Penodontics

The treatment of acute neerotizing ulcerative gingivitisAnne C. Hartnett* / Jacob Shiloah**

The destruction of tbe interdental papillae and formation of permanent gingiva! craierxare common sequelae of acute neerotizing uleerative gingivitis. These craters ean bedisfiguring, especially in the anterior gingiva, and ean act as a nidus for recurrent epi-sodes. Traditional therapy has emphasized a stirgieal approach for elimination of Ihesedefects, often increasing the esthelie problems. The pwpose of this paper is to reviewthe treatment modalities of acitte neerotizing itlcerative gingivitis and ¡Ilústrate an al-ternative treatment approach of periodic sealing, root planing, and antimicrohiai rinseswith 0.12% chlorhexidine. With this therapeutic regimen, the disease proeess ean bereversed and damaged papillae may regenérale. (Quintessence Int 1991:22:95-100.)

Introduction

Acute neerotizing ulcerative gingivitis (ANUG) is arapidly destructive, noncommunicable, gingival infec-tion of complex etiology. It is characterized by necrosisof the crest of the gingival papillae, spontaneousbleeding, pain, and halitosis. If left untreated, it mayspread laterally and apically to involve the entire gin-gival complex, including the alveolar mucosa andbone, leading to neerotizing ulcerative periodontitis(NUP).' Although known since ancient times by amultitude of names, ANUG was first described byPlaut in 1894 and Vincent in 1896.--̂ While nearly acentury of investigation has shed some light on itsetiology, pathogenesis, and treatment, many aspectsof this disease remain obscure. In fact, current theoriesof causative mechanisms differ httle from those pro-posed by Vincent: that of an endogenous, opportu-nistic fusospirochetal infecfion,"*^ Although spiro-

* Senior Resident. Postgraduate Periodontology, University ofTennessee, College of Dentistry, 875 Union Avenue, Memphis,Tennessee 38163.

** Professor, Department of Periodontology, University of Ten-nessee.

Address all correspondence to Dr Jacob Shiloah.

chetes, fusifonn bacteria, and species of Bacteroidesare the organisms most frequently cultivated fromthese lesions,' a definitive periodontal pathogen hasyet to be tmplicated in the onset or progression ofANUG. A susceptible animal model in which to studyANUG has not been found.

Previous studies have speculated on the importanceof secondary predisposing etiologic factors,*'' such asstress,'" '̂ impaired chemotaxis,'^ poor oral hygiene,'̂alcohol consumption, smoking" general debilitation,and malnutrition.'^ In the past, differing criteria fordiagnosis have led to confusion and to highly variableresults as to the epidemiology, demography, and mi-crobiology of ANUG."'* In 1984, Stevens et al'̂ out-lined a triad of criteria that are diagnostic for ANUG.These included acute necrosis and ulcération of theinterdental papillae, pain, and bleeding. While theseare the generally accepted criteria, other signs may bepresent, including halitosis, pseudomernbrane, lymph-adenopathy, and elevated body temperature.

The study of ANUG has been as diverse as itscomplex and tnultifactorial nature. Several reviewson the epidemiology, diagnosis, and etiology ofANUG"'*"*^-' have been written. Although relativelyfew reports focusing on treatment modalities havebeen published,"-^-''treatment recommendations havebeen as varied as the developing etiologic theories.

The purpose of this paper is to review the treatmentof ANUG and to illustrate the therapy currently used

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by the authors for papillary regeneration: ,';caling, rootplaning, and antimicrobial rinses with 0,12% chlor-hexidine.

Historical aspects of treatment

Early reports on the treattnent of ANUG focused onmanagement of the microbial aspects of the diseasewith available antimicrobial and chemical agents. Ini-tially, arsenicals were used becattse of their effective-ness against spirochetes associated with venereal dis-ease. Vincent̂ '̂ employed topical iodine applicationsand rinses of boric acid solution. In the first two dec-ades of this century, oxidizing agents, especiallychromic acid, were a popular mode of therapy, sincethe involved microorganisms are anaerobtc.-' Mercury,silver compounds, and anihne dyes were also used,-'

In 1930, Hirschfeld"" recommended debridementand use of sodium perborate rinses until the infiatn-mation subsided. This approach was in direct conñictwith the widely held behef that instrumentation of theinfected tissues eotild cause bacterial transmission intouninvolved areas^* and possibly even lead lo hfe-threatening Vincent's angina. In 1949, Schluger" re-ported treatment of his patients by deep and thoroughcurettage, followed by hydrogen peroxide and watermouthrinses six to eight times a day,̂ ^ However, be-cause of the preconceived notions of potential bacter-emia and spread of infection, scaling and root planingdid not gain wide acceptance by the profession as atreatment of choice for ANUG. In fact, tn 1944, Fishrecommended resting the tissues beneath periodontaldressings,̂ ^ and, as late as 1950, Miller's text' rec-ommended very careful scaling to prevent systemicspreading of infection.

