RESUMO
Inflammation is a driven force in modulating microbial communities, but little is known about the interplay between colonizing microorganisms and the immune response in periodontitis. Since local and systemic inflammation may play a whole role in disease, we aimed to evaluate the oral and fecal microbiome of patients with periodontitis and to correlate the oral microbiome data with levels of inflammatory mediator in saliva. Methods: Nine patients with periodontitis (P) in Stage 3/Grade B and nine age-matched non-affected controls (H) were evaluated. Microbial communities of oral biofilms (the supra and subgingival from affected and non-affected sites) and feces were determined by sequencing analysis of the 16SrRNA V3-V4 region. Salivary levels of 40 chemokines and cytokines were correlated with oral microbiome data. Results: Supragingival microbial communities of P differed from H (Pielou's evenness index, and Beta diversity, and weighted UniFrac), since relative abundance (RA) of Defluviitaleaceae, Desulfobulbaceae, Mycoplasmataceae, Peptostreococcales-Tissierellales, and Campylobacteraceae was higher in P, whereas Muribaculaceae and Streptococcaceae were more abundant in H. Subgingival non-affected sites of P did not differ from H, except for a lower abundance of Gemellaceae. The microbiome of affected periodontitis sites (PD ≥ 4 mm) clustered apart from the subgingival sites of H. Oral pathobionts was more abundant in sub and supragingival biofilms of P than H. Fecal samples of P were enriched with Acidaminococcus, Clostridium, Lactobacillus, Bifidobacterium, Megasphaera, and Romboutsia when compared to H. The salivary levels of interleukin 6 (IL-6) and inflammatory chemokines were positively correlated with the RA of several recognized and putative pathobionts, whereas the RA of beneficial species, such as Rothia aeria and Haemophilus parainfluenzae was negatively correlated with the levels of Chemokine C-C motif Ligand 2 (CCL2), which is considered protective. Dysbiosis in patients with periodontitis was not restricted to periodontal pockets but was also seen in the supragingival and subgingival non-affected sites and feces. Subgingival dysbiosis revealed microbial signatures characteristic of different immune profiles, suggesting a role for candidate pathogens and beneficial organisms in the inflammatory process of periodontitis.
RESUMO
AIM: Periodontitis is correlated with type 2 diabetes mellitus (T2DM), but little is known about glycaemic status effect on subgingival microbiota associated with periodontitis. This study evaluated if periodontal microbiome of T2DM patients is affected by glycaemic status. MATERIALS AND METHODS: Twenty-one T2DM non-smoking patients with chronic periodontitis and body mass index ≤40 kg/m2 were allocated into two groups according to systemic glycaemic status: inadequate (DMI- HbA1c ≥ 8%) and adequate (DMA- HbA1c <7.8%). Subgingival biofilm was collected from sites with moderate (PD = 4-6 mm) and severe disease (PD ≥ 7 mm) in two quadrants. The V5-V6 hypervariable region of the 16SrRNA was sequenced using the GS-FLX-454 Titanium platform. Sequences were compared with HOMD database using QIIME and PhyloToAST pipelines. Statistical comparisons were made using two-sample t-tests. RESULTS: DMA microbiome presented higher diversity than DMI. Inadequate glycaemic control favoured fermenting species, especially those associated with propionate/succinate production, whereas those forming butyrate/pyruvate was decreased in DMI. Higher abundances of anginosus group and Streptococcus agalactiae in DMI may indicate that subgingival sites can be reservoir of potentially invasive pathogens. Altered subgingival microbiome in DMI may represent an additional challenge in the periodontal treatment of these patients and in the prevention of more invasive infections. CONCLUSION: Glycaemic status in T2DM patients seems to modulate subgingival biofilm composition.