Aphthous Ulcers

Also known as: Mouth ulcers, Canker sores

Recurrent painful ulceration of the non keratinised oral mucosa, occurring in the absence of systemic disease in the majority, and affecting up to 25 percent of the population.

Pathogenesis

Not fully established. The current understanding is of a T cell mediated immune response with tumour necrosis factor alpha as a central mediator, triggered in a genetically susceptible individual by local and systemic factors. There is a strong familial component, with a positive family history in around 40 percent. It is not an infection and is not transmissible, which is worth stating explicitly to patients.

Classification

Minor aphthous ulcers, accounting for 80 to 85 percent: round or oval ulcers under 10 mm with a grey white pseudomembrane and an erythematous halo, occurring on non keratinised mucosa, that is the labial and buccal mucosa, the floor of mouth, the ventral tongue and the soft palate. They heal in 7 to 14 days without scarring.
Major aphthous ulcers, that is periadenitis mucosa necrotica recurrens or Sutton disease, accounting for 10 to 15 percent: larger than 10 mm, deep, often involving keratinised mucosa including the dorsum of the tongue and the hard palate, lasting weeks to months and healing with scarring. They are severely painful and cause substantial functional impairment.
Herpetiform ulcers, accounting for 5 to 10 percent: crops of 10 to 100 pinhead ulcers of 1 to 3 mm which coalesce into larger irregular ulcers, occurring anywhere on non keratinised mucosa. Despite the name they are not herpetic and have no viral association.

The critical anatomical rule: aphthous ulcers occur on non keratinised, mobile, non attached mucosa. Ulcers on keratinised mucosa, that is the hard palate, the attached gingiva and the dorsum of the tongue, are not typical aphthae and suggest herpetic infection, trauma, malignancy or a vesiculobullous disorder.

Predisposing and associated factors

Local trauma from toothbrushing, sharp teeth, orthodontic appliances and biting.
Sodium lauryl sulphate in toothpaste, which is a genuine and easily removed trigger in a proportion of patients.
Stress and sleep deprivation.
Hormonal fluctuation, with some women experiencing a cyclical pattern.
Cessation of smoking, which characteristically precipitates or worsens aphthous ulceration through loss of mucosal keratinisation.
Haematinic deficiency: iron, folate, vitamin B12 and, less commonly, zinc, present in up to 20 percent of patients with recurrent aphthous stomatitis, and worth seeking because correction cures the ulceration.
Coeliac disease, which may present with recurrent aphthous ulceration as its only manifestation.
Certain foods, including chocolate, nuts, tomatoes, cheese and citrus, in individual patients.

Systemic conditions producing aphthous like ulceration, which must be excluded

Behçet disease: recurrent oral ulceration plus two of recurrent genital ulceration, ocular inflammation with uveitis or retinal vasculitis, skin lesions including erythema nodosum and pseudofolliculitis, and a positive pathergy test. Oral ulceration is the presenting feature in the great majority and precedes other features by years.
Coeliac disease and inflammatory bowel disease, particularly Crohn disease.
HIV infection, in which large persistent aphthous ulcers occur with advanced immunosuppression.
Cyclic neutropenia, with ulceration recurring at regular 3 weekly intervals.
PFAPA syndrome in children.
Systemic lupus erythematosus.
Reactive arthritis.
Sweet syndrome.
MAGIC syndrome, that is mouth and genital ulcers with inflamed cartilage.
Drug induced ulceration: nicorandil, which produces large deep painful ulcers that resolve on withdrawal and which is a frequently missed cause; nonsteroidal anti inflammatory drugs; methotrexate; alendronate; and chemotherapy.

Prodromal burning or tingling for 24 to 48 hours before the ulcer appears.
Pain out of proportion to size, aggravated by eating, particularly acidic, salty and spicy food, by speaking and by toothbrushing.
Recurrence at intervals, with the frequency ranging from a few episodes per year to continuous ulceration with no ulcer free interval.
Onset typically in childhood or adolescence, with a tendency to reduce in frequency with age. New onset in an older adult is atypical and requires more careful evaluation.
Absence of systemic upset in idiopathic disease. Fever, malaise, weight loss and diarrhoea point to a systemic cause.

