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Spring 2004

Clinical Case Discussions

Contributed by Dr. Beatrice Gandara, University of Washington.

Oral Lichen Planus: A Potential Premalignant Lesion

Case Histories
Case # 1: This is a 49-year-old Vietnamese male with white lesion with striae involving bilateral buccal mucosa clinically consistent with lichen planus. The patient has several years history of tobacco use—cigarettes a few per day. He presented recently with a white patch on the buccal mucosa (Fig 1). An incisional biopsy showed carcinoma in situ with probable superficially invasive squamous cell carcinoma (Fig 2) arising in lichen planus. Three previous biopsies showed progression from mild epithelial dysplasia to carcinoma in situ. Lichen planus was confirmed with immunofluoresence studies.

Lichen planus, a common chronic immune mediated disease affecting 1-2% of the population, has a variety of clinical presentations, management, and predisposing factors that render it a family of diseases rather than one entity with a specific treatment modality (1,2). To be specific, lichen planus can be immune mediated, drug induced, associated with transplant rejection (also known as graft verses host disease), or associated with galvanic effect (when two separate restorations are in opposite contact with each other). It is also seen in families (though rarely), and is known to undergo a malignant transformation in about 2.5% of cases. Given the versatility of this disease, it is difficult to apply one treatment modality for all presentations (2,3).

The most common type of LP is the chronic T-lymphocyte-mediated disease where CD4 (early stage) and CD8 (later stages) T-lymphocytes are stimulated, releasing lymphokines such as tumor necrosis factor which lead to the destruction of the cells in the basal and parabasal cell layers (2). This type of oral LP tends to come and go, sometimes lasting a lifetime. Lichen planus of the skin usually resolve within 1-3 years while only 20% of oral LP cases resolve in that period of time. Lichen planus occurs in adults between 30 and 70 years of age with a strong female predilection (1-3). It is often associated with stressful lifestyles. Skin LP presents as purplish, pruritic papules with a white keratotic surface, commonly on the flexor surfaces of the wrists, trunk and the genitalia. Oral LP presents as keratotic and reticular (the reticular pattern is the most common type), atrophic or erosive (the erosive type is the most important clinically), or plaque-like (the hypertrophic type, which is the least common). Oral LP presents most commonly in a symmetrical manner on the bilateral buccal mucosa, followed by tongue and gingiva. Reticular type LP is asymptomatic and presents with interlacing lines against an erythematosus bluish background; the lines are known as the striae of Wickham. Erosive type LP, on the other hand, is symptomatic—patients complain of sensitivity to hot and cold, spicy, acidic, and alcoholic food and beverages. Erosive LP also presents in locations similar to those of the reticular type. At times, erosive LP can be hard to distinguish from other mucocutaneous diseases such as benign mucous membrane pemphigoid (BMMP) and pemphigus vulgaris (PV). Hyperplastic or plaque LP is uncommon and presents as a confluent white plaque often mistaken for leukoplakia. The hyperplastic type is more common on the dorsal surface of the tongue, gingiva, and palate, making a clinical diagnosis of LP difficult at times, especially if the patient is a smoker. LP can also present on the gingiva alone as a thin and atrophic lesion known as desquamative gingivitis. The clinical differential diagnosis for desquamative gingivitis should include BMMP and PV.

A discussion of LP would be incomplete without addressing Lichenoid Drug Reaction, a condition that is especially common in elderly patients. It most frequently present as erosive lichen planus on the bilateral buccal mucosa. It is associated with the ingestion of a number of medications including antibiotics, antihypertensive drugs, allopurinol (gout), diuretics, antidiabetics, gold, mercury, antibiotics, antihistamines and many others. The malignant potential of oral LP is a significant clinical concern, especially in long-term erosive lichen planus patients; transformation in reticular LP has also been documented, but rarely (4). The World Health Organization (WHO) defines oral LP as a precancerous condition (5) with the full understanding that the risk for transformation is very small, around 2.5%. The locations of transformation are not in the high-risk locations of the conventional oral SCC, but rather involve the buccal mucosa, tongue and gingiva—same locations as conventional lichen planus.

We have recently encountered three cases: one from the buccal mucosa (Figs 1-2), one from the gingiva, and one from the tongue. Two out of three of our patients were smokers, a risk factor encountered in oral LP patients with SCC, but not necessarily a major risk factor in the transformation of LP.

Lichen planus is a disease that requires both clinical and histological features to arrive to a definitive diagnosis. Depending on the LP type, the epithelium ranges from thin and erosive to thick and keratotic (2,3). All types have a band-like infiltrate of T-lymphocytes. The basal cell layer shows evidence of degeneration; rete pegs are or are not present, basement membrane zone is thickened, and cytoid bodies (Civatte bodies) may be present. The immunofluorescence (IMF) features (technique described in Oral Pathology newsletter, Jan 04 issue) include positive staining with antibody to fibrinogen present along the basement membrane. Treatment ranges from no treatment for the asymptomatic reticular type, to topical steroids, to intralesional steroid therapy (rarely used), to systemic steroid therapy (if the condition is severe such as in erosive LP). The best treatment for lichenoid drug reaction is replacement of the causing medication with a substitute. Treatment for transformation would follow the criteria for the treatment of oral squamous cell carcinoma, which are described in the April 2004 Case of the Month.

References

  1. Silverman S, Gorsky M et al. A retrospective study of findings and management in 214 patients with oral lichen planus. Oral Surg Oral Med Oral Pathol 1991; 72:665–670.
  2. Chiappelli F, Kung MA et al. Cellular immune correlates of clinical severity in oral lichen planus: preliminary association with mood states. Oral Dis. 1997; 3:64-70.
  3. Silverman S. Oral lichen planus: a potentially premalignant lesion. J Oral Maxillofac Surg 2000; 58:1286–1288.
  4. Duffey DC, Eversole LR et al. Oral lichen planus and its association with squamous cell carcinoma: an update on pathogenesis and treatment implications. Laryngoscope. 1996; 106:357-362.
  5. Pindborg JJ, Reichart PA et al. WHO International histological Clasification of Tumours. Histological typing of cancer and precancer of the oral mucosa. Springer, Berlin (1997).

For questions or comments, please email Dolphine Oda at doda@washington.edu