Analysis of subgingival microbial community structure in MAFLD patients with periodontitis

To investigate the potential pathological associations of subgingival microbiota in metabolic associated fatty liver disease (MAFLD) patients with periodontitis (PD), as well as in patients with PD alone, and to analyze the composition, diversity, and functional differences of the subgingival microbiota.

Fifteen patients suffering from MAFLD and PD (MAFLD-PD) and fifteen patients with PD were recruited. The microbial community structure was determined by collecting and analyzing subgingival plaque samples using 16 S rRNA gene sequencing. In conjunction with statistical methods, intergroup differences were analyzed using Alpha/Beta diversity analysis, LEfSe multi-level species discrimination, PICRUSt2 functional prediction, and BugBase phenotype prediction.

Significant differences were observed in Alpha diversity indices between the MAFLD-PD group and the PD group (Chao1, p = 0.04094; Shannon, p = 0.01606; Simpson, p = 0.03689). Beta diversity analysis revealed significant differences in community structure between the two groups (PCoA; R² = 0.09443, p = 0.008). The relative abundance of certain bacterial taxa, such as Proteobacteria, Actinobacteriota, and others, was numerically higher in MAFLD-PD patients compared to PD-only patients. In comparison, the relative abundance of Bacteroidota, Porphyromonas, Treponema, and others was numerically lower in MAFLD-PD patients compared to PD-only patients. Without correction, the MAFLD-PD group and PD group showed significant differences in 19 KEGG pathways (p < 0.05). After FDR correction, these differences indicated a potential differential trend (0.05 < corrected p < 0.12), with significant differences in 4 phenotypes between the two groups.

The microbial communities of subgingival plaque in MAFLD-PD patients are characterized by a predominance of pro-inflammatory bacterial communities, metabolic pathway disorders, and enhanced pathogenicity. This indicates that MAFLD may exacerbate the progression of MAFLD-PD by altering the microbial community structure.

This study establishes a crucial theoretical foundation for microbiota-targeted therapy and multidisciplinary interventions in MAFLD-PD.