Oral lichen planus
OLP; "Wickham striae of the oral cavity"; (with cancer transformation, "OLP-related SCC"); oral lichenoid lesions (OLL โ overlap with drug / restoration / GVHD reactions)
Oral lichen planus is a chronic T-cell-mediated inflammatory disorder of the oral mucosa, affecting ~1โ2% of adults globally with a strong female predominance (3:1) and onset typically in middle age. The clinical phenotype spans six WHO subtypes โ reticular (the commonest, with characteristic Wickham striae), plaque-like, papular, atrophic, erosive / ulcerative and bullous โ with the atrophic and erosive subtypes producing painful symptoms and the reticular subtype often asymptomatic. The skin-oncology importance is the recognition by the World Health Organization that OLP is a "potentially malignant disorder" with a lifetime SCC transformation rate estimated at ~1โ3%, particularly for the atrophic and erosive subtypes on the lateral / ventral tongue, and especially in long-standing disease. The chronic inflammation, microbiome changes, and lichenoid inflammatory infiltrate are the postulated mechanisms. Surveillance, biopsy of any change, smoking cessation and effective inflammatory control with topical corticosteroids and calcineurin inhibitors are the cornerstones. Oral lichenoid drug reactions (lichenoid lesions adjacent to dental amalgam, or related to systemic medications) and chronic oral GVHD are clinical / histological mimics with overlapping malignant potential.
Clinical features & subtypes
- Bilateral, symmetrical involvement of buccal mucosa, lateral / dorsal tongue, gingiva, lips and floor of mouth.
- Six WHO subtypes:
- Reticular OLP โ fine white "Wickham striae" in a lacy, reticular network on buccal mucosa; commonest; usually asymptomatic.
- Plaque-like OLP โ thicker white plaques, especially on dorsal tongue.
- Papular OLP โ small individual white papules.
- Atrophic OLP โ red atrophic mucosa with surrounding white striae; symptomatic.
- Erosive / ulcerative OLP โ painful erosions / ulcers with surrounding white striae; the most clinically significant variant; substantial functional impact.
- Bullous OLP โ uncommon; sub-epithelial bullae with surrounding striae.
- Cutaneous lichen planus, nail / scalp / vulval / penile / oesophageal involvement may co-exist.
- Median age 40โ60; F:M ~3:1.
Risk of malignant transformation
- WHO recognises OLP as a "potentially malignant disorder" with lifetime SCC transformation rate ~1โ3%.
- Risk factors for transformation:
- Atrophic / erosive / ulcerative subtype.
- Lateral / ventral tongue location โ the highest-risk anatomical site.
- Long-standing disease (>5 years).
- Tobacco / alcohol use.
- HPV co-infection.
- Immunosuppression.
- Chronic Candida co-infection.
- Concomitant oral leukoplakia or erythroplakia.
- The transformation rate is contested โ some authors argue that "OLP-related SCC" cases reflect misdiagnosis of OLP-mimicking lichenoid dysplasia, and that strict-diagnosis OLP carries lower risk than commonly cited.
- Regardless of the specific transformation rate, surveillance and biopsy of any change are mandatory.
Diagnosis
- Clinical recognition of the characteristic bilateral symmetrical reticular / atrophic / erosive features.
- Biopsy โ incisional from edge of lesion, including some clinically uninvolved mucosa for comparison.
- Histology โ band-like ("lichenoid") sub-epithelial lymphocytic infiltrate at the basement membrane, basal cell vacuolar degeneration, civatte (apoptotic) bodies, hyperkeratosis / parakeratosis.
- Direct immunofluorescence โ fibrinogen along basement membrane in shaggy linear pattern; rules out other vesiculobullous diseases.
- Differential โ oral lichenoid drug reaction (lichenoid features adjacent to dental amalgam or systemic drug โ ACEi, NSAIDs, ฮฒ-blockers, antimalarials, gold), chronic oral GVHD, lupus, leukoplakia, candidiasis.
- Investigate for triggers โ drug history, dental amalgam pattern, hepatitis C serology (debated association in some populations).
Management
- Multidisciplinary care โ oral medicine, dermatology, dental surgery, ENT.
- First-line:
- Topical ultrapotent corticosteroid (clobetasol propionate 0.05% gel / orabase) applied to lesions 2โ3 times daily until controlled then reducing.
- Topical calcineurin inhibitor (tacrolimus 0.1% in orabase, pimecrolimus 1%).
- Topical anaesthetic / analgesic (lignocaine gel, viscous) for symptomatic relief.
- Optimise oral hygiene โ soft toothbrush, atraumatic dental care.
- Refractory disease:
- Intralesional triamcinolone injections.
- Systemic corticosteroid pulse (prednisolone 0.5โ1 mg/kg/day, taper over weeks).
- Hydroxychloroquine, mycophenolate, azathioprine, methotrexate.
- Photodynamic therapy.
- Topical retinoids.
- JAK inhibitors (tofacitinib, baricitinib) โ emerging.
- Biologics (rituximab, anti-IL-23) โ refractory / multisite disease.
- Trigger management โ withdraw / substitute lichenoid-inducing drugs; replace amalgam restorations with gold / ceramic if patch test positive.
- Smoking and alcohol cessation.
- Surveillance:
- 3โ6-monthly clinical review by oral medicine.
- Biopsy any change, ulceration, focal thickening, induration.
- Lifelong.
- Refer suspicious lesions to head and neck cancer MDT.
References
- Carrozzo M et al. Oral lichen planus โ a disease or a spectrum of tissue reactions? Periodontol 2000; 2019.
- Warnakulasuriya S et al. Oral potentially malignant disorders โ consensus report from an international seminar on nomenclature and classification. Oral Dis; 2021.
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