In the early 1960s, Fitch et aP^ suggested that ultra-sonic instrumentation was effective in managingANUG. Goldhaber,^' in 1968, proposed repeatedgentle scalings, diluted hydrogen peroxide rinses, andestablishtnent of good oral hygiene programs. He stat-ed that "the more meticulous and complete the subgin-gival curettage, the more complete will be the re-sponse,"^''

The role of antibiotics in ANUG

Given the microbial basis of ANUG, antibioticsseemed a logical treatment option when they becameavailable. Penicillin was first used to treat ANUG inmilitary personnel in the mid 1940s, Its dramatic ef-fects were quickly realized. However. Schluger" ree-

ognized that when penicilhn was employed as the onlymode of therapy, the condition could reappear or lapseinto a chronie state, Curettage alone, he noted, was amore definitive treatment modality. Tn 1945, a reportof the Research Commission of the Ameiucan DentalAssociation on Vincent's infection relegated chemo-therapy to the role of an adjunct to rational treat-ment,"

Goldhabcr-^ warned that antibiotics are not anal-gesics and should not be prescribed simply to mini-mize the discomfort of local therapy Discriminatinguse of these potentially life-saving drugs was recom-mended due to the possibility that the host might de-velop resistant strains of bacteria or hypersensitivereactions. As a result, antibiotics were recommendedonly for patients with systemic signs and symptotns(fever, lymphadenopathy, and/or malaise) or in acutefulminating cases that were slow to respond to localtherapy. However, these symptoms may be an indica-tion of other systetnic conditions (acute herpetic gin-givostomatitis, blood dyscrasias) if antibiotics therapyis not effective,̂ '"'''-*

Several antibiotics have been proposed for the treat-ment of ANUG,^' Reports in the mid-1960s advocatedthe use of metronidazole,-'''"-^' originally described fortreatment of trichomonal infections of the vagina.This drug was usually effective in alleviating the acutephase of ANUG in 48 hours,^" The recommended reg-imen consisted of 200 mg, three times a day, for 7days. After comparing the effectiveness of five rec-ommended drugs for the management of ANUG,Wade et al'° concluded that penicillin was the anti-biotic of choice. Forty-eight hours following tbe initialdose, patients responded well to penicilhn therapy,whereas one patient out of eight that received met-ronidazole did not show any improvement, Loescheet al' found that metronidazole treatment was effectivein all eight patients studied, providing prompt reso-lution of clinical symptoms and decreased proportionsof Treponema. Bacieroides intermedius. and Fusobac-terium Species for 2 to 3 months post treatment. How-ever, hke penicillin treatment, metronidazole does noteliminate local contributing etiologic factors or thegingival deformities (craters) resulting from ANUG,Consequently, systemic antibiotics are recommendedonly as an adjunct to compliment local treatment ofANUG, namely scahng and root planing, and not asa substitute for local therapy

Topical antibiotics have also been widely used. Re-ports in the hterature include local application of pen-icillin, vancomycin, metronidazole, and the sulfon-

96 Quintessence Internationai Volume 22. Number 2/1991

Periodontics

Fig la Permanent destruction farrows) of the interdentalpapilla in a 36-year-oid woman 15 years following ANUG,

Figib Gingival craters and compromised esthetics (ar-rows) are common results ol ANUG, Plaque retention isevident.

amides,''-" As many as 40% of patients treated withtopical penicillin have reported local irritations, chei-litis, and glossitis,' Side effects from the use of topicalmetronidazole include the oecurrence of black tongue,generalized erythema, and thrush,-' Generally, the top-ical mode of antibiotic therapy is not recommendedbecause of the increased risk of sensitivity and poten-tial development of resistant strains in thenormal oralflora.^'

Current treatment

The most frequent eonsequence of single or recurrentepisodes of ANUG is the destruction of gingival pa-pillae and the formation of an interdental gingivalcrater (Fig 1). Many researchers believe that recurrentattacks of ANUG occur at these gingival cra-ters. ̂ ''•̂ •̂̂ '•" Repeated curettage and the establishmentof good plaque control may result in regeneration ofdestroyed papillae-''-* However, the most common rea-son for failure in the treatment of ANUG is prematuretermination of therapy after the acute symptoms havesubsided,'' Once the acute symptoms have resolved,patients with ANUG may not comply with prescribedtherapy and subsequent dental appointments. There-fore, the patient must be properly informed at theinitial presentation of the potential risk of permanentgingival deformities and a high recurrence rate andthe importance of follow-up therapy- If treatment issought early, and is prompt and thorough, gingivaldeformities can be prevented. Crater formation willmost hkely result if there is a delay in therapy or re-peated exacerbations occur, as is often the case.

Because of the relationship of recurrences of ANUGto persistent gingival deformities, emphasis has beenplaced on surgical elimination of these gingival de-fects, Gingivoplasty has often been recommended asearly as 1 month after the acnte infection, to permitadequate plaque control and lo recreate a physiologicgingival form and contour,-^ However, extensive gin-givoplasty to correct reversed gingival architecturemay require the sacrifice of healthy tissue from thefacial and lingual marginal gingiva. In anterior areas,where esthetics are an important consideration, suchsurgery might accentuate unesthetic open gingival em-brasures and elongate the clinical crowns.

