吉林大学学报(医学版) ›› 2026, Vol. 52 ›› Issue (4): 1187-1194.doi: 10.13481/j.1671-587X.20260432

• 综述 • 上一篇    

慢性牙周炎对代谢相关脂肪性肝病发生发展影响的研究进展

刘欣,刘雨晴,李慧()   

  1. 吉林大学中日联谊医院口腔科,吉林 长春 130033
  • 收稿日期:2033-03-12 接受日期:2025-03-10 出版日期:2026-07-28 发布日期:2026-07-27
  • 通讯作者: 李慧 E-mail:liuhui99@jlu.edu.cn
  • 作者简介:刘 欣(1995-),女,吉林省长春市人,在读硕士研究生,主要从事牙周病的治疗和预防方面的研究。
  • 基金资助:
    吉林省科技厅科技发展计划项目(20230508073RC)

Research progress in effect of chronic periodontitis on occurrence and development of metabolic fatty liver disease

Xin LIU,Yuqing LIU,Hui LI()   

  1. Department of Stomatology,China-Japan Union Hospital,Jilin University,Changchun 130033,China
  • Received:2033-03-12 Accepted:2025-03-10 Online:2026-07-28 Published:2026-07-27
  • Contact: Hui LI E-mail:liuhui99@jlu.edu.cn

摘要:

代谢相关脂肪性肝病(MAFLD)作为一种常见肝脏疾病,其发病率随着肥胖和糖尿病等代谢性疾病的增多而持续升高。慢性牙周炎(CP)作为常见口腔疾病,也被证实与全身健康密切相关。CP与MAFLD之间存在一定关联。CP可能经多种途径影响肝脏脂肪代谢,进而增加MAFLD发病风险。牙周致病菌及其代谢产物可能直接作用于肝脏,抑制胰岛素信号通路,致使肝糖原合成减少、血糖升高;CP引发的慢性炎症反应会提高血液中促炎细胞因子水平,如肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6),上述因子会破坏脂肪细胞,影响脂肪因子平衡,进而导致肝脏胰岛素抵抗;CP可增加血液中活性氧(ROS)水平,引发系统性氧化应激,损伤肝脏细胞,加重MAFLD病情;CP可能通过激活核因子κB(NF-κB)、c-Jun氨基末端激酶(JNK)和高迁移率族蛋白B1-Toll样受体(HMGB1-TLR)等信号通路,影响肝脏脂肪代谢和炎症反应,推动MAFLD的发生发展。未来需进一步深入探讨CP与MAFLD间的关联机制,开展队列研究和前瞻性研究,评估CP治疗对MAFLD患者的影响。同时,还需探讨联合治疗策略,如饮食调整、锻炼和抗炎药物治疗等,以提高治疗效果。现综述CP与MAFLD间的关联性,为临床实践提供新思路,并提示临床工作者在治疗MAFLD时,应关注患者牙周健康状况,采取相应预防治疗措施。

关键词: 慢性牙周炎, 代谢性脂肪肝, 流行病学, 炎症反应, 氧化应激

Abstract:

Metabolic-associated fatty liver disease (MAFLD) is a common liver disorder, and its incidence continues to rise along with the increasing prevalence of metabolic diseases such as obesity and diabetes. chronic periodontitis(CP), a prevalent oral disease, has also been confirmed to be closely associated with overall health. A certain correlation exists between CP and MAFLD. CP may affect hepatic fat metabolism through multiple pathways, thereby increasing the risk of MAFLD. Periodontal pathogens and their metabolites may directly act on the liver, inhibiting the insulin signaling pathway, reducing hepatic glycogen synthesis, and leading to hyperglycemia. The chronic inflammatory response induced by CP elevates the levels of pro-inflammatory cytokines in the blood, such as tumor necrosis factor α(TNF-α) and interleukin-6 (IL-6). These factors can disrupt the adipocytes and affect the balance of adipokines, thus leading to hepatic insulin resistance. CP also increases the level of reactive oxygen species (ROS) in the blood, triggering systemic oxidative stress, damaging liver cells, and exacerbating the condition of MAFLD. Furthermore, CP may influence hepatic fat metabolism and inflammatory response by activating signaling pathways such as nuclear factor κB (NF-κB), c-Jun N-terminal kinase (JNK), and high mobility group box 1-Toll-like receptors (HMGB1-TLR), thereby promoting the occurrence and development of MAFLD. Future studies are needed to explore the association mechanism between CP and MAFLD, and to conduct cohort studies and prospective studies to evaluate the impact of CP treatment on the patients with MAFLD. Additionally, combined treatment strategies, such as dietary adjustments, exercise, and anti-inflammatory drug therapy, should be explored to improve therapeutic outcomes. This review summarized the correlation between CP and MAFLD, providing new insights for clinical practice, and reminding clinicians to pay attention to the periodontal health status of patients and take appropriate preventive and therapeutic measures when treating MAFLD.

Key words: Chronic periodontitis, Metabolic fatty liver disease, Epidemiology, Inflammatory response, Oxidative stress

中图分类号: 

  • R781.4