Examination

Round or oval ulcers with a yellow grey fibrinous base, a well defined margin and an erythematous halo, on non keratinised mucosa.
Absence of induration, which is the key finding. An indurated ulcer is malignant until proven otherwise.
Assess the number, size, distribution and duration.
Examine the whole oral cavity, the skin, the eyes, and where appropriate the genitalia.
Look for signs of nutritional deficiency including glossitis, angular cheilitis and pallor.

Red flags requiring urgent investigation

Any single ulcer persisting beyond 3 weeks, which requires biopsy for squamous cell carcinoma regardless of appearance. This is the single most important rule in oral ulceration.
Induration, a rolled everted edge, fixation to underlying tissue or a mass.
Ulceration on keratinised mucosa, on the lateral tongue, or on the floor of mouth, which are high risk sites for carcinoma.
Associated cervical lymphadenopathy.
Weight loss, night sweats or systemic symptoms.
Genital ulceration, ocular inflammation or skin lesions, indicating Behçet disease.
Diarrhoea, abdominal pain, weight loss or anaemia, indicating coeliac or inflammatory bowel disease.
New onset in an older adult, particularly a smoker.
Ulcers in a patient on nicorandil.

Clinical, with investigation directed at excluding deficiency and systemic disease.

Full blood count with mean corpuscular volume.
Ferritin, vitamin B12, folate and, where indicated, zinc. Test these in every patient with recurrent aphthous stomatitis, since deficiency is present in up to 20 percent and correction is curative in that group.
Coeliac serology with tissue transglutaminase immunoglobulin A antibodies and total immunoglobulin A to exclude deficiency causing a false negative.
HIV testing in extensive, atypical or persistent disease.
Inflammatory markers, and faecal calprotectin where inflammatory bowel disease is suspected.
Serial full blood counts twice weekly for 6 weeks where cyclic neutropenia is suspected, timed to capture the nadir.
Autoimmune screen where connective tissue disease is suspected.
Pathergy test and ophthalmological assessment where Behçet disease is suspected, with referral to rheumatology.
Biopsy is not required for typical recurrent aphthous ulceration and its histology is non specific. It is mandatory for any ulcer persisting beyond 3 weeks, for atypical ulcers, for suspected vesiculobullous disease where direct immunofluorescence on perilesional tissue is needed, and where malignancy is a possibility.
Medication review, specifically for nicorandil, which should be prompted by large persistent ulcers in a patient with angina.

Differential diagnosis and the discriminating feature

Traumatic ulceration: a clear cause such as a sharp tooth or denture, with irregular margins, healing within 10 days of removing the cause. If it does not heal, biopsy.
Squamous cell carcinoma: indurated, persistent, often painless initially, on the lateral tongue or floor of mouth, in a smoker or drinker.
Primary herpetic gingivostomatitis: vesicles progressing to ulcers on keratinised and non keratinised mucosa with gingivitis, fever and lymphadenopathy, in a first episode.
Recurrent intraoral herpes: clustered vesicles then ulcers on keratinised mucosa, typically the hard palate and attached gingiva, which is the distribution that separates it from aphthae.
Herpangina and hand foot and mouth disease: vesicles on the soft palate and pillars in a child with fever.
Erythema multiforme: target lesions on skin, haemorrhagic crusted lips, widespread oral ulceration, often precipitated by herpes simplex or drugs.
Pemphigus vulgaris: flaccid bullae rupturing to widespread ragged erosions, positive Nikolsky sign, with direct immunofluorescence showing intercellular immunoglobulin G. Oral lesions precede skin lesions in most patients, so the dentist or otolaryngologist frequently sees this first.
Mucous membrane pemphigoid: subepithelial blisters with desquamative gingivitis and ocular involvement with symblepharon, which threatens sight and requires ophthalmology involvement.
Erosive lichen planus: white striae at the periphery of erosions, bilateral distribution.
Necrotising ulcerative gingivitis: punched out interdental papillae, halitosis, in a smoker or immunocompromised patient.
Syphilis, tuberculosis and deep fungal infection.

Treatment is stepwise, aimed at reducing pain, duration and frequency, since there is no cure for idiopathic recurrent aphthous stomatitis.

