📋 Key Information Summary
- Most mouth ulcers are benign: Minor aphthous ulcers (miRAS) account for ~80% of recurrent oral ulceration and are self-limiting within 7–14 days; a systematic diagnostic approach is essential to exclude sinister causes.
- Red-flag ulcers require urgent referral: Any non-healing oral ulcer persisting >3 weeks, a painless indurated ulcer, or an ulcer in a patient with risk factors for malignancy (smoking, alcohol, betel nut) warrants same-week oral medicine or ENT review.
- Traumatic ulceration is the most common cause of acute solitary oral ulceration — always assess for sharp dental edges, ill-fitting prostheses, or chemical injury before attributing to aphthous disease.
- Topical corticosteroids are first-line for aphthous ulcers: triamcinolone acetonide in orabase (Kenalog in Orabase®), betamethasone soluble tablet as a mouth rinse, or clobetasol gel for major aphthae. PBS-listed options should be prioritised.
- Oral candidiasis presents as white plaques that scrape off (pseudomembranous) or erythematous mucosa; risk factors include inhaled corticosteroid use, denture wearing, diabetes, and immunosuppression. Nystatin suspension or miconazole oral gel are first-line; fluconazole for refractory cases.
- Oral lichen planus affects ~1–2% of the population; the reticular (Wickham striae) form is usually asymptomatic, but erosive forms cause significant pain and carry a small (~1%) malignant transformation risk requiring long-term surveillance.
- Angular cheilitis most commonly reflects Candida albicans infection in the setting of denture-related stomatitis, diabetes, or iron/B12/folate deficiency — treat the underlying cause plus topical miconazole or a combination antifungal-corticosteroid cream.
- Herpes simplex gingivostomatitis is the most common cause of acute diffuse oral ulceration in children; oral aciclovir within 72 hours of onset shortens duration. Valaciclovir is an alternative with improved bioavailability and simpler dosing.
- Burning mouth syndrome (glossodynia) is a diagnosis of exclusion — normal-appearing oral mucosa with persistent burning pain for ≥2 hours/day for ≥3 months; investigate for candidiasis, nutritional deficiency, and medication side effects before diagnosis.
- Investigate recurrent or severe aphthous ulcers for underlying causes: coeliac disease, inflammatory bowel disease, Behçet disease, haematinic deficiency (iron, folate, B12), and HIV infection.
- Oral lichenoid reactions may be drug-induced (NSAIDs, ACE inhibitors, beta-blockers, sulfonylureas) or represent a contact reaction to dental materials (amalgam); medication review is essential.
- ATSI populations have higher rates of oral health disease, limited access to dental and specialist services, and higher prevalence of betel nut use in some Torres Strait Islander communities — consider these factors in assessment and referral.
- Chlorhexidine 0.12–0.2% mouthwash (Savacol®) reduces secondary infection and aids healing in most oral ulceration; avoid prolonged use (>2 weeks) due to taste disturbance and tooth staining.
Introduction & Australian Epidemiology
Oral complaints including sore mouth, tongue discomfort, and mucosal ulceration are among the most common presentations in Australian general practice. The oral mucosa is a readily visible and accessible tissue that reflects both local pathology and systemic disease. A structured clinical approach — combining history, examination, and targeted investigation — enables accurate diagnosis and timely management of conditions ranging from benign self-limiting aphthous ulcers to oral malignancy.
In Australia, oral health conditions affect a significant proportion of the population across all age groups:
- Recurrent aphthous stomatitis (RAS) affects approximately 20–25% of the general population, with onset typically in childhood or adolescence and peak prevalence in the second and third decades of life.
- Oral candidiasis is reported in 35–60% of denture wearers and is a frequent complication of inhaled corticosteroid use in the estimated 2.7 million Australians with asthma.
- Oral lichen planus has a prevalence of approximately 1–2%, with a female-to-male ratio of approximately 1.4:1 and peak incidence between ages 30 and 60.
