White and Red Oral Lesions: Keratotic, Erythematous, and Ulcerative Conditions

Core Review

The Clinical Significance of White and Red Lesions

White and red lesions represent the most common category of oral mucosal pathology encountered in dental practice. The clinical significance ranges from entirely benign (frictional keratosis) to premalignant (leukoplakia/erythroplakia) to malignant (squamous cell carcinoma). The central clinical question is always: Is this lesion benign/reactive, or does it require biopsy?

White Lesions

Frictional (Traumatic) Keratosis

Clinical appearance: White, rough, hyperkeratotic plaque at a site of chronic, low-grade mechanical irritation. The white color results from increased keratin production (hyperkeratosis). The surface may be rough but is not verrucous.

Common examples and locations:

• Linea alba: White line on buccal mucosa at the occlusal plane (friction from teeth)
• Morsicatio buccarum (cheek biting): Irregular, ragged white patches on the buccal mucosa; often bilateral. History of habitual cheek biting/chewing. May have areas of erythema, erosion, or superficial ulceration intermixed.
• Morsicatio linguarum (tongue biting): White, ragged patches on the lateral tongue borders.
• Toothbrush trauma: Linear white streaks or erosions on the gingiva (overzealous brushing)
• Denture-induced keratosis: White lesion on the denture-bearing area or flange area

Key clinical feature: The lesion can be DIRECTLY attributed to a mechanical cause. If the irritant is removed, the lesion should RESOLVE within 2 weeks (the "two-week removal rule").

Management: Identify and remove the source of trauma. Re-evaluate in 2 weeks. If the lesion resolves, no further action is needed. If it persists, biopsy is indicated because persistent "frictional keratosis" may actually be idiopathic leukoplakia with superimposed trauma.

NBDHE trap: A question may describe a white lesion on the buccal mucosa at the occlusal plane that disappears when the patient stops cheek biting. The answer is likely frictional keratosis, not leukoplakia.

Leukoplakia

Definition (WHO): "A white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer." Leukoplakia is a CLINICAL term, not a histologic diagnosis. It is a diagnosis of exclusion.

Clinical features:

• White plaque that CANNOT be wiped off and cannot be characterized as any other specific white lesion
• May be homogeneous (uniformly white, smooth or finely wrinkled, thin — lower malignant risk) or non-homogeneous (speckled/erythroleukoplakia, verrucous, nodular — HIGHER malignant risk)
• May occur on any oral mucosal surface
• Most common in middle-aged to older adults, strong association with tobacco use (smoking > smokeless tobacco)

Epidemiology: Prevalence approximately 2-3% of the general population. Malignant transformation rate overall ~1-4% over 10 years, but varies significantly by subtype, location, and presence of epithelial dysplasia.

Risk factors for malignant transformation:

• Non-homogeneous (speckled) appearance — HIGHEST risk subtype
• Location: Floor of mouth, lateral/ventral tongue, soft palate complex are HIGH-RISK sites
• Size >200 mm²
• Presence of epithelial dysplasia (moderate to severe)
• Female gender
• Long duration
• No identifiable etiological factor (idiopathic leukoplakia carries higher risk than tobacco-associated)
• Non-smokers (paradoxically — idiopathic leukoplakia in non-smokers may have higher risk)

Management: ALL leukoplakia requires biopsy to establish the histologic diagnosis and rule out dysplasia or carcinoma. The pathologist's report will indicate whether dysplasia is present and its grade (mild, moderate, severe/carcinoma in situ). Management depends on the histology: no dysplasia → periodic observation; dysplasia → complete removal (excision, laser ablation) and close follow-up.

NBDHE critical concept: Leukoplakia does NOT automatically mean cancer or precancer. It means "a white patch that needs to be investigated." Many leukoplakias (50-70%) are benign hyperkeratosis without dysplasia. However, because a subset harbor dysplasia or carcinoma, ALL require biopsy.

Proliferative Verrucous Leukoplakia (PVL)

A particularly aggressive, multifocal variant of leukoplakia characterized by:

• Persistent/recurrent, multifocal involvement
• Progression from flat hyperkeratosis → verrucous (warty) hyperplasia → verrucous carcinoma or squamous cell carcinoma over years
• Strong female predilection
• Often NOT associated with tobacco use
• Very high malignant transformation rate (>70% in long-term follow-up)

NBDHE significance: PVL is a distinct entity from conventional leukoplakia with a much worse prognosis.

Hairy Leukoplakia

Clinical appearance: White, corrugated ("hairy"), vertically oriented plaque that CANNOT be wiped off. Unlike leukoplakia, it has a distinctive corrugated, shaggy surface texture. Usually bilateral.

