unless first diagnosed.In this regard, it is interesting to notethat at least one study has reported a dis-connect between dentists’ perception oftreatment rendered and actual treatmentas recorded in patient records.10 As anexample, prophylactic procedures out-number periodontal procedures by aratio of 20:111,12 and yet the prevalence ofchronic periodontitis (slight, moderate,and severe) is estimated to range from alow of 7% (aged > 18 years)13 up to 35%(aged > 30-90 years)14 of the US adultpopulation.

Cobb et al.3 compared the pattern ofreferral of periodontitis patients in 1980vs 2000 using patient record data from3 geographically-diverse private peri-odontal practices. Results showed thefollowing trends occurring over the 20-year time span: decreased use oftobacco; increase in the percentage ofcases exhibiting advanced chronic peri-

odontitis with a concomitant decreasein the percentage of mild-moderate dis-ease cases; increase in the average num-ber of missing teeth per patient; andincrease in the average number of teethscheduled for extraction per patient. Asimilar study by Docktor et al4 based onpatient records from 3 private peri-odontal practices located within a majormetropolitan area reported the follow-ing: 74% of referred cases were con-sidered advanced periodontitis, ofwhich 30% were treatment planned forextraction of 2 or more teeth; periodon-tal treatment provided by the general

dental office did not vary because ofdisease severity; and the average num-ber of periodontal maintenance vis-its/patient/year in the general dentaloffice was less than the standard of careaccording to severity of disease, eg,68% of advanced periodontitis casesreported between 0 and 2 periodontalmaintenance visits per year rather thanthe recommended every 3 months.Viewed in aggregate, the trendsreported by Cobb et al3 and Docktor etal4 support the assertion that timelydiagnosis and appropriate and timelytreatment of chronic periodontitis have

AbstractA sequence of interrelated steps is inherent to effective periodontaltreatment: early and accurate diagnosis, comprehensive treatment, andcontinued periodontal maintenance and monitoring. A primary goal ofperiodontal therapy is to reduce the burden of pathogenic bacteria andthereby reduce the potential for progressive inflammation and recur-rence of disease. Emerging evidence of possible perio-systemic linksfurther reinforces the need for good periodontal health. In the privatepractice setting, the treatment of patients with periodontal disease is bestaccomplished within the structure of a uniform and consistent Peri-odontal Treatment Protocol (PTP). Such a protocol would reinforceaccurate and timely diagnosis, treatment needs based on a specificdiagnosis, and continual assessment and monitoring of outcomes. Thisis best achieved if everyone in the practice setting has a general under-standing of the etiology of periodontal diseases, the benefits of treat-ment, and potential consequences of nontreatment. Communicationskills and patient education are vital components of effective therapysince slight and even moderate stages of the disease often have fewnoticeable symptoms to the patient. Accurate documentation and report-ing of procedures for dental insurance reimbursement, coupled withscheduling considerations, assist general practice settings in effectivelymanaging the increasing volume of patients that can benefit from earlydiagnosis and treatment of periodontal diseases. This article presentsthe essential elements of a PTP including diagnosis, treatment planning,implementation of therapy, assessment and monitoring of therapy, insur-ance coding, introduction of the patient to periodontal therapy, andenhanced verbal skills. In addition, considerations for implementation ofadjunctive local delivery antimicrobials is presented.

Key Words: periodontal diseases, periodontal diagnosis, treatmentprotocol, periodontal maintenance, periodontal assessment, patienteducation

Periodontal Treatment Protocol (PTP) for the General Dental PracticeLarry A. Sweeting, DDS; Karen Davis, RDH, BSDH; Charles M. Cobb, DDS, PhD


not significantly improved over time. Amajor reason for the reported scarcity oftimely diagnosis and appropriate treat-ment may be the lack of a well-estab-lished office protocol for the diagnosis,treatment, maintenance, and monitor-ing of periodontal disease, and involve-ment of the patient through education.Obviously, this requires dedication ofenergy, resources, effective communi-cation skills, and a change in practicephilosophy.

The PeriodontalTreatment Protocol(PTP)

Diagnosis

Regardless of recent advances in ourunderstanding of the etiology and patho-genesis of the periodontal diseases, theassessment of traditional clinical param-eters remain the foundation for peri-odontal diagnosis.15 Generally, such clin-ical parameters include probing depth(PD), bleeding on probing (BOP), clin-ical attachment level (CAL), degree offurcation involvement, extent of gingi-val recession, tooth mobility, and plaquescore. Clinicians typically utilize theresults from the periodontal exam, radi-ographs, and the patient’s medical anddental histories to establish a diagnosisand evolve a goal/diagnosis-directedtreatment plan. It has been clearlydemonstrated that different interpreta-tions of the same diagnostic informationcan have a dramatic impact on treatmentdecisions.16 For this reason, a standard-ized approach to periodontal assess-ments and a working protocol as to treat-ment parameters would fill a logicalneed in the average general practice set-ting. However, due to extensive over-laps in most classification systems, anystandardized approach is subject to vari-ations in both clinical assessments (eg,variations in probing depth among cli-nicians) as well as the interpretationthereof.

All effective treatment protocolsbegin with a thorough and timely diag-nosis. Six-point probing to measure PDand BOP is the standard of care. Basedon the needs of the patient, current radi-ographs should be evaluated to deter-mine the location and percentage of bone

loss. The presence, location, and extentof furcation invasions should be noted, aswell as the location of the gingival mar-gin or CAL. Also, the patient’s age is animportant factor, especially in cases ofrapidly progressing disease and deter-mining overall long-term prognosis.