- Oral cancer accounts for approximately 4,000 new cases annually in Australia, with a 5-year survival rate of ~68% — late presentation remains a significant concern, particularly in regional and remote areas.
- The Australian Institute of Health and Welfare (AIHW) reports that Aboriginal and Torres Strait Islander peoples experience oral disease at 1.5–2 times the rate of non-Indigenous Australians, with significantly higher rates of tooth loss and untreated decay.
This guideline provides a practical, evidence-based framework for the diagnosis and management of the most common oral mucosal and tongue conditions presenting in Australian primary care, with attention to PBS-listed therapies, appropriate referral pathways, and health equity considerations.
Mouth Ulcers Diagnostic Model
A systematic diagnostic approach is essential when evaluating patients with oral ulceration. The majority of mouth ulcers encountered in general practice are benign, but the differential diagnosis is broad and includes infectious, autoimmune, traumatic, and malignant aetiologies. The following model organises the clinical assessment into key diagnostic domains.
History — Key Diagnostic Questions
| Domain | Questions to Ask | Diagnostic Significance |
|---|---|---|
| Duration | How long has the ulcer been present? Has it changed in size? | >3 weeks non-healing → suspect malignancy; recurrent episodes → RAS |
| Number | Single vs. multiple? Clustered or scattered? | Single → traumatic, malignancy; multiple/scattered → aphthous, herpetic, Behçet |
| Location | Lip, buccal mucosa, tongue, palate, gingivae? | Non-keratinised mucosa (buccal, soft palate) → aphthae; attached gingiva/palate → herpetic |
| Pain | Severity? Interfering with eating/drinking/sleeping? | Painless indurated ulcer → malignancy (urgent referral) |
| Recurrence | Previous episodes? Frequency? Family history? | Recurrent pattern with healing between episodes → RAS; family history in 30–40% of RAS |
| Triggers | Stress, trauma, foods, menstrual cycle, medications? | Food triggers (citrus, cinnamon, chocolate) → aphthae; new medication → lichenoid reaction |
| Systemic symptoms | Fevers, rash, genital ulcers, eye symptoms, diarrhoea, weight loss? | Behçet, IBD, coeliac disease, SLE, HIV |
| Risk factors | Smoking, alcohol, betel nut, immunosuppression, dentures? | Malignancy risk, candidiasis risk |
Clinical Examination Approach
Diagnostic Classification of Oral Ulcers
| Category | Key Features | Typical Duration | Action |
|---|---|---|---|
| Minor aphthous | Round/oval, <10 mm, yellow-grey base, erythematous halo; non-keratinised mucosa | 7–14 days, heals without scarring | Topical treatment; investigate if frequent/severe |
| Major aphthous (Sutton's) | >10 mm, deep, punched-out; may scar; lips, soft palate, fauces | Weeks to months | Systemic steroids; oral medicine referral |
| Herpetiform | 1–3 mm, multiple (10–100), may coalesce; recurrent pattern | 7–14 days | Topical steroids; consider aciclovir if herpetic |
| Herpetic (HSV) | Vesicles → shallow ulcers; attached gingiva, palate; children: acute gingivostomatitis with fever | 10–14 days (primary) | Antivirals within 72 hours of onset |
| Traumatic | Corresponds to mechanical/chemical injury site; irregular shape; heals when cause removed | 7–14 days after cause removal | Remove cause; chlorhexidine rinse |
| Immune-mediated | Lichen planus (Wickham striae), pemphigoid (desquamative gingivitis), pemphigus (flaccid blisters) | Chronic/recurrent | Oral medicine / dermatology referral |
| Malignant | Painless, indurated, rolled/everted edges, non-healing (>3 weeks); floor of mouth, lateral tongue, soft palate complex | Persistent, progressive | Urgent oral medicine / ENT / head & neck referral |
Recurrent Aphthous Ulceration & Traumatic Ulceration
Recurrent Aphthous Stomatitis (RAS)
RAS is the most common oral mucosal disease, characterised by recurrent episodes of discrete, painful ulcers on non-keratinised oral mucosa with intervening ulcer-free periods. The pathogenesis is multifactorial, involving T-cell-mediated immune dysregulation against oral epithelial antigens, with genetic predisposition (positive family history in 30–40% of cases).
