16S rRNA gene sequencing-based preliminary study on the differences in the microbiota between children with rampant caries and those with arrested caries

基于16S rRNA基因测序的初步研究:龋齿猖獗儿童与龋齿停止发展儿童肠道菌群差异

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Abstract

OBJECTIVE: In clinical practice, arrested caries (AC) poses less harm to children than rampant caries (RC), as the development of caries is arrested. However, there is limited research on the microbiology of the two types of caries. This research study the differences in microbial profiles among AC, caries-free (CF)and RC patients. METHODS: Thirty-six children aged 3–5 years were selected, grouped into AC, CF, and RC groups, with 12 children in each group. A total of 72 samples, including non-stimulated saliva and dental plaque, were collected. Microbial DNA was extracted, and the V3-V4 region of the 16S rRNA gene was sequenced using the Illumina MiSeq platform. Bioinformatics analysis was performed with QIIME2, and taxonomic classification was based on the SILVA database. Alpha and beta diversity were assessed, and the Kruskal–Wallis test (with Benjamini-Hochberg correction) was used to identify taxonomic abundance differences. RESULTS: The α-diversity in plaque was significantly lower than in saliva. While the salivary microbiome showed minimal variation across different caries states, the plaque microbiome displayed distinct structural differences. At the taxonomic level, Bacteroidota and Prevotella were enriched in the RCP group, while Fusobacteriota and Leptotrichia were more abundant in the ACP and CFP groups, with Corynebacterium being most abundant in the arrested caries group. Differential abundance analysis identified five putative species-level biomarkers associated with specific clinical states in dental plaque. CONCLUSION: This study suggests that different caries statuses are linked to distinct microbial profiles in dental plaque. The analysis revealed clear differences in microbial community structures across the three clinical groups, highlighting a potential connection between caries activity and plaque dysbiosis.

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