Address triggers and deficiencies

Correct iron, vitamin B12, folate and zinc deficiency, which resolves ulceration in the deficient group.
Treat coeliac disease with a gluten free diet.
Switch to a sodium lauryl sulphate free toothpaste, which reduces frequency in a proportion of patients and costs nothing to try.
Avoid identified food triggers using a diary rather than blanket elimination.
Eliminate mechanical trauma: smooth sharp teeth, adjust dentures and orthodontic appliances, use a soft toothbrush.
Stress management.
Withdraw nicorandil in discussion with the cardiologist, substituting an alternative antianginal.

Topical therapy, first line

Chlorhexidine gluconate 0.2 percent mouthwash, 10 mL twice daily, which reduces secondary infection, pain and duration. Warn about tooth staining and taste disturbance with prolonged use.
Benzydamine hydrochloride 0.15 percent mouthwash or spray as required for analgesia.
Lidocaine 2 percent gel or 5 percent ointment applied before meals.
Topical corticosteroid, which is the mainstay and which shortens healing time when applied at the prodromal stage:
Hydrocortisone oromucosal tablets 2.5 mg, dissolved next to the ulcer four times daily.
Triamcinolone acetonide 0.1 percent in an adhesive paste, applied two to four times daily.
Betamethasone sodium phosphate 500 microgram tablets dissolved in 10 mL water as a mouthwash, rinsed for 2 to 3 minutes and spat out, two to four times daily, which is useful for widespread ulceration where topical application is impractical.
Beclometasone or fluticasone metered dose inhaler sprayed directly onto the ulcer.
Clobetasol propionate 0.05 percent in an adhesive base for major ulcers.
Topical tetracycline: a doxycycline 100 mg capsule dissolved in 10 mL water used as a mouthwash for 2 to 3 minutes four times daily, which reduces pain and duration, particularly in herpetiform ulceration. Avoid in children under 12 years and in pregnancy.
Protective barrier pastes and bioadhesive gels containing hyaluronic acid.
Topical amlexanox 5 percent paste where available.

Systemic therapy

Reserved for severe, frequent, major or disabling disease with functional impairment, and initiated after excluding systemic causes.

Prednisolone 25 to 50 mg daily for 5 days then tapered over 1 to 2 weeks for a severe episode, and used sparingly given cumulative toxicity.
Colchicine 500 micrograms two or three times daily, which reduces frequency and is particularly useful in Behçet disease. Adverse effects are diarrhoea, which is dose limiting, and myelosuppression. Reduce in renal and hepatic impairment and review interactions with statins, macrolides and ciclosporin.
Pentoxifylline 400 mg three times daily.
Dapsone 50 to 100 mg daily, with glucose 6 phosphate dehydrogenase testing before starting and monitoring for haemolysis and methaemoglobinaemia.
Azathioprine, methotrexate or mycophenolate for refractory disease under specialist supervision, with thiopurine methyltransferase testing before azathioprine.
Thalidomide 50 to 100 mg daily, which is highly effective for major aphthous ulceration and for HIV associated ulceration, but which is severely teratogenic and requires strict pregnancy prevention programmes, and which causes irreversible peripheral neuropathy requiring regular neurological monitoring. It is a specialist prescription only.
Biologic therapy with tumour necrosis factor alpha inhibitors such as adalimumab or infliximab for severe Behçet disease and refractory ulceration, and apremilast, which is licensed for oral ulcers in Behçet disease.

Behçet disease

Refer to rheumatology. Requires systemic immunosuppression, ophthalmological surveillance given the risk of blindness from posterior uveitis and retinal vasculitis, and assessment for vascular, neurological and gastrointestinal involvement.

HIV associated ulceration

Large persistent aphthous ulcers in advanced HIV respond to thalidomide, but the definitive treatment is antiretroviral therapy with immune reconstitution.

Follow up and counselling

Explain that this is not an infection, is not transmissible, and is not caused by poor hygiene, since patients frequently believe all three.
Explain the chronic relapsing course and that treatment controls rather than cures.
Review at 6 to 8 weeks after initiating treatment.
Biopsy without hesitation any ulcer persisting beyond 3 weeks, and re examine any patient who reports a change in the pattern of their ulceration, since a long history of aphthous ulceration does not protect against developing a carcinoma.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Halitosis

Offensive breath odour. It is a common complaint with a well defined and largely treatable set of causes, and the clinical failure in this area is the tendency to dismiss it as trivial when it produces genuine social withdrawal, occupational difficulty and psychological distress.