Predisposing and Exacerbating Factors
- Nutritional deficiency: Iron, vitamin B12, folate, zinc — check FBC, serum ferritin, serum B12, red cell folate, zinc
- Haematological: Anaemia (iron deficiency, B12/folate deficiency), cyclic neutropenia
- Gastrointestinal: Coeliac disease (prevalence of RAS up to 25% in coeliac patients), inflammatory bowel disease
- Immunological: Behçet disease, HIV, cyclic neutropenia, MAGIC syndrome
- Medications: NSAIDs, nicorandil, methotrexate, immune checkpoint inhibitors
- Lifestyle: Psychological stress, local trauma, smoking cessation (paradoxical increase), sodium lauryl sulphate in toothpaste
Treatment of Aphthous Ulceration
Mild (Minor Aphthae) — Symptomatic & Barrier Measures
Moderate — Topical Corticosteroid Therapy
Severe / Refractory — Systemic Therapy
Traumatic Ulceration
Traumatic ulceration is the most common cause of solitary oral ulceration in general practice. Causes include mechanical trauma (sharp dental cusps, broken restorations, ill-fitting dentures, cheek biting), thermal burns (hot food/drink), and chemical injury (aspirin held against mucosa, caustic substances).
Management Principles
- Identify and remove the cause: Sharp dental edges → dental referral for smoothing/polishing; ill-fitting denture → denture adjustment or relining; cheek biting → occlusal splint if bruxism-related.
- Topical analgesia: Benzydamine 0.15% mouthwash (Difflam®) QID for pain relief.
- Antiseptic mouthwash: Chlorhexidine 0.12–0.2% (Savacol®) to prevent secondary infection.
- If no healing within 2–3 weeks after cause removal: Biopsy to exclude malignancy, especially in patients with risk factors.
Oral Candidiasis, Lichen Planus & Angular Cheilitis
Oral Candidiasis
Oral candidiasis (oral thrush) is a fungal infection of the oral mucosa caused predominantly by Candida albicans. It is the most common oral fungal infection in Australia and affects immunocompromised and immunocompetent individuals alike.
Risk Factors
- Inhaled corticosteroid use (especially without mouth rinsing after use) — the most common iatrogenic cause
- Denture wearing (especially overnight) — denture-related stomatitis
- Diabetes mellitus (poorly controlled)
- Immunosuppression: HIV/AIDS (oral candidiasis is an AIDS-defining illness), chemotherapy, organ transplant, corticosteroid use
- Xerostomia (medication-induced, Sjögren syndrome, post-radiotherapy)
- Antibiotic use (broad-spectrum disrupting oral flora)
- Iron deficiency, vitamin B12 / folate deficiency
- Smoking
- Neonates and elderly
Clinical Forms
| Form | Appearance | Key Features |
|---|---|---|
| Pseudomembranous | Creamy white plaques that wipe off leaving erythematous base | Classic "thrush"; most common form; any mucosal surface |
| Erythematous (atrophic) | Red, smooth, raw-looking patches; often on palate (denture-related) or tongue dorsum | May be asymptomatic or burning; common with inhaled corticosteroids |
| Chronic hyperplastic | White, non-wipeable plaques, typically on buccal mucosa commissure | Does NOT scrape off; requires biopsy to differentiate from leukoplakia; may be premalignant |
| Denture stomatitis | Erythema and petechiae under upper denture fitting surface | Often asymptomatic; associated with Candida colonisation; may cause angular cheilitis |
Treatment of Oral Candidiasis
Oral Lichen Planus
Oral lichen planus (OLP) is a chronic T-cell-mediated inflammatory disease affecting the oral mucosa, with an estimated prevalence of 1–2% in Australia. It predominantly affects middle-aged adults, with a female-to-male ratio of approximately 1.4:1. OLP is classified as a potentially malignant disorder by the WHO, with malignant transformation rates reported at approximately 1–2% over long-term follow-up.
