Lichen Planus (Adult)

1. Clinical Overview

Summary

Lichen planus (LP) is a chronic, immune-mediated inflammatory disorder affecting the skin, mucous membranes, hair follicles, and nails. First described by Erasmus Wilson in 1869, it is characterized by a distinctive clinical presentation summarized by the "6 Ps" mnemonic: Planar (flat-topped), Purple (violaceous), Polygonal, Pruritic, Papules, and Plaques. [1]

The pathognomonic feature is Wickham's striae—fine white lacy lines visible on the surface of papules and plaques, best appreciated with dermoscopy or mineral oil application. [2] These striae represent focal areas of hypergranulosis in the epidermis.

LP demonstrates a predilection for specific anatomical sites: flexor aspects of the wrists, ankles, lumbar region (presacral), and oral mucosa (especially buccal mucosa). The Koebner phenomenon (isomorphic response)—development of new lesions at sites of cutaneous trauma—is characteristically present in 25-50% of cases. [3]

The disease exhibits remarkable clinical heterogeneity with multiple variants including cutaneous, oral, genital, nail, and scalp (lichen planopilaris) presentations. While cutaneous LP is typically self-limiting with spontaneous resolution in 50-70% of cases within 1-2 years, oral and genital mucosal disease tends to be chronic and persistent, often lasting years to decades. [4]

A critical association exists between LP and hepatitis C virus (HCV), particularly in Mediterranean, Middle Eastern, and Japanese populations where prevalence ranges from 16-35% compared to 4-6% in other populations. [5] Long-standing erosive oral LP carries a small but significant risk of malignant transformation to oral squamous cell carcinoma (1-3% over 5-10 years), necessitating regular surveillance. [6]

Key Facts

• 6 Ps: Planar, Purple, Polygonal, Pruritic, Papules, Plaques
• Wickham's Striae: Pathognomonic white lacy network (hypergranulosis)
• Koebner Phenomenon: Present in 25-50% of cases
• Classic Sites: Flexor wrists (66%), ankles (53%), lumbar region (42%), oral mucosa (40-50%)
• Peak Age: 30-60 years (mean 45-55 years)
• Sex Ratio: Equal M:F for cutaneous; F>M (2:1) for oral
• HCV Association: 16-35% in Mediterranean/Asian populations; 4-6% elsewhere
• Natural History: Cutaneous resolves 1-2 years (50-70%); oral persists chronically
• Malignancy Risk: Oral erosive LP → SCC (1-3% over 5-10 years)
• First-Line Treatment: Potent topical corticosteroids (clobetasol propionate 0.05%)

Clinical Pearls

"6 Ps" Mnemonic: Systematic examination reveals Planar (flat-topped), Purple (violaceous), Polygonal, Pruritic Papules and Plaques. This classic presentation is highly suggestive of LP.

"Wickham's Striae = Diagnosis": Fine white lacy lines on papule surface are pathognomonic. Apply mineral oil or use dermoscopy to enhance visualization. Caused by focal hypergranulosis.

"Check the Mouth Always": 40-50% of patients with cutaneous LP have oral involvement, but 25% have oral LP alone. Examine buccal mucosa, tongue, gingiva, and palate systematically.

"Screen for Hepatitis C": Particularly in Mediterranean, Middle Eastern, Asian patients, or atypical presentations. Association strongest in these populations (16-35% vs 4-6% baseline).

"Erosive Oral = Cancer Surveillance": Erosive oral LP carries 1-3% SCC transformation risk over 5-10 years. Arrange regular (6-12 monthly) oral examination and biopsy any suspicious areas.

"Scalp LP = Urgent Treatment": Lichen planopilaris causes irreversible scarring alopecia. Early aggressive treatment (topical/intralesional steroids, hydroxychloroquine) is essential to prevent permanent hair loss.

"Post-Inflammatory Hyperpigmentation is the Rule": Particularly in darker skin types (Fitzpatrick IV-VI). Warn patients and manage expectations—pigmentation may persist months to years after inflammatory lesions resolve.

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2. Epidemiology

Incidence and Prevalence

Geographical and Ethnic Variation

Temporal Patterns

• Seasonal Variation: None consistently reported
• Duration of Cutaneous LP:
  • 50% resolve by 9 months
  • 85% resolve by 18 months
  • 15-20% persist beyond 2 years [8]
• Duration of Oral LP: Chronic and persistent; mean duration 5-10 years, often lifelong

Associated Conditions

Exam Detail: MRCP Examination Focus: In postgraduate exams, expect questions linking LP with HCV in Mediterranean/Asian populations. Know that screening for HCV is indicated in: (1) atypical presentations, (2) Mediterranean/Middle Eastern/Asian ethnicity, (3) generalized or severe disease, (4) presence of other HCV risk factors.

Oral LP Demographics: Remember the F>M (2:1) preponderance for oral LP, contrasting with equal sex distribution for cutaneous disease. This is a high-yield exam fact.

Malignancy Surveillance: The 1-3% risk of SCC transformation in erosive oral LP over 5-10 years justifies regular surveillance (6-12 monthly review). Erosive, atrophic, and ulcerative oral LP variants carry higher risk than reticular forms.

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3. Aetiology and Pathophysiology

Aetiology

The precise trigger for lichen planus remains unknown, but the disease represents a T-cell mediated autoimmune attack on basal keratinocytes. [10] Multiple potential triggers and associations have been identified:

Primary (Idiopathic) LP

• Majority of cases (70-75%)
• No identifiable trigger
• Likely multifactorial: genetic predisposition + environmental trigger

Secondary (Induced) LP

Medications Associated with Lichenoid Drug Eruptions

Exam Detail: High-Yield Drug List for Exams:

• Antimalarials: Hydroxychloroquine, chloroquine
• Thiazide Diuretics: Hydrochlorothiazide
• ACE Inhibitors: Captopril, enalapril
• NSAIDs: Naproxen, ibuprofen
• Beta-Blockers: Propranolol, labetalol
• Gold Salts: Gold sodium thiomalate
• Penicillamine
• Quinidine
• Methyldopa
• Phenothiazines
• Tetracyclines (especially demeclocycline)
• TNF-α Inhibitors: Adalimumab, etanercept

Exam Pearl: Lichenoid drug eruptions differ from idiopathic LP by: (1) photodistributed pattern, (2) eczematous/psoriasiform features, (3) resolution 6-12 weeks after drug cessation, (4) histology may show eosinophils and parakeratosis.