Biochemistry

Odour arises predominantly from volatile sulphur compounds produced by anaerobic Gram negative bacteria degrading sulphur containing amino acids:

Hydrogen sulphide, from cysteine, with the smell of rotten eggs.
Methyl mercaptan, from methionine, with the smell of decaying cabbage, which is the compound most strongly associated with periodontal disease.
Dimethyl sulphide, which is the predominant compound in extraoral and blood borne halitosis, and which is therefore a diagnostic pointer when it dominates.

Other contributors include cadaverine, putrescine, indole, skatole and short chain fatty acids including butyric and propionic acid.

The organisms responsible are anaerobes including Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Treponema denticola, Tannerella forsythia and Solobacterium moorei.

Classification

Genuine halitosis, subdivided into:
Physiological halitosis: morning breath and hunger breath, resulting from reduced salivary flow and increased bacterial metabolism overnight, which resolves with eating and oral hygiene and is not pathological.
Pathological halitosis, oral in origin, which accounts for 85 to 90 percent of genuine halitosis.
Pathological halitosis, extraoral in origin, accounting for 10 to 15 percent.
Pseudohalitosis: the patient believes they have halitosis but it cannot be demonstrated objectively, and they accept reassurance and objective evidence.
Halitophobia: persistent belief in halitosis despite objective evidence to the contrary and despite treatment and reassurance. This is a psychiatric condition on the spectrum of olfactory reference syndrome and body dysmorphic disorder, and it requires psychiatric rather than dental or otolaryngological management. Repeatedly investigating and treating these patients reinforces the belief and causes harm.

Causes

Oral, 85 to 90 percent:

Tongue coating, which is the single largest contributor. The posterior dorsum of the tongue has a large surface area with papillary crypts harbouring anaerobes, desquamated epithelium and food debris.
Periodontal disease and gingivitis, with periodontal pockets providing an anaerobic environment.
Dental caries and food impaction.
Pericoronitis around partially erupted third molars.
Necrotising ulcerative gingivitis, which produces a characteristic and intense foetor.
Dry socket after extraction.
Ill fitting or unclean dentures and orthodontic appliances.
Xerostomia from drugs, radiotherapy, Sjögren syndrome, mouth breathing and dehydration.
Oral candidiasis.
Oral malignancy with necrotic tissue.

Otolaryngological:

Tonsilloliths and chronic cryptic tonsillitis, which are a specific and frequently overlooked cause.
Chronic rhinosinusitis with postnasal purulent discharge.
Nasal foreign body, particularly in a child with unilateral foul discharge.
Atrophic rhinitis with crusting.
Nasopharyngeal and oropharyngeal malignancy with necrosis.
Adenoiditis.
Zenker diverticulum, in which retained decomposing food produces halitosis together with dysphagia and regurgitation.

Gastrointestinal:

Gastro oesophageal reflux disease and laryngopharyngeal reflux.
Helicobacter pylori infection, whose contribution is debated but which is worth treating where present with other indications.
Achalasia and oesophageal stricture with food retention.
The general belief that halitosis commonly originates in the stomach is largely wrong. The oesophagus is normally collapsed, and gastric gas reaches the mouth only on belching. Attributing halitosis to the stomach without evidence delays the correct diagnosis.

Systemic and blood borne, in which the odorant is carried in the blood and excreted through the lungs. These characteristically produce dimethyl sulphide and are unaffected by oral hygiene measures:

Diabetic ketoacidosis, with a sweet acetone odour.
Uraemia in chronic kidney disease, with an ammoniacal fishy odour.
Hepatic failure, with foetor hepaticus described as sweet and musty.
Trimethylaminuria, that is fish odour syndrome, a metabolic disorder with a defect in flavin containing monooxygenase 3, producing a fishy odour in breath, sweat and urine.
Bronchiectasis, lung abscess and empyema.
Certain foods and drugs: garlic, onion, alcohol, dimethyl sulphoxide, disulfiram, and drugs causing xerostomia.