Location: LATERAL BORDER of the tongue (most characteristic). May extend to dorsal and ventral surfaces.

Etiology: Epstein-Barr virus (EBV) reactivation in the setting of immunosuppression. NOT a premalignant lesion.

Clinical significance: Hairy leukoplakia is an AIDS-defining condition and a marker of immunosuppression. It was historically one of the most common oral manifestations of HIV/AIDS. It can also occur in other immunosuppressed states (transplant, chemotherapy, high-dose corticosteroids).

Distinguish from: Frictional keratosis of the lateral tongue (does not have the corrugated "hairy" surface); leukoplakia (lack of EBV association, different clinical context).

Management: Does NOT require biopsy if clinical diagnosis is clear. Resolves with effective antiretroviral therapy (ART) or improvement of immune status. Antiviral therapy (acyclovir, valacyclovir) may be used.

Oral Lichen Planus

Clinical forms (oral):

1. Reticular (most common): Network of interlacing white lines (Wickham striae), often bilaterally on the BUCCAL MUCOSA. This is the classic, most recognizable form. Usually asymptomatic.
2. Erosive/atrophic: Erythematous, eroded, painful areas. Often superimposed on reticular striae. The MOST SYMPTOMATIC form.
3. Plaque: White, homogeneous plaques resembling leukoplakia. Often on the dorsum of the tongue.
4. Papular: Small, white papules.
5. Bullous: Rare; fluid-filled bullae that rupture to form erosions.

Key clinical features:

• BILATERAL involvement (often symmetric)
• Multifocal (multiple sites in the mouth)
• Wickham striae (reticular white lines) — pathognomonic
• Skin lesions may be present (violaceous, pruritic, polygonal papules — "purple, pruritic, polygonal, papules/plaques" — flexor surfaces of wrists, shins)
• Female predominance
• Middle-aged to older adults

Etiology: T cell-mediated autoimmune disorder targeting basal keratinocytes. Chronic inflammatory condition. NOT infectious, NOT contagious.

Malignant transformation risk: Slightly increased risk (approximately 1-2% over 5-10 years), particularly with erosive/atrophic forms. Patients with oral lichen planus require periodic monitoring.

Management: Asymptomatic reticular form: no treatment, periodic observation. Symptomatic erosive form: topical corticosteroids (triamcinolone paste, fluocinonide gel, clobetasol gel). Severe cases: systemic corticosteroids, immunomodulators.

Distinguish from:

• Lichenoid reaction (drug-induced or contact): Unilateral, related to specific medication or dental material (amalgam); resolves when the trigger is removed
• Leukoplakia: Does not have reticular Wickham striae; often associated with tobacco
• Candidiasis: Pseudomembranous type can be wiped off

Smokeless Tobacco Keratosis

Clinical appearance: White, wrinkled, translucent plaque precisely localized to the site where smokeless tobacco (snuff, dip, chewing tobacco) is habitually placed. The mucosa appears granular or "cobblestone-like."

Location: Corresponds to the site of tobacco placement — typically the mandibular buccal vestibule or labial vestibule.

Clinical significance: The lesion is thought to be reactive hyperkeratosis from chemical irritation. It carries a risk of malignant transformation, particularly with long-term use. The risk is lower than smoking-related oral cancer risk but is still significant (approximately 4% malignant transformation rate). Biopsy is indicated if there are areas of erythema, ulceration, induration, or verrucous change within the lesion.

Management: Smoking/tobacco cessation counseling. Biopsy any suspicious areas. Monitor for changes.

Red Lesions

Erythroplakia

Definition (WHO): "A fiery red patch that cannot be characterized clinically or pathologically as any other definable disease." The RED ANALOGUE of leukoplakia.

Clinical appearance: A well-demarcated, velvety red patch. May be flat or slightly depressed. Often has an irregular border. May be speckled (erythroleukoplakia — mixed red and white).

Clinical significance — THIS IS THE MOST DANGEROUS ORAL POTENTIALLY MALIGNANT LESION:

• On biopsy, 50-90% already show dysplasia, carcinoma in situ, or invasive squamous cell carcinoma
• HIGHER risk than leukoplakia for malignant transformation
• Less common than leukoplakia
• Any persistent red patch that cannot be definitively diagnosed as something else (candidiasis, vascular, geographic tongue, inflammatory) MUST be biopsied

NBDHE critical concept: If a question asks "Which oral lesion has the highest risk of dysplasia or malignancy?", the answer is erythroplakia.

Location: High-risk sites: floor of mouth, lateral/ventral tongue, soft palate. These are the same high-risk sites as for oral cancer.