A modified version of the AmericanAcademy of Periodontology (AAP)proposed guidelines for a comprehen-sive periodontal examination is pre-sented in Table 1.17 However, withrespect to a functional PTP for the gen-

eral dental practice, only the followingprincipal diagnostic criteria can beaddressed: age, PD, CAL, BOP, toothmobility, furcation involvement, andpercentage of radiographic bone loss. Itmust be emphasized that these criteriarepresent the minimal parameters fordetermining a periodontal diagnosis.There are many other important risk andmodifying factors that will impactdevelopment and progression of diseaseand all such factors must be taken intoconsideration when establishing a defin-

Assessment of medical history

Assessment of dental history

Assessment of periodontal risk factors1. Age2. Gender3. Medications4. Presence of plaque and calculus (quantity and distribution)5. Smoking6. Race/Ethnicity7. Systemic disease (eg, diabetes)8. Oral hygiene9. Socioeconomic status and level of education

Assessment of extraoral and intraoral structures and tissues

Assessment of teeth1. Mobility2. Caries3. Furcation involvement4. Position in dental arch and within alveolus5. Occlusal relationships6. Evidence of trauma from occlusion

Assessment of periodontal soft tissues including peri-implant tissues1. Color2. Contour3. Consistency (fibrotic or edematous)4. Presence of purulence (suppuration)5. Amount of keratinized and attached tissue gingiva6. Probing depths7. Bleeding on probing8. Clinical attachment levels9. Presence and severity of gingival recession

Radiographic evaluation of alveolar bone loss, bone density, furcations,root shape, and proximity, etc.

Table 1. Modified Version of the AmericanAcademy of Periodontology Suggested Guidelinesfor a Comprehensive Periodontal Examination.18


itive diagnosis and a diagnosis-driventreatment plan.18

Age is of relative value in thatadvanced amounts of periodontaldestruction at an earlier age tend to indi-cate a more aggressive form of peri-odontitis. In contrast, chronic periodon-titis may slowly progress towardsseverity over several years or decades.Young age combined with moderate tosevere bone loss presents a tenuouslong-term prognosis and requires moreaggressive therapy compared to theolder patient presenting with a chronicform of periodontitis.19

Probing depth (PD) is defined asthe distance from the gingival marginto the base of the gingival crevice.20 Theperiodontal pocket, represented by aprobing depth > 3 mm, is the principlehabitat for gram-negative, anaerobicpathogenic bacteria.20 Deeper pocketstend to represent more extensivedestruction of the underlying periodon-tium and, therefore, a potentially greaterpathenogenic burden.

Clinical Attachment Level (CAL) isdefined as the distance from the CEJ tothe base of the probable crevice/pocket.In cases of gingival recession, the amountof recession is added to the PD to yieldthe total amount of CAL. Although moredifficult to obtain, it is a better measure ofthe total extent of damage to the under-lying periodontium.20-22

Mobility is best measured by theblunt end of 2 instruments alternatingpressure in a facial-lingual direction andan apical direction to assess abnormalmovement of the tooth. Simplyassessed: Grade I mobility is slightlymore than normal; Grade II is moder-ately more than normal; Grade III issevere mobility facial-lingually plus api-cal displacement.23 Mobility patterns aresuggestive of possible occlusal trauma,severe inflammation, and/or loss of sup-porting alveolar bone.

Furcations represent bone lossbetween the roots of multi-rooted teeth.A deeply invasive furcation lesion is theequivalent of a poor long-term progno-sis for the involved tooth. Simply put, aGrade 1 furcation involvement is incip-ient bone loss only; a Grade 2 is partialloss of bone producing a cul-de-sac; aGrade 3 is total bone loss with through-and-through opening of the furcation;and a Grade 4 is similar to a Grade 3, butwith gingival recession that visuallyexposes the furcation opening.24

Radiographic Evidence of BoneLoss is best determined with adequateand current radiographs,17 most typicallya full-mouth periapical survey, includingvertical bite-wings, or a panographicradiograph supplemented with verticalbite-wings and selected periapical films.By definition, true periodontitis does notbegin until bone loss occurs.25 Radi-ographic evaluation of the distributionand severity of bone loss, bone density,root anatomy, and approximation to otherteeth provides specific information thatwill help in determining a proper diag-nosis, treatment plan, and prognosis.

Bleeding on Probing (BOP) is asimple assessment of the inflammatorystatus of the gingiva.15,26 In patients withdeeper pockets and/or loss of clinicalattachment, the chances of disease pro-gression are greater as the percentage ofbleeding sites increase.27 Conversely,lack of BOP is highly correlated withstability and a lack of inflammation.28

This latter statement, however, does notapply to smokers as they tend to bleedless when compared to nonsmokers withequal amounts of disease.29

In addition to the usual clinicalparameters, the clinician is well advisedto consider other risk factors and theirpotential impact on the development andprogression of plaque-induced peri-odontal diseases.18 Risk factors that aresometimes overlooked in the diagnosis,treatment plan, and prognosis equationinclude, among others: diabetes, smok-ing, osteoporosis, compromised immunesystem, drug-induced gingival condi-tions, hormonal changes, and genetics.Patients at risk for periodontal diseaseare often allowed to “slip between thecracks” during a routine visit becausethey may be in the early stages of thedisease. Risk factors increase a patient’schance of developing periodontitis. Thepresence of one or more of these riskfactors may also indicate a benefit fromspecialty referral in some patients.

Case Types and PeriodontalDiagnosis

As part of a PTP it is necessary toestablish diagnostic guidelines that willprovide a framework for organizing thetreatment needs of the patient. Guide-lines are not meant to replace clinicalknowledge or skills, nor do they imply aone-size-fits-all treatment plan for peri-

odontal disease. It is recognized thateach dental practice setting is different.Consequently, guidelines are intendedto be used in a manner that best meetsthe needs of the specific patient.

