Gingival Erosive Lichen Planus: Case Report


Regina Garcia DORTA1
João Batista de SOUZA2
Denise Tostes OLIVEIRA1

1Department of Stomatology, Area of Pathology, Faculty of Dentistry of Bauru, University of São Paulo, Bauru, SP, Brazil

2Department of Prevention and Oral Rehabilitation, Faculty of Dentistry, Federal University of Goiâs, Goiânia, GO, Brazil


Correspondence: Dra. Denise Tostes Oliveira, Av. Getúlio Vargas 4-82, apto 301-B, 17045-000 Bauru, SP, Brasil. e-mail: d.tostes@travelnet.com.br


Braz Dent J (2001) 12(1): 63-66 ISSN 0103-6440

INTRODUCTION | CASE REPORT | DISCUSSION | RESUMO | REFERENCES


A case of gingival erosive lichen planus is presented with special emphasis on its clinical and microscopic characteristics. The differential diagnosis and the controversy associated with the malignant potential of oral lichen planus is also discussed.

Key Words: lichen planus, desquamative gingivitis, oral cancer, premalignancy.


INTRODUCTION

A broad range of systemic diseases may have gingival lesions, including lichen planus. The oral manifestation of lichen planus generally has typical clinical aspects and distribution, but the atrophic and erosive forms may be challenging even for the most experienced dental practitioner (1).

Atrophic lesions account for 5% to 44% of oral lichen planus manifestations, while the erosive and/or ulcerative ones vary between 9% and 46% of cases (1). This higher frequency of erosive lichen planus compared to the reticular and atrophic forms, as previously observed by Silverman and Bahl (2), is probably the result of the symptomatic nature of this lesion, which often prompts an evaluation visit.

The occurrence of erosive lichen planus confined to the gingival mucosa is characterized by the presence of diffuse erythematous areas that may or may not be interspersed with desquamative and ulcerated foci. The lesions may occur following the gingival outline and hyperkeratotic radiating striae can be found at the periphery of the erosive regions, simplifying diagnosis. This clinical appearance known as desquamative gingivitis is not pathognomonic of oral erosive lichen planus and may represent the gingival manifestation of many other diseases such as cicatricial
pemphigoid, pemphigus vulgaris, lupus erythematosus, epidermolysis bullosa acquisita, and linear IgA disease. Hormonal dysfunction, candidosis, lichenoid lesions and the vulvo-vaginal-gingival syndrome must also be included in the differential diagnosis of oral erosive gingival lichen planus (3-6). In addition, lichenoid lesions must be distinguished from oral lichen planus because these lesions are similar both clinically and microscopically. Generally, lichenoid lesions resolve after removal of the inciting agent, such as dental amalgams or drugs (5), while lichen planus usually requires the use of topical or systemic corticosteroids for improvement.

Frequently, the atrophic and erosive forms of lichen planus cause pain and burning in the affected area. Difficulties in the establishment of diagnosis of gingival lichen planus may arise if gingivitis and periodontitis are superimposed on the lesions (4). Biopsy is mandatory in cases of oral erosive lichen planus because the clinical characteristics simulate a wide spectrum of systemic diseases.

The precise etiology of the disease, however, remains elusive, but initial lesions are the result of the destruction of basement membrane and basal cell layer of the epithelium by immune cells. It appears that an early event in lichen planus is the change in the plasma membrane of the keratinocytes resulting in altered antigen expression and the appearance of new surface antigens. It has not yet been established whether alterations are primary changes, induced by a variety of external agents such as drugs and contact allergens, or secondary events, induced by cytokines such as gamma-interferon released by the inflammatory cell infiltrate (7).

The malignant potential of lichen planus is still controversial in the literature and it has been commonly associated with the atrophic and erosive forms (1,2,5,8). Most cases of reported malignant transformation are rather poorly documented. Some of these cases may not have been true lichen planus, but rather may have actually been dysplastic leukoplakias with secondary lichenoid inflammatory infiltrate that mimicked lichen planus (5).

A case of gingival erosive lichen planus, with special emphasis on its clinical and microscopic features, is presented. The importance of periodic disease reevaluation and malignant potential of lichen planus is also discussed.


