White Lesions

💡Master classification

💡NORMAL WHITE VARIANTS

💡Leukoedema

• A common developmental variation of the oral mucosa.
• Appears as a bilateral, diffuse, grey-white or opalescent film, especially on the buccal mucosa.
• More common in dark-skinned individuals.
• Histology shows intracellular edema of superficial epithelial cells.

Hallmark: The lesion disappears or markedly diminishes when the cheek is stretched.

FCPS tip: White buccal mucosa that disappears on stretching = leukoedema.

💡Fordyce granules

• Ectopic sebaceous glands within the oral mucosa.
• Present in a large proportion of adults.
• Multiple small, yellowish-white papules, often bilateral.
• Common on buccal mucosa opposite the molars and upper lip.
• No associated hair follicles.

💡White sponge nevus

• An inherited disorder with autosomal dominant transmission.
• Associated with mutations in keratin 4 (K4) or keratin 13 (K13).
• Usually begins in childhood or adolescence and persists throughout life.
• Produces bilateral, thick, white, folded or corrugated plaques.
• Buccal mucosa is the most common site; other mucosal surfaces can be affected.
• Histology shows marked intracellular edema of spinous cells and epithelial thickening.

MCQ tip: Young patient + lifelong bilateral spongy white plaques + family history = white sponge nevus.

💡FRICTIONAL AND TRAUMATIC WHITE LESIONS

💡Frictional keratosis

A reactive thickening of the oral epithelium caused by chronic mechanical irritation.

Causes

• Sharp tooth edges.
• Cheek biting.
• Poorly fitting dentures.
• Habitual chewing or friction against a restoration.

Clinical features

• White patch with a rough or irregular surface.
• Usually located where the irritant contacts the mucosa.
• Common sites include the lateral tongue, buccal mucosa along the occlusal line and edentulous alveolar ridges.

Management

1. Identify and remove the cause.
2. Reassess after approximately 2–4 weeks.
3. If the lesion persists after eliminating trauma, biopsy to exclude dysplasia or malignancy.

FCPS tip: A presumed traumatic white lesion that fails to resolve after removal of the irritant requires further investigation.

💡Morsicatio buccarum (cheek biting)

• Caused by habitual biting or chewing of the buccal mucosa, lips or tongue.
• Produces ragged, shredded, macerated white tissue.
• Usually affects the buccal mucosa bilaterally or the lower lip.
• The roughened surface may contain irregular white tags.
• No inherent malignant potential is described in the notes.

Management: Reassurance, habit modification and removal of contributing factors.

Comparison: frictional keratosis vs morsicatio

💡CANDIDA-RELATED WHITE LESIONS

💡Pseudomembranous candidiasis (thrush)

Caused most commonly by Candida albicans, an opportunistic fungal organism.

Predisposing factors

• Broad-spectrum antibiotics.
• Inhaled or systemic corticosteroids.
• HIV/AIDS and other forms of immunosuppression.
• Diabetes mellitus.
• Xerostomia.
• Denture wearing and poor denture hygiene.
• Extremes of age.

Clinical features

• Creamy white plaques on the buccal mucosa, palate, tongue or oropharynx.
• Plaques can be wiped or scraped off.
• The underlying mucosa is erythematous and may bleed.

Diagnosis and treatment

• Diagnosis is often clinical.
• KOH smear can demonstrate yeast and pseudohyphae.
• PAS staining and fungal culture may be used when needed.
• Topical nystatin or miconazole is commonly used; systemic fluconazole may be required in selected severe or immunocompromised cases.

💡Chronic hyperplastic candidiasis (candidal leukoplakia)

• Produces a firm, adherent white plaque, commonly on the buccal mucosa or commissural region.
• Cannot be wiped off, unlike pseudomembranous candidiasis.
• Associated with chronic fungal infection and epithelial hyperplasia.
• Dysplasia may develop; biopsy is important to assess the lesion.

Key comparison

Exam pearl: Do not label every non-removable white plaque as Candida. Leukoplakia and other potentially malignant lesions must be considered, and persistent lesions need appropriate assessment.

💡ORAL POTENTIALLY MALIGNANT DISORDERS

💡Leukoplakia

Definition

A predominantly white plaque of the oral mucosa that cannot be characterized clinically or pathologically as another definable disease. It is a diagnosis of exclusion.

Risk factors

• Tobacco use — a major risk factor.
• Alcohol use.
• Betel quid and areca nut chewing.
• High-risk HPV in selected oral lesions.
• Ultraviolet exposure for lip lesions.

Prevalence is approximately 1–5% in adults, with peak occurrence around 40–70 years.

Clinical types and malignant potential

These figures are approximate estimates; individual risk depends on clinical and histological findings.

High-risk features for malignant transformation

• Non-homogeneous or speckled appearance.
• Location on the floor of the mouth or ventrolateral tongue.
• Large lesion, particularly over 200 mm².
• Epithelial dysplasia on biopsy.
• Candidal superinfection.
• Leukoplakia in a non-smoking woman, sometimes termed idiopathic leukoplakia.

Management

1. Biopsy is mandatory to establish the diagnosis and assess dysplasia.
2. Remove risk factors, especially tobacco, areca nut and betel quid.
3. If no dysplasia is identified, arrange regular clinical follow-up, commonly every 3–6 months.
4. Mild dysplasia may be managed with close monitoring or excision, depending on risk and clinical findings.
5. Moderate or severe dysplasia generally warrants specialist assessment and consideration of excision.
6. Continue long-term surveillance because lesions may recur or develop additional areas.

