Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba, Departamento de Prótese e Periodontia, Piracicaba, Brasil.
Universidade Estadual de Campinas, Centro de Pesquisas em Engenharias e Ciências Computacionais, Campinas, Brasil.
J Appl Oral Sci. 2024 Aug 16;32:e20240031. doi: 10.1590/1678-7757-2024-0031. eCollection 2024.
This study aimed to assess the influence of smoking on the subgingival metatranscriptomic profile of young patients affected by stage III/IV and generalized periodontal disease.
In total, six young patients, both smokers and non-smokers (n=3/group), who were affected by periodontitis were chosen. The STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) guidelines for case-control reporting were followed. Periodontal clinical measurements and subgingival biofilm samples were collected. RNA was extracted from the biofilm and sequenced via Illumina HiSeq. Differential expression analysis used Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and differentially expressed genes were identified using the Sleuth package in R, with a statistical cutoff of ≤0.05.
This study found 3351 KEGGs in the subgingival biofilm of both groups. Smoking habits altered the functional behavior of subgingival biofilm, resulting in 304 differentially expressed KEGGs between groups. Moreover, seven pathways were modulated: glycan degradation, galactose metabolism, glycosaminoglycan degradation, oxidative phosphorylation, peptidoglycan biosynthesis, butanoate metabolism, and glycosphingolipid biosynthesis. Smoking also altered antibiotic resistance gene levels in subgingival biofilm by significantly overexpressing genes related to beta-lactamase, permeability, antibiotic efflux pumps, and antibiotic-resistant synthetases.
Due to the limitations of a small sample size, our data suggest that smoking may influence the functional behavior of subgingival biofilm, modifying pathways that negatively impact the behavior of subgingival biofilm, which may lead to a more virulent community.
本研究旨在评估吸烟对患有 III/IV 期和广泛性牙周病的年轻患者龈下元转录组谱的影响。
共选择了 6 名年轻患者,包括吸烟者和非吸烟者(n=3/组),他们均患有牙周炎。遵循 STROBE(加强观察性研究在流行病学中的报告)报告准则。收集牙周临床测量值和龈下生物膜样本。从生物膜中提取 RNA 并通过 Illumina HiSeq 进行测序。使用京都基因与基因组百科全书(KEGG)富集进行差异表达分析,并使用 R 中的 Sleuth 包识别差异表达基因,统计截止值为≤0.05。
本研究在两组龈下生物膜中发现了 3351 个 KEGG。吸烟习惯改变了龈下生物膜的功能行为,导致两组之间有 304 个 KEGG 存在差异表达。此外,有 7 条途径被调节:糖降解、半乳糖代谢、糖胺聚糖降解、氧化磷酸化、肽聚糖生物合成、丁酸代谢和糖脂生物合成。吸烟还通过显著过表达与β-内酰胺酶、通透性、抗生素外排泵和抗生素抗性合成酶相关的基因,改变了龈下生物膜中抗生素耐药基因的水平。
由于样本量小的限制,我们的数据表明吸烟可能影响龈下生物膜的功能行为,改变对龈下生物膜行为产生负面影响的途径,从而导致更具毒力的群落。