Pathophysiology

Molecular Pathogenesis

Lichen planus is mediated by CD8+ cytotoxic T lymphocytes that target basal keratinocytes, resulting in apoptosis and characteristic histological changes. [10]

┌─────────────────────────────────────────────────────────────────┐
│         PATHOGENIC MECHANISM OF LICHEN PLANUS                   │
├─────────────────────────────────────────────────────────────────┤
│                                                                 │
│  1. TRIGGER (Unknown/HCV/Drug)                                  │
│     ↓                                                           │
│  2. ALTERED KERATINOCYTE ANTIGEN EXPRESSION                     │
│     • Stress proteins (HSP65)                                   │
│     • Altered self-antigens on MHC Class I                      │
│     ↓                                                           │
│  3. ANTIGEN PRESENTATION TO T CELLS                             │
│     • Langerhans cells activate CD4+ helper T cells             │
│     • CD4+ cells recruit CD8+ cytotoxic T cells                 │
│     ↓                                                           │
│  4. CD8+ T CELL INFILTRATION                                    │
│     • Migration to dermoepidermal junction                      │
│     • Release of cytotoxic mediators:                           │
│       - Perforin/granzyme B → apoptosis                         │
│       - TNF-α → inflammation                                    │
│       - IFN-γ → keratinocyte damage                             │
│     ↓                                                           │
│  5. BASAL KERATINOCYTE APOPTOSIS                                │
│     • Civatte bodies (apoptotic keratinocytes)                  │
│     • Disruption of basement membrane                           │
│     ↓                                                           │
│  6. COMPENSATORY EPIDERMAL CHANGES                              │
│     • Hypergranulosis (Wickham's striae)                        │
│     • Acanthosis                                                │
│     • Saw-tooth rete ridges                                     │
│     ↓                                                           │
│  7. CLINICAL LESION: Purple polygonal papule with striae        │
│                                                                 │
└─────────────────────────────────────────────────────────────────┘

Key Immunological Features

Histopathological Correlates

The distinctive histological pattern is termed "interface dermatitis" or "lichenoid tissue reaction": [2]

Direct Immunofluorescence (DIF)

• Fibrinogen: Linear deposition at basement membrane zone (most common)
• IgM: Colloid bodies (Civatte bodies)
• IgA, IgG, C3: Occasionally at basement membrane
• Pattern: NOT diagnostic (unlike pemphigus/pemphigoid); supportive finding

Exam Detail: Viva Question: "How does lichen planus cause Wickham's striae?"

Model Answer: "Wickham's striae are the clinical manifestation of focal areas of hypergranulosis in the stratum granulosum. Histologically, LP shows irregular acanthosis with a thickened granular layer. The hypergranulosis appears white on the surface due to increased refractile keratohyalin granules. This is a compensatory epidermal response to the underlying chronic inflammation and basal cell destruction. The striae are best visualized with dermoscopy or by applying mineral oil to the lesion surface, which eliminates surface reflection and enhances the white lacy pattern. Their presence is pathognomonic for LP."

Viva Question: "What is the Koebner phenomenon and why does it occur in lichen planus?"

Model Answer: "The Koebner phenomenon, or isomorphic response, is the development of new lesions at sites of cutaneous trauma. It occurs in 25-50% of LP patients. The mechanism involves local immune activation at sites of skin injury—trauma causes keratinocyte damage and stress protein expression (e.g., heat shock proteins), which act as danger signals. This recruits CD8+ cytotoxic T lymphocytes to the area in genetically susceptible individuals, triggering the same pathogenic cascade seen in spontaneous lesions. Classic sites include scratch marks, surgical scars, and pressure areas. Other conditions demonstrating Koebner include psoriasis, vitiligo, and viral warts."

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4. Clinical Presentation

Classical Cutaneous Lichen Planus

The hallmark presentation remembered by the "6 Ps":

Distribution

Wickham's Striae

• Appearance: Fine white lacy lines on papule/plaque surface
• Mechanism: Focal hypergranulosis
• Visualization: Best seen with dermoscopy or mineral oil application
• Diagnostic Value: Pathognomonic when present
• Frequency: Present in 60-70% of cutaneous lesions

Clinical Variants

1. Hypertrophic (Verrucous) LP

2. Oral Lichen Planus

Prevalence: 40-50% of cutaneous LP patients; 25% oral-only disease

Reticular Oral LP (Most Common - 80%)

Erosive (Ulcerative) Oral LP (15-20%)

Atrophic Oral LP

Desquamative Gingivitis

• Specific manifestation of oral LP affecting gingiva
• Erythematous, friable gingiva; bleeds easily
• Differential: Pemphigoid, pemphigus vulgaris, linear IgA disease
• Requires biopsy + DIF to distinguish

Exam Detail: Exam Pearl - Oral LP Variants:

• Reticular: White lacy network; asymptomatic; low malignancy risk → observe
• Erosive: Painful ulcers; eating difficulty; 1-3% SCC risk → high-potency steroids + surveillance
• Atrophic: Red shiny patches; mild symptoms → topical steroids

Viva Question: "How do you counsel a patient with erosive oral lichen planus about malignancy risk?"

Model Answer: "I would explain that erosive oral lichen planus carries a small but significant risk of developing oral cancer—specifically squamous cell carcinoma—estimated at 1-3% over 5-10 years. While the absolute risk is low, it is higher than the general population. For this reason, I recommend regular oral examinations every 6-12 months with a dermatologist or oral medicine specialist. I advise the patient to avoid known risk factors such as smoking and excessive alcohol, both of which substantially increase cancer risk. I would also counsel them to report any changes immediately, including non-healing ulcers, persistent lumps, or areas that bleed easily. Any suspicious areas will be biopsied. Despite the small risk, the majority of patients do not develop cancer, and with good surveillance, any malignancy can be detected early when treatment is most effective."

3. Genital Lichen Planus

Penile LP

Vulvovaginal LP

4. Nail Lichen Planus (10% of LP cases)

Exam Detail: Red Flag - Nail LP: Pterygium formation (fusion of ventral nail fold to nail bed with obliteration of nail matrix) is irreversible and leads to permanent nail loss. Early aggressive treatment (intralesional or systemic steroids) is essential to prevent this complication. This is a high-yield exam scenario.

5. Lichen Planopilaris (Scalp LP)

Lichen planopilaris (LPP) is a scarring alopecia caused by LP affecting hair follicles.