Generally speaking, plaque-inducedperiodontal diseases have historicallybeen categorized into gingivitis versusperiodontitis based upon whether attach-ment loss has occurred. The 1999 Inter-national Workshop for Classification ofPeriodontal Diseases21 reclassified theplaque-induced periodontal diseases into7 different classifications. In considera-tion of a working PTP that addressesonly the common periodontal diseases,this paper will address health, gingivitis,chronic periodontitis (formerly adultperiodontitis), and aggressive periodon-titis (formerly early-onset periodontitis).The first 7 entries in Table 2 (see backcover) constitute a set of clinical criteria(PD, BOP, percent bone loss, toothmobility, degree of furcation involve-ment, and CAL) that will facilitate dif-ferentiation of health from gingivitis andbetween the various levels of severityof chronic periodontitis. Further, Table 2can aid the clinician in differentiatingbetween chronic and aggressive peri-odontitis.

Some practice settings may prefer asystem of “Periodontal Case Types” forpurposes of diagnosis and record keep-ing. Table 3 presents the diagnostic clin-ical criteria as applied to Case Types forhealth, gingivitis, chronic periodontitis(slight, moderate, and severe), andaggressive periodontitis. These criteriaand Case Types are generally appropri-ate but should be considered as guide-lines only and not as a definitive diag-nosis. As mentioned before, there arenumerous modifying and risk factors toconsider prior to evolving a diagnosisand a diagnosis-driven treatment plan.

Treatment Planning

Development of a logical and prop-erly sequenced treatment plan is a deriv-ative of the periodontal assessment anddiagnosis. Periodontal therapy is diag-nosis-driven and, to the extent possible,should address all modifying factors andrisk factors that impact development andprogression of plaque-induced peri-odontal disease. An overview of a typi-cal periodontal treatment plan is pre-sented in Table 4.30

PD BOP Bone Mobility Furcations CAL VisualCase Type (mm) (Yes/No) Loss (%) (Grade) (Grade) (mm) Inflammation

0 (Health) 0-3 No 0 None None 0 No

I (Gingivitis) 0-4 Yes 0 None None 0 Yes (localized orgeneralized)*

II (Slight Chronic Periodontitis)† 4-5 Yes 10 I 1 1-2 Yes (localized orgeneralized)*

III (Moderate Chronic Periodontitis)† 5-6 Yes 33 I and II 1 and 2 3-4 Yes (localized orgeneralized)*

IV (Severe Chronic Periodontitis)† > 6 Yes > 33 I, II, or III 1, 2, 3, or 4 > 5 Yes (localized orgeneralized)*

V (Aggressive Periodontitis)†_ > 6 Yes > 33 I, II, or III 1, 2, 3, or 4 > 5 Yes (localized or(age is significant factor) generalized)*

* Localized disease is defined as < 30% of sites are involved; and generalized disease infers >30% of sites are involved.21

† Specialty referral may be indicated for additional treatment beyond initial therapy.†_ Specialty referral should be considered.

Table 3. Clinical Criteria Assigned to Periodontal Case Types of Health, Gingivitis, Chronic Periodontitis (slight, moderate, and severe),and Aggressive Periodontitis.

Sequence of Major Phases

1. Address acute periodontal problems and/or pain

2. Review and update medical and dental histories

3. Assessment of systemic risk factors and refer for medical consultation as needed

4. Extraoral examination

5. Oral cancer evaluation

6. Assessment of periodontal risk and modifying factors

7. Periodontal examination to include dental implants

8. Dental examination to include occlusal relationships and dental implants

9. Radiographic examination

10. Establish a definitive diagnosis

11 Generate a diagnosis-driven periodontal treatment plan and sequence of treatment

12. Determine required adjunctive restorative, prosthetic, orthodontic, and/or endodontic treatments andsequence

13. Execute Phase I therapy (aka anti-infective or nonsurgical therapy) with consideration given to adjunc-tive use of chemotherapeutic agents

14. Re-evaluation (assessment) of Phase I therapy

15. If end-points are not achieved, consider selective retreatment, need for surgical therapy, specialty refer-ral, or use of adjunctive diagnostic aides, eg, microbial, genetic, medical lab tests, etc.

16. Determine interval for periodontal maintenance and continued assessment of periodontal status

Table 4. General Overview of the Major Steps in a Typical PeriodontalTreatment Plan.3


Implementation of Therapy

There are a wide variety of treatmentoptions to be considered when con-fronted with gingivitis or chronic oraggressive periodontitis. However, thor-ough scaling and root planing (SRP) isstill considered the gold standard in peri-odontal therapy. Beyond SRP, no onetreatment modality is the answer inevery case. However, the clinician musthave specific endpoints or goals thattherapy should achieve. If such end-points are not achieved, then therapymust be re-evaluated and a decisionmade concerning retreatment or spe-cialty referral for consideration of moreadvanced therapy options. Treatmentoptions that should be consideredinclude:30

• Patient education including plaquecontrol and counseling in manage-ment of periodontal and systemicrisk factors

• Scaling and root planing

• Consideration of adjunctive chemo-therapeutic agents, eg, locally orsystemically administered antibi-otics and host response modifica-tion agents.

• Re-evaluation

• Consideration of referral to a spe-cialist is an option that must be con-sidered for both legal and ethicalreasons.31 There are a variety of rea-sons to consider referral to a peri-odontist, such as, SRP in the pres-ence of extreme amounts of dentalcalculus or SRP with complicationsof systemic disease, gingival over-growth and/or inflammatory hyper-plasia, resective surgery, regenera-tive procedures for soft and hardtissues, periodontal plastic surgery,occlusal therapy, pre-prosthetic sur-gery, dental implants, managementof perio-systemic complications,phobic patients requiring conscioussedation, etc.

