Acute recurrent gingivitis

Acute recurrent gingivitis A cilnkal

entity

Lawrence R. Page, D.D.S., Ph.D., * C. Warner Bosman, B.Ch.D., M.Sc., ** James F. Drummond, D.D.S., M.S.D., Ph.D.,*** and Ky. and Buffalo, N. Y. Sebastian G. Ciancio, D.D.S., M.S.D., ****Lexington, UNIVERSITY NEW

YORK

OF KENTUCKY

COLLEGE

OF DENTISTRY

AND

STATE

UNIVERSITY

OF

AT BUFFALO

A typical case of a previously undescribed form of gingivitis which is self-limittng and recurrent is discussed. The signs and symptoms include acute pain and swelling of intetientel papfllae with regional lymphadenopathy. As the disease progresses the locaked swelling qukkly spreads to the adjacent marginal and papikty ghgiva. Ulceration is infrequent and without pseudomembrane formation or interdental cratering. We believe this to be a unique form of gingivitis and suggest the name acute recurrent gingivitis (ARG).

n recent years, we have noted a pattern of gingivitis Iwhich differs from either simple inflammatory gingivitis or necrotizing ulcerative gingivitis (NUG). ‘Ibis gingivitis is characterizedby an acutecourse, its occurrence despite excellent piaque control, and its recurrent nature. A thorough searchof the literature has failed to produce any reports of a similar nature. Four persons from within the faculty/student population of the University of Kentucky College of Dentistry have presentedwith this unusual form of gingivitis; one of them hasheen followed for the past 9 years and is the subject of the following case report. CASEREPORT The patient is a 35-year-old white man without known medical problems other than mild atopia and occasional migraine headaches.Oral examinations consistently reveal the patient to have excellent plaque control and clinically healthy gingiva. The patient recalls first having the condition at the age of 25, with other epiosdesoccurring in either rapid successionor months apart. Symptoms appear suddenly, with the patient *Departments of PeriodonticsandOral Biology, Universityof Kentucky Collegeof Dentistry. **Departmentof Periodontics,University of KentuckyCollegeof Dentistry. ***Dqartments of Oral PathologyandOral Biology, Universityof KentuckyCollegeof Dentistry. ****Departmentof Periodontologyand Endodontology,StateUniversityof New York at Buffalo. 0030-4220/80/040337+04$00.40/0 @!I198OTheC. V. Mot&y Co.

usually able to recall the particular time of day or night when the processbegan. The initial lesion is usually locatedin a singleinterdental areaand spreadsto adjacentareaswithin 12 to 48 hours. As theprocessspreads,it mayaffecttwo or three

adjacentgingival unitsor theentirearch.Theprocessmaybe localizedto the facial or the palatal/lingualaspectsof the gingiva during acFive episodes. Clinically, the gingiva appearsreddenedandgrosslyedematous (Fig. 1)but usuallyhas

an intact gritheM surface.Occasionallyoneor moresmall ulcerationsmay he seen. Cytologic smearsof these uicerations failed to reveal evidence of a viral etiology. The ulcers probably are a result of toothbrush abrasion, since the patient refuses to discontinue plaque control during these episodes. Although there is no fever, regionallymphadenqatbydoes occur, and both the iymphadenopathy and the edematous

gingiva canbe painful enoughto interferewith eating.The swelling and pain resolve spontaneously in about a week. However, resolution can be hastenedby penicillin therapy. A biopsy of a typical early lesion on the p&W aspectof the maxillaryright first premolarshowedh and crevicularepithelium(Figs. 2 and 3). The underlying iamina propria consistedof densecollagen bundles containing a heavy infiltrate of lymphocytes and a few plasmacells (Fig.

4). A Brown andBrennstainrevealedno id&tiffabte microorganismswithin the tissue. Differential blood studies were performed during six separate episodesof the disease.Samplesweretakenat intervals of 1, 3, and 7 days after the appearanceof initial ~ymptoma. .