Exam Detail: Exam Pearl - LPP: This is a scarring (cicatricial) alopecia. Once the follicle is destroyed, hair loss is permanent. Early recognition and aggressive treatment are critical. Frontal fibrosing alopecia (FFA) is a variant of LPP characterized by receding frontal hairline and eyebrow loss, predominantly affecting postmenopausal women.

6. Other Rare Variants

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5. Differential Diagnosis

Cutaneous LP Differentials

Oral LP Differentials

Nail LP Differentials

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6. Clinical Examination

Systematic Approach to Examining Lichen Planus

1. Cutaneous Examination

Inspection:

• Distribution: Flexor wrists, ankles, lumbar region
• Morphology: Flat-topped, polygonal, violaceous papules/plaques
• Size: Typically 2-5mm papules; may coalesce
• Color: Purple, violaceous, or purple-pink
• Surface: Look for Wickham's striae (white lacy lines)

Palpation:

• Firm papules/plaques
• Assess for Koebner phenomenon (lesions in scars, scratch marks)

Enhancement of Wickham's Striae:

• Apply mineral oil to lesion surface
• Use dermoscopy for magnified visualization

2. Oral Examination (Always Examine)

Systematic Sites:

1. Buccal Mucosa (most common site - 90%):
   • Reticular: White lacy network bilaterally
   • Erosive: Ulcers with surrounding striae
2. Tongue:
   • Lateral borders (reticular pattern)
   • Dorsum (atrophic patches)
3. Gingiva:
   • Desquamative gingivitis (erythematous, friable)
4. Palate:
   • Less common; reticular pattern
5. Lips:
   • Vermilion border involvement

Erosive Disease Assessment:

• Extent of erosions
• Pain level (impact on eating/speaking)
• Rule out malignancy (induration, bleeding, non-healing)

3. Nail Examination

Inspection (All 20 Nails):

• Longitudinal Ridging: Fine parallel grooves
• Thinning: Fragile, semi-transparent nail plate
• Pterygium: Scar tissue obliterating nail; irreversible
• Onycholysis: Nail separation
• Complete Loss: Anonychia

Severity Grading:

• Mild: Ridging/thinning only
• Moderate: Progressive thinning with onycholysis
• Severe: Pterygium formation or nail loss (urgent treatment required)

4. Scalp Examination (Lichen Planopilaris)

Inspection:

• Patches of alopecia
• Perifollicular erythema and scale
• Loss of follicular ostia (scarring)
• Violaceous border (active inflammation)

Dermoscopy:

• Perifollicular scale
• Loss of follicular openings
• White dots (fibrosis)

Assessment:

• Extent of hair loss
• Active vs. burnt-out disease (erythema vs. white scarring)
• Urgency: Active LPP requires immediate treatment

5. Genital Examination

Vulvovaginal LP (Female):

• Erosions on vestibule, labia minora
• Vaginal involvement (speculum examination)
• Assess for stenosis/adhesions
• Pain assessment

Penile LP (Male):

• Annular lesions on glans
• White striae or purple papules
• Erosions (rare)

6. General Examination

• Skin: Post-inflammatory hyperpigmentation (especially darker skin types)
• Hair: Eyebrow loss (frontal fibrosing alopecia variant)
• Koebner Sites: Scars, scratches, tattoos

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7. Investigations

Clinical Diagnosis

Lichen planus is primarily a clinical diagnosis based on characteristic morphology (6 Ps), distribution (flexor wrists/ankles), and Wickham's striae. Investigations are reserved for:

• Atypical presentations
• Diagnostic uncertainty
• Exclusion of differentials
• Assessment of complications (oral SCC)
• Screening for HCV

Skin Biopsy

Indications:

• Diagnostic uncertainty
• Atypical features
• Exclude malignancy (oral erosive LP)
• Distinguish from lichenoid drug eruption, lupus, GVHD

Histopathology (Classic "Interface Dermatitis"):

Immunohistochemistry:

• Infiltrate is predominantly CD8+ T lymphocytes
• CD4+ cells also present but fewer
• Not routinely required for diagnosis

Direct Immunofluorescence (DIF)

Findings in LP (Non-Diagnostic; Supportive):

• Fibrinogen: Linear deposition at basement membrane zone (70%)
• IgM: Civatte bodies (colloid bodies)
• IgA, IgG, C3: Occasionally at BMZ (weak)

Utility:

• DIF is NOT diagnostic for LP (unlike pemphigus/pemphigoid)
• Main use: Exclude other conditions (pemphigoid, pemphigus, lupus)

Oral LP DIF:

• Often performed to exclude mucous membrane pemphigoid
• Linear IgG/C3 at BMZ = pemphigoid (NOT LP)

Laboratory Investigations

Dermoscopy

Cutaneous LP:

• Wickham's Striae: White dots and lines in criss-cross pattern
• Vascular Pattern: Red dots/globules
• Pigmentation: Brown/grey dots (melanin incontinence)

Scalp (LPP):

• Perifollicular scale (follicular red dots)
• Loss of follicular openings
• White dots (fibrosis/scarring)

Oral LP:

• Oral dermoscopy not widely used; clinical examination sufficient

Oral LP Surveillance

For Erosive/Ulcerative Oral LP (SCC Risk 1-3% over 5-10 years):

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8. Classification and Staging

Clinical Classification by Site

Morphological Classification

Oral LP Classification (WHO)

Severity Grading (Not Standardized)

Mild:

• Localized cutaneous lesions
• Asymptomatic oral reticular LP
• Minimal impact on quality of life

Moderate:

• Widespread cutaneous lesions
• Symptomatic oral LP (non-erosive)
• Nail ridging/thinning
• Moderate pruritus

Severe:

• Erosive oral/genital LP (severe pain, functional impairment)
• Active lichen planopilaris (progressive hair loss)
• Severe nail involvement (pterygium, nail loss)
• Widespread hypertrophic LP (intractable pruritus)
• Significant impact on quality of life

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9. Management

General Principles

1. Cutaneous LP: Often self-limiting (50-70% resolve 1-2 years); symptomatic treatment
2. Oral LP: Chronic; aims are symptom control and malignancy surveillance
3. Scalp LP (LPP): Urgent treatment to prevent irreversible scarring
4. Nail LP: Early aggressive treatment to prevent pterygium
5. Erosive Genital LP: Prevent scarring and sexual dysfunction
6. Drug-Induced: Identify and stop offending drug

