口腔疾病防治 ›› 2021, Vol. 29 ›› Issue (7): 485-489.DOI: 10.12016/j.issn.2096-1456.2021.07.009

• 综述 • 上一篇    下一篇

白细胞介素-18与慢性牙周炎相关性的研究进展

单超1,2(),王婷婷1,2,赵今1,2,3()   

  1. 1.新疆医科大学,新疆维吾尔自治区 乌鲁木齐(830011)
    2.新疆医科大学第一附属医院(附属口腔医院)牙体牙髓科,新疆维吾尔自治区 乌鲁木齐(830054)
    3.新疆维吾尔自治区口腔医学研究所,新疆维吾尔自治区 乌鲁木齐(830011)
  • 收稿日期:2020-07-19 修回日期:2020-10-16 出版日期:2021-07-20 发布日期:2021-04-19
  • 通讯作者: 赵今
  • 作者简介:单超,硕士研究生,Email: 1016181652@qq.com
  • 基金资助:
    国家自然科学基金项目(81760194);自治区研究生科研创新项目项目(XJ2019G180);自治区重点研发计划项目(2016B03049-1)

Research progress on the correlation between interleukin-18 and chronic periodontitis

SHAN Chao1,2(),WANG Tingting1,2,ZHAO Jin1,2,3()   

  1. 1. Xinjiang Medical University, Urumqi 830011, China
    2. Department of Endodontics, The First Affiliated Hospital of Xinjiang Medical University (Affiliated Stomatological Hospital), Urumqi 830054, China
    3. Xinjiang Uygur Autonomous Region Institute of Stomatology, Urumqi 830011, China
  • Received:2020-07-19 Revised:2020-10-16 Online:2021-07-20 Published:2021-04-19
  • Contact: Jin ZHAO
  • Supported by:
    National Natural Science Foundation of China(81760194);Graduate Student Scientific Research Innovation Project of Autonomous region(XJ2019G180);Key Research and Development Projects of Autonomous Region(2016B03049-1)

摘要:

慢性牙周炎作为一种以菌斑为始动因素的慢性感染性疾病,临床表现为硬组织的不可逆丧失以及周围软组织的破坏,包括深牙周袋、附着丧失,最终导致牙齿的丢失。白细胞介素-18(interleukin-18,IL-18)具有促进炎症和调节免疫功能,在介导宿主免疫应答及炎症反应中发挥重要作用。体内IL-18的升高可诱导干扰素及炎症因子如白细胞介素、肿瘤坏死因子、基质金属蛋白酶的生成,从而介导免疫与炎症的双重反应,这些炎症因子均参与慢性牙周炎的发生发展。许多临床研究已表明,慢性牙周炎患者的血清、唾液、龈沟液以及牙龈组织样本中的IL-18水平可能与牙周炎严重程度成正相关;而IL-18作为候选基因参与牙周炎的易感多态性研究至今结论不一。如何在临床研究中量化IL-18的水平并将其应用于诊断工具,以及利用全基因组关联研究、组学研究等新方法甄别出新的位点,将有助于加深对IL-18在慢性牙周炎的致病机制的认识,可为未来的精准医疗和制定个性化方案提供新思路。

关键词: 慢性牙周炎, 白细胞介素-18, 干扰素-γ, 适应性免疫, 炎症反应, 转录水平, 基因多态性

Abstract:

Chronic periodontitis is an infectious disease caused by plaque as the initiating factor. Clinically, it manifests as irreversible loss of hard tissue, leading to the destruction of surrounding periodontal tissue, including the deep periodontal pocket, loss of attachment, and finally, tooth loss. Interleukin-18 (IL-18) can promote inflammation and regulate immune function and plays an important role in mediating the host immune response and inflammatory response. An increase in IL-18 in vivo can induce the production of interferon and inflammatory factors, such as interleukin, tumor necrosis factor and matrix metalloproteinase, thus mediating the dual reaction of immunity and inflammation. These inflammatory factors are involved in the occurrence and development of chronic periodontitis. Many clinical studies have shown that the levels of IL-18 in serum, saliva, gingival crevicular fluid and gingival tissue samples of patients with chronic periodontitis may be positively correlated with the severity of periodontitis; however, as a candidate gene, IL-18 is involved in the susceptibility polymorphism of periodontitis. Understanding how to quantify the level of IL-18 in clinical studies and apply it to diagnostic tools and new sites identified by new methods (genome-wide association studies and omics research) will also deepen our understanding of the pathogenesis of IL-18 in chronic periodontitis and provide new ideas for future precision medicine and the formulation of personalized programs. In this paper, the structure, biological function and association between IL-18 and periodontitis are reviewed.

Key words: chronic periodontitis, interleukin-18, interferon-γ, adaptive immunity, inflammation, transcriptional level, gene polymorphism

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