Oral Lichen Planus

§ overviewOverview

A chronic, immunologically mediated mucocutaneous disease characterised by CD8+ T-cell-directed apoptosis of basal keratinocytes, presenting with bilateral, symmetrical white striae and/or erosions of oral mucosa.

§ icdICD Classification

ICD-10 L43.9

§ etiologyEtiology

• 01Idiopathic — T-cell autoimmune reaction against basal keratinocytes
• 02Hepatitis C virus association (particularly in Mediterranean populations)
• 03Drug reactions (lichenoid): ACE inhibitors, NSAIDs, β-blockers, antimalarials, sulphonylureas
• 04Dental materials (amalgam, gold, composites — lichenoid contact reaction)
• 05Stress and anxiety (exacerbating factor)

§ riskRisk Factors

• 01Female, 30–60 years
• 02Hepatitis C infection
• 03Psychological stress
• 04Autoimmune comorbidity (diabetes, thyroid disease)

§ geneticsGenetics & Molecular Biology

• 01HLA-DR1, HLA-DQ1 associations
• 02Polymorphisms in TNF-α, IFN-γ, IL-10 genes

§ epidemiologyEpidemiology

Prevalence 1–2%; female:male 2:1; peak 4th–6th decade. Cutaneous involvement in ~15% of oral cases.

§ pathogenesisPathogenesis

Antigen presentation by basal keratinocytes activates CD8+ cytotoxic T cells → band-like sub-epithelial lymphocytic infiltrate → apoptosis of basal keratinocytes (Civatte bodies) → basement membrane damage. Chronic inflammation drives hyperkeratosis (reticular striae).

§ clinicalClinical Features

• 01Bilateral, symmetrical distribution — hallmark feature
• 02Reticular — interlacing white Wickham striae (most common, asymptomatic)
• 03Papular — small white papules
• 04Plaque-like — homogeneous white plaque mimicking leukoplakia
• 05Atrophic — red, thinned mucosa with striae at margins
• 06Erosive — painful ulcers with peripheral striae
• 07Bullous — rare, fluid-filled blisters that rupture
• 08Common sites: posterior buccal mucosa (bilaterally), tongue, gingiva (desquamative gingivitis)
• 09Skin: purple, pruritic, polygonal, planar papules (6 Ps) on flexor surfaces
• 10Nails, scalp (lichen planopilaris), genital mucosa may be involved

§ signsSigns & Symptoms

• 01Asymptomatic in reticular type
• 02Burning, roughness, pain (atrophic/erosive)
• 03Sensitivity to spicy/acidic foods
• 04Bleeding from erosive lesions

§ differentialDifferential Diagnosis

• 01Leukoplakia
• 02Lichenoid drug/contact reaction
• 03Lupus erythematosus (discoid)
• 04Chronic graft-versus-host disease
• 05Mucous membrane pemphigoid
• 06Pemphigus vulgaris
• 07Candidiasis
• 08Erythema multiforme

§ criteriaDiagnostic Criteria

• 01Modified WHO 2003 criteria — clinical (bilateral, symmetric, reticular) + histological (band-like lymphocytic infiltrate, basal cell liquefaction, no dysplasia) required
• 02Direct immunofluorescence to exclude vesiculobullous diseases

§ histopathHistopathology

• 01Hyperkeratosis (ortho- or para-)
• 02Saw-tooth (irregular acanthosis) rete ridges
• 03Liquefactive degeneration of basal cell layer
• 04Civatte (colloid) bodies — apoptotic keratinocytes
• 05Dense band-like sub-epithelial lymphocytic infiltrate (mainly CD8+ T cells)
• 06Absence of epithelial dysplasia (if present, re-classify as lichenoid dysplasia)

§ investigationsInvestigations

• 01Incisional biopsy including intact epithelium and lamina propria
• 02Direct immunofluorescence: shaggy fibrinogen deposition at BMZ, Civatte bodies stain for IgM
• 03Hepatitis C serology (endemic areas)
• 04Patch testing if contact lichenoid reaction suspected

§ ihcIHC / Special Stains

• 01CD8+ T-cell predominance in infiltrate
• 02Cytokeratin markers to confirm epithelial origin
• 03Ki-67 to exclude dysplasia

§ whoWHO Classification

Included as OPMD (WHO 2022) — erosive and atrophic subtypes carry the highest risk.