Treatment Ladder

┌──────────────────────────────────────────────────────────────────┐
│              LICHEN PLANUS MANAGEMENT ALGORITHM                  │
├──────────────────────────────────────────────────────────────────┤
│                                                                  │
│  CUTANEOUS LP:                                                   │
│                                                                  │
│  Step 1: FIRST-LINE                                              │
│    • Potent topical corticosteroid (Clobetasol propionate        │
│      0.05% ointment BD) [12]                                     │
│    • Emollients (reduce dryness)                                 │
│    • Sedating antihistamines (pruritus; night-time)              │
│                                                                  │
│  Step 2: SECOND-LINE (Widespread/Resistant)                      │
│    • Phototherapy (Narrowband UVB 3x/week) [13]                  │
│    • Systemic corticosteroids (Prednisolone 0.5mg/kg for         │
│      4-6 weeks, taper) [14]                                      │
│                                                                  │
│  Step 3: THIRD-LINE (Refractory)                                 │
│    • Acitretin 25-50mg daily (especially hypertrophic LP)        │
│    • Methotrexate 10-25mg weekly                                 │
│    • Ciclosporin 3-5mg/kg/day (rarely used)                      │
│    • Hydroxychloroquine 200-400mg daily                          │
│                                                                  │
│ ─────────────────────────────────────────────────────────────────│
│                                                                  │
│  ORAL LP:                                                        │
│                                                                  │
│  RETICULAR (Asymptomatic):                                       │
│    • Observation + patient education                             │
│    • Avoid triggers (spicy food, alcohol, smoking)               │
│    • 6-12 monthly surveillance                                   │
│                                                                  │
│  EROSIVE/SYMPTOMATIC:                                            │
│    Step 1: Topical corticosteroids                               │
│      • Clobetasol propionate 0.05% gel/ointment BD [15]          │
│      • Betamethasone sodium phosphate 0.5mg mouthwash            │
│        (dissolve tablet, rinse 2-3 min, spit) QDS                │
│                                                                  │
│    Step 2: Calcineurin inhibitors                                │
│      • Tacrolimus 0.1% ointment BD (steroid-sparing) [16]        │
│                                                                  │
│    Step 3: Systemic therapy (Severe erosive)                     │
│      • Prednisolone 0.5mg/kg for 2-4 weeks, taper [14]           │
│      • Hydroxychloroquine 200-400mg daily                        │
│      • Mycophenolate mofetil 1-2g daily                          │
│      • Ciclosporin 3-5mg/kg/day (refractory cases)               │
│                                                                  │
│    Surveillance: 6-12 monthly; biopsy suspicious areas           │
│                                                                  │
│ ─────────────────────────────────────────────────────────────────│
│                                                                  │
│  GENITAL LP:                                                     │
│    • High-potency topical corticosteroids (Clobetasol 0.05%)    │
│    • Tacrolimus 0.1% (vulval erosive LP)                         │
│    • Vaginal dilators (prevent stenosis)                         │
│    • Systemic therapy if refractory (as per oral LP)             │
│                                                                  │
│ ─────────────────────────────────────────────────────────────────│
│                                                                  │
│  NAIL LP:                                                        │
│    • Early aggressive treatment (prevent pterygium)              │
│    • Intralesional triamcinolone 2.5-5mg/ml (proximal nail       │
│      fold monthly) [17]                                          │
│    • Potent topical corticosteroids under occlusion              │
│    • Systemic corticosteroids (Prednisolone 0.5mg/kg if severe)  │
│    • Acitretin (refractory)                                      │
│                                                                  │
│ ─────────────────────────────────────────────────────────────────│
│                                                                  │
│  LICHEN PLANOPILARIS (SCALP):                                    │
│    • URGENT treatment (prevent irreversible scarring)            │
│    • Potent topical corticosteroids (Clobetasol 0.05% solution)  │
│    • Intralesional triamcinolone 5-10mg/ml monthly [18]          │
│    • Hydroxychloroquine 200-400mg daily (disease-modifying)      │
│    • Oral steroids (active inflammation)                         │
│    • Doxycycline 100mg BD (anti-inflammatory)                    │
│    • Finasteride 2.5-5mg daily (frontal fibrosing alopecia)      │
│                                                                  │
│ ─────────────────────────────────────────────────────────────────│
│                                                                  │
│  LICHENOID DRUG ERUPTION:                                        │
│    • Identify and STOP offending drug                            │
│    • Symptomatic treatment (topical steroids, antihistamines)    │
│    • Resolves 6-12 weeks post-drug cessation [11]                │
│                                                                  │
└──────────────────────────────────────────────────────────────────┘

Specific Treatment Modalities

1. Topical Corticosteroids

Precautions:

• Skin atrophy with prolonged use (especially thin skin areas)
• Oral mucosa: atrophy less of a concern; can use long-term
• Occlusion increases potency (useful for hypertrophic LP)

2. Intralesional Corticosteroids

Precautions: Atrophy, hypopigmentation (dilute in darker skin)

3. Systemic Corticosteroids

Indications:

• Severe widespread cutaneous LP
• Severe erosive oral/genital LP
• Active lichen planopilaris
• Severe nail LP (prevent pterygium)

Regimen:

• Prednisolone 0.5mg/kg/day for 2-6 weeks, then taper over 2-4 weeks [14]
• Maintenance: Avoid if possible (side effects)

Precautions: Diabetes, osteoporosis, hypertension, weight gain, immunosuppression

4. Topical Calcineurin Inhibitors

Advantages:

• No atrophy (unlike steroids)
• Safe for long-term use
• Useful for facial/genital/oral sites

Precautions:

• Burning sensation initially (resolves in 1-2 weeks)
• Theoretical (unproven) malignancy risk with prolonged use

5. Phototherapy

Narrowband UVB (NB-UVB):

• Indication: Widespread cutaneous LP unresponsive to topical therapy [13]
• Regimen: 3 times/week for 8-12 weeks
• Efficacy: 70-80% improvement
• Precautions: Erythema, pruritus, hyperpigmentation (darker skin), photoaging, skin cancer risk (cumulative)

PUVA (Psoralen + UVA):

• Second-line to NB-UVB
• More side effects

6. Systemic Retinoids

Acitretin:

• Indication: Hypertrophic LP (first-line systemic); widespread cutaneous LP [19]
• Dose: 25-50mg daily
• Efficacy: 60-70% improvement over 3-6 months
• Precautions: Teratogenic (contraception 3 years post-cessation in women); dry lips/skin; hyperlipidemia; hepatotoxicity; monitor LFTs, lipids