Theresultsshowedno significantchangescomparedto blood samplestakenduringperiodsof remission.ARW~FS to casually relatethe episodesto particularfoodsor bevemgesor to contact with other substanceshave been unsuccessful.

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Oral Surg. April, 1980

Fig. 1. ARC affecting marginal and papillary gingiva as comparedto the samegingiva after remission. A andbl, Maxillary palatal gingiva. C and D, Mandibular anterior facial gingiva.

Flg. 2. Parakeratinized gingival epithelium with an infiltration of lymphocytes and a few plasma cells in the subjacent fibrous connective tissue. (Hematoxylin and eosin stain. Original magnification, X 40.)

DISCUSSION

We believe this to be a unique gingival disease and suggest the name acute recurrent gingivitis (ARG). The signs and symptoms of ARG are acute pain and edema of the marginal and papillary gingiva, with little or no ulceration, spread to adjacent marginal and papillary gingiva, regional lymphadenopathy, and resolution within 10 days.

Since epidemiologic surveys have not been carried out, the incidence and demographic patterns of ARG are not known. Most of the patients with ARG observed thus far were dental students with high levels of plaque control. There are similarities between ARG and NUG. Clinically, both diseases present with a sudden onset of pain, inflammation and lymphadenopathy and run an

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Acute recurrent gingivitis

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Fig. 3. Crevicular epithelium with inflammatory cell infiltration of subjacent fibrous connective tissue. (Hematoxylin and eosin stain. Original magnification, x 40.)

acute course. Like NUG,le3 ARG may be stress related. Fig. 5 shows the occurrence of ARG over a l-year period. The patient claims to have been under greater stressfrom Decemberto May. As can be seen, that is the time when most of the ARG episodes occurred. (Other patients with ARG also tend to relate occurrences with stress.) The progressive patterns of spread, the lymphadenopathy, and the rapid resolution of ARG with penicillin therapy are suggestive of bacterial etiology. There are also distinct clinical differences between ARG and NUG. ARG does not result in necrosis or pseudomembraneformation, and ulceration is rare. ARG is usually localized, with a pattern of slow spreading after the initial lesion appears,while NUG usually is not as localized and does not have a slow-spreading pattern. A possible hypothesis is that the samepredisposing conditions responsible for NUG may result in ARG when the gingiva is initially healthy with little mature plaque accumulation-in contrast to the initial poor plaque control and high levels of inflammation in persons susceptible to NUG. The clinical and histologic differences in the two diseasescould conceivably be explained by the relative difference in the numbers and types of opportunistic pathogenic bacteria present. However, such a hypothesis is far from confirmed. All that can be stated at this time is that ARG is a specific clinical entity, whether or not it is a variant of NUG.

Fig. 4. Inflammatory cell infiltrate consisting of lymphocytes and a few plasma cells. Hematoxylin and eosin stain. Original magnification, X 100.)

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Page et al.

Oral Surg. April, 1980

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Fig. 5. Occurrence of ARG over a l-year period. 1, Maxillary right; 2, Maxillary Mandibular left; 5, Mandibular anterior; 6, Mandibular right. REFERENCES 1. Barnes, G. W., and Bowles, H. C.: Acute Necrotizing Ulcerative Gingivitis: A Survey of 218 Cases, J. Periodontol 44: 35-42, 1973. 2. Formicola A., Witte, E. and Curran P.: A Study of Personality Traits and Acute Necrotizing Ulcerative Gingivitis, J. Periodontol. 41: 3638, 1970. 3. Schields, W.: Acute Necrotizing Ulcerative Gingivitis: A Study

anterior; 3, Maxillary left; 4,

of Some of the Contributing Factors and Theii Validity in an Army Population, J. Periodontal. 4%: 346349, 1977.

Reprintrequeststo: Dr. Lawrence R. Page University of Kentucky College of Dentistry Department of Periodontics Lexington, Ky. 40536