Case Letter

Oral Lichen Planus With Malignant Transformation to Invasive Squamous Cell Carcinoma

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Clinically, OLP lesions are known to be more chronic in nature than cutaneous lichen planus.7 There are 6 classifications of OLP: reticular (lacy white with Wickham striae), plaquelike, papular, atrophic, bullous, and erosive. The latter 3 are known to be the more symptomatic manifestations.3,7 Of note, the atrophic and erosive forms are believed to account for the vast majority of cases of malignant transformation of OLP to OSCC. Approximately 90% of patients have involvement of multiple oral sites, with the most common affected areas being the buccal mucosa (90%), gingival margin (56%), and dorsal tongue (34%).7 Symptoms include increased sensitivity to foods, intense local pain, and coarse-feeling mucosa. The nature of the disease favors an active-quiescent-active course, with flares occurring after direct irritation (ie, dental procedures, Köbner phenomenon), emotional stress, medication use, and systemic illness.7 The differential diagnosis of OLP includes bite trauma, candidiasis, pemphigus, leukoplakia, lichenoid drug reaction, pemphigoid, and graft-versus-host disease.4 Red flags of malignant transformation include induration, worsening ulceration in the setting of previously effective therapy, and presence of constitutional symptoms.

Regarding the behavior of OSCC after malignant transformation, the literature seems to suggest a tendency for well-differentiated noninvasive tumors that most often occur on the buccal mucosa (43%), tongue (33%), gingiva (19%), and palate (4.8%).8 Interestingly, one study described that only 1 (4.8%) of 21 patients with OLP and OSCC was deemed as having stage II or higher disease at time of diagnosis. Likewise, 90% of the biopsied samples revealed well-differentiated carcinomas.8 These findings clearly contrast with our case in which the patient experienced rapid conversion of localized OSCC to more invasive disease. Also of consequence in this study was the finding that a relatively high proportion of patients (29% [6/21]) developed at least one other primary OSCC lesion over the course of follow-up.8 This finding is consistent with our patient.

Last, management of OLP lesions is most commonly accomplished with topical steroids such as fluocinolone acetonide or triamcinolone acetonide.3 Treatment of gingival disease may be enhanced with the use of form-fitting trays.2 For refractory erosive disease, tacrolimus ointment has been demonstrated as a useful backup therapy but may actually be associated with the development of OSCC through alteration of MAPK and p53.3 Some investigators suggest regular 4-month 
follow-up of OLP patients to detect if acute worsening and or refractoriness to treatment have signified early dysplastic change. Various scoring systems also have been suggested for following up on the severity of OLP lesions.3

The management of OSCC usually is accomplished via surgery, radiation, or both. The decision is dependent on tumor stage and the patient’s individual limitations. It is highly recommended that patients with OSCC arising from OLP be closely followed after diagnosis of cancer, with some sources suggesting follow-up every 2 months for the first 6 to 9 months after diagnosis due to the relatively high rate of discovery of nodal metastases and new primary lesions in that critical time span.8 Thereafter, an examination every 4 months is suggested as sufficient for detecting future complications.


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