Periodontal Maintenance Therapy and Continual Assessment

In general, data suggests that patientswho have undergone definitive therapyfor either localized or generalized peri-

odontitis should be managed by peri-odontal maintenance (PM), performedat an interval of 3 months for an indefi-nite period of time following active ther-apy.32 The 3-month interval is critical(and the standard of care for moderateand severe chronic periodontitis andaggressive periodontitis) as it has beenrepeatedly shown to be effective inreducing disease progression, preserv-ing teeth, and controlling the subgingi-val bacterial burden.33-35 Nonetheless, thePM schedule should be individualizedand tailored to meet the needs of eachpatient. Factors such as home care, pre-vious level of disease, tendency towardrefraction, stability indicators, etc,should be used in making this assess-ment. More fragile patients may needintervals of 2 months or less, and con-versely, patients intercepted in early dis-ease states who demonstrate consistentstability may need less frequent inter-vals of 4-6 months. Regardless of theinterval between appointments, the peri-odontal status of each patient should bere-evaluated at every maintenanceappointment. Only through close moni-toring can disease recurrence be detectedand the maintenance interval adjustedaccordingly. Continual assessment of theperiodontium during maintenanceaffords the best opportunity for assur-ing long-term stability or providinginterceptive care.34,35

Insurance Coding

The American Academy of Peri-odontology’s Parameters of Care 200036

and the American Dental Association’sCurrent Dental Terminology37 are avail-able to clinicians to guide decision-mak-ing related to providing therapeutic peri-

odontal treatment and subsequentreporting of services for insurance reim-bursement. In terms of nonsurgical peri-odontal therapy, familiarity with dentalinsurance codes provides a clear methodto document treatment and select appro-priate procedures to maximize insurancereimbursement for the patient.

Table 5 presents a modified descrip-tion of the ADA insurance codes mostcommonly used in Phase I periodontaltherapy (aka anti-infective therapy ornonsurgical therapy). The descriptionsare intended to reveal distinctive differ-ences between procedures, and guide theclinician in reimbursement procedures.

To simplify decisions made bypatients, dental insurance should bereferred to as “reimbursement,” “bene-fit,” or “assistance” by the clinician andother staff members rather than “cover-age” since the word implies complete.Most patients with dental insurance willfind it necessary to supplement what-ever insurance benefit they receivetoward lifetime periodontal care, asmany plans have contract limitations forthe percentage of reimbursement asso-ciated with various procedures and/orthe length of time those benefits apply.For example, limitations of some insur-ance plans assign benefits for PM fol-lowing SRP but only for 24 months fol-lowing active therapy. As anotherexample, exclusions found in otherinsurance plans assign benefits for SRPfor generalized periodontal disease butnot for localized infection. Manypatients are reticent to proceed withtreatment unless their insurance will“pay for it.” Consequently, it is advan-tageous for practices to have clear expla-nations about the reality of dental insur-ance. Figure 2 presents a sampleexplanation of dental insurance that can

Figure 2. Facts about dental insurance to share with patients.

Understanding Dental Insurance1. Dental insurance is a contractual agreement between the employer

and insurance company. The percentage of reimbursement variesgreatly dependent upon the premiums paid for a particular plan andlimitations of the agreement.

2. Maximum payable benefits around $1000 - $1500 commonly foundtoday with dental insurance plans are almost identical to the annualmaximum benefit of dental insurance plans 40 years ago.

3. Dental insurance is a benefit designed to help defray the costs ofquality dental care, but is not all-inclusive of what an individual mayneed or desire to obtain optimal dental health for a lifetime.



CodeNumber Treatment Procedure DescriptionD0180 Comprehensive Indicated for new or established patients showing signs or symptoms of

Periodontal Evaluation periodontal disease and for patients with risk factors such as smokingor diabetes. It includes evaluation of periodontal conditions, probing andcharting, evaluation and recording of the patient’s dental and medicalhistory and general health assessment. It may include the evaluationand recording of dental caries, missing or unerupted teeth, restorations,occlusal relationships and oral cancer evaluation.

D1110 Adult Prophylaxis Includes the removal of plaque, stain and calculus from tooth structuresand is intended to control local irritation to gingival tissues, thereby preventing disease initiation.

D4355 Full Mouth Debridement Initial removal of plaque and calculus that interfere with the ability toto Enable Comprehen- perform a comprehensive oral evaluation. This preliminary procedure is sive Evaluation and generally followed by a comprehensive periodontal evaluation forDiagnosis diagnosis and subsequent therapeutic periodontal procedures.

D4341 Scaling and Root Involves therapeutic treatment of 4 or more periodontally involved teethPlaning per quadrant through definitive removal of subgingival plaque biofilm andGeneralized per root preparation in order to halt the disease from progressing, therebyQuadrant creating an opportunity for healing. To be reported per quadrant inclusive

of updated periodontal charting and radiographs for reimbursement.

D4342 Scaling and Involves therapeutic treatment of 1 to 3 periodontally involved teeth perRoot Planing quadrant through definitive removal of subgingival plaque biofilm andLocalized per root preparation in order to halt the disease from progressing, therebyQuadrant creating an opportunity for healing. To be reported per quadrant with

identification of specific teeth being treated inclusive of updated peri-odontal charting and radiographs for reimbursement.

D4381 Localized Delivery of Subgingival insertion of antimicrobial medications of a therapeutic con-Antimicrobial Agents via centration into periodontal pockets that are released over a sufficienta Controlled Release length of time in order to suppress the pathogenic burden, and are Vehicle into Diseased intended to enhance the clinical results of scaling and root planing alone.Crevicular Tissue To be reported per tooth, identifying multiple treatment sites per tooth, if

indicated, inclusive of a narrative describing systemic considerations forreimbursement such as tobacco usage, diabetes, or heart disease.

D4999 Unspecified Periodontal In the absence of a specific ADA code for complete periodontalProcedure, by Report re-assessment following definitive periodontal therapy, this procedure

code is being utilized to determine healing response and future treat-ment recommendations.