Management: BIOPSY ALL erythroplakic lesions — do NOT delay, do NOT observe.

Erythematous Candidiasis

Red patches that may mimic erythroplakia. Key distinguishing features: history of predisposing factors (antibiotics, corticosteroids, xerostomia, dentures), diffuse rather than focal, responds to antifungal therapy. If antifungal therapy fails to resolve the lesion, biopsy is mandatory.

Vascular Lesions

• Hemangioma: Benign proliferation of blood vessels; red/purple, blanches on pressure (diascopy), may be congenital or acquired
• Varix: Dilated vein; purple/blue, blanches, common on ventral tongue and lips in older adults
• Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu): Multiple small telangiectasias on lips, tongue, and buccal mucosa; associated with recurrent epistaxis and GI bleeding; autosomal dominant

Ulcerative Lesions (Red with Tissue Loss)

Recurrent Aphthous Stomatitis (RAS, Aphthous Ulcers, Canker Sores)

One of the most common oral mucosal conditions. Affects 10-20% of the population. Unknown etiology (T cell-mediated immune dysregulation, NOT infectious, NOT viral). Triggers: stress, trauma, certain foods (nuts, chocolate, acidic foods), sodium lauryl sulfate (SLS) in toothpaste, nutritional deficiencies (B12, folate, iron), hormonal fluctuations, and some systemic conditions (Behçet disease, Crohn disease, celiac disease, HIV).

Three clinical subtypes:

Key NBDHE distinctions from HSV:

• RAS: NO vesicles (never a blister phase), NON-KERATINIZED mucosa, NO fever/lymphadenopathy (minor type), recurrent episodes, deep well-defined ulcers
• HSV: Preceded by VESICLES, involves KERATINIZED mucosa (in recurrent form), acute onset, systemic symptoms in primary form, shallow punctate ulcers

Management: Topical corticosteroids (triamcinolone paste — first line for minor RAS). Topical anesthetics (benzocaine, viscous lidocaine) for symptomatic relief. Protective pastes (Orabase). Severe cases: systemic corticosteroids, immunomodulators. Identify and supplement nutritional deficiencies.

Systemic associations requiring workup for "complex aphthosis":

• Behçet disease: Recurrent oral AND genital aphthae + ocular lesions (uveitis) + skin lesions + positive pathergy test
• Crohn disease: GI symptoms, aphthous-like ulcers
• Celiac disease: Gluten sensitivity, aphthous-like ulcers
• Cyclic neutropenia: Cyclic fever, oral ulcers, neutropenia
• HIV/AIDS: Severe, persistent aphthous-like ulcers

Traumatic Ulcer

Clinical appearance: Irregular ulcer with ragged borders. Cause is identifiable: sharp tooth, fractured restoration, ill-fitting denture, accidental bite, burn from hot food. Heals within 2 weeks after removal of the cause. If it persists beyond 2 weeks, BIOPSY.

Squamous Cell Carcinoma (SCC) — Early Presentation

SCC may present as:

• Non-healing ulcer with rolled, indurated borders
• Exophytic (mass-like) lesion
• Erythroplakia or erythroleukoplakia
• Persistent white lesion that changes in appearance

Red flags for SCC: Persistence >2 weeks, induration (hardness), fixation, bleeding, paresthesia, lymphadenopathy, weight loss, voice changes, dysphagia. Any lesion with these features requires urgent biopsy.

Clinical Application

The dental hygienist's role is detection and appropriate referral. A systematic approach: (1) Identify the lesion, (2) Remove any potential traumatic cause if applicable, (3) Re-evaluate in 2 weeks. If the lesion resolves, document and continue monitoring. If it persists or has high-risk features (erythroplakia, non-homogeneous leukoplakia, floor of mouth/ventral tongue location, induration, ulceration, bleeding), refer for biopsy WITHOUT the 2-week observation period. The most common error is delaying biopsy of a potentially malignant lesion.

Common Traps

• Thinking every white lesion needs immediate biopsy — frictional keratosis resolves with removal of the cause
• Thinking leukoplakia = cancer — most leukoplakias are benign hyperkeratosis; biopsy tells the story
• Not biopsying erythroplakia because it "looks benign" — it's the highest-risk lesion
• Confusing HSV ulcers with aphthous ulcers — the key is vesicles (HSV yes, aphthous no) and location (keratinized vs. non-keratinized)
• Forgetting that lichen planus requires periodic monitoring due to slight increased SCC risk
• Calling every white lesion "leukoplakia" — leukoplakia is a diagnosis of exclusion; first rule out frictional keratosis, candidiasis, lichen planus, etc.