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:
- 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
- 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
- Simple aphthosis
Epidemiology
- Common worldwide - highest prevalence in Middle East, Mediterranean and South Asia [1]
- 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 |
Differential Diagnosis
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 [2]
- 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
Management
Prognosis and Complications
Images
References
- ↑ Chattopadhyay, Amit, and Kishore V Shetty. “Recurrent aphthous stomatitis.” Otolaryngologic clinics of North America vol. 44,1 (2011): 79-88, v. doi:10.1016/j.otc.2010.09.003
- ↑ Slebioda, Zuzanna et al. “Etiopathogenesis of recurrent aphthous stomatitis and the role of immunologic aspects: literature review.” Archivum immunologiae et therapiae experimentalis vol. 62,3 (2014): 205-15. doi:10.1007/s00005-013-0261-y