Clinical Forms
| Form | Appearance | Symptoms |
|---|---|---|
| Reticular | White, lace-like (Wickham) striae; bilateral buccal mucosa, gingivae, tongue | Usually asymptomatic; patient may notice white patches |
| Erosive | Erythematous, ulcerated areas surrounded by white striae | Painful; burning; difficulty eating spicy/acidic foods |
| Atrophic | Thin, erythematous mucosa with minimal striae | Burning, sensitivity |
| Plaque-like | Homogeneous white plaques (resembles leukoplakia) | Usually asymptomatic; requires biopsy |
| Bullous | Fluid-filled bullae that rupture to form erosions | Painful; rare form |
Treatment of Oral Lichen Planus
Treatment is indicated for symptomatic (erosive/atrophic) forms. Asymptomatic reticular OLP does not require treatment but warrants long-term monitoring.
Angular Cheilitis
Angular cheilitis (angular stomatitis, perlèche) presents as erythema, fissuring, and maceration at the oral commissures. It is most commonly caused by Candida albicans, often in the context of denture-related stomatitis, but may also involve Staphylococcus aureus or Streptococcus species, or be multifactorial.
Underlying Causes to Investigate
- Denture-related stomatitis (most common association) — loss of vertical dimension creating moisture/fold at commissures
- Iron deficiency anaemia
- Vitamin B12 or folate deficiency
- Diabetes mellitus
- Immunosuppression (HIV, corticosteroids)
- Drooling in children with atopic dermatitis or in elderly with sagging facial skin
Treatment
The Painful Tongue & Oral Dermatoses
Burning Mouth Syndrome (Glossodynia)
Burning mouth syndrome (BMS) is characterised by a persistent burning sensation of the oral mucosa (most commonly the tongue) in the absence of clinically identifiable mucosal lesions. It is a neuropathic pain disorder affecting an estimated 1–5% of the general population, with a strong female predominance (especially postmenopausal women, F:M ratio ~7:1).
Diagnostic Criteria (International Headache Society)
- Oral pain recurring daily for ≥2 hours per day for >3 months
- Burning quality, with or without dysgeusia (altered taste) or xerostomia (dry mouth)
- Clinically normal oral mucosa on examination
- Not better explained by another oral or systemic condition
Differential Diagnosis — Conditions to Exclude Before Diagnosing BMS
| Category | Condition | Investigation |
|---|---|---|
| Local | Oral candidiasis (erythematous), lichen planus (atrophic), geographic tongue, contact allergy (dental materials, toothpaste) | Examination ± swab ± patch testing |
| Nutritional | Iron deficiency, B12 deficiency, folate deficiency, zinc deficiency | FBC, serum ferritin, B12, red cell folate, zinc |
| Endocrine | Diabetes mellitus, hypothyroidism, menopause | Fasting glucose / HbA1c, TFTs |
| Medication-related | ACE inhibitors, SSRIs, antihypertensives, antiretrovirals (dysgeusia) | Medication review |
| Neurological | Glossopharyngeal neuralgia, trigeminal neuropathy, multiple sclerosis | Neurological examination ± MRI |
| Psychological | Anxiety, depression (common comorbidity, may be cause or consequence) | PHQ-9, GAD-7 screening |
Management of Burning Mouth Syndrome
- Reassurance and education: Explain that BMS is a real neuropathic condition, not imagined. Identify and address comorbid anxiety/depression.
- Address treatable causes: Correct nutritional deficiencies, manage candidiasis, adjust medications where possible.
- Topical therapies: Benzydamine 0.15% mouthwash (Difflam®) for symptomatic relief; capsaicin rinse (0.025% capsaicin in 5 mL water, TDS) — evidence limited but may reduce pain perception.
