10.1 Oral Mucosal Disease & Lichen Planus
Key Takeaways
- Oral lichen planus (OLP) presents in four clinical forms — reticular (Wickham striae), erosive, atrophic, and plaque-like — with the erosive/atrophic forms carrying roughly a 1-2% malignant transformation risk over years, mandating long-term follow-up
- OLP pathogenesis is cell-mediated: CD8+ T cells attack basal keratinocytes; first-line management is a topical corticosteroid (betamethasone rinse or fluticasone spray), reserving systemic agents for severe disease
- Lichenoid reactions mimic OLP but are triggered by drugs (NSAIDs, ACE inhibitors, antimalarials, gold) or amalgam contact and usually resolve on removing the trigger
- Recurrent aphthous stomatitis has three forms (minor, major, herpetiform) and warrants checking iron, vitamin B12, and folate plus screening for coeliac disease, Crohn disease, and Behçet syndrome
- Any oral ulcer that has not healed within three weeks must be referred to exclude malignancy — the cornerstone of UK oral medicine triage
Oral Lichen Planus: Clinical Forms
Oral lichen planus (OLP) is a chronic T-cell-mediated inflammatory mucocutaneous disease of stratified squamous epithelium. UK guidance (British Association of Dermatologists, updated 2023) classifies four clinical forms, which may coexist in the same patient:
| Form | Appearance | Typical Site | Symptom |
|---|---|---|---|
| Reticular | White Wickham striae (lace-like network) | Buccal mucosa (bilateral) | Often asymptomatic |
| Atrophic | Red, thinned epithelium with striae at margins | Buccal mucosa, gingiva | Soreness |
| Erosive | Erythematous erosions with peripheral striae | Anywhere, often buccal | Painful, interferes with eating |
| Plaque-like | Smooth white homogeneous plaque | Tongue, buccal mucosa | Asymptomatic |
Bilateral symmetry and Wickham striae are the diagnostic anchors. The atrophic and erosive forms are the symptomatic, higher-risk variants.
Pathogenesis
OLP is a cell-mediated autoimmune process. Autoreactive CD8+ T cells attack basal and parabasal keratinocytes, triggering apoptosis and producing the characteristic sawtooth rete-ridge pattern and basal cell liquefactive degeneration seen on histology. A dense band-like lymphohistiocytic infiltrate immediately beneath the epithelium is the histological hallmark. Hepatitis C association is recognised internationally but is uncommon in the UK population.
Management
- First-line: topical corticosteroid — betamethasone (as a rinse or dissolved tablet), fluticasone propionate spray, or an adcortyl-in-orabase preparation applied to erosions
- Second-line / severe erosive disease: systemic corticosteroid (short prednisolone course) plus a steroid-sparing agent such as azathioprine, mycophenolate, or methotrexate
- Monitoring: UK primary-care guidance recommends 6-monthly review for stable reticular disease and urgent referral for non-healing ulceration, induration, or texture change
Malignant Transformation
The UK BAD patient information leaflet cites a ~1% risk of cancerous change over 10 years. The 2024 González-Moles meta-analysis pooled estimate is 1.43% (95% CI 1.09-1.80), rising in higher-quality studies. Risk is concentrated in the erosive and atrophic forms, on the tongue, and with smoking and alcohol. All patients with OLP need long-term follow-up and smoking/alcohol counselling.
Lichenoid Reactions
Lichenoid lesions are clinically and histologically near-identical to OLP but have an identifiable external trigger:
- Drug-induced — NSAIDs, ACE inhibitors (especially lisinopril), antimalarials (hydroxychloroquine), gold, beta-blockers, sulfonylureas
- Amalgam contact — lesions abutting an amalgam restoration, often on the buccal mucosa or lateral tongue; resolve on replacement with a non-amalgam material and patch-test positivity to mercury salts
- GVHD — oral lichenoid lesions in graft-versus-host disease post-haematopoietic stem-cell transplant
Resolution on removing the trigger confirms the diagnosis.