D4910 Periodontal Maintenance Follows the completion of active therapy to treat periodontal infectionfor the lifetime of the dentition or implant replacements and includesremoval of plaque biofilm and calculus from supra and subgingival sur-faces. It may also include site specific scaling and root planing for areasof localized disease recurrence. It is intended to keep periodontal dis-eases under control; therefore a patient may move from active therapyto periodontal maintenance and back to active therapy and/or referralduring the lifetime of the dentition or implant replacements. It is not syn-onymous with prophylaxis, and is required at varying intervals to man-age periodontal diseases and modify risk factors. To be reported byboth general and periodontal practices on patients having undergoneactive therapy irrespective of where the procedure is performed. Cur-rent periodontal charting documenting the patient’s on-going periodon-tal status should be submitted for reimbursement.

Table 5. Modified Description of ADA Insurance Codes Commonly Used for Phase I Periodontal Therapy (aka anti-infective therapy or nonsurgical therapy).


be shared with patients, assisting them inmaking independent decisions abouttreatment, regardless of the insurancereimbursement schedule.

Patient Education and Introduction to Periodontal Therapy

Effective implementation of theaforementioned concepts requiresexpertise in effective patient educationand introduction of periodontal therapyso that patients are prepared to makewise health decisions. Being proficientin SRP procedures has little value to thepatient who assumes they are visitingthe dental hygienist for a “routine clean-ing.” This is particularly true if thepatient already has a developing or exist-ing periodontal infection and does notunderstand the need for therapeuticintervention. Chronic periodontal dis-eases often provide few noticeablesymptoms, especially in earlier stagesof development. Thus, the need foreffective communication, education, andlistening skills are of particular impor-tance to today’s dental patient.

The incidence of moderate andsevere generalized chronic periodonti-tis in the US appears to affect only 5%to 15% of the adult population, whereasslight disease affects approximately 35%of the adult population.13,14,38 Thus, mostnew patients and even many existingpatients will ultimately be diagnosedwith periodontal diseases. To be effec-tive at enrolling patients into active ther-apy everyone in the practice setting musthave a basic understanding of the etiol-ogy of periodontal diseases, treatmentoptions, consequences of nontreatment,and direct benefits of therapy. Patientsare more motivated to accept treatmentrecommendations when a clear diagno-sis has been established, they are giventhe opportunity to see infection in theirown mouths, their questions have beenanswered, and they understand the valueof treating periodontal infection in rela-tion to their overall health.

Many clinicians inform patients oftheir periodontal status while workingin their mouths with sharp instruments,or give a summary of findings at the endof the visit. Most patients are visuallearners. Consequently, patients need tosee the condition of their own mouth.At the beginning of every appointment,

during data collection and tissue assess-ment, the patient should be provided amirror to visualize with the clinician theevidence of periodontal disease, caries,gingival recession, tooth mobility, fur-cation involvement, etc. (Figure 1). Dur-ing periodontal probing, the patientshould hear the pocket measurements asdata is being collected and recorded. Ina similar manner, during examination ofthe radiographs, the patient should beshown evidence of permanent bone loss,and contrast that to areas without boneloss. Involving the patient in the dis-covery process visually and audibly is apowerful tool to help patients take own-ership in their own health.

This is also an opportune time for theclinician to introduce adjunctive thera-pies to the patient such as the use oflocally delivered antimicrobials andother agents. For example, the cliniciancan communicate that locally deliveredantimicrobials have been on the US mar-ket for many years and have been shownto be a safe, effective treatment option.Important information to conveyincludes the ease of application; the highpotency of the drug at levels that willkill bacteria; it does not affect the rest ofthe body; and there is no need for anadditional appointment to remove theproduct since the agent biodegrades.Educating the patient to all of their treat-ment options is vital to clear and evi-dence-based communication.

Enhanced Communication Skills

Each clinician will develop his/herown style of case presentation for peri-odontal therapy and will individualizethe message to different patients. How-ever, there is significant advantage ifthe entire office staff has continuity inkey words that are used when dis-cussing periodontal therapy withpatients. Equally important is the avoid-ance of minimizing messages such as“just a little bit of bleeding,” or “a littlebone loss,” or “just a little bit ofplaque.” It is advisable to use languagethat does not trivialize conditions thatare not yet severe. Terms such as “slight

bleeding,” “early bone loss,” or “slightplaque” accurately describe findingswithout overstating them. Periodontaldisease is a bacterial infection leading toa host immune response that is charac-terized by inflammation and degrada-tion of periodontal tissues.22 Wheninforming patients of periodontal dis-ease, using the word “infection” is morepowerful than “gum inflammation” andcan create a sense of urgency regardingtreatment. The word “hemorrhage”indicates heavy bleeding and implies acondition outside healthy parameters.When the patient’s gingival tissueshemorrhage easily upon provocation,“hemorrhage” rather than “bleedinggum tissue” should be verbalized to thepatient. The words “scaling and root

Figure 1. Dental hygienist showing patient periodontal conditions inpatient’s own mouth.


Where to use locally delivered antimicrobials:➢ Pockets > 5 mm with bleeding on probing (BOP).

• The locally delivered antimicrobial may be used atthe time of scaling and root planing (SRP) or at there-evaluation appointment 4-6 weeks following SRP.If used first at the re-evaluation appointment, the sitemust have additional SRP to remove biofilm and harddeposits that may have re-accumulated.

➢ Residual pockets of > 5 mm with BOP or any site > 6mm following initial SRP.• Determined at re-evaluation appointment.• If > 4 residual pockets in a given quadrant then con-

sider either retreatment (SRP) with locally deliveredantimicrobial or surgical intervention.

➢ Sites treatment planned for osseous grafting.• Locally delivered antimicrobial placed 3 weeks prior

to surgical procedure.➢ Periodontal abscess➢ Probing depth at the distal-facial line-angle of 2nd

molars related to 3rd molar extractions where surgicalintervention will yield a compromised result.