The last decade has witnessed a resurgence of re-ports documenting the effectiveness of nonsurgicaltherapy in the management of periodontal diseases.This therapy, consisting primarily of seahng and rootplaning, has an obvious advantage in the esthetic re-sult when eompared with most surgieal modes, espe-eially in anterior segments, Shapiro'"" has proposed atechnique, developed by Kramer, that uses periodiccurettage to stimulate regeneration of the interdentalpapillae to eliminate or lessen the need for surgicalintervention in the management of ANUG, Thismethod requires approximately 9 months of aetivetherapy for maximal gingival regeneration to oeenrand has varying and unpredictable degrees of success.Some papillae may regenerate to a convex, or flatform, while others may not respond at all.

Recently, a major emphasis has been placed on therole of topical antimicrobial agents in periodontics.Currently, chlorhexidine gluconate is the tnost effec-tive topical chemotherapeutic agent'^-* available for

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Fig 2 Preoperative view ot a 17-year-old boy witti ANUG.Infiammation, bleeding, necrosis of the interdental papilla,and crater formation are present. Poor orai hygiene, stress,smoking, and alcohoi abuse contribute to the catjse in thispatient

Fig 3 Same patient as in Fig 2 immediately following grossdebridement at fhe initial visit. Patient was instructed inpiaque control, including brushing, fiossihg, and 0.12%chlorhexidine rinses, twice daiiy.

Fig 4 Same patient at 4 months. Gingival health has im-proved and early signs of papillary regeneration are pres-ent. Area was retreated with scaling and root pianing andthe previous plaque-control regimen was reinforced.

Fig 5 Finai resuit 7 months postoperatively. Regenerationof the interdental papilla is completed with return of para-bolic gingival architecture. These changes occurred in spiteof marginal gingivitis.

Fig 6 A 32-year-oid HIV-positive man exhibiting signs olHIV-associated periodontifis, including inflammation, se-vere attachment loss, soft tissue ulcération into the aiveolarmucosa, and advanced bone loss.

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Pehodontics

the control of plaque and gingivitis. It has been ac-cepted by both the Council on Dental Therapeuticsof the American Dental Association and the Food andDrug Administration. Although no controlled studieshave testeti the efficacy of chlorhexidine treatment inANUG patients, we have found it to be quite prom-ising. Periodic chlorhexidine rinses may complementmechanical plaque control during the crucial periodof wound healing of the damaged gingiva after scalingor curettage. Figures 2 to 5 illustrate the potentialbenefits of combining scaling and root planing withdaily rinses of 0.12% chlorhexidine in the treatmentof ANUG and the associated gingival deformities.

Acquired immunodeficiency syndrome and ANUG

Patients with acquired immunodeficiency syndromeexhibit neutrophil abnormalities, as well as lympho-cyte and mononuclear phagocyte defects, and oftenhave a severe form of ulcerative periodontal disease.^'Recent data suggest that ANUG may be an earlysign of infection with human immunodeficiency virus(HIV)'*-̂ ** and that ANUG occurs in about 20% ofpatients with acquired immunodeficiency syndrome.''Silverman et aP^ reported a high incidence of rapidlyprogressive periodontal disease in a group of 375 malehomosexual patients. This has heen termed HlV-re-lated gingivitis and often initially manifests itself asANUG or a chronic persistent erythematous gingi-vitis. These lesions can quickly progress to HlV-as-sociated penodontitis characterized by inflammation,cratered papillae, attachment loss, soft tissue ulcéra-tion and necrosis, advanced bone loss, and a tendencytoward spontaneous bleeding (Fig 6). A recent reportby Murray et al"" found the microorganisms associatedwith HIV-periodontitis and HIV-associated gingivitisto he similar to those of classic adult periodontitis.Eariy detection and treatment of HIV gingivitis mayprevent rapid tissue destruction associated with HIV-periodontitis. Recommended treatment is similar tothat of non-HIV ANUG: oral hygiene, local debride-ment, and rinses with antimicrobials such as chlor-hexidine and povidone-iodine. Ultrasonic use has notbeen recommended in this group of patients becauseof the contaminated aerosol produced- Systemic an-tibiotics are usually avoided to prevent an increase inthe risk of opportunistic infections.

Summary

Interdental craters that result from ANUG can bepermanently disfiguring, especially in the anterior gin-

giva. Traditional therapy has emphasized the impor-tance of surgical elimination of these local predispos-ing factors (craters), which are thought to serve as anidus for leeurrent episodes common after the reso-lution of the acute symptoms. The second phase ofsurgical correction, although an attempt to eliminatenegative gingival architecture, would often amplifydispleasing esthetics. An alternative therapeutic modeinvolving nonsurgical treatment—periodic scalingand root planing combined with daily rinses withchlorhexidine—is prescribed. Satisfactory results canoften be achieved using this conservative approach totherapy

Acknowledgments

The authors gratefully acknowledge the editorial assistance of DrMark Patters and Dt Hiram Fry in the preparation of this tnanu-scripl.

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