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How Does Epstein-Barr Virus Contribute to Chronic Periodontitis?

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2020 Mar 18
PMID 32178406
Citations 14
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Abstract

Chronic periodontitis is spreading worldwide and mutually interacts with systemic diseases like diabetes mellitus. Although periodontopathic bacteria are inevitable pathogens in their onset and progression, many cases are not ascribable to the virulence of these bacteria because the effect of plaque control is limited. In contrast, Epstein-Barr virus (EBV) in the periodontium has been correlated with chronic periodontitis and has recently been considered as a promising pathogenic candidate for this disease. However, several important questions have yet to be addressed. For instance, although EBV latently infects more than 90% of individuals over the world, why do patients with chronic periodontitis exclusively harbor progeny EBV in the oral cavity? In addition, how does latently infected or reactivated EBV in the periodontium relate to the onset or progression of chronic periodontitis? Finally, is periodontitis incurable because EBV is the pathogen for chronic periodontitis? In this review, we attempt to answer these questions by reporting the current understanding of molecular relations and mechanisms between periodontopathic bacteria and EBV reactivation in the context of how this relationship may pertain to the etiology of chronic periodontitis.

Citing Articles

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References
1.
Li B, Carey M, Workman J . The role of chromatin during transcription. Cell. 2007; 128(4):707-19. DOI: 10.1016/j.cell.2007.01.015. View

2.
Slots J, Saygun I, Sabeti M, Kubar A . Epstein-Barr virus in oral diseases. J Periodontal Res. 2006; 41(4):235-44. DOI: 10.1111/j.1600-0765.2006.00865.x. View

3.
Himi K, Takeichi O, Imai K, Hatori K, Tamura T, Ogiso B . Epstein-Barr virus reactivation by persistent apical periodontal pathogens. Int Endod J. 2019; 53(4):492-505. DOI: 10.1111/iej.13255. View

4.
Abusleme L, Dupuy A, Dutzan N, Silva N, Burleson J, Strausbaugh L . The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation. ISME J. 2013; 7(5):1016-25. PMC: 3635234. DOI: 10.1038/ismej.2012.174. View

5.
Makino K, Takeichi O, Hatori K, Imai K, Ochiai K, Ogiso B . Epstein-Barr virus infection in chronically inflamed periapical granulomas. PLoS One. 2015; 10(4):e0121548. PMC: 4401687. DOI: 10.1371/journal.pone.0121548. View