➢ Ailing/failing dental implants (peri-implantitis) where sur-gical intervention is not indicated or will yield a compro-mised result.

➢ Grade II furcation involvements (shallow or deep) whensurgical intervention is not planned.

Who might benefit from use of locally deliveredantimicrobials:➢ Periodontal maintenance

patients with isolatedprobing depths of > 5 mmthat exhibit BOP or anypocket > 6 mm (Figure 3).

➢ Patients wanting to avoidperiodontal surgery.

➢ High risk surgery patients.• Poorly controlled (brit-

tle) diabetic patients• Patients with a history

of recent or recurrentcoronary or cere-brovascular events.

• Patients with a compromised immune system due todisease or medications.

• Kidney dialysis patients.• Heavy smokers (>1/2 pack/day)• Patients with physical disability that impacts oral

hygiene efficiency• Mentally handicapped patients

➢ Patient’s with marginal oral hygiene that is not likely toimprove and thereby represent a poor surgical risk.

➢ Please note that locally applied antimicrobials may needto be placed more than one time to achieve the desiredresult.

How to apply locally delivered antimicrobials: ➢ For optimal effect from locally delivered antimicrobials

the following must be achieved:• Oral hygiene instructions and patient compliance

regarding the necessary oral hygiene procedures, ie,tooth brushing, use of interdental hygiene aids suchas dental floss and proxabrushes, and use of antimi-crobial oral rinses.

• Supragingival scaling and polishing.• Definitive subgingival SRP (generally under local

anesthesia).• Place locally delivered antimicrobial according to

manufacturer’s directions. For example, in the caseof minocycline microspheres, place one pre-meas-ured dose per pocket. If the tooth has 2 pockets thatneed local delivery, 2 full doses should be adminis-tered.

• The pocket should be as biofilm and deposit free aspossible prior to insertion.

• Insert the locally delivery product to the base of thepocket. In the case of minocycline microspheres, thetip should be placed as far into the pocket as possi-ble before activatingthe syringe/handle(Figures 4 and 5).

Addendum:➢ If probing depths are < 4

mm, the clinician shouldconsider a conventionaladult prophylaxis coupledwith oral hygiene recom-mendations and/or rein-forcement.• If the patient exhibits

multiple probingdepths of 4 mm a peri-odontal maintenanceinterval of 3-4 monthsshould be considereduntil it can be deter-mined if the patient’speriodontal status isstable and/or improv-ing.

Guide for Use of Locally Delivered Antimicrobials

Figure 3. Pre-treatmentclinical presentationshowing PD of 6 mm

Figure 4. Initial Inser-tion of the pre-meas-ured tip for adminis-tration of minocyclinemicrospheres

Figure 5.Tip place-ment to base ofpocket for administra-tion of minocyclinemicrospheres.


References1. Hujoel PP, Bergström J, del Aguila MA, DeRouen TA. A hid-

den periodontitis epidemic during the 20th century? Com-munity Dent Oral Epidemiol 2003;31:1-6.

2. Mendez D, Warner KE. Adult cigarette smoking preva-lence: Declining as expected (not as desired). Am J PubHealth 2004;94:251-252.

3. Cobb CM, Carrara A, El-Annan E, et al. Periodontal refer-ral patterns, 1980 versus 2000: A preliminary study. J Peri-odontol 2003:74:1470-1474.

4. Dockter KM, Williams KB, Bray KS, Cobb CM. Relation-ship between pre-referral periodontal care and peri-odontal status at time of referral. J Periodontol2006:77:1708-1716.

5. Bader JD, Rozier G, McFall WT, Jr., Sams DH, GravesRC, Slome BA, Ramsey DL. Evaluating and influenc-ing periodontal diagnostic and treatment behaviors ingeneral practice. J Am Dent Assoc 1990;121:720-724.

6. Cury PR, Martins MT, Bonecker M, De Araujo NS. Inci-dence of periodontal diagnosis in private dental practice.Am J Dent 2006;19:163-165.

7. Heins PJ, Fuller WW, Fries SE. Periodontal probe use ingeneral practice in Florida. J Am Dent Assoc 1989;119:147-150.

8. McFall WT, Jr., Bader JD, Rozier G, Ramsey D. Presenceof periodontal data in patient records of general practi-tioners. J Periodontol 1988;59:445-449.

9. Brown LJ, Johns BA, Wall TP. The economics of peri-odontal diseases. Periodontol 2000. 2002;29:223-234.

10. Helminen SE, Vehkalahti M, Murtomaa H. Dentists’ per-ception of their treatment practices versus documentedevidence. Int Dent J 2002;52:71-74.

11. Blair, C. The economic impact of the under diagnosis ofperiodontal disease in general practice. Triage 2005;1:21-25.

12. American Dental Association, Survey Center. 1999 Surveyof Dental Services Rendered. Chicago IL: American Den-tal Association; 1999.

13. Borrell LN, Burt BA, Taylor GW. Prevalence and trends inperiodontitis in the USA: The NHANES, 1988 to 2000. JDent Res 2005;84:924-930.

14. Albandar JM, Brunelle JA, Kingman A. Destructive peri-odontal disease in adults 30 years of age and older in theUnited States, 1988-1994. J Periodontol 1999;70:13-29.

15. Armitage GC. Periodontal diseases: Diagnosis. Ann Peri-odontol 1996;1:37-215.

16. Papapanou PN, Wennstrom JL, Sellen A, Hirooka H, Gron-dahl K, Johnsson T. Periodontal treatment needs assessedby the use of clinical and radiographic criteria. CommunityDent Oral Epedimiol 1990;18:113-119.

17. American Academy of Periodontology. Parameter on com-prehensive periodontal examination. J Periodontol2000;71(Suppl.);847-848.

