Plasma-cell gingivitis

Plasma-cell gingivitis

Plasma-cell gingivitis R. M. Palmer, B.D.S., F.D.S.R.C.S.(Eng.),* and J. W. Eveson, B.Sc., B.D.S., Ph.D., F.D.S.R.C.P.S.(Glas.), London, England ROYAL...

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Plasma-cell gingivitis R. M. Palmer, B.D.S., F.D.S.R.C.S.(Eng.),* and J. W. Eveson, B.Sc., B.D.S., Ph.D., F.D.S.R.C.P.S.(Glas.), London, England ROYAL

DENTAL.

HOSPITAL

OF LONDON

AND

GUY’S

M.R.C.Path.,**

HOSPITAL

Two cases of plasma-cell gingivitis identical to those previously reported as so-called “allergic gingivostomatitis” are presented. Glossitis and cheilitis were absent in the present cases, however. There wasno evidence that the lesions were allergic in nature. The distinctive clinical and histologic features of the lesion are described.

T

he presenceof large numbersof plasmacells in the establishedlesion of chronic inflammatory periodontal diseasecan occasionally lead to difficulty in distinguishing this common condition from the more exotic plasma-cell lesions reported to affect the gingiva. These include rare cases of extramedullary plasmacytoma, plasmacytosisof the gingiva,’ plasma-cell gingivitis,2 and plasma-cell granuloma.3 Plasma-cell gingivitis has been described under a variety of names, including atypical gingivo-stomatitis,4, 5 idiopathic gingivostomatitis,6 and allergic gingivostomatitis. 7The condition wasfrequently associated with cheilitis and glossitis, and many cases were thought to be an allergic reaction to a component of chewing gum. However, the condition, which appeared to be prevalent between 1966 and 1971, suddenly disappeared,and in 1977 Silverman and Lozada wrote an epilogue to plasma-cellgingivitis. It was presumedthat an allergen producing a hypersensitivity reaction had been present in the suspectedproducts for a limited period of time. Two casesof “plasma-cell gingivitis,” identical to the condition previously described in associationwith the symptom complex of allergic gingivostomatitis but without glossitis or cheilitis, are presented. CASE REPORTS CASE

1

A 29-year-oldwomanwasreferredfor investigationof red, swollengingivaein the upperanteriorregion. The medical historyshowedthat the patientwasallergicto housedustand sufferedfrom asthma,for which shetook salbutamol.Routine hematologicinvestigationsshowedno abnormality. *Lecturer in Periodontology, Royal Dental Hospital of London. **Senior Lecturer, Department of Oral Medicine and Pathology, Guy’s Hospital. 0030-4220/81/020187+03$00.30/0

0

1981 The C. V. Mosby

Co.

Fig. 1. Case1. Photographshowingerythematpus,faintly mottledinvolvementof attachedgingivain the upperanterior region.

On examination,the patienthada bright red, faintly mottled areaaffectingthe labialattachedgingivafrom themaxillary left canineto the right canine(Fig. 1). The lesionresembledlocalizedchronicatrophiccandidosis,but a smeartaken from the areashowedno candidalhyphae. The lesionwas painless,andtherewasno cheilitisor glossitis.Therewasan associated marginalgingivitis, which resolvedwhenthe patient’s oral hygiene improved. Despite the severely inflamed appearance of the affected gingiva, there was no significant loss of periodontal attachment. Elsewhere in the mouth there was early pocketing 2 to 4 mm. deep, which was most severe in the molar regions. The patient did not chew gum, and there was no obvious dietary cause. The patient was asked to discontinue the use of toothpaste, but the lesion did not resolve. A biopsy specimen was taken from the gingiva, and the wound healed uneventfully. Histology

There was epithelialhyperplasia,elongationof the rete ridges, and thinning of the suprapapillary epithelium, giving a psoriasiform appearance (Fig. 2). There was severe spon187

Oral Sure. February.

Fig. 2. Psoriasiform hyperplasia and eosin stain. Magnification,

of the epithelium x40.)

and dense

plasma-cell

infiltration

of the corium.

IWI

(Hematoxylin

giosis and infiltration of the epithelium by inflammatory cells. The infiltrate in the deeper layers was predominantly lymphocytic, but in the superficial layers neutrophils were conspicuous (Fig. 3). There was a dense, mainly plasma-cell infiltration of the corium. Dilated capillaries with neutrophil margination were present in the papillary corium. Special stains failed to show candidal hyphae.

Manfbgwwnt The patient is undergoing treatment for chronic marginal periodontitis. A high standard of plaque control is being maintained in the affected area, but there has been no change in the clinical appearance. Empirical antifungal treatment has been ineffective. CASE

Fig. 3. Higher-power photomicrograph showing in the superficial epithelium and characteristic infltration of the corium. (Hematoxylin and Magnification, x 350.)

neutrophils plasma-cell eosin stain.