CASE REPORT

A 41-year-old female patient was referred to the Dental School of Bauru, University of São Paulo for restorative treatment. Oral examination showed the presence of multiple bilateral erythematous and desquamative areas on both upper and lower buccal gingival mucosa (Figure 1). The lesions were slightly symptomatic and followed the gingival outline without involvement of the gingival margin. There was good dental plaque control and gingival alterations were not
directly associated with dental restorations or any evident systemic disease, drugs, smoking or genetic predisposition. On anamnesis, the patient did not report any history of allergy to amalgam or other dental materials. An incisional punch biopsy was performed from the periphery of the posterior upper gingival lesion. The histopathologic examination of the gingival lesion showed a flattened epithelium with liquefaction of the basal layer and juxtaepithelial areas of chronic inflammatory infiltrate. The diagnosis was gingival erosive lichen planus according to both clinical and histopathological patterns.

The patient was treated with a corticosteroid applied topically to the gingiva twice daily (triamcinolone acetonide, Omcilon-A, Bristol-Myers Squibb Brasil S/A, São Paulo, SP, Brazil). The complete remission of lesions was observed after two months (Figure 2) and a one-year follow-up did not detect exacerbation of the lesions.


DISCUSSION

Gingival lesions of lichen planus, as described in this case, may cause difficulties in diagnosis. When considering the site chosen for biopsy, ulcerated areas should be avoided, because they make microscopic features confusing. Furthermore, initial lesions may have an unspecific histopathologic pattern represented by chronic inflammatory infiltrate (4). A second biopsy or immunohistochemical and immunofluorescence evaluation may be necessary for the differential diagnosis with those systemic diseases which can mimic, clinically or microscopically, lichen planus (6,9).

The presence of gingival erosive lichen planus in women may be associated with the vulvo-vaginal-syndrome. It has been characterized by erosion and desquamation of the vulva, vagina and gingiva (3). All patients presenting oral lesions of lichen planus should be questioned about and examined specifically for signs of genital involvement. In the present case, the patient did not have any other signs, except for the gingival lesions.

Most cases of oral lichen planus are often asymptomatic but the atrophic and/or erosive forms cause varied degrees of discomfort, which prompts the search for early professional care. However, as in the present case, patients may have the disease for a long time because lichen planus is a chronic condition characterized by recurrent exacerbation and remission periods.

The malignant transformation of oral erosive and atrophic lesions has been described between 0.3% to 12.5% depending on different criteria adopted by the authors. The development of squamous cell carcinoma may occur in areas directly affected by lichen planus, as well as in other areas of the oral mucosa (10). However, it is not established if atrophic and erosive forms of lichen planus have an intrinsic potential for malignant transformation or if the disorder facilitates the development of oral mucosa squamous cell carcinoma by influence of exogenous carcinogens (11).

It has been suggested that the close cell-to-cell interaction observed in lichen planus and the subsequent release of cytokines by keratinocytes, mononuclear inflammatory cells and dendritic cells modifies the tissue and cell surface proteins to the effect that the tissue becomes more prone to dysplastic or malignant transformation. The close cell contact with intrinsically released chemicals may change the amplification and structure of cell surface proto-oncogene proteins and/or proto-oncogenes so that the control of cell growth is distorted, eventually leading to malignancy. The external factors affecting oral soft tissues (for example tobacco and alcohol) also cannot be excluded from co-influencing the tissue transformation (11).

As stated before, there is no consensus of the malignant potential of oral lichen planus, and some authors believe that this assumption arose as a result of misconceptions, misdiagnosis and misinterpretations reported in the literature and legitimized with time. Many published cases of oral lichen planus with malignant transformation occurred in patients with a known history of exposure to carcinogens, others represented diagnostic errors or even insufficient evidence to prove that lichen planus was present at the outset. The most important failures would probably occur in microscopic identification of changes in epithelial maturation with cellular aberrations that range from mild atypia to frank dysplasia (12).

Since the etiology of lichen planus is not totally clarified (1,11), the therapeutic goal is palliative rather than curative. Symptomatic lichen planus is usually treated with anti-inflammatory medication, while gingival lesions are treated with topical corticosteroids. Patients should be advised to maintain good control of dental plaque in order to avoid superimposed gingivitis and periodontitis.

