IADR Abstract Archives
Bacterial Dysbiosis in Patients with Recurrent Aphthous Stomatitis
Objectives: Aetiology of recurrent aphthous stomatitis (RAS) is unknown but several factors have been implicated, all of which influence the composition of oral mucosal microbiota which in turn modulates immunity and thereby affects disease progression. Although no individual pathogens have been conclusively shown to be causative agents of RAS, microbial dysbiosis may play a key role. In this study we sought to determine the relationship between total composition of bacterial microbiota in the oral mucosa and patients’ susceptibility to RAS.
Methods: Using high-throughput 16S rRNA gene sequencing we have characterised the most abundant bacterial populations residing on healthy mucosae and ulcerated mucosae in 16 patients with RAS and no associated systemic condition, and also compared these profiles to the mucosal microbiota of healthy controls (HC).
Results: No differences were seen in bacterial richness indices between healthy and ulcerated mucosal sites. Phylum-level diversity comparisons revealed decreased Firmicutes and increased Proteobacteria (P= 0.034 and 0.032, respectively) in ulcerated compared to healthy sites in RAS patients. Genus-level analysis demonstrated higher abundance of Bacteroidales members in RAS patients healthy sites over HC (61.9±88.6 vs 12.9±17.8 reads, P=0.04). Porphyromonadaceae comprising species associated with periodontal disease predominated only in ulcerated sites over HC (mean 17.5±20.6 vs 3.6± 4.3 reads, P = 0.014), but not in RAS patients healthy sites over HC. Streptococcaceae comprising species associated with oral health predominated in HC over ulcerated sites (mean 5.7±4.0 vs 2.2±1.4 reads, P=0.01), but not in HC over RAS patients healthy sites.
Conclusions: This study confirms a role for dysbiosis in pathogenesis of RAS and suggests that increased abundance of Bacteroidales species is associated with increased RAS susceptibility. Increased Porphyromonadaceae and decreased Streptococcaceae species were only seen in ulcerated tissue suggesting that these changes are associated with perpetuation of established acute inflammation rather than the aetiological trigger of RAS.
Methods: Using high-throughput 16S rRNA gene sequencing we have characterised the most abundant bacterial populations residing on healthy mucosae and ulcerated mucosae in 16 patients with RAS and no associated systemic condition, and also compared these profiles to the mucosal microbiota of healthy controls (HC).
Results: No differences were seen in bacterial richness indices between healthy and ulcerated mucosal sites. Phylum-level diversity comparisons revealed decreased Firmicutes and increased Proteobacteria (P= 0.034 and 0.032, respectively) in ulcerated compared to healthy sites in RAS patients. Genus-level analysis demonstrated higher abundance of Bacteroidales members in RAS patients healthy sites over HC (61.9±88.6 vs 12.9±17.8 reads, P=0.04). Porphyromonadaceae comprising species associated with periodontal disease predominated only in ulcerated sites over HC (mean 17.5±20.6 vs 3.6± 4.3 reads, P = 0.014), but not in RAS patients healthy sites over HC. Streptococcaceae comprising species associated with oral health predominated in HC over ulcerated sites (mean 5.7±4.0 vs 2.2±1.4 reads, P=0.01), but not in HC over RAS patients healthy sites.
Conclusions: This study confirms a role for dysbiosis in pathogenesis of RAS and suggests that increased abundance of Bacteroidales species is associated with increased RAS susceptibility. Increased Porphyromonadaceae and decreased Streptococcaceae species were only seen in ulcerated tissue suggesting that these changes are associated with perpetuation of established acute inflammation rather than the aetiological trigger of RAS.