The subgingival microbiome associated with periodontitis in type 2 diabetes mellitus

Abstract

Type 2 diabetes mellitus (T2DM) is a systemic disease, predisposing patients to other inflammatory conditions including periodontitis. The subgingival microbiome, a key player in periodontitis pathogenesis, is not well characterized in T2DM population. To better understand whether the subgingival microbiome is different between T2DM and systemically healthy, nondiabetic (ND) subjects, we performed a longitudinal analysis of the subgingival microbiome in T2DM patients (n = 15) compared with ND subjects (n = 16). Using metagenomic shotgun sequencing, we investigated the microbiome in the healthy periodontal state, periodontitis state, and resolved state after treatment. We found that in the periodontitis state, the shift in the subgingival microbiome from the healthy state was less prominent in T2DM compared with ND subjects, yet the clinical signs of disease were similar for both. Furthermore, we revealed highly correlated presence of pathogenic species in relative abundance not only in the periodontitis state, but also in the healthy state in T2DM, suggesting an elevated risk of progression to periodontitis in this cohort. We further investigated the functional potentials of the subgingival microbiome and identified a set of microbial marker genes associated with the clinical states. These genes were significantly enriched in 21 pathways, some of which are associated with periodontitis and some potentially link T2DM and periodontitis. This study identified the longitudinal changes of the subgingival microbiome associated with periodontitis in T2DM and suggests that T2DM patients are more susceptible to shifts in the subgingival microbiome toward dysbiosis, potentially due to impaired host metabolic and immune regulation.

Impact of systemic factors in shaping the periodontal microbiome

“…16 were observed in diabetic patients 16 Furthermore, the shift in composition of the subgingival microbiome from the healthy to the periodontitis state appears to be less prominent in diabetic patients than in normoglycemic individuals, even under similar clinical conditions, with the presence of pathogenic species in the subgingival microbiome being highly correlated between the periodontitis state and the healthy state in diabetic patients. 87 Collectively, these findings indicate that glucose availability may favor the increase in levels of saccharolytic commensals and that this "less traditionally pathogenic" Figure 2C and Figure 3B). 16 Overall, studies utilizing next-generation sequencing revealed reduced microbial diversity in the subgingival microbiome of subjects with diabetes compared with that of healthy controls or nondiabetic subjects with periodontitis, and support the notion that a dysbiotic oral microbiome is a plausible contributory factor in the pathogenesis of diabetes-induced periodontal disease.…”

Did Omics change periodontal therapy?

“…More recently, investigators started to use this method to evaluate the effects of different treatment protocols in modulating the oral microbiome. 67,[71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87][88][89] Next-generation sequencing has also enabled rapid expansion of the oral microbial reference genomes available, including uncultured phylotypes. Critical for the study of the oral microbiome was the development of the Human Oral Microbial Database (HOMD, http://www.homd.org).…”

Management of periodontal disease in patients with diabetes- good clinical practice guidelines: A joint statement by Indian Society of Periodontology and Research Society for the Study of Diabetes in India

“…[ 13 ] Quantitative and qualitative changes in pathogenic periodontal microflora have been observed by various researchers, leading to an oral diabetic dysbiotic state with an increased number of organisms such as Porphyromonas . [ 14 15 16 17 18 ]…”

“…[ 20 ] Hence, subjects with uncontrolled DM are more prone to a shift toward microbial dysbiosis due to impaired immunity and metabolism. [ 16 ]…”