Ulcers and Lesions

Oral Pathology & Medicine6 min read
On this page 39 sections

💡Traumatic Ulcers

Causes

  • Mechanical trauma: sharp teeth, broken restorations, dental appliances.
  • Chemical trauma: aspirin burns.
  • Thermal injury.
  • Self-inflicted trauma, e.g., morsicatio buccarum (cheek biting).

Clinical features

  • Usually a single ulcer at the site of trauma.
  • Painful, with irregular margins and a yellowish-white fibrinous base.

Healing

  • Usually heals within 7–14 days after removal of the cause.
  • An ulcer persisting for more than 3 weeks requires biopsy to exclude squamous cell carcinoma (SCC).

💡Recurrent Aphthous Stomatitis (RAS)

Definition: The most common inflammatory ulcerative condition of the oral mucosa, affecting approximately 20–25% of the population.

Etiology and predisposing factors

  • Genetic predisposition — family history in approximately 40%.
  • Hematological deficiencies: iron, vitamin B12, and folate.
  • Stress and hormonal changes.
  • Food sensitivity.
  • Sodium lauryl sulfate (SLS) in toothpaste may contribute.

Important: RAS is not caused by herpes simplex virus (HSV).

Sites: Non-keratinized mucosa, including buccal mucosa, labial mucosa, floor of mouth, and ventral tongue.

Types of RAS

TypeSizeNumberHealingScarring
Minor (80%)10 mm1–3Weeks to monthsYes
Herpetiform (5–10%)1–3 mm10–100+10–14 daysNo, unless coalesced

Differential diagnosis: RAS vs primary herpetic gingivostomatitis

FeatureRASPrimary herpetic gingivostomatitis
MucosaNon-keratinizedKeratinized and non-keratinized
VesiclesAbsentPresent before ulceration
FeverNot characteristicMay occur
GingivitisNot characteristicOften diffuse
ContagiousnessNoYes

Investigations

  • CBC.
  • Serum ferritin and iron studies.
  • Vitamin B12 and folate.
  • Celiac disease screening: anti-tTG and EMA.
  • HLA-B51 testing when Behçet disease is suspected.

Treatment

Local treatment

  • Topical corticosteroids are first-line: triamcinolone 0.1% in Orabase, 3–4 times daily.
  • Chlorhexidine 0.2% mouthwash.
  • Benzydamine for analgesia.

Systemic treatment for severe disease

  • Colchicine.
  • Dapsone.
  • Thalidomide — teratogenic.
  • Short courses of prednisolone.
  • Azathioprine in selected cases.
  • Minor RAS is the commonest form.
  • Herpetiform RAS consists of numerous tiny ulcers but has no preceding vesicles and is not contagious.
  • Major aphthae may heal with scarring.
  • Investigate iron, B12, folate, and celiac disease in recurrent or severe cases.

💡Behçet Disease

Definition: A chronic, relapsing, multisystem vasculitis.

Classic triad

  1. Recurrent oral ulcers.
  2. Genital ulcers.
  3. Ocular inflammation, particularly uveitis, which can lead to blindness.

Other manifestations

  • Skin: Erythema nodosum, papulopustular lesions.
  • Joints: Arthritis.
  • CNS: Neuro-Behçet disease.
  • Vascular: Venous thrombosis and arterial aneurysms.
  • Gastrointestinal: GI ulceration.

Pathergy test

  • A pustule develops at a needle-prick site within approximately 24–48 hours.
  • Positive in around 50% of patients according to the notes.

Association

  • HLA-B51.

Diagnosis

Consider Behçet disease in a patient with recurrent oral ulcers plus genital ulcers, ocular disease, skin manifestations, or a positive pathergy test.

Treatment

  • Corticosteroids.
  • Colchicine.
  • Azathioprine.
  • Cyclosporine.
  • Anti-TNF agents, e.g., infliximab and adalimumab.

💡Vesiculobulous Diseases

💡Pemphigus Vulgaris

Definition: An autoimmune intraepithelial blistering disease caused by antibodies against desmosomal proteins.

Pathogenesis

  • Anti-desmoglein 3 antibodies → predominantly mucosal disease.
  • Anti-desmoglein 1 antibodies → cutaneous involvement.
  • Both antibodies may be present in mucocutaneous disease.

Clinical features

  • Oral lesions are the initial manifestation in approximately 60% of cases.
  • Oral disease may precede skin lesions by months.
  • Flaccid bullae rupture easily, producing persistent, irregular, painful erosions.

Clinical signs

  • Nikolsky sign: Positive — lateral pressure on apparently normal skin or mucosa may cause epithelial separation.
  • Asboe-Hansen sign: Pressure on an intact blister causes it to extend into surrounding tissue.

Histopathology

  • Suprabasal acantholysis.
  • Basal cells remain attached to the basement membrane, producing a “row of tombstones” appearance.
  • Tzanck cells may be present.

