The subgingival microbiome associated with periodontitis in type 2 diabetes mellitus

牙周炎 微生物群 生物 失调 口腔微生物群 免疫学 基因组 牙龈和牙周袋 糖尿病 人口 二、侵袭性牙周炎 生物信息学 内科学 医学 遗传学 基因 内分泌学 环境卫生
作者
Baochen Shi,Renate Lux,Perry R. Klokkevold,Michaela Chang,Emma Barnard,Susan Kinder Haake,Huiying Li
出处
期刊:The ISME Journal [Springer Nature]
卷期号:14 (2): 519-530 被引量:65
标识
DOI:10.1038/s41396-019-0544-3
摘要

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.

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