Int J Stomatol ›› 2026, Vol. 53 ›› Issue (6): 866-873.doi: 10.7518/gjkq.2026601

• Review • Previous Articles    

MicroRNA and oral microenvironment: research progress in microbiota dysbiosis and oral disease regulation

Keyi Zhang(),Jieyu Zhou,Yafei Wu()   

  1. State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Dept. of Periodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2025-03-27 Revised:2026-01-13 Online:2026-11-01 Published:2026-10-29
  • Contact: Yafei Wu E-mail:634646274@qq.com;Yfw1110@163.com
  • Supported by:
    National Natural Science Foundation of China(82170970);Exploration and R&D Project of West China Hospital of Stomatology, Sichuan University(RD-02-202407)

Abstract:

The human oral cavity harbors a highly complex microbial community, whose dynamic balance of composition and function is a central factor in maintaining oral health. Oral symbiotic microbiota refers to the microbial communities that naturally reside in the human oral cavity and engage in a mutually beneficial relationship with the host. However, when host or environmental factors change, microbial dysbiosis may occur, contributing to the pathological processes of various oral diseases such as periodontitis and oral cancer. Recent studies have shown that microRNA (miRNA), as post-transcriptional regulators of gene expression, can mediate bidirectional interactions between microbes and the host. This review summarizes and discusses the molecular regulatory mechanisms of oral dysbiosis and miRNA in typical oral diseases, while also reviewing and prospecting the progress of miRNA-based probiotic therapies for oral diseases.

Key words: oral microecology, microbiota dysbiosis, microRNA, periodontitis, oral cancer, probiotic therapy

CLC Number: 

  • R780.2

TrendMD: 

Fig 1

Oral microbiota dysbiosis-miRNA-oral diseases regulatory axis"

Tab 1

Representative regulatory mechanisms of miRNA in oral diseases"

口腔疾病miRNA调控机制参考文献
牙周炎miRNA-146通过TLRs/NF-κB信号通路调控促炎因子分泌[34-35]
miR-128通过p38信号通路调控TNF-α分泌[13]
miR-543-3p靶向KLF-6调控炎症反应[36]
miR-203靶向SOCS3调控RANKL介导的破骨细胞生成[14]
miR-1246维持Th17/Treg稳态[38]
miR-26a-5p靶向磷脂酶Cβ1影响组织重建[37]
miR-495-3p靶向TRAF6介导细胞功能障碍[40]
口腔癌miR-214靶向ULK1调控癌细胞增殖和侵袭[42]
miR-210-3p通过PI3K/AKT信号通路调控血管生成[43]
miR-150靶向HMGA2抑制癌细胞增殖、侵袭及上皮—间充质转化[45]
miR-205,miR-296调控癌细胞侵袭[46]
miRNA-21调控癌细胞增殖、侵袭及凋亡[47]
龋病SmsR-1532, SmsR-1785调控细胞内金属离子稳态与毒力基因[29]
牙髓炎miR-21-5p靶向TRAF6/PDCD4调控NF-κB信号通路介导的炎症反应[50]
根尖周炎miR-10a-5p调控巨噬细胞相关炎症及凝血反应[51]
miR-200a-3p靶向FOXJ1调控骨髓间充质干细胞的迁移[52]
miR-199a-5p靶向IFIT2调控根尖区成骨分化[53]
口腔黏膜病miR-155调控IL-6/TNF-α/CD106信号传导[54]
miR-17-5p通过TGF-β纤维化途径诱导上皮紊乱[55]
miR-503通过RAS/RAF/MEK/ERK信号通路调控成纤维细胞分化[56]
miR-23a-3p靶向CCND1调控上皮增殖[57]
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