7. Other Systemic Agents

8. Hepatitis C Treatment

• If HCV-positive LP, treat HCV with direct-acting antivirals (DAAs)
• 30-50% of LP improves or resolves after HCV eradication [5]
• Liaise with hepatology

Patient Education and Self-Management

Key Messages:

1. Natural History: Skin LP often resolves 1-2 years; oral LP chronic
2. Pigmentation: Expect dark marks after lesions heal (especially darker skin); gradual fading over months-years
3. Triggers: Avoid identified triggers (drugs, dental materials)
4. Oral Hygiene: Maintain excellent oral hygiene; avoid smoking, alcohol, spicy foods (erosive oral LP)
5. Surveillance: Regular follow-up for erosive oral LP (cancer risk)
6. Koebner: Avoid trauma to skin (scratching, tattoos)

Special Scenarios

Drug-Induced Lichenoid Eruption

Vulvovaginal-Gingival Syndrome

• Triad: Erosive vulval + vaginal + gingival LP
• Management:
  • High-potency topical steroids (clobetasol)
  • Vaginal dilators (prevent stenosis)
  • Tacrolimus (steroid-sparing)
  • Systemic therapy (prednisolone, mycophenolate, ciclosporin) if refractory
  • "Multidisciplinary: Dermatology + Gynaecology + Oral Medicine"

Pregnancy and LP

• Mild cutaneous LP: Continue topical steroids (safe)
• Oral LP: Topical steroids safe
• Avoid systemic retinoids (teratogenic)
• Avoid methotrexate (teratogenic)
• Prednisolone: safe if required (short course)

Exam Detail: Viva Question: "How would you manage a 45-year-old woman with severe erosive oral lichen planus affecting her buccal mucosa, tongue, and gingiva, causing significant pain and difficulty eating?"

Model Answer:

"I would adopt a stepwise approach starting with topical therapy and escalating to systemic agents if necessary.

First-line: High-potency topical corticosteroids are the mainstay. I would prescribe clobetasol propionate 0.05% gel or ointment applied directly to the erosions twice daily. Additionally, I would use betamethasone sodium phosphate 0.5mg mouthwash—the patient dissolves one tablet in water, rinses for 2-3 minutes, and spits it out four times daily. This provides widespread mucosal coverage.

Adjunctive measures: I would advise avoidance of triggers such as spicy foods, citrus, alcohol, and smoking, all of which can exacerbate symptoms. Excellent oral hygiene is essential.

Second-line: If topical steroids are inadequate after 4-6 weeks, I would add tacrolimus 0.1% ointment applied to the erosions twice daily. Tacrolimus is effective and steroid-sparing, though patients should be warned about initial burning.

Third-line: For severe, refractory disease causing significant functional impairment (inability to eat), I would consider systemic corticosteroids—prednisolone 0.5mg/kg daily (e.g., 30-40mg) for 2-4 weeks, then a slow taper. If maintenance therapy is needed, I would use a steroid-sparing agent such as hydroxychloroquine 200-400mg daily or mycophenolate mofetil 1-2g daily. In very refractory cases, ciclosporin may be considered, though this requires monitoring for nephrotoxicity and hypertension.

Surveillance: Given the 1-3% risk of squamous cell carcinoma transformation over 5-10 years, I would arrange 6-12 monthly oral examination and biopsy any suspicious areas (non-healing ulcers, induration, exophytic lesions).

Multidisciplinary approach: I would involve oral medicine or oral surgery if available for co-management.

Patient education: I would counsel the patient about the chronic nature of oral LP, the low but present malignancy risk, the importance of avoiding smoking and alcohol (which increase cancer risk), and the need for long-term follow-up."

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10. Complications

Complications of Disease

Complications of Treatment

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11. Prognosis and Outcomes

Natural History

Prognostic Factors

Favorable Prognosis (Shorter Duration):

• Classic cutaneous LP
• Localized disease
• Acute onset
• Absence of mucosal involvement
• Younger age

Unfavorable Prognosis (Prolonged/Chronic):

• Oral erosive LP
• Genital erosive LP
• Hypertrophic variant
• Lichen planopilaris
• Widespread disease
• HCV-associated LP (may persist despite HCV treatment)

Quality of Life Impact

Mortality

• Lichen planus itself is not life-threatening
• Mortality risk related to:
  • Oral SCC (1-3% of erosive oral LP) [6]
  • Complications of systemic therapy (immunosuppression, hepatotoxicity)
  • HCV-associated complications (cirrhosis, HCC) if untreated

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12. Prevention and Screening

Primary Prevention

No specific primary prevention (aetiology unknown). General measures:

• Avoid known triggers (smoking, alcohol—exacerbate oral LP)
• Caution with medications known to cause lichenoid eruptions
• HCV vaccination (where available) may reduce HCV-associated LP

Secondary Prevention (Early Detection)

Tertiary Prevention (Prevent Complications)

Screening for Hepatitis C

Indications for HCV Screening:

1. Mediterranean, Middle Eastern, or Asian ethnicity
2. Atypical or severe LP
3. Generalized/widespread disease
4. Other HCV risk factors (IVDU, transfusion pre-1992, tattoos)

Action if HCV Positive:

• Refer to hepatology for HCV treatment (direct-acting antivirals)
• 30-50% of LP cases improve/resolve after HCV eradication [5]
• Monitor liver function; screen for cirrhosis/HCC

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13. Key Guidelines and Evidence

International Guidelines

Key Evidence

Treatment Efficacy

Malignancy Risk

Hepatitis C Association

Exam Detail: High-Yield Evidence for Exams:

1. Topical Clobetasol: First-line for cutaneous and oral LP (Level I evidence from RCTs) [12,15]
2. Oral LP SCC Risk: 1-3% over 5-10 years; erosive/atrophic variants higher risk (Level II evidence) [6,21]
3. HCV Association: Strong in Mediterranean (16-35%), weak in Northern Europe (4-6%); treat HCV improves LP in 30-50% (Level II-III evidence) [5]
4. NB-UVB: Effective for widespread cutaneous LP (70-80% improvement; Level II evidence) [13]
5. Tacrolimus: Effective for oral LP; steroid-sparing (Level I evidence from RCTs) [16]
6. LPP: Early treatment essential; hydroxychloroquine stabilizes disease (Level III evidence) [18]

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14. Examination Focus

OSCE/PACES Scenarios

Scenario 1: Cutaneous LP History and Examination

Stem: "This 52-year-old woman has noticed itchy spots on her wrists and ankles for 3 months. Please examine the rash and discuss your findings."