Investigations

  • Direct immunofluorescence (DIF): Intercellular IgG and C3 in a chicken-wire or fish-net pattern.
  • Indirect immunofluorescence (IIF): Circulating antibodies against epithelial antigens.
  • Anti-desmoglein antibody titers may correlate with disease activity.

Treatment

  • High-dose systemic corticosteroids, e.g., prednisolone approximately 1–2 mg/kg/day in severe disease.
  • Steroid-sparing immunosuppressants: azathioprine or mycophenolate.
  • Rituximab.

Prognosis: Potentially fatal if untreated.

💡Mucous Membrane Pemphigoid (MMP)

Definition: An autoimmune subepithelial blistering disease that predominantly affects mucous membranes.

Target antigens

  • BP180.
  • Laminin 332.

Clinical features

  • Tense bullae because the split occurs beneath the epithelium.
  • Desquamative gingivitis is a common oral presentation.
  • Nikolsky sign is usually negative or weakly positive.

Ocular involvement

  • Conjunctival scarring.
  • Symblepharon formation (adhesion between conjunctival surfaces).
  • Progressive scarring may cause blindness.

Important: Ocular involvement requires ophthalmological assessment.

Investigations

  • DIF: Linear IgG and/or C3 deposition along the basement membrane zone.
  • Salt-split skin: Antibody binding on the dermal (floor) side may occur, depending on the target antigen.

Treatment

  • Topical clobetasol for localized oral disease.
  • Dapsone.
  • Systemic immunosuppressants for severe disease.
  • Ophthalmological co-management for ocular involvement.

Pemphigus vulgaris vs mucous membrane pemphigoid

FeaturePemphigus vulgarisMucous membrane pemphigoid
Level of splitIntraepithelial, suprabasalSubepithelial
BlistersFlaccidTense
Nikolsky signStrongly positiveNegative or weak
DIFIntercellular, chicken-wireLinear basement membrane pattern
Main targetDesmoglein 1 and/or 3BP180, laminin 332
ScarringUsually absentCommon, particularly ocular
Major dangerSevere disease may be fatal untreatedOcular scarring and blindness

Memory aid

  • Pemphigus: Intraepithelial, flaccid bullae, positive Nikolsky, chicken-wire DIF.
  • Pemphigoid: Subepithelial, tense bullae, linear DIF, scarring.

💡Erythema Multiforme (EM)

Etiology

  • HSV is the leading trigger of recurrent erythema multiforme, accounting for approximately 90% of recurrent cases in the notes.
  • Medications may also trigger EM, particularly sulfonamides and NSAIDs.

Clinical features

  • Acute onset.
  • Target or iris lesions, classically involving the skin.
  • Oral hemorrhagic lip crusting.
  • Diffuse oral erosions.

Classification

TypeMucosal involvement
EM minorOne mucosal site or less extensive involvement
EM majorTwo or more mucosal sites

Treatment

  • Supportive care.
  • Topical corticosteroids for oral inflammation.
  • Acyclovir prophylaxis for recurrent HSV-associated disease: the notes list 400 mg twice daily for 6–12 months.

Exam pearl: HSV-associated recurrent EM classically presents with target lesions and hemorrhagic crusting of the lips.

💡Other Conditions

💡Linear IgA Disease

  • Rare autoimmune subepithelial blistering disorder.
  • DIF: Linear IgA deposition along the basement membrane zone.
  • Classic drug trigger: Vancomycin.
  • Treatment: Dapsone.

💡Allergic/Contact Stomatitis

Mechanism: Type IV delayed hypersensitivity reaction.

Common allergens

  • Dental materials: nickel, mercury, acrylic.
  • Flavouring agents, particularly cinnamon.

Diagnosis

  • Patch testing, with readings at 48–72 hours.

Treatment

  • Identify and eliminate the offending allergen.

💡Quick-Recall Table

ConditionHallmark featureKey investigation/signImportant association or treatment
Traumatic ulcerLocalized ulcer at site of traumaPersistent lesion requires biopsyRemove cause
RASRecurrent ulcers on non-keratinized mucosaScreen iron, B12, folateTopical corticosteroids
Behçet diseaseOral + genital ulcers + ocular diseasePathergy testHLA-B51 association
Pemphigus vulgarisFlaccid bullae and erosionsPositive Nikolsky; chicken-wire DIFDesmoglein antibodies
Mucous membrane pemphigoidTense bullae, desquamative gingivitisLinear DIFOcular scarring
Erythema multiformeTarget lesions, hemorrhagic lip crustsClinical diagnosisHSV trigger
Linear IgA diseaseSubepithelial blisteringLinear IgA on DIFVancomycin; dapsone
Contact stomatitisReaction to dental material or flavouringPatch testAllergen removal

Essential biopsy rule

Any oral ulcer that fails to heal after 3 weeks requires biopsy to exclude malignancy, particularly SCC.