18. Krebs KA, Clem DS, III. American Academy of Periodon-tology. Guidelines for the management of patients withperiodontal diseases. J Periodontol 2006;77:1607-1611.

19. Novak KF, Goodman SF, Takei HH. Determination of prog-nosis. In: Newman MG, Takei H, Klokkevold PR, CarranzaFA, eds. Clinical Periodontology, 10th ed. Philadelphia:Saunders/Elsevier; 2006; pp. 614-625.

planing” may sound confusing topatients or imply discomfort. The words“periodontal therapy” are effectivesemantic choices when informingpatients about necessary periodontaltreatment. “We now know” are wordsthat can introduce patients to new ideasor treatment options to explain whyinformation may be different than whatthey have heard in the past, or expectedto hear at their current visit. “Halting”or “arresting disease” can be used todescribe a measurable goal for treatingperiodontal diseases that should beobtained through intervention. “Dailydisease control” communicates to thepatient that they share in the role in theeffective removal of plaque bacteriabeyond what it achieve through peri-odontal treatment.

Even though some states requirewritten consent, effective communica-tion between the clinician and the patientis the important consideration ofinformed consent,39 not the completionof a form. Therefore, deliberate seman-tic choices should be shared by all mem-bers of the office staff to optimizepatient understanding of their periodon-tal conditions.

Suggestions forImplementation of aPeriodontal Treatment Protocol in the General Practice Setting

• General dentists and dental hygien-ists should schedule a meeting withreferring periodontists and theirdental hygienists to share philoso-phies of periodontal treatment andestablish clarity for referrals.

• Schedule a team meeting workshopto bring all office staff up-to-dateregarding periodontal assessments,diagnosis, case types, periodontalrisk factors, individualized treat-ment of periodontal diseases, con-sequences of nontreatment (toothloss and possible systemic involve-ment), and the value of periodontalmaintenance.

• Establish continuity of the verbalskills and terminology the officestaff will utilize to communicateeffectively to patients about peri-odontal conditions.

• Include assessments and diagnosisof periodontal diseases in all newpatient visits, routine prophylaxisappointments, and ongoing peri-odontal maintenance to insure nopatient is overlooked regardingdiagnosis of developing periodontaldisease or recurring disease.

• Select appropriate ADA InsuranceProcedure Codes for reporting peri-odontal procedures in order to max-imize the patient’s benefit.

• Share insurance information withpatients to assist them in reducingtheir dependence on dental insur-ance benefits, thereby enablingthem to make independent healthdecisions related to treatment ofperiodontal diseases.

Disclosure

Dr. Sweeting, Ms. Davis, and Dr.Cobb are scientific advisors forOraPharma, Inc.

20. Carranza FA, Camargo PM. The periodontal pocket. In:Newman MG, Takei H, Klokkevold PR, Carranza FA, eds.Clinical Periodontology, 10th ed. Philadelphia: Saun-ders/Elsevier; 2006, pp. 434-451.

21. Armitage GC. Development of a classification system forperiodontal diseases and conditions. Ann Periodontol1999;4:1-6.

22. American Academy of Periodontology. Position paper:Diagnosis of periodontal diseases. J Periodontol2003;74:1237-1247.

23. Carranza FA, Takei HH. Clinical diagnosis. In: NewmanMG, Takei H, Klokkevold PR, Carranza FA, eds. ClinicalPeriodontology, 10th ed. Philadelphia: Saunders/ Elsevier; 2006, pp. 540-560.

24. Carranza FA, Takei HH. Bone loss and patterns of bonedestruction. In: Newman MG, Takei H, Klokkevold PR,Carranza FA, eds. Clinical Periodontology, 10th ed.Philadelphia: Saunders/Elsevier; 2006, pp. 452-466.

25. Armitage GC. Clinical evaluation of periodontal diseases.Periodontol 2000 1995;7:39-53

26. Haffajee AD, Socransky SS, Lindhe J, Kent RL, OkamotoH, Yoneyama T. Clinical risk indicators for periodontalattachment loss. J Clinical Periodontol 1991;18:117-125.

27. Claffey N, Egelberg J. Clinical indicators of probing attach-ment loss following initial periodontal treatment inadvanced periodontitis patients. J Clin Periodontol1995;22: 690-696.

28. Lang NP, Adler R, Joss A, Nyman S. Absence of bleedingon probing – an indicator of periodontal stability. J ClinPeriodontol 1990;17:714-721.

29. Muller HP, Stadermann S. Multivariate multilevel models forrepeated measures in the study of smoking effects on the

association between plaque and gingival bleeding. ClinOral Invest 2006;10:311-316.

30. American Academy of Periodontology. Position paper.Guidelines for periodontal therapy. J Periodontol2001;72:1624-1628.

31. American Dental Association. Principles of ethics and codeof professional conduct. January 2005. Available at:http://www.ada.org/prof/prac/law/code/index.asp. AccessedAugust 28, 2008.

32. American Academy of Periodontology. Position paper. Peri-odontal maintenance. J Periodontol 2003;74:1395-1401

33. Greenwell H, Bissada NB, Wittwer JW. Periodontics ingeneral practice: Perspectives on periodontal diagnosis. JAm Dent Assoc 1989:119:537-541.

34. Hirschfeld L, Wasserman B. A long-term survey of toothloss in 600 treated periodontal patients. J Periodontol1978;49:225-237.

35. Tonetti MS, Muller-Campanile V, Lang NP. Changes in theprevalence of residual pockets and tooth loss in treatedperiodontal patients during a supportive maintenance careprogram. J Clin Periodontol 1998;25:1008-1016.

36. American Academy of Periodontology. Parameters of care.J Periodontol 2000;71: 847-880.

37. American Dental Association. Current Dental Terminology.2007-2008;3-27.

38. American Academy of Periodontology. Position paper. Epi-demiology of periodontal diseases. J Periodontol2005;76:1406-1419.

