已发表论文

口腔微生物群及其对炎症性肠病的影响:文献综述

 

Authors Chen XK, Mao T, Song X, Ren LL

Received 25 June 2025

Accepted for publication 27 October 2025

Published 3 December 2025 Volume 2025:18 Pages 7213—7229

DOI https://doi.org/10.2147/IJGM.S549434

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Gopal Krishna Dhali

Xiao-Kai Chen,* Tao Mao,* Xiang Song,* Lin-Lin Ren* 

Department of Gastroenterology, Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Lin-Lin Ren, Department of Gastroenterology, the Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, Shandong, 266000, People’s Republic of China, Email renlinlin@qdu.edu.cn

Abstract: Background: Inflammatory bowel disease (IBD) encompasses Crohn’s disease (CD) and ulcerative colitis (UC) and represents a heterogeneous spectrum of chronic intestinal inflammation with no exclusive etiology. Emerging evidence underscores that IBD arises from complex interactions between host factors and microbial communities. The disruption of microbial homeostasis facilitates the colonization and invasion of opportunistic pathogens within the gut, precipitating an exaggerated host immune response and driving disease progression. While extensive research has elucidated the role of the gut microbiota in IBD pathogenesis, the contribution of the oral microbiota to this process is garnering increasing attention. Oral microbes can translocate to the intestine via the swallowing of saliva, and harmful oral bacteria and proinflammatory immune cells from the oral mucosa may migrate to the gut, eliciting immune activation. This review explores the emerging role of the oral microbiota in IBD pathogenesis and synthesizes recent advancements in understanding the intricate relationship between oral microbial communities and IBD.

Keywords: oral-gut axis, microbial translocation, dysbiosis, impaired intestinal barrier function