Examination Approach:

1. Inspect wrists (flexor aspect), ankles, lower back
2. Describe lesions: "Violaceous, flat-topped, polygonal papules"
3. Look for Wickham's striae (apply mineral oil; use dermoscopy)
4. Assess Koebner phenomenon (scratch marks, scars)
5. Examine oral mucosa (50% have oral involvement)
6. Examine nails (ridging, pterygium)
7. Examine scalp (lichen planopilaris)

Expected Findings:

• Violaceous polygonal papules on flexor wrists and ankles
• Wickham's striae visible
• Possible oral reticular LP (buccal mucosa)

Diagnosis: "These findings are consistent with lichen planus, characterized by the 6 Ps: Planar, Purple, Polygonal, Pruritic Papules and Plaques, with pathognomonic Wickham's striae."

Management Discussion:

• First-line: Potent topical steroids (clobetasol 0.05%)
• Emollients and antihistamines for pruritus
• Natural history: Likely to resolve in 1-2 years
• Check mouth regularly (oral involvement may persist)
• Consider HCV screening (ethnicity-dependent)

Scenario 2: Oral LP Communication Station

Stem: "This 48-year-old woman has been diagnosed with erosive oral lichen planus. Please discuss her diagnosis, treatment, and long-term management."

Key Points to Cover:

1. Explain condition: Immune system attacking mouth lining; chronic; not contagious
2. Symptoms: Painful ulcers; difficulty eating spicy/acidic foods
3. Treatment:
   • Steroid mouthwashes/gels (first-line)
   • Avoid triggers (spicy food, alcohol, smoking)
   • Tacrolimus if steroids insufficient
   • Systemic therapy if severe
4. Long-term:
   • Chronic; requires long-term management
   • Small risk of oral cancer (1-3% over 5-10 years)
   • Regular check-ups (6-12 monthly)
   • Biopsy any suspicious areas
   • Avoid smoking/alcohol (increase cancer risk)
5. Address concerns: Reassure most patients do not develop cancer; surveillance detects early

Viva Voce Questions and Model Answers

Question 1: "What is the pathophysiology of lichen planus?"

Model Answer:

"Lichen planus is a T-cell mediated autoimmune disorder targeting basal keratinocytes. The primary effector cells are CD8+ cytotoxic T lymphocytes that infiltrate the dermoepidermal junction.

The pathogenic mechanism involves:

1. An unknown trigger (possibly viral antigen, drug, or altered self-antigen) causes altered antigen expression on basal keratinocytes via MHC Class I.
2. Langerhans cells present antigens to CD4+ helper T cells, which then recruit CD8+ cytotoxic T cells.
3. CD8+ T cells migrate to the dermoepidermal junction and release cytotoxic mediators—perforin, granzyme B, TNF-α, and IFN-γ—causing apoptosis of basal keratinocytes.
4. This creates the characteristic histological pattern termed 'interface dermatitis': a band-like lymphocytic infiltrate at the dermoepidermal junction, with apoptotic keratinocytes (Civatte bodies) and basal cell vacuolization.
5. Compensatory epidermal changes include hypergranulosis (which manifests as Wickham's striae), acanthosis, and saw-tooth rete ridges.
6. Melanin incontinence (pigment dropping into the dermis) explains the post-inflammatory hyperpigmentation.

The target antigen remains unknown, but the process is similar to graft-versus-host disease, where donor T cells attack host keratinocytes."

Question 2: "How would you differentiate lichen planus from a lichenoid drug eruption?"

Model Answer:

"While the histology is virtually identical, several clinical and histological clues help distinguish:

Clinical Differences:

1. Distribution: Lichenoid drug eruptions are often photodistributed (face, arms, V-neck), whereas classic LP favors flexor wrists, ankles, and lumbar region.
2. Morphology: Drug eruptions may have eczematous or psoriasiform features, whereas LP is classically violaceous and polygonal.
3. Temporal: Drug eruptions occur weeks to months after starting the medication, and resolve 6-12 weeks after drug cessation. LP persists despite stopping potential triggers.
4. Drug History: NSAIDs, antimalarials, ACE inhibitors, thiazides, beta-blockers, and gold are common culprits.

Histological Clues:

1. Eosinophils: Presence of eosinophils in the infiltrate suggests drug eruption (absent in classic LP).
2. Parakeratosis: Focal parakeratosis favors drug eruption (LP typically has hypergranulosis and orthokeratosis).
3. Deeper Infiltrate: Drug reactions may have a deeper dermal infiltrate extending beyond the papillary dermis.

Management: The critical step is identifying and stopping the suspected drug. Symptomatic treatment with topical steroids is similar. Re-challenge is generally avoided due to recurrence risk."

Question 3: "What is the malignant potential of oral lichen planus, and how would you manage it?"

Model Answer:

"Oral lichen planus, particularly the erosive, ulcerative, and atrophic variants, carries a malignant transformation risk of approximately 1-3% over 5-10 years to oral squamous cell carcinoma. The reticular variant has a much lower risk.

Risk Factors for Malignancy:

1. Erosive or ulcerative oral LP
2. Smoking
3. Alcohol consumption
4. Chronic inflammation (long-standing disease)
5. Possibly certain HLA types (population-dependent)

Surveillance Strategy:

1. Regular Examination: 6-12 monthly oral examination by a dermatologist or oral medicine specialist.
2. Patient Education: Instruct the patient to report any changes—non-healing ulcers, persistent lumps, areas of induration, or unexplained bleeding.
3. Avoidance of Risk Factors: Strongly advise smoking cessation and moderation/avoidance of alcohol, both of which substantially increase cancer risk.
4. Low Threshold for Biopsy: Any area that changes character (becomes indurated, exophytic, or fails to heal) should be biopsied to exclude dysplasia or SCC.
5. Photographic Documentation: Serial photographs can help track changes over time.

Management of Oral LP:

• Symptomatic treatment with high-potency topical steroids (clobetasol gel) or tacrolimus
• Systemic therapy if severe
• The goal is both symptom control and close surveillance for malignancy.

While the absolute risk is low, vigilance is essential to detect any transformation early when treatment is most effective."

Question 4: "Describe the management of lichen planopilaris."

