Lichen planus is a chronic mucocutaneous inflammatory disease that often affects the oral mucosa and is the most common dermatologic disease to affect the oral cavity.19 The etiopathogenesis is unknown, but the prevailing view postulates there is an underlying dysregulated T-lymphocyte response to autologous keratinocyte antigens or exogenous triggers.20 OLP is estimated to affect 0.5 -2.2% of the population and there is a distinct female predilection.13 OLP is associated with an increased risk of malignant transformation of about 1.1%.21
In some cases of OLP, extrinsic antigens such as dental materials, medications (e.g., antimalarials, NSAIDs, cardiovascular agents, and hypoglycemics) have been identified as causative triggers. Lesions with an identifiable trigger are more appropriately termed oral lichenoid reactions (OLRs). ORLs are allergic reactions that usually resolve upon removal of the trigger and do not maintain the chronic character of OLP.22
The cutaneous component of lichen planus is characteristically described as purple, polygonal, pruritic, plaques or papules affecting the trunk or extremities.19 Up to 65% of patients with cutaneous lichen planus will develop oral lesions concomitantly.19 OLP is typically bilateral and may be categorized as reticular, atrophic or erosive. Reticular OLP is the most recognizable pattern and manifests hyperkeratotic striations in a characteristic lacey pattern (Wickhams striae), keratotic plaques and papules. Atrophic OLP presents as erythematous patches and erosive OLP presents as shallow ulcerations.
The clinical manifestation of OLP is dynamic and patients often present with a combination of reticular, atrophic or erosive forms. The most commonly affected site is the buccal mucosa, but any area may be affected (Figure 4). Gingival OLP often presents as desquamative gingivitis, a clincal description that is also frequently observed in mucous membrane pemphigoid and pemphigus vulgaris. Pain and sensitivity to spicey foods is often observed, most typically with the atrophic and erosive forms.
Figure 4. Oral Lichen Planus 65-year-old Male.
There is no cure for OLP and therapeutic strategies are aimed to decrease inflammation, promote healing and alleviate symptoms. Asymptomatic OLP only requires routine monitoring for change. Mild or intermittent symptomatic localized cases often respond to topical glucocorticoid gels or ointments (0.1% triamcinalone acetonide, 0.1% betamethasone valerate, 0.05% fluocinonide, 0.05% clobetasol) on an as needed basis.19,23
The use of a soft resilient splint as a medication delivery tray facilitates the administration of the medication in cases of gingival OLP. Dexamethasone elixir (0.5mg/5mL) may be a more convenient and effective choice for widepsread eruptions or lesions affecting the tongue. As a rule, therapy should be titrated to the minimal amount necessary to provide symptom relief.19
For lesions resistent to topical steroid therapy or where glucocorticoids are contraindicated, the use a topical calcineurin inhibitor may be beneficial. Calcineurin inhibitors (e.g., tacrolimus, pimecrolimus) suppress cellular immunity (inhibit T-lymphocyte activation).24,25 Topical tacrolimus and pimecrolimus can be administered to the affected area 2 times a day.
The most common side effect reported is burning after application. Patients should be advised of the potential increased risk for malignancy associated with the use of tacrolimus.23 Either drug should be used as a second-line option and therapy should be titrated to the minimal amount necessary to provide symptom relief.23 Isolated recalcitrant lesions, may respond well to intra-lesion injection of triamcinolone acetonide (10mg/mL, injecting 0.1mg/cm3).13
For recalcitrant OLP, an empirical short-term course of a systemic glucocorticoid such as prednisone 0.5 mg/kg/day as a single dose in the morning, tapered down over 2 weeks may be prescribed in conjunction with a topical maintenance regimen described above.19 Patient with OLP not responding to short-term systemic steroid therapy should be referred to a dermatologist for long-term combination immunopharmacotherapy, which may include glucocorticoids, azathioprine, cyclosporine, methotrexate, TNF-α inhibitors, and others immunomodulators.23