2

The patient, a 52-year-old man, complained of red, shiny gingivae which he had noticed for 5 months. The medical history showed that the patient had previously suffered from psoriasis and had Paget’s disease of bone. Examination showed that the labial gingiva from the maxillary right canine region to the left premolar region was bright red and had a spongy texture. The full width of the attached gingiva was affected, and there was sharp demarcation at the mucogingival junction. Patches of attached gingiva within the affected area were normal in appearance. The condition was painless, and there was no cheilitis or glossitis. There was chronic marginal gingivitis as a result of poor oral hygiene but no significant loss of periodontal attachment. Improvement of the oral hygiene led to resolution of the marginal gingivitis. but the underlying condition was unchanged. Dietary analysis did not show any obvious causative agents, and discontinuation of the use of toothpaste had no effect. The results of routine hematologic examination and serologic investigations

Volume Number

Plasma-cell

51 2

for iron, B12, and folate were within normal limits. After a biopsy specimen was taken from the affected area, the wound healed uneventfully. The histologic features were similar to those described in Case 1, but the inflammatory cell infiltration of the epithelium was more severe. Special stains failed to show candidal hyphae. In the deeper corium there was perivascular plasmacell infiltration but no vasculitis. Management

Topical ttiamcinolonein Orabaseproduceda limited improvementin the condition.As the affectedareawaspainless anddid not progressto lossof periodontalattachmentover a periodof 2 years, no further treatmentwasundertaken. DISCUSSION

The foregoing casesillustrate a distinctive plasmacell lesion of the gingiva but without other features associatedwith atypical or allergic gingivostomatitis. The lesion has characteristic clinical features. The involved mucosahas a bright red, faintly stippled surface. It is sharply demarcatedfrom the adjacent tissue and may extend from the gingival margin onto and beyond the mucogingival junction. There are no vesicles, bullae, ulcers, or associatedwhite lesions. The lesionsdo not appearto be related to plaque accumulation. The clinical differential diagnosis includes mucous membrane pemphigoid, atrophic lichen planus, ’ ‘desquamative gingivitis” related to the climacteric, and candidosis. The histologic differential diagnosis includes candidosis, geographic stomatitis, intraoral psoriasis, and extramedullary plasmacytoma. The causeof the condition is unknown, but it does not seem to be related to dental plaque. Both of the present patients had generalized chronic marginal gingivitis due to plaque accumulation. Although the mar-

gingivitis

189

ginal gingivitis resolved when the patients’ plaque control improved, the underlying condition remained unchanged. The characteristic gingivitis, with a dense plasma-cell infiltrate, haspreviously been describedin associationwith cheilitis and glossitis. It was assumed that this symptom complex was an allergic responseto an unidentified antigen. No allergic basisfor the lesions was detected in the present cases. The authorsthank Mr. R. P. Juniperfor permissionto report Case2, Mr. M. B. Edwardsfor supplyinghistologic materialfrom Case2, ProfessorR. A. Cawsonfor his constructivecriticismof the manuscript,and Mr. J. Mercer for his invaluableassistance with the photomicrographs. REFERENCES

1. Poswillo, D.: Plasmacytosis of theGingiva,Br. .I. OralSurg.5: 194202,1968. 2. Vickers,R. A., andHudson, C. D.: A Clinicopathologic Investigationof “Plasma CellGingivitis,”I.A.D.R. Abstr. 755, p. 241, 1971. 3. Bhaskar, S. N., Levin,M., andFrisch,J.: Plasma CellGranulomaof Periodontal Tissues: Reportof 45 Cases, Periodontics 6: 272-276,

1968.

211-217,

1977.

Owings,J. R.: An AtypicalGingivostomatitis: A Reportof Four Cases, J. Periodontol. 40: 538542,1969. 5. Perry,H. O., Deffner,N. F., andSheridan, P. J.: AtypicalGingivostomatitis, Arch.Dermatol.107:872-878,1973. 6. Kerr, D. A., McClatchey, K. D., andRegezi,J. A.: Idiopathic Gingivostomatitis, ORAL SURG. 32: 402-423, 1971. 7. Kerr, D. A., McClatchey,K. D., andRegezi,J. A.: Allergic Gingivostomatitis (Dueto GumChewing),J. Periodontol. 42: 709-712,1971. 8. Silverman, S., andLozada,F.: An Epilogue to Plasma-Cell Gingivostomatitis (Allergic Gingivostomatitis), ORAL SURG. 43: 4.

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Dr. J. W. Eveson

Department of OralMedicineandPathology Guy’sHospital LondonSE19RT,England