Bad breath reported by the patient, or more often by a family member, partner or colleague. The source of the complaint matters diagnostically: halitosis reported only by the patient, with no confirmation from others, raises the possibility of pseudohalitosis or halitophobia.
Bad taste, which frequently accompanies genuine halitosis.
Social avoidance, covering the mouth when speaking, excessive use of mints and mouthwash, and reluctance to be close to others.
Anxiety and depression, which may be secondary to the halitosis or, in halitophobia, primary.

History that directs investigation

Who noticed it, and has anyone else confirmed it.
Duration, timing through the day, and relation to meals, hunger and sleep.
Oral hygiene practices including frequency of brushing, interdental cleaning and tongue cleaning.
Dental history, dentures, and time since the last dental visit.
Nasal and sinus symptoms, tonsilloliths, and recurrent sore throats.
Reflux symptoms, dysphagia and regurgitation.
Systemic symptoms and known renal, hepatic, respiratory and metabolic disease.
Medication list, with attention to xerostomia inducing agents: anticholinergics, antidepressants, antihistamines, antipsychotics, diuretics and antihypertensives.
Smoking, alcohol and dietary habits.
Psychiatric history and the degree of preoccupation with the symptom.

Examination

Full oral examination including the tongue dorsum with attention to coating, the periodontium, all teeth, the dentures and the fitting surfaces.
Tonsils examined for cryptic debris and tonsilloliths, with gentle pressure on the anterior pillar to express material.
Nasal examination and flexible nasoendoscopy in adults, assessing the nasopharynx, postnasal space, hypopharynx and larynx. This step is essential and is frequently skipped, and it is what identifies sinus disease, tonsilloliths, malignancy and a foreign body.
Assessment of salivary flow and the salivary duct orifices.
General examination directed by the history.

Organoleptic assessment, which remains the reference standard. The examiner smells the patient's exhaled breath at a distance of around 10 cm through a tube, scoring intensity on a 0 to 5 scale. Compare mouth breath with nose breath: odour predominantly from the mouth indicates an oral or oropharyngeal source; odour predominantly from the nose indicates a nasal or sinus source; equal odour from both indicates a systemic or blood borne source. This simple comparison is the single most useful discriminating test and requires no equipment.
Patients should avoid eating, drinking, smoking, oral hygiene products and scented cosmetics for at least 2 to 3 hours before assessment, and should avoid antibiotics for 3 weeks and garlic, onion and spicy food for 48 hours.
Portable sulphide monitors, which quantify total volatile sulphur compounds, giving an objective and reproducible measure that is particularly useful for demonstrating absence of odour to a patient with suspected pseudohalitosis.
Gas chromatography, which separates and quantifies individual compounds, and which is the definitive method. A dimethyl sulphide predominant pattern points strongly to an extraoral or blood borne source.
Tongue coating index, scoring coating across the tongue dorsum.
Periodontal assessment with probing depths, bleeding on probing and radiographs, by a dentist.
Full blood count, glucose and HbA1c, renal function, liver function.
Helicobacter pylori testing where there are dyspeptic symptoms.
Sinus computed tomography where sinusitis is suspected.
Upper gastrointestinal endoscopy or a barium swallow where dysphagia, regurgitation or a pharyngeal pouch is suspected.
Chest imaging where bronchiectasis or lung abscess is possible.
Urinary trimethylamine to creatinine ratio after a choline load where trimethylaminuria is suspected.
Psychiatric assessment where halitophobia is suspected.

The great majority is oral in origin and responds to mechanical measures. Antimicrobial mouthwashes alone, without mechanical debridement, fail.

Tongue cleaning, which is the highest yield single intervention

Clean the posterior dorsum of the tongue daily using a tongue scraper, which is more effective than a toothbrush and provokes less gagging.
Scrape from posterior to anterior with light pressure, repeated 5 to 10 times, rinsing between strokes.
Reach as far posteriorly as tolerated, since the posterior third harbours most of the coating and is the part usually missed.
Explain and demonstrate the technique, since patients who are simply told to clean their tongue generally clean only the anterior visible part, which achieves little.

Oral hygiene and dental treatment

Twice daily brushing with a fluoride toothpaste, and daily interdental cleaning with floss or interdental brushes.
Professional scaling, root planing and periodontal treatment for periodontal disease, which produces substantial improvement.
Treat caries, extract unrestorable teeth, and address food traps and overhanging restorations.
Denture hygiene: remove overnight, clean daily, soak in chlorhexidine 0.2 percent or dilute hypochlorite for acrylic dentures, and assess fit.
Treat pericoronitis, with extraction of the impacted tooth where recurrent.
Treat oral candidiasis.