§ classificationClassification

• 01Andreasen 6 types: reticular, papular, plaque-like, atrophic, erosive, bullous
• 02Clinically: keratotic (reticular/papular/plaque) vs non-keratotic (atrophic/erosive/bullous)

§ planTreatment Planning

• 01Confirm diagnosis histologically + DIF
• 02Identify and eliminate lichenoid triggers (drugs, dental materials)
• 03Symptomatic control based on severity
• 04Long-term surveillance for malignant transformation

§ treatmentTreatment

• 01Reticular / asymptomatic: reassurance, oral hygiene, observation
• 02Symptomatic (atrophic/erosive): topical high-potency corticosteroids (clobetasol 0.05%, fluocinonide) as gel or in orabase
• 03Intralesional triamcinolone for localised persistent erosions
• 04Systemic corticosteroids (prednisolone 40–60 mg/day tapering) for severe widespread disease
• 05Topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus) — steroid-sparing
• 06Systemic immunomodulators: azathioprine, mycophenolate, hydroxychloroquine, methotrexate, retinoids for refractory cases
• 07Chlorhexidine mouthwash; antifungals to cover steroid-induced candidiasis

§ medicalMedical Management

• 01Topical clobetasol propionate 0.05% BD–TDS
• 02Topical tacrolimus 0.1% BD (short courses)
• 03Systemic prednisolone in severe erosive disease
• 04Nystatin/miconazole to prevent secondary candidiasis

§ surgicalSurgical Management

• 01Excision only for isolated dysplastic plaque-like lesions
• 02CO2 laser for refractory erosions (limited evidence)

§ complicationsComplications

• 01Malignant transformation to oral SCC
• 02Secondary candidiasis (from steroid use)
• 03Steroid mucosal atrophy
• 04Chronic pain and impaired quality of life

§ recurrenceRecurrence Rate

Chronic relapsing–remitting course; complete remission uncommon. Requires long-term maintenance.

§ followupFollow-up Protocol

• 013-monthly during active disease
• 026-monthly once controlled
• 03Annual review lifelong with re-biopsy of any changing lesion

§ prognosisPrognosis

Chronic disease; malignant transformation ≈ 1% over 5 years (higher for erosive/atrophic types).

§ preventionPrevention

• 01Identify and remove drug/dental material triggers
• 02Stress management
• 03Regular oral cancer surveillance

§ examKey Examination Points

• 01Bilateral symmetry?
• 02Type of lesion (reticular/atrophic/erosive)?
• 03Skin, nail, genital involvement?
• 04Drug and dental history?

§ revisionQuick Revision Summary

• 016 Andreasen types
• 026 Ps of cutaneous LP: Purple, Pruritic, Polygonal, Planar, Papules
• 03Basal cell degeneration + saw-tooth rete + band-like infiltrate
• 04Topical clobetasol = first line
• 051% MT over 5 years

§ vivaBDS Viva Questions

• 01Define OLP and list Andreasen's 6 types.
• 02What are Wickham striae?
• 03Describe histopathology of OLP.
• 04Difference between OLP and lichenoid reaction.
• 05Role of direct immunofluorescence in OLP.
• 06First-line treatment of erosive OLP.
• 07Malignant transformation risk of OLP.
• 08What is desquamative gingivitis?
• 09Name systemic drugs causing lichenoid reactions.
• 10Skin manifestations of lichen planus (6 Ps).

§ bdsBDS Professional Examination

• 01Classify OLP. Describe the clinical features, histopathology and management of erosive lichen planus (10 marks).
• 02Short note: Wickham striae.

§ fcpsFCPS Residency Questions

• 01Discuss the immunopathogenesis of oral lichen planus and evidence-based management of steroid-refractory disease.
• 02Debate the malignant potential of OLP.

§ pearlsClinical Pearls

• 01Bilateral, symmetric, reticular — think OLP first.
• 02Steroid + antifungal together — steroids provoke candidiasis.
• 03Re-biopsy any long-standing lesion that changes character.

§ mnemonicsMnemonics

• 016 Ps of LP: Purple, Pruritic, Polygonal, Planar, Papules, (+ Plaque)

§ readingSuggested Reading

• 01Sugerman PB et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med 2002.
• 02Al-Hashimi I et al. Oral lichen planus and lichenoid lesions — consensus report. OOOOE 2007.

§ differentialDifferential Comparison

§ mcqsMCQs — Assessment (8)

§ relatedRelated Diseases

References

1. Neville BW. Oral & Maxillofacial Pathology, 4e
2. Regezi JA. Oral Pathology, 7e
3. WHO Head & Neck Tumours 5e (2022)