Recurrent Aphthous Stomatitis (RAS)
RAS affects up to 20% of the population and presents as painful, recurrent, round or oval ulcers on non-keratinised mucosa with an erythematous halo:
| Type | Size | Number | Healing |
|---|---|---|---|
| Minor | <10 mm | 1-5 | 7-14 days, no scarring |
| Major | >10 mm | 1-3 | Weeks-months, may scar |
| Herpetiform | 1-3 mm | 10-100 clusters | 7-14 days |
Associations to screen for
- Iron, vitamin B12, and folate deficiency (baseline bloods for every RAS patient)
- Coeliac disease (serology ± duodenal biopsy if warranted)
- Crohn disease / orofacial granulomatosis
- Behçet syndrome (RAS plus genital ulceration, eye signs, skin lesions — refer)
- Stress, trauma, sodium lauryl sulphate in toothpaste, food hypersensitivity
Treatment is symptom-focused: chlorhexidine mouthwash, topical benzylamine, topical steroid (hydrocortisone lozenges, betamethasone), and for major RAS, systemic agents.
Other Common Mucosal Conditions
- Geographic tongue (benign migratory glossitis): asymptomatic or mildly sore smooth red patches with white wandering borders; benign, reassurance only
- Frictional keratosis: white plaque from chronic mechanical irritation (cheek biting, sharp tooth); homogenous, wipes-revealed, not premalignant; remove the cause and review
- Candidiasis vs leukoplakia: candidal plaques wipe off leaving erythema; leukoplakia is a non-wipeable white plaque requiring biopsy to exclude dysplasia
The Three-Week Ulcer Rule
Any oral ulcer that persists beyond three weeks must be referred urgently (2-week-wait pathway in the UK) to exclude squamous cell carcinoma — irrespective of patient age or risk factors. This single rule underpins oral medicine triage in primary dental and medical care.
Diagnosing OLP - Clinical and Histopathological Criteria
The modified World Health Organization criteria combine clinical and histological features. Clinically, OLP is bilateral and symmetrical with the characteristic reticular striae; histologically there is a band-like lymphohistiocytic infiltrate in the lamina propria, basal cell liquefactive degeneration, Civatte bodies, and sawtooth rete ridges. A biopsy is recommended for atypical, unilateral, erosive, or non-striated lesions to exclude dysplasia, a lichenoid drug reaction, or mimics such as chronic ulcerative stomatitis and pemphigoid. Direct immunofluorescence is often performed on erosive presentations to exclude immunobullous disease.
Other White Lesions to Distinguish
Differentiating white lesions is a common exam stem:
| Lesion | Key feature |
|---|---|
| Idiopathic leukoplakia | Non-wipeable homogeneous or nodular white plaque; biopsy mandatory; premalignant |
| Oral submucous fibrosis | Stiff pale mucosa with restricted opening; areca nut chewing; premalignant |
| White sponge naevus | Benign autosomal-dominant white folded mucosa from birth; buccal mucosa; no treatment |
| Oral hairy leukoplakia | EBV-driven white vertical folds on lateral tongue; implies immunosuppression or HIV; not premalignant |
| Chemical (aspirin) burn | White slough from topical aspirin misuse; resolves on withdrawal |
The non-wipeable lesions (leukoplakia, submucous fibrosis, chronic hyperplastic candidiasis, hairy leukoplakia) all warrant a definitive diagnosis rather than empirical antifungal.
A 56-year-old woman has bilateral white lace-like striae on her buccal mucosa with central erythematous erosions that have been sore for four months. Which form of oral lichen planus is this, and what is the key long-term management implication?
A patient with well-controlled hypertension develops new bilateral lichenoid oral lesions three months after a medication change. Which drug class is the most likely culprit?
A 24-year-old reports 3-4 small (<5 mm) painful round ulcers on the labial mucosa every few weeks, each healing within 10 days. Baseline bloods are normal. What is the most likely diagnosis and initial management?
A 62-year-old man has a unilateral 1.5 cm white plaque on the lateral tongue that has not changed in six weeks. The plaque cannot be wiped off with gauze. What is the correct next step?