39. American Academy of Periodontology. American Acad-emy of Pediatric Dentistry. Guideline for periodontaltherapy. Pediatr Dent 2005-2006;27(7 Reference Man-ual):197-201.

Case Slight Moderate AdvancedIndicator Healthy Gingivitis Periodontitis Periodontitis Periodontitis Aggressive/Refractory

Pocket Deptha < 3 mm < 4 mm 4 - 5 mm 5 -6 mm > 6mm > 6mm

Bleeding Upon No Yesb Yesb Yesb Yesb Yesb

Probing

Six-Point Yes Yes Yes Yes Yes YesProbing

Bone Loss None None < 10% < 33% > 33% > 33%

Tooth None None None < Grade II < Grade III < Grade IIIMobilityc

Furcationd None None < Grade I < Grade II < Grade III/IV < Grade III/IV

Clinical None None 1 - 2 mm CAL 3 - 4 mm CAL > 5 mm CAL > 5 mm CALAttachmentLoss (CAL)e

Other No Only gingival Signs of inflammation Signs of inflammation Signs of inflammation Signs of inflammationinflammation tissues affected may be present, including may be present, including may be present, including may be present, including

by the • Edema • Edema • Edema • Edemainflammatory • Redness • Redness • Redness • Rednessprocess • Suppuration • Suppuration • Suppuration • Suppuration

• Alveolar bone level is • Alveolar bone level is • Alveolar bone level is • Same clinical signs as• No alveolar 3 - 4 mm from CEJ 4 - 6 mm from CEJ • > 6 mm from CEJ advanced but includes

bone loss • Radiographic bone loss • Radiographic bone loss • Radiographic bone loss adolescents or• Localized or present present present young adults

generalized • Localized or generalized • Localized or generalized • Localized or generalized • Localized or generalized• Rapid cycles of disease

progression

Assessment • Prophy • Prophy • Comp. Oral Eval D0150 • Comp. Oral Eval D0150 • Comp. Oral Eval D0150 • Comp. Oral Eval D0150• OHI • OHI • Comp. Perio Eval D0180 • Comp. Perio Eval D0180 • Comp. Perio Eval D0180 • Comp. Perio Eval D0180

• Four bitewings D0274 • Four bitewings D0274 • Four bitewings D0274 • Four bitewings D0274• Eight bitewings D0277 • Eight bitewings D0277 • Eight bitewings D0277 • Eight bitewings D0277• FMX D0210 • FMX D0210 • FMX D0210 • FMX D0210• Panoramic Film D0330 • Panoramic Film D0330 • Panoramic Film D0330 • Panoramic Film D0330

• Full Mouth Debride D4355 • Full Mouth Debride D4355 • Full Mouth Debride D4355• Occlusal Analysis D9950 • Occlusal Analysis D9950 • Occlusal Analysis D9950

• Specialty Referral • Specialty Referral

Active • Prophy • Prophy • Quadrant SRP D4341 • Quadrant SRP D4341 • Quadrant SRP D4341Therapy • OHI • OHI - UR, UL, LR, LL - UR, UL, LR, LL - UR, UL, LR, LL

• Localized SRP D4342 • Localized SRP D4342 • Localized SRP D4342- UR, UL, LR, LL - UR, UL, LR, LL - UR, UL, LR, LL

• Locally Administered D4381 • Locally Administered D4381 • Locally Administered D4381 • Specialty ReferralAntimicrobials Antimicrobials Antimicrobials

• OHI D1330 • OHI D1330 • OHI D1330• Specialty Referral • Specialty Referral • Specialty Referral• Other Treatments • Other Treatments • Other Treatments

Ongoing 6 Months 6 Months • Perio Maintenance D4910 • Perio Maintenance D4910 • Perio Maintenance D4910 • Perio Maintenance D4910Maintenance • Prophy • Prophy - 3/4/6 months - 3/4/6 months - 3/4/6 months - 3/4/6 months

• OHI • OHI • OHI D1330 • OHI D1330 • OHI D1330 • OHI D1330• Locally Administered D4381 • Locally Administered D4381 • Locally Administered D4381 • Locally Administered D4381Antimicrobials Antimicrobials Antimicrobials Antimicrobials

• Localized SRP D4342 • Localized SRP D4342 • Localized SRP D4342 • Localized SRP D4342- UR, UL, LR, LL - UR, UL, LR, LL - UR, UL, LR, LL - UR, UL, LR, LL

• Other Treatments • Other Treatments • Other Treatments • Host Modulation

©OraPharma, Inc. 2008aExcluding gingival overgrowth and recessionbBleeding upon probing may not be present in individuals with periodontal disease who are smokers.c Tooth Mobility: Grade I: Slightly more than normal; Grade II: Moderately more than normal; Grade III: Severe mobility faciolingually and mesiodistally, combined with vertical displacement. Adaptedfrom Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology 10th ed. Philadelphia, PA: Elsevier; 2006.

d Furcation Grades: Grade I: Initial attachment loss with most of the bone still intact in the furcation. No radiographic changes seen; Grade II: The bone defect is definite horizontal bone loss that doesnot extend all the way through. Vertical bone loss may also be present. There is an opening into the furca with a bony wall at the deepest portion. Grade III: Bone is lost across the whole width of thefurcation so no bone is attached to the furcation roof; Grade IV: Bone loss across the furcation, accompanied with gingival recession at the furcation, is clinically visible. Adapted from Newman MG,Takei H, Klokkevold PR, Carranza FA. Carranza’s Clinical Periodontology 10th ed. Philadelphia, PA: Elsevier; 2006.

eAdapted from Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999; 4(I):1-6

Adapted from Periodontal Diagnostic Guidelines ©OraPharma, Inc. 2008

Table 2. Periodontal Diagnostic Guidelines.

Rationale for Comprehensive Nonsurgical Periodontal Therapy

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