Severe periodontitis patients with well-controlled type 2 diabetes display a distinct subgingival microbiome with increased Saccharibacteria compared to systemically healthy controls

患有严重牙周炎且2型糖尿病控制良好的患者,其龈下微生物群落组成与全身健康对照组相比存在显著差异,表现为糖杆菌属(Saccharibacteria)菌群增多。

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Abstract

INTRODUCTION: Type 2 diabetes mellitus (T2DM) is a major systemic risk factor that exacerbates periodontitis, with microbial dysbiosis recognized as an important mechanism. However, whether a well-controlled diabetic state still exerts a distinct influence on the subgingival microbiome remains to be fully elucidated. METHODS: This study compared the subgingival microbiota composition in patients with generalized Stage III/IV periodontitis, categorized into a systemically healthy Control group (n = 30) and a well-controlled T2DM group (HbA1c < 8%, n = 30). Subgingival plaque samples were collected using curettes from the deepest diseased sites. The V4 hypervariable region of the 16S rRNA gene was sequenced using Illumina NovaSeq 6000 platform. RESULTS: Demographic characteristics and periodontal parameters were comparable between groups, except for glycemic indices. Alpha and beta diversity analyses demonstrated no significant differences in overall microbial diversity or community structure (ANOSIM, P > 0.05). However, the T2DM group exhibited a distinct diabetic-associated microbial signature. The T2DM group showed a significant enrichment of the phylum Saccharibacteria (formerly TM7), particularly Nanosynbacter lyticus. In contrast, the phylum Actinomycetota, predominantly represented by the genus Actinomyces, was significantly reduced in the T2DM group. Notably, classical "Red Complex" pathogens were not identified as discriminative biomarkers between the groups. Additionally, correlation analysis revealed that Saccharibacteria abundance was positively associated with HbA1c and fasting blood glucose levels. DISCUSSION: These findings demonstrate that even with adequate glycemic control, the diabetic microenvironment exerts a unique selective pressure on the subgingival microbiome, favoring the expansion of specific epibiotic bacteria like Saccharibacteria while reducing commensal Actinomyces.

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