Model Answer:

"Lichen planopilaris (LPP) is a scarring (cicatricial) alopecia caused by LP affecting hair follicles. It is a dermatological emergency because follicular destruction is irreversible, leading to permanent hair loss. The goal is to halt disease progression and preserve remaining follicles.

Clinical Assessment:

1. Identify active inflammation: perifollicular erythema, scale, pustules, pruritus, burning.
2. Assess extent of scarring: loss of follicular ostia, white smooth patches (burnt-out disease).
3. Dermoscopy: perifollicular scale, red dots (active); white dots, loss of follicles (scarring).

Treatment Strategy:

Active Disease (Inflammation Present):

1. Topical Corticosteroids: Clobetasol propionate 0.05% solution applied to scalp daily.
2. Intralesional Corticosteroids: Triamcinolone acetonide 5-10mg/ml injected into active areas monthly. This is often the most effective treatment.
3. Systemic Corticosteroids: Prednisolone 0.5mg/kg daily for 4-6 weeks if widespread or rapidly progressive, then taper.
4. Hydroxychloroquine: 200-400mg daily as a disease-modifying agent. This is first-line systemic therapy for LPP and has good evidence for stabilizing disease. Requires annual ophthalmology screening for retinal toxicity.
5. Doxycycline: 100mg twice daily for anti-inflammatory effects (alternative to hydroxychloroquine).
6. Frontal Fibrosing Alopecia (LPP variant): Finasteride 2.5-5mg daily may slow progression in postmenopausal women.

Burnt-Out Disease (No Active Inflammation):

• Treatment is ineffective once scarring has occurred.
• Cosmetic options: wigs, hair transplantation (controversial; may Koebnerize).

Monitoring:

• Clinical photographs at each visit to assess progression
• If stable on treatment for 1-2 years, may cautiously taper therapy
• Relapse is common

Patient Counseling:

• Explain that hair loss is permanent once the follicle is destroyed.
• Early aggressive treatment is essential to preserve remaining hair.
• Long-term treatment may be needed (months to years).
• Realistic expectations: treatment aims to stop progression, not regrow lost hair."

Question 5: "What are the '6 Ps' of lichen planus and why are they useful?"

Model Answer:

"The '6 Ps' is a classic mnemonic that describes the key clinical features of cutaneous lichen planus:

1. Planar: Flat-topped (not dome-shaped like molluscum or warts)
2. Purple: Violaceous or purple-pink hue due to dermal inflammation
3. Polygonal: Angular borders (reflecting the saw-tooth rete ridge pattern)
4. Pruritic: Intensely itchy (a major symptom)
5. Papules: Small raised lesions (2-5mm)
6. Plaques: Larger confluent areas when papules coalesce

Clinical Utility: The 6 Ps provide a rapid, systematic framework for recognizing classic cutaneous LP. When you see violaceous, flat-topped, polygonal, itchy papules on the flexor wrists or ankles, you immediately think LP. Combined with Wickham's striae (white lacy lines on the surface—pathognomonic), the diagnosis is often clinical without requiring biopsy.

Limitations: The 6 Ps apply primarily to classic cutaneous LP. They are less useful for variants such as hypertrophic LP (thick warty plaques), oral LP (mucosal striae or erosions), lichen planopilaris (follicular papules and scarring alopecia), or nail LP (ridging and pterygium). However, the mnemonic remains an essential starting point for medical students and trainees learning dermatology."

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15. Patient/Layperson Explanation

What is Lichen Planus?

Lichen planus (LP) is a condition where the immune system mistakenly attacks the skin, mouth, nails, or hair. It causes itchy, purple, flat-topped bumps on the skin and white lacy patterns or painful sores in the mouth. It's not contagious—you can't catch it from someone else or pass it on.

What Causes It?

We don't know the exact cause. It's related to an overactive immune response, where immune cells attack healthy skin cells. Sometimes it's linked to:

• Hepatitis C virus (a liver infection)
• Certain medications (e.g., blood pressure tablets, anti-inflammatory drugs)
• Dental fillings (in the mouth)
• Stress (may trigger flare-ups)

What Does It Look Like?

On the Skin:

• Small, shiny, purple-pink bumps
• Often on the wrists (inner side), ankles, and lower back
• Very itchy
• Fine white lines on the surface (called Wickham's striae)

In the Mouth:

• White lacy patterns on the inside of the cheeks (usually painless)
• Painful red sores or ulcers (erosive type)
• Sore gums

On the Nails:

• Ridges or thinning
• Nail may lift or be destroyed in severe cases

On the Scalp:

• Hair loss with scarring (permanent if not treated early)

How Long Does It Last?

• Skin: Usually clears up on its own within 1-2 years, but may leave dark marks (especially on darker skin).
• Mouth: Often lasts much longer (years or lifelong) and needs ongoing treatment.
• Scalp/Nails: Can be permanent if not treated early.

Is It Serious?

Most cases are not dangerous, but:

• Mouth sores can be very painful and make eating difficult.
• Erosive oral LP (painful sores in the mouth) has a small risk (1-3%) of turning into mouth cancer over 5-10 years. Regular check-ups are important.
• Scalp LP causes permanent hair loss if not treated quickly.

How is It Treated?

Skin LP:

• Strong steroid creams (e.g., clobetasol) to reduce inflammation and itching
• Moisturizers and antihistamine tablets for itchiness
• Light therapy (UVB) if widespread
• Steroid tablets for severe cases

Mouth LP:

• Steroid gel, ointment, or mouthwash applied to sores
• Tacrolimus ointment (an alternative to steroids)
• Avoid spicy foods, alcohol, and smoking (make it worse)
• Regular dentist/doctor check-ups to monitor for mouth cancer

Scalp LP:

• Steroid creams, injections, or tablets
• Hydroxychloroquine tablets (used for malaria; also helps hair loss)
• Early treatment is critical to prevent permanent hair loss

Nail LP:

• Steroid injections or tablets
• Difficult to treat; may need long-term care

What Should I Avoid?

• Smoking and alcohol (especially if you have mouth LP—increases cancer risk)
• Spicy, acidic, or hot foods (if you have mouth sores)
• Scratching (can cause new spots to appear)
• Certain medications (ask your doctor if your medicines could be causing it)

Will It Come Back?

• Skin LP clears up in most people (50-85%) within 1-2 years, but it can come back (15-20% chance).
• Mouth LP is usually long-lasting and needs ongoing management.

When Should I See a Doctor Urgently?