FCPS tip: Leukoplakia is not a histological diagnosis. It is a clinical diagnosis of exclusion; biopsy is required.

💡Erythroplakia

Definition

A well-demarcated red patch that cannot be diagnosed as another definable disease.

Clinical features

• Bright-red, velvety, often homogeneous patch.
• May be asymptomatic.
• Common sites include the floor of the mouth, ventrolateral tongue, soft palate and retromolar area.

Histology and malignant potential

• Approximately 90% of biopsied erythroplakias show severe dysplasia, carcinoma in situ or invasive squamous cell carcinoma.
• It has the highest malignant potential among the oral lesions discussed here.

Management

• Urgent incisional biopsy.
• Specialist assessment and appropriate definitive treatment.
• Close follow-up.

MCQ tip: A red, velvety patch is more concerning than a simple homogeneous white plaque. Erythroplakia warrants urgent biopsy.

💡Speckled leukoplakia (erythroleukoplakia)

• Mixed red and white lesion.
• Combines the clinical features of leukoplakia and erythroplakia.
• Has a higher malignant risk than homogeneous leukoplakia.
• Biopsy is essential.

Important exam pearl: Sample the red component, which is more likely to reveal significant dysplasia.

Leukoplakia vs erythroplakia

💡EPITHELIAL DYSPLASIA

💡Definition and histological features

Epithelial dysplasia refers to disordered epithelial maturation and cellular atypia. It is a potentially precancerous change that increases the risk of malignant transformation but does not guarantee that cancer will develop.

Architectural changes

• Drop-shaped or bulbous rete ridges.
• Irregular epithelial stratification.
• Loss of basal-cell polarity.
• Premature keratinization of individual cells below the normal keratinized layer.

Cytological changes

• Nuclear hyperchromatism.
• Increased nuclear-to-cytoplasmic ratio.
• Cellular and nuclear pleomorphism.
• Abnormal mitotic figures, including atypical mitoses.
• Mitoses above the basal layer.
• Increased nuclear abnormalities.

Grading of epithelial dysplasia

Remember: Carcinoma in situ involves the full thickness of the epithelium but has not invaded through the basement membrane. Invasive squamous cell carcinoma crosses the basement membrane.

💡ORAL SUBMUCOUS FIBROSIS (OSMF)

Definition and etiology

OSMF is a chronic, progressive fibrotic disorder of the oral mucosa strongly associated with areca nut or betel quid chewing.

Arecoline, an alkaloid in areca nut, stimulates fibroblasts and increases collagen production.

Pathogenesis

1. Arecoline stimulates fibroblast proliferation and collagen synthesis.
2. Flavonoids in areca nut may inhibit collagen breakdown.
3. Collagen cross-linking contributes to dense, inelastic fibrous tissue.
4. The overlying epithelium becomes atrophic and more vulnerable to carcinogens.

OSMF has significant malignant potential and requires long-term surveillance.

Clinical features

Staging by interincisal opening

These thresholds are a study framework; clinical staging systems may use additional features.

Management of OSMF

1. Stop areca nut, betel quid and tobacco exposure.
2. Improve nutritional status and correct documented deficiencies.
3. Use jaw physiotherapy, stretching and mouth-opening exercises.
4. Intralesional corticosteroids and hyaluronidase may be considered in selected cases.
5. Severe trismus may require surgical release of fibrous bands, sometimes with reconstruction.
6. Maintain regular surveillance for malignant transformation.

FCPS tip: Areca nut chewing + burning mouth + palpable fibrous bands + progressive trismus = OSMF.

Remember: Stopping areca nut is essential; medication or surgery does not remove the need for ongoing surveillance.

💡ORAL LICHEN PLANUS (OLP)

Definition and pathogenesis

Oral lichen planus is a chronic, T-cell-mediated inflammatory mucocutaneous disorder of uncertain etiology.

• Commonly affects middle-aged adults, particularly women.
• The posterior buccal mucosa is a classic site.
• Lesions are often bilateral and symmetrical.
• It is a chronic condition that may require long-term follow-up.

Clinical types

Hallmark clinical features

• Bilateral, symmetrical white Wickham striae.
• Commonly affects posterior buccal mucosa.
• Erosive disease may cause painful ulcers.
• Desquamative gingivitis may occur.

Histopathology

The classic histological findings are:

1. Band-like lymphocytic infiltrate at the epithelial–connective tissue interface.
2. Saw-tooth-shaped rete ridges.
3. Civatte bodies — apoptotic keratinocytes.
4. Basal-cell degeneration.
5. Max-Joseph spaces may occur because of separation at the epithelial–connective tissue interface.

Direct immunofluorescence may show shaggy fibrinogen deposition along the basement membrane zone.

Malignant potential

The estimated malignant transformation risk is approximately 0.4–5%.

• Erosive and atrophic forms are considered more concerning than the typical reticular form.
• Long-term clinical follow-up is important.
• Persistent ulcers, induration, changing appearance or a focal suspicious area require reassessment and possible biopsy.

Oral lichen planus vs lichenoid reaction

Potential triggers for lichenoid reactions include certain NSAIDs, antihypertensives, antimalarials and contact with dental restorative materials.

Management of OLP

FCPS tip: Bilateral Wickham striae suggest OLP. A unilateral lesion directly adjacent to a restoration raises suspicion of a lichenoid contact reaction.

💡MASTER COMPARISON TABLE

💡White lesions and potentially malignant disorders