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抗生素暴露会使牙周炎菌斑生物膜中携带耐药基因的链球菌增多。

Antibiotic exposure enriches streptococci carrying resistance genes in periodontitis plaque biofilms.

作者信息

Zhang Qian, Zhen Min, Wang Xiaochen, Zhao FengXiang, Dong Yang, Wang Xiaoya, Gao Shengtao, Wang Jinfeng, Shi Wenyu, Zhang Yifei

机构信息

Central Laboratory, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.

Department of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China.

出版信息

PeerJ. 2025 Jan 20;13:e18835. doi: 10.7717/peerj.18835. eCollection 2025.

DOI:10.7717/peerj.18835
PMID:39850835
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11756365/
Abstract

BACKGROUND

Periodontitis is not always satisfactorily treated with conventional scaling and root planing, and adjunctive use of antibiotics is required in clinical practice. Therefore, it is important for clinicians to understand the diversity and the antibiotic resistance of subgingival microbiota when exposed to different antibiotics.

MATERIALS AND METHODS

In this study, subgingival plaques were collected from 10 periodontitis patients and 11 periodontally healthy volunteers, and their microbiota response to selective pressure of four antibiotics (amoxicillin, metronidazole, clindamycin, and tetracycline) were evaluated through 16S rRNA gene amplicon and metagenomic sequencing analysis. Additionally, sensitive and resistant strains were isolated and cultured for resistance evaluation.

RESULTS

Cultivation of subgingival microbiota revealed the oral microbiota from periodontitis patients were more resistant to antibiotics than that of healthy. Significant differences were also observed for the microbial community between with and without antibiotics (especially amoxicillin and tetracycline) treated in periodontitis group.

CONCLUSION

Overall, after the two antibiotics (amoxicillin and tetracycline) exposed, the oral subgingival microbiota in periodontitis patients exhibited different diversity and composition. may account for oral biofilm-specific antibiotic resistance in periodontitis. This provides information for personalized treatment of periodontitis.

摘要

背景

传统的龈下刮治和根面平整术对牙周炎的治疗效果往往不尽人意,临床实践中需要辅助使用抗生素。因此,对于临床医生来说,了解龈下微生物群在接触不同抗生素时的多样性和抗生素耐药性非常重要。

材料与方法

在本研究中,从10名牙周炎患者和11名牙周健康志愿者中收集龈下菌斑,并通过16S rRNA基因扩增子和宏基因组测序分析评估其微生物群对四种抗生素(阿莫西林、甲硝唑、克林霉素和四环素)选择性压力的反应。此外,分离并培养敏感和耐药菌株以进行耐药性评估。

结果

龈下微生物群的培养显示,牙周炎患者的口腔微生物群比健康人的口腔微生物群对抗生素更具耐药性。在牙周炎组中,使用和未使用抗生素(尤其是阿莫西林和四环素)治疗的微生物群落之间也观察到显著差异。

结论

总体而言,在暴露于两种抗生素(阿莫西林和四环素)后,牙周炎患者的口腔龈下微生物群表现出不同的多样性和组成。这可能是牙周炎中口腔生物膜特异性抗生素耐药性的原因。这为牙周炎的个性化治疗提供了信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/197af2fdc7d7/peerj-13-18835-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/ac60226fa017/peerj-13-18835-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/d8101aaf94ff/peerj-13-18835-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/a9d59f1c5a93/peerj-13-18835-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/64f6f65ec434/peerj-13-18835-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/197af2fdc7d7/peerj-13-18835-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/ac60226fa017/peerj-13-18835-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/d8101aaf94ff/peerj-13-18835-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/a9d59f1c5a93/peerj-13-18835-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/64f6f65ec434/peerj-13-18835-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f5c/11756365/197af2fdc7d7/peerj-13-18835-g005.jpg

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Antibiotic resistance in periodontitis patients: A systematic scoping review of randomized clinical trials.
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Oral Dis. 2023 Oct;29(7):2501-2511. doi: 10.1111/odi.14288. Epub 2022 Jul 4.
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