Int J Stomatol ›› 2020, Vol. 47 ›› Issue (5): 607-615.doi: 10.7518/gjkq.2020022

• Reviews • Previous Articles     Next Articles

Regulation of osteoimmunology by MicroRNA 155 and research progress of its possible mechanism in periodontitis

Sun Jianwei(),Lei Lihong,Tan Jingyi,Chen Lili()   

  1. Dept. of Periodontics, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China
  • Received:2019-11-30 Revised:2020-03-25 Online:2020-09-01 Published:2020-09-16
  • Contact: Lili Chen E-mail:21818178@zju.edu.cn;chenlili_1030@zju.edu.cn
  • Supported by:
    National Natural Science Foundation of China(81771072);the Science and Technology Program of Zhejiang Province(2017C33141)

Abstract:

Periodontitis is a chronic infectious disease that is characterised by the inflammation of gingiva and the progressive destruction of alveolar bone. The interaction between plaque microbes and host defence affects the process of the disease. As a new interdisciplinary field, osteoimmunology mainly studies the molecular interaction mechanism between skeletal and immune systems, which are related to the occurrence of periodontitis. MicroRNA 155 (miR-155) is an endogenous noncoding single-stranded RNA in eukaryotic organisms. miR-155 combines with the 3’-untranslated region of target mRNA to negatively regulate the expression of mRNA. miR-155 can participate in multiple physiological and pathological processes, such as immunity, haematopoiesis and inflammation. A large number of studies have shown that the expression level of miR-155 can be altered during periodontitis development, but results reported in literature are inconsistent. miR-155 can also regulate the skeletal system through multiple pathways. This review elaborates the modulation of miR-155 in osteoimmunology and periodontitis. We aim to offer novel insights and strategies for clinical therapy of periodontitis.

Key words: MicroRNA, osteoimmunology, periodontitis, bone metabolism, osteoblast, osteoclast

CLC Number: 

  • R781.4+2

TrendMD: 
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