10.1 White, Red & Ulcerative Mucosal Lesions

Key Takeaways

  • Leukoplakia is a white plaque that cannot be wiped off and cannot be attributed to another defined disease—it is a clinical term, not a histologic diagnosis, and requires risk-stratified biopsy.
  • Oral lichen planus is a chronic T-cell–mediated mucocutaneous disease; reticular (Wickham striae) is common and often asymptomatic, while erosive forms cause pain and need active management plus cancer surveillance.
  • Candidiasis presents as wipeable white plaques (pseudomembranous), red mucosa (erythematous/atrophic), or angular cheilitis—treat predisposing factors plus antifungals.
  • Geographic tongue (benign migratory glossitis) shows map-like red patches with white borders that migrate; it is benign and usually needs only reassurance.
  • Traumatic ulcers have a clear local cause and heal when the insult is removed; aphthous ulcers are recurrent, non-keratinized-site lesions without primary vesicles; HSV shows primary gingivostomatitis or recurrent cold sores with vesicles.
Last updated: July 2026

10.1 White, Red & Ulcerative Mucosal Lesions

Quick Answer: Sort mucosal lesions by color, wipeability, site (keratinized vs non-keratinized), duration, and symptoms. Leukoplakia = persistent white plaque that cannot be wiped or explained by another disease → risk-based biopsy. Candidiasis white plaques wipe off. Lichen planus shows Wickham striae or painful erosions. Aphthae are recurrent ulcers on non-keratinized mucosa without vesicles; HSV starts with vesicles; traumatic ulcers resolve after removing the cause.

Oral medicine on the AFK rewards systematic differentials, not memorized brand names. Mucosal disease is a large share of the Oral Medicine/Oral Pathology domain (~15% blueprint weight with radiology). Build a habit: history (onset, pain, recurrence, drugs, tobacco, dentures, systemic disease) → clinical morphology → provisional diagnosis → when to biopsy or culture → first-line care.

Framework: How to Approach Any Mucosal Lesion

FeatureQuestions to askExam implication
ColorWhite, red, mixed, pigmented, vesicular?White: keratin, fungus, scar, material alba; red: atrophy, inflammation, dysplasia/erythroplakia risk
WipeabilityDoes white material rub off?Wipeable → candidiasis/material alba; non-wipeable → leukoplakia, lichen planus, frictional keratosis
SiteKeratinized (hard palate, gingiva, dorsum tongue) vs non-keratinized (buccal, floor, ventral tongue, soft palate)?Aphthae prefer non-keratinized; recurrent HSV on keratinized movable mucosa (lip vermilion, hard palate, attached gingiva)
DurationAcute days vs chronic weeks/months?>2 weeks without clear healing trajectory → investigate (biopsy if suspicious)
SymptomsPain, burning, none?Asymptomatic white plaque can still be dysplasia; pain ≠ benign
MultiplicitySingle vs multiple, migrating?Migrating map lesions → geographic tongue; widespread ulcers → viral, EM, systemic

Biopsy rule of thumb: any persistent unexplained white/red lesion, non-healing ulcer >2 weeks after removing local irritants, or lesion with induration, fixation, rolled borders, or high-risk site (floor of mouth, ventrolateral tongue, soft palate) warrants tissue diagnosis. Cytology is not a substitute for biopsy of suspected premalignancy/cancer.

Leukoplakia (Clinical Term)

Definition (WHO concept): a white plaque of questionable risk, having excluded other known diseases/disorders that carry no increased cancer risk. It is not a histopathology diagnosis—histology may show hyperkeratosis only, dysplasia, or even carcinoma.

FeatureTeaching points
ClinicalWhite (or mixed red-white = speckled), cannot wipe off, variable thickness
High-risk sitesFloor of mouth, ventrolateral tongue, soft palate/oropharynx
Risk factorsTobacco (smoked and smokeless), alcohol, areca nut/betel quid; HPV association stronger for oropharyngeal SCC than classic oral leukoplakia
Speckled leukoplakiaMixed red-white; higher dysplasia/malignancy risk than homogeneous white
Proliferative verrucous leukoplakia (PVL)Multifocal, progressive, often in older women, high malignant transformation—needs aggressive surveillance
ManagementEliminate risk habits; biopsy (incisional for large/heterogeneous; excisional for small); treat dysplasia per grade; long-term follow-up

Frictional (reactive) keratosis along a bite line or under a sharp cusp can look white and non-wipeable but has a clear mechanical cause and usually resolves with elimination of trauma. If in doubt, especially at high-risk sites, biopsy.

Hairy leukoplakia (EBV-related, often lateral tongue, immunocompromised/HIV) is a distinct entity—corrugated white plaques that do not wipe; manage underlying immune status; not the same as idiopathic leukoplakia.

Oral Lichen Planus (OLP)

OLP is a chronic immune-mediated (T-cell) mucocutaneous disease. Skin may show purple polygonal pruritic papules with Wickham striae; oral disease may occur alone.