Antimicrobial adjuncts

Chlorhexidine gluconate 0.12 to 0.2 percent mouthwash, 10 mL twice daily, which is the most effective antimicrobial mouthwash. Warn about tooth staining, taste disturbance and, with prolonged use, calculus formation. Use for defined periods rather than indefinitely.
Cetylpyridinium chloride mouthwash.
Zinc containing mouthwashes and toothpastes, which chemically neutralise volatile sulphur compounds by forming insoluble sulphides. Combined zinc and chlorhexidine preparations are more effective than either alone.
Chlorine dioxide and sodium chlorite rinses, which oxidise sulphur compounds.
Essential oil mouthwashes.
Avoid alcohol containing mouthwashes in patients with xerostomia, since they worsen dryness and therefore worsen halitosis.
Mints and chewing gum give brief masking only; sugar free gum has some benefit by stimulating salivary flow.

Management of xerostomia

Frequent sips of water, sugar free gum, saliva substitutes and gels.
Review and substitute xerostomia inducing medications where feasible.
Pilocarpine 5 mg three times daily where there is residual gland function, with attention to contraindications including asthma, chronic obstructive pulmonary disease, bradycardia and narrow angle glaucoma.
Treat Sjögren syndrome with rheumatology involvement.

Otolaryngological causes

Tonsilloliths: oral irrigation with a water flosser directed at the crypts, salt water gargles, and manual expression. Laser or coblation cryptolysis under local anaesthesia for persistent cases. Tonsillectomy where conservative measures fail and the tonsils are demonstrably the source, with the important caveat that dental and tongue causes must be excluded and treated first, since tonsillectomy performed for halitosis of dental origin fails and leaves a dissatisfied patient who has undergone a painful operation for nothing.
Chronic rhinosinusitis: intranasal corticosteroid, saline irrigation, antibiotics for exacerbations, and endoscopic sinus surgery for medically refractory disease.
Nasal foreign body: removal.
Atrophic rhinitis: alkaline nasal irrigation, emollients and glucose in glycerine drops.
Zenker diverticulum: endoscopic stapling or laser cricopharyngeal myotomy with diverticulotomy, or open diverticulectomy with myotomy.
Malignancy: oncological management.

Systemic causes

Optimise diabetes control.
Manage renal and hepatic disease.
Treat bronchiectasis and lung abscess.
Trimethylaminuria: dietary restriction of choline, carnitine, trimethylamine N oxide and lecithin, avoiding eggs, offal, seafood and legumes; low dose metronidazole or neomycin to reduce gut bacterial trimethylamine production; riboflavin supplementation to maximise residual enzyme activity; and acidic soaps and lotions to trap trimethylamine on the skin. Genetic counselling and psychological support are important, since the condition is lifelong and socially disabling.
Reflux: proton pump inhibitor such as omeprazole 20 mg twice daily for 8 to 12 weeks with lifestyle modification, and alginates after meals.

Pseudohalitosis and halitophobia

For pseudohalitosis, provide objective evidence with organoleptic scoring and sulphide monitoring, explain the results, reinforce normal oral hygiene, and most patients accept the reassurance.
For halitophobia, recognise it and stop investigating. Repeated tests, mouthwashes, antibiotics and surgery reinforce the belief and cause harm. Refer for psychiatric assessment, since the condition responds to cognitive behavioural therapy and to selective serotonin reuptake inhibitors, and it sits within the olfactory reference syndrome and body dysmorphic disorder spectrum.
Handle the referral carefully and without dismissiveness, since these patients are genuinely distressed and often have long histories of feeling disbelieved. Frame it as treatment for the distress rather than as a statement that the problem is imaginary.

Follow up

Review at 4 to 6 weeks with repeat organoleptic and sulphide assessment to demonstrate objective improvement, which is both a clinical measure and a therapeutic reassurance. Persistent halitosis after adequate oral treatment requires reassessment for an extraoral source, with particular attention to the nose, sinuses, tonsils, pharyngeal pouch and systemic disease.

Aphthous Ulcers

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management