Aphthous stomatitis

• Common condition characterised by the repeated formation of benign and non-contagious aphthae (mouth ulcers)
• Also known as "canker sores" (especially in North America)
• Classification:
  1. Simple aphthosis
     • Most common form of the disease
     • This is also called Mikulicz ulcers
     • Individual usually experiences several episodes per year
     • Usually one to several ulcers lasting up to 14 days
     • Ulcers limited to oral mucosa
  2. Complex aphthosis
     • Ulcers can involve oral and genital mucosa
     • Usually ulcers are larger (>1cm) and can take several weeks to resolve
     • Some experience such frequent episodes that they are rarely without ulcers
     • Must exclude diagnosis of Behçet's syndrome before diagnosis is made

Epidemiology

• Common worldwide - highest prevalence in Middle East, Mediterranean and South Asia
• Most individuals start developing recurrent aphthae during adolescence
  • May decrease in later years and may spontaneously resolve for some
• More common in higher socioeconomic group
• ♀ > ♂

Clinical Features

• Regular, round/oval ulcers
• Painful
• Erythematous border
• Recur on regular basis
• Three different ulcer morphologies exist:

Minor	<1cm ∅ (usually 3-5mm) Classically grey ulcer base that becomes yellow with an erythematous halo as it heals Usually solitary but can occur in clusters of up to ~6 Occur predominantly on non-keratinised mucosa 7-10 days to heal Heal without scarring Recur at intervals of 1-4 months
Major	>1cm ∅ More painful than minor morphology Keratinised and non-keratinised mucosa equally involved Recur more regularly than minor Can take up to 1 month to heal Can heal with scarring Recur frequently
Herpetiform	Clusters of small ulcers (1-2mm) ← initially present as crops of vesicles that quickly develop into ulcers Can coalesce to form larger ulcers Keratinised and non-keratinised mucosa equally involved Heal in ~10 days Can recur very frequently

Aetiology and Pathogenesis

• Aetiology and pathogenesis are largely unknown (likely multifactorial)
• Theories suggest altered immune regulation involving oral mucosa → exaggerated pro-inflammatory process and/or weak anti-inflammatory response
• Genetic predisposition possible (common for patients to have family history of RAS)
• Certain foods as well as vitamin/mineral deficiencies have been implicated but no strong evidence
• Sodium lauryl sulfate (found in toothpastes) can make RAS worse/more frequent for some patients3
• Some observational evidence suggesting smoking confers some protection
• Stress and hormonal disturbances can also be predisposing factors