Although oral lichen planus is not considered a premalignant condition by some authors (12-14), the erosive and atrophic forms lack the normal epithelial protective barrier and thus may be more vulnerable to exogenous carcinogens. For this reason constant follow-up of erosive lichen planus is recommended for early diagnosis of suspected transformed lesions. Other authors, however, believe that oral lichen planus is undoubtedly a premalignant condition, justifying more aggressive treatment and strict follow-up for long periods (2,15,16).

Finally, since this issue will remain controversial for some time, it must be emphasized that although a strict follow-up of erosive lichen planus is necessary, dissemination of cancerophobia among both professionals and patients should be avoided.


RESUMO

Dorta RG, de Souza JB, Oliveira DT. Líquen plano erosivo gengival. Relato de caso. Braz Dent J 2001;12(1):63-66.

Um caso de líquen plano erosivo será apresentado com especial ênfase para suas características clínicas e microscópicas. O diagnóstico diferencial e a controvérsia relacionada ao potencial de malignização do líquen plano também serão revisados.

Unitermos: líquen plano, gengivite descamativa, câncer bucal, condição cancerizável.


REFERENCES

1. Scully C, Beyli M, Ferreiro MC, Ficarra G, Gill Y, Griffiths M, Holmstrup P, Mutlu S, Porter S, Wray D. Update on oral lichen planus: etiopathogenesis and management. Crit Rev Oral Biol Med 1998;9:86-122.

2. Silverman Jr S, Bahl S. Oral lichen planus update: clinical characteristics, treatment responses, and malignant transformation. Am J Dent 1997;10:259-263.

3. Pelisse M. The vulvo-vaginal-gingival syndrome: a new form of erosive lichen planus. Int J Dermatol 1989;28:381-384.

4. Rubira IR, Gobetti JP. Gingival lichen planus: a diagnostic problem. J Mich Dent Assoc 1994;76:44-48.

5. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral & Maxillofacial Pathology. Philadelphia: W.B. Saunders Company; 1995.

6. Yih W, Maier T, Kratochvil FJ, Zieper B. Analysis of desquamative gingivitis using direct immunofluorescence in conjunction with histology. J Periodontol 1998;69:678-685.

7. Soames JV, Southam JC. Oral Pathology. 2nd ed. New York: Oxford University Press; 1996.

8. Vallejo MJG, Lapiedra C. Liquen plano de la mucosa oral. Rev Clin Esp 1998;198:448-457.

9. Markopoulos AK, Antoniades D, Papanayotou P, Trigonidis G. Desquamative gingivitis: a clinical, histopathologic, and immunologic study. Quintessence Int 1996;27:763-767.

10. Duffley DC, Eversole LR, Abemayor E. Oral lichen planus and its
association with squamous cell carcinoma: an update on pathogenesis and treatment implications. Laryngoscope 1996;106:357-362.

11. Kilpi A, Rich AM, Reade PC, Konttinen YT. Studies of the inflammatory process and potential of oral mucosal lichen planus. Aust Dent J 1996;41:87-90.

12. Eisenberg E, Krutchkoff DJ. Lichenoid lesions of the oral mucosa. Diagnostic criteria and their importance in the alleged relationship to oral cancer. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1992;73:699-704.

13. Krutchkoff DJ, Eisenberg E. Lichenoid dysplasia: a distinct histopathologic entity. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1985;30:308-315.

14. Allen CM. Is lichen planus really premalignant? (editorial): Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:347.

15. Doyle JL, Miele JF, Ford AS. Diagnosis and treatment of erosive lichen planus: report of two cases. J Oral Med 1985;40:18-22.

16. Lo Muziu L, Mignogna MD, Favia G, Procaccini M, Testa NF, Bucci E. The possible association between oral lichen planus and oral squamous cell carcinoma: a clinical evaluation on 14 cases and a review of the literature. Oral Oncol 1998;34:239-246.


Accepted April 5, 2000
Braz Dent J 12(1) 2001


BACK TO CONTENTS