Diagnosis: oral lichen planus
Compared with the more self-limited nature of its cutaneous counterpart, oral lichen planus (OLP) causes more chronic inflammatory lesions, resulting in increased morbidity and a greater therapeutic challenge for physicians. Of the 3 basic clinical morphologies of the disease (reticular, erythematous, and erosive), the last form tends to be more symptomatic and prompts patients to seek treatment.1,2 The more asymptomatic reticular form is the most easily recognizable variant and may cause increased symptoms when involving the tongue, typically manifesting on the dorsal surface.1
In contrast to reticular lesions in other oral sites, tongue lesions do not usually exhibit the characteristic interlacing pattern of white, raised striae; instead they manifest as well-demarcated areas with a patch-like pattern of erythematous, atrophic, and keratotic regions. 3 Erosive OLP more commonly involves the lateral tongue and displays erythematous or ulcerated areas with peripheral keratosis, forming fine centrifugal striae.3
Oral lichen planus affects approximately 1% to 4% of the population 4 and is seen most commonly in older women.1,5,6 It has a predilection for bilateral involvement of the buccal mucosa but may also affect (in descending order of frequency) the tongue, gingiva, lips, floor of the mouth, and palate.1,2 Isolated involvement of only 1 oral site is infrequent, with the exception of gingival lesions.1 Extraoral cutaneous lichen planus has been reported in 16% to 44% of patients with oral disease; it most frequently involves the genital mucosa, as well as the scalp, nails, and esophageal and ocular mucosae.4 A multidisciplinary approach including generalists, dermatologists, otolaryngologists, ophthalmologists, and gynecologists may be necessary for patient evaluation and management.
Pathogenesis of oral lichen planus
Although the precise cause of OLP is unknown, its pathogenesis has been linked to an autoimmune mechanism involving autocytotoxic CD8+ T cells, which trigger apoptosis (programmed cell death) of basal keratinocytes.4,7 An imbalance between T cell helper and suppressor activity has also been observed.1,7
Complications: Carcinoma, chronic liver disease
Malignant transformation to squamous cell carcinoma (SCC) is seen in 0.4% to 5% of patients with OLP, particularly those with erosive and erythematous disease.1,2 Increased risk factors for SCC have not been identified in these patients, but a greater prevalence of Candida albicansmay be associated with carcinogenesis, as may herpes simplex and human papilloma viruses, immunosuppressive therapy, and an inflammatory cytokine-rich microenvironment.1