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关志炜, 徐天琪, 沈松, 等. 牙周炎促进不良妊娠结局的途径与作用机制[J]. koko体育app 学报(医学版), 2023, 54(1): 39-48. DOI:
引用本文: 关志炜, 徐天琪, 沈松, 等. 牙周炎促进不良妊娠结局的途径与作用机制[J]. koko体育app 学报(医学版), 2023, 54(1): 39-48. DOI:
GUAN Zhi-wei, XU Tian-qi, SHEN Song, et al. Pathways and Mechanisms of Periodontitis Contributing to Adverse Pregnancy Outcomes[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(1): 39-48. DOI:
Citation: GUAN Zhi-wei, XU Tian-qi, SHEN Song, et al. Pathways and Mechanisms of Periodontitis Contributing to Adverse Pregnancy Outcomes[J]. Journal of Sichuan University (Medical Sciences), 202👍3, 54(1): 39-48. DOI:

牙周炎促进不良妊娠结局的途径与作用机制

Pathways and Mechanisms of Periodontitis Contributing to Adverse Pregnancy Outcomes

  • 摘要: 牙周炎是人群中高发的口腔慢性感染性疾病,牙周致病菌可通过血液传播途径异位定植并感染多个人体组织器官,是多种全身系统性疾病的风险因素。近年来,牙周炎与不良妊娠结局(adverse pregnancy outcomes, APOs)间的关系引起越来越多的关注。本文系统回顾牙周炎与APOs相互关系的研究历程,总结已有牙周炎促进APOs的致病途径和机制,阐明口腔致病菌经血液传播造成宫内感染是牙周炎干扰妊娠过程的重要途径。未来如要深入解析牙周炎影响APOs的具体分子机制,可将研究重点放在APOs相关口腔致病菌及其毒力因子的发现、致病菌与胎盘组织的相互作用分析及侵袭胎儿的致病途径等方向。此外,通过动物和细胞实验验证人群研究的结果并将其转化为行之有效的干预措施对防控APOs的发生、发展具有重要的临床意义。  
    Abstract: Periodontitis is a chronic oral inflammatory disease with a high incidence in the global population. Periodontal pathogens can colonize and infect multiple human tissues and organs through blood transmission, which is an important risk factor of many systemic diseases. Recently, the correlation between periodontitis and adverse pregnancy outcomes (APOs) has attracted growing research interest. Herein, we systematically reviewed the research progress in the relationship between periodontitis and APOs and summarized reported findings on the pathways and mechanisms by which periodontitis contributes to APOs. We also clarified that intrauterine infection caused by oral pathogens transmitted through blood is an important pathway by which periodontitis interferes with pregnancy. In addition, further research focused on the discovery of more APOs-related oral pathogenic bacteria and their virulence factors, analysis of the interaction between pathogenic bacteria and placental tissue, and pathogenic pathways of oral bacterial invasion of the fetus will promote thorough analysis of the specific molecular mechanism of how periodontitis affects APOs. Furthermore, the validation of the results of human population-based studies through animal/cell experiments and the translation into effective intervention strategies are of great clinical significance to the prevention and control of the occurrence and development of APOs.  
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