- Systemic therapy (for refractory cases):
Geographic Tongue (Benign Migratory Glossitis)
Geographic tongue affects approximately 1–3% of the Australian population and is characterised by irregular, erythematous patches with elevated yellow-white borders on the dorsum and lateral aspects of the tongue. The pattern migrates over days to weeks (the "wandering rash" of the tongue). Most cases are asymptomatic; a minority report burning or irritation, especially with spicy or acidic foods.
- No treatment is usually required. Reassurance is the primary intervention.
- If symptomatic: benzydamine 0.15% mouthwash (Difflam®) PRN for pain; avoid known triggers (spicy, acidic foods).
- Associated with psoriasis (up to 10% of patients with geographic tongue have psoriasis) — screen for skin and nail changes.
- Topical corticosteroids are rarely indicated but may be used for severe symptomatic flares.
Oral Herpes Simplex Virus (HSV)
Primary herpetic gingivostomatitis is the most common cause of acute diffuse oral ulceration in children, caused by HSV-1 (or HSV-2). It presents with fever, irritability, submandibular lymphadenopathy, and widespread painful vesicles and ulcers affecting the oral mucosa, gingivae, tongue, and palate. Recurrent herpes labialis (cold sores) affects the vermillion border of the lips.
Treatment
Other Oral Dermatoses
Oral Manifestations of Lichenoid Drug Reactions
Lichenoid drug reactions mimic oral lichen planus clinically and histologically, but are caused by systemically administered medications or contact with dental materials. Common causative medications include:
- NSAIDs (ibuprofen, naproxen, diclofenac)
- ACE inhibitors (enalapril, ramipril, perindopril)
- Beta-blockers (atenolol, metoprolol, propranolol)
- Sulfonylureas (glibenclamide, gliclazide)
- Thiazide diuretics
- TNF-alpha inhibitors (infliximab, adalimumab)
- Dental amalgam (contact lichenoid reaction — unilateral, adjacent to amalgam restoration)
Management: Medication review and switch to an alternative agent if possible. Contact reactions to amalgam may resolve with replacement of amalgam restorations with composite or porcelain (refer to dentist). Topical corticosteroids for symptomatic relief while the causative agent is being addressed.
Oral Pemphigoid and Pemphigus
Investigations & Referral Indications
Investigations for Recurrent / Severe Oral Ulceration
When to Refer
| Referral | Indication | Timeframe |
|---|---|---|
| Oral medicine specialist | Refractory aphthous ulcers, erosive lichen planus, blistering conditions, BMS, diagnostic uncertainty, biopsy | Routine to semi-urgent (2–4 weeks) |
| Oral & maxillofacial surgery / ENT head & neck | Suspected oral malignancy (ulcer >3 weeks, induration, rolled edges, cervical lymphadenopathy) | Urgent — within 2 weeks |
| Dermatology | Oral lichen planus with skin involvement, pemphigus, mucous membrane pemphigoid | Semi-urgent (2–4 weeks) |
| Gastroenterology | Positive coeliac serology, suspected IBD, Behçet disease | Routine (4–6 weeks) |
| Dentist / Prosthodontist | Denture-related stomatitis, traumatic ulcers from dental causes, replacement of amalgam restorations | Routine (2–4 weeks) |
| Ophthalmology | Suspected Behçet disease (anterior uveitis), mucous membrane pemphigoid (conjunctival involvement) | Semi-urgent (within 1–2 weeks) |
Special Populations
Pregnancy
Paediatrics
Elderly
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health Considerations
📚 References
- 1. Australian Institute of Health and Welfare. Oral health and dental care in Australia. Canberra: AIHW; 2024. Available from: https://www.aihw.gov.au/reports/dental-oral-health
- 2. Scully C, Felix DH. Oral medicine — update for the dental practitioner: oral white patches. British Dental Journal. 2005;199(9):565–572.
- 3. Ship JA, Chavez EM, Doerr PA, Henson BS, Sarmadi M. Recurrent aphthous stomatitis. Quintessence International. 2000;31(2):95–112.
- 4. Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology. 2005;100(2):164