• Mouth: A sore that doesn't heal, bleeds, or has a lump (could be cancer—rare but possible)
• Scalp: Hair loss with redness, soreness, or scarring (needs urgent treatment to prevent permanent baldness)
• Severe pain in the mouth or genitals that stops you eating or having sex

Living with Lichen Planus

• Good oral hygiene: Brush teeth gently, use soft toothbrush, avoid harsh mouthwashes.
• Moisturize skin: Helps with dryness and itching.
• Sun protection: Sun can darken the marks left behind.
• Regular check-ups: Especially for mouth LP (cancer surveillance).
• Support groups: Talking to others with LP can help.

Key Takeaways

• LP is a long-term condition where the immune system attacks the skin/mouth/nails/hair.
• Skin LP usually clears within 1-2 years; mouth LP is chronic.
• Treatment focuses on symptom control (steroids, tacrolimus).
• Mouth sores have a small cancer risk (1-3%)—regular check-ups are vital.
• Scalp and nail LP need urgent treatment to prevent permanent damage.
• It's not contagious, and most people manage well with treatment.

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16. References

Systematic Reviews and Meta-Analyses

1. Le Cleach L, Chosidow O. Lichen Planus. N Engl J Med. 2012;366(8):723-732. doi:10.1056/NEJMcp1103641. PMID: 22356325

2. Gorouhi F, Davari P, Fazel N. Cutaneous and mucosal lichen planus: a comprehensive review of clinical subtypes, risk factors, diagnosis, and prognosis. Sci World J. 2014;2014:742826. doi:10.1155/2014/742826. PMID: 24551873

Epidemiology and Associations

3. Boyd AS, Neldner KH. Lichen planus. J Am Acad Dermatol. 1991;25(4):593-619. doi:10.1016/0190-9622(91)70241-s. PMID: 1791218

4. Sugerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Rev Oral Biol Med. 2002;13(4):350-365. doi:10.1177/154411130201300405. PMID: 12191961

5. Lodi G, Pellicano R, Carrozzo M. Hepatitis C virus infection and lichen planus: a systematic review with meta-analysis. Oral Dis. 2010;16(7):601-612. doi:10.1111/j.1601-0825.2010.01670.x. PMID: 20412447

Malignancy Risk

6. Eisen D. The clinical features, malignant potential, and systemic associations of oral lichen planus: a study of 723 patients. J Am Acad Dermatol. 2002;46(2):207-214. doi:10.1067/mjd.2002.120452. PMID: 11807431

7. Aghbari SMH, Abushouk AI, Attia A, et al. Malignant transformation of oral lichen planus and oral lichenoid lesions: A meta-analysis of 20095 patient data. Oral Oncol. 2017;68:92-102. doi:10.1016/j.oraloncology.2017.03.012. PMID: 28438299

Pathophysiology

7. Shiohara T, Kano Y. Lichen planus and lichenoid dermatoses. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:183-203.

8. Wenzel J, Scheler M, Proelss J, et al. Type I interferon-associated cytotoxic inflammation in lichen planus. J Cutan Pathol. 2006;33(10):672-678. doi:10.1111/j.1600-0560.2006.00527.x. PMID: 17026519

Natural History

8. Chuang TY, Stitle LE, Brashear R, Lewis C. Hepatitis C virus and lichen planus: a case-control study of 340 patients. J Am Acad Dermatol. 1999;41(5 Pt 1):787-789. doi:10.1016/s0190-9622(99)70025-3. PMID: 10534647

Associated Conditions

9. Mozaffari HR, Sharifi R, Sadeghi M. Prevalence of oral lichen planus in diabetes mellitus: a meta-analysis study. Acta Inform Med. 2016;24(6):390-393. doi:10.5455/aim.2016.24.390-393. PMID: 28077885

Drug-Induced Lichenoid Eruptions

11. Shiohara T, Kano Y. Lichenoid dermatoses. In: Griffiths CEM, Barker J, Bleiker T, Chalmers R, Creamer D, eds. Rook's Textbook of Dermatology. 9th ed. Wiley-Blackwell; 2016:38.1-38.37.

Treatment Evidence

12. Atzmony L, Reiter O, Hodak E, Gdalevich M, Mimouni D. Treatments for cutaneous lichen planus: a systematic review and meta-analysis. Am J Clin Dermatol. 2016;17(1):11-22. doi:10.1007/s40257-015-0160-6. PMID: 26547913

13. Pavlotsky F, Nathansohn N, Kriger G, Shpiro D, Trau H. Ultraviolet-B treatment for cutaneous lichen planus: our experience with 50 patients. Photodermatol Photoimmunol Photomed. 2008;24(2):83-86. doi:10.1111/j.1600-0781.2008.00345.x. PMID: 18353089

14. Cribier B, Frances C, Chosidow O. Treatment of lichen planus. An evidence-based medicine analysis of efficacy. Arch Dermatol. 1998;134(12):1521-1530. doi:10.1001/archderm.134.12.1521. PMID: 9875189

15. Thongprasom K, Dhanuthai K. Steroids in the treatment of lichen planus: a review. J Oral Sci. 2008;50(4):377-385. doi:10.2334/josnusd.50.377. PMID: 19106464

16. Laeijendecker R, Tank B, Dekker SK, Neumann HA. A comparison of treatment of oral lichen planus with topical tacrolimus and triamcinolone acetonide ointment. Acta Derm Venereol. 2006;86(3):227-229. doi:10.2340/00015555-0073. PMID: 16710578

17. Tosti A, Piraccini BM, Iorizzo M, Misciali C. The nail in lichen planus: short review and classification. G Ital Dermatol Venereol. 2008;143(3):151-156. PMID: 18833068

18. Chieregato C, Zini A, Barba A, Magnanini M, Rosina P. Lichen planopilaris: report of 30 cases and review of the literature. Int J Dermatol. 2003;42(5):342-345. doi:10.1046/j.1365-4362.2003.01850.x. PMID: 12755967

19. Laurberg G, Geiger JM, Hjorth N, et al. Treatment of lichen planus with acitretin. A double-blind, placebo-controlled study in 65 patients. J Am Acad Dermatol. 1991;24(3):434-437. doi:10.1016/0190-9622(91)70069-a. PMID: 1829480

20. Harpenau LA, Plemons JM, Rees TD. Effectiveness of a low dose of cyclosporine in the management of patients with erosive oral lichen planus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995;80(2):161-167. doi:10.1016/s1079-2104(05)80198-0. PMID: 7552858

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