FormClinicalSymptomsNotes
ReticularWhite lace-like Wickham striae, often bilateral buccal mucosaOften asymptomaticMost common oral form
Papular / plaqueWhite papules or plaquesVariableMay mimic leukoplakia
Erythematous / atrophicRed mucosa with striaeBurning, sensitivity
Erosive / ulcerativePainful erosions, sometimes desquamative gingivitisSignificant pain, eating difficultyHigher morbidity; cancer surveillance important
BullousRare bullaePain when rupture

Lichenoid reactions: drug-related (e.g., antihypertensives, antimalarials, NSAIDs, gold historically), dental restorative materials (amalgam contact lichenoid), and graft-versus-host disease can mimic OLP. Unilateral contact lesions adjacent to a restoration suggest lichenoid contact reaction—consider replacement if symptomatic and biopsy-supported.

Diagnosis: clinical pattern often sufficient for classic bilateral reticular disease; biopsy when atypical, unilateral, erosive, or to exclude dysplasia/carcinoma. Histology: band-like lymphocytic infiltrate, basal cell degeneration, saw-tooth rete ridges (skin more classic).

Management principles:

  1. Confirm diagnosis / rule out dysplasia in suspicious areas
  2. Eliminate triggers (drugs when feasible, plaque control, replace culprit restorations)
  3. Topical corticosteroids first-line for symptomatic disease (gels, ointments, steroid mouthrinses; occlusive trays for desquamative gingivitis)
  4. Topical calcineurin inhibitors in selected refractory cases (off-label patterns; specialist care)
  5. Systemic therapy for severe refractory disease (specialist)
  6. Surveillance: OLP, especially erosive, carries a small but real malignant transformation risk → periodic exam and biopsy of changing areas

Oral Candidiasis

Candida albicans (and other species) overgrow when host defenses or local ecology change.

TypeAppearanceWipeable?Classic associations
Pseudomembranous (thrush)Creamy white plaquesYes → red baseInfants, antibiotics, steroids, immunosuppression, xerostomia
Erythematous / atrophicRed painful mucosaN/ADenture stomatitis, antibiotic use, HIV (acute erythematous)
Chronic hyperplasticPersistent white plaquesPoorly wipeableMay need biopsy to exclude dysplasia; smoking
Angular cheilitisCracks/erythema at commissuresDenture vertical dimension loss, Candida ± Staph, nutritional deficiency
Median rhomboid glossitisMidline dorsal tongue red rhomboid patchCandida-associated; often asymptomatic

Predisposing factors (memorize): broad-spectrum antibiotics, inhaled/systemic corticosteroids (rinse after inhalers), diabetes, xerostomia, ill-fitting dentures worn overnight, immunosuppression/HIV, iron/B12 deficiency, smoking.

Treatment: topical antifungals (nystatin suspension/pastilles, clotrimazole troches) for uncomplicated disease; systemic azoles (e.g., fluconazole) when extensive, esophageal involvement, or refractory—watch drug interactions. Always treat the cause (denture hygiene, leave dentures out at night, disinfect dentures, steroid inhaler technique, glycemic control). Culture or specialist referral if atypical/refractory (non-albicans species, resistance).

Geographic Tongue (Benign Migratory Glossitis)

FeatureDetail
ClinicalMap-like red patches (filiform papilla atrophy) with slightly raised white/yellow borders; pattern migrates over days–weeks
SiteDorsal/lateral tongue; ectopic geographic stomatitis can involve other mucosa
SymptomsOften asymptomatic; some have burning with spicy/acidic foods
AssociationsAtopy, psoriasis in some patients; not infectious or premalignant
ManagementReassure; avoid triggers; topical steroids only if significantly symptomatic

Differential: candidiasis (does not migrate in map pattern with classic borders), erythroplakia (fixed high-risk red patch—biopsy), median rhomboid glossitis (midline fixed).

Traumatic Ulcers

CauseExamplesClue
MechanicalSharp tooth, broken restoration, ill-fitting denture, cheek bitingAdjacent culprit; often single
ChemicalAspirin burn, improper etchant/whitening misuseHistory of application
ThermalHot foods, pizza burnPalate common
Factitial / iatrogenicCotton roll injury, suction traumaProcedure history

Course: remove cause → healing usually within 7–14 days. If no healing after elimination of trauma or if indurated/suspicious → biopsy. Traumatic ulcerative granuloma with stromal eosinophilia (TUGSE) is a deep chronic traumatic ulcer (often tongue) that may need biopsy to exclude malignancy/lymphoma.

Aphthous Ulcers (Recurrent Aphthous Stomatitis, RAS)

TypeSizeDurationScarring
Minor<1 cm7–14 daysNo
Major≥1 cmWeeksOften yes
HerpetiformMany 1–2 mm ulcers that coalesceVariableUncommon

Key clinical rules:

  • Prefer non-keratinized mucosa (buccal, labial, floor of mouth, ventral tongue, soft palate)
  • No primary vesicle stage (contrast with HSV)
  • Prodrome of tingling may occur; yellow-gray fibrin base with erythematous halo
  • Triggers: stress, trauma, hormonal change, sodium lauryl sulfate toothpaste, food sensitivities; systemic associations include Behçet, IBD, celiac, HIV, cyclic neutropenia, nutritional deficiencies

Management: identify systemic red flags (genital ulcers, uveitis, GI disease, severe recurrent major aphthae → medical workup). Local care: topical corticosteroids, barrier agents, analgesics; chlorhexidine for secondary infection control (not curative); systemic steroids/immunomodulators for major/refractory disease under specialist care. Rule out HSV when ulcers are on keratinized mucosa or vesicles are present.

Herpes Simplex Virus (HSV)

EntityHostClinical
Primary herpetic gingivostomatitisOften children/young adults; non-immuneFever, malaise, widespread vesicles/ulcers on keratinized and non-keratinized mucosa, painful gingivitis, lymphadenopathy
Recurrent herpes labialisImmune hostsVermilion/perioral vesicles → crusts; triggers: UV, stress, illness
Recurrent intraoral HSVImmune hostsAlmost always keratinized bound mucosa (hard palate, attached gingiva); cluster of small ulcers
Immunocompromised HSVHIV, transplant, etc.Atypical large chronic ulcers; any site

Diagnosis: clinical; viral culture/PCR/DFA when atypical. Tzanck smear shows multinucleated giant cells but does not distinguish HSV from VZV.

Treatment: supportive care for mild primary disease; systemic antivirals (acyclovir, valacyclovir, famciclovir) best if started early (prodrome/first 48–72 h) for significant primary disease, frequent recurrence, or immunocompromised patients. Avoid elective dental care during active contagious vesicular stages when possible; infection control for aerosols/contact.

Herpes Zoster (Shingles, VZV Reactivation)

FeatureTeaching point
PatternUnilateral vesicles/ulcers strictly in a dermatome (trigeminal divisions V1/V2/V3)
OralV2/V3: unilateral palatal/gingival/vestibular vesicles ending at midline
PainOften severe prodromal pain; post-herpetic neuralgia risk rises with age
Hutchinson signVesicles on nasal tip (nasociliary, V1) → urgent ophthalmic risk
Ramsay HuntGeniculate ganglion: ear vesicles + facial palsy ± oral lesions
TreatmentEarly systemic antivirals; analgesics; ophthalmology/medical referral as indicated

AFK differential: zoster is unilateral dermatomal; primary HSV is more diffuse with systemic illness in non-immune hosts; aphthae lack vesicles and dermatomal restriction.

Master Differential: White, Red, Ulcerative

LesionWipe off?Vesicles?Site preferenceFirst action
Pseudomembranous candidiasisYesNoAny; soft tissuesAntifungal + risk factors
LeukoplakiaNoNoAny; risk sites criticalBiopsy / risk reduction
Reticular lichen planusNoNoBilateral buccal commonOften observe if asymptomatic
Erosive lichen planusNoRare bullaeVariable; gingivaSteroids + surveillance
Geographic tongueNoNoDorsum tongue, migratesReassure
Traumatic ulcerN/ANoAdjacent to causeRemove cause; recheck
Minor aphthousN/ANoNon-keratinizedTopical steroid; triggers
Primary HSVN/AYesWidespread + gingivaSupportive ± antiviral
Recurrent intraoral HSVN/AYes earlyKeratinized onlyEarly antiviral if severe
Herpes zosterN/AYesUnilateral dermatomeEarly antiviral; refer if eye

Rapid review list

  • Leukoplakia: non-wipeable unexplained white plaque → clinical term → biopsy
  • Speckled / high-risk site / PVL → higher malignancy concern
  • Lichen planus: Wickham striae; erosive needs treatment + follow-up
  • Candida: wipeable plaques; fix dentures/steroids/diabetes
  • Geographic tongue migrates and is benign
  • Aphthae = non-keratinized, no vesicles; HSV vesicles; zoster = unilateral dermatome
  • Non-healing ulcer >2 weeks after removing trauma → biopsy

Section 10.2 focuses on cancer and premalignancy; 10.3 covers autoimmune vesiculobullous disease that can mimic erosive lichen planus and severe aphthae.

Test Your Knowledge

A white plaque on the buccal mucosa cannot be wiped off and is not explained by cheek biting or another defined disease. Which label and next step are most appropriate?

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Test Your Knowledge

Which clinical feature best supports recurrent intraoral herpes simplex rather than minor aphthous ulceration?

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D
Test Your Knowledge

Which statement about oral lichen planus is most accurate for AFK-level management?

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D
Test Your Knowledge

A 68-year-old develops severe unilateral facial pain followed by vesicles strictly limited to the right hard palate ending at the midline. The most likely diagnosis is:

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D