Contribution of herpesviruses in the progression of periodontal and peri‐implant diseases in systemically healthy individuals

Abstract

The aim of this review was to assess the contribution of herpesviruses in the subgingival oral biofilm in the progression of periodontal and peri-implant diseases in systemically healthy individuals. The literature review was customized to summarize the pertinent information for the following reasons: (1) A systematic review regarding the role of herpesviruses in the etiopathogenesis of periodontal disease has recently been published; and (2) a limited number of studies have assessed the association of herpesviruses with peri-implant diseases. To date, five observational studies have assessed the presence of herpesviruses in the subgingival oral biofilm of individuals with peri-implant diseases. In these studies, dental implants were in place for up to approximately 8 years. In two studies, human cytomegalovirus (HCMV) was more often isolated from the peri-implant sulci of sites with than without peri-implantitis. In one study, a low prevalence of HCMV compared with Epstein-Barr virus (EBV) was associated with the progression of peri-implantitis. In previous studies, the presence of EBV in the subgingival oral biofilm was associated with the onset of peri-implantitis and peri-implant mucositis, respectively. Major limitations of the studies assessed were the absence of blinding and lack of power analysis for sample size estimation. In conclusion, the presence of herpesviruses in the periodontal and peri-implant subgingival oral biofilm is an indicator of periodontal and peri-implant diseases in systemically healthy individuals; however, further studies with a statistically justified sample-size are needed to understand and refine this association.

A brief history of periodontics in the United States of America: Pioneers and thought‐leaders of the past, and current challenges

“…Dysbiotic bacterial communities have been strongly implicated in the initiation and progression of periodontitis . In addition to the role played by bacteria in the development of periodontal diseases, there is a growing body of evidence demonstrating that viruses which prey on host cells (ie, eukaryotic viruses) are part of the etiological story . However, currently there is no defined group of bacteria, viruses, or bacteria‐virus combinations that can be said to be stand‐alone causes of periodontal disease.…”

“…Viruses are ubiquitous components and drivers of ecological change in all oral biofilms. The human oral virobiota includes bacteriophages and mammalian (eukaryotic) viruses . The genes, or virome, that these viruses possess add significantly to the genetic repertoire of oral biofilms …”

“…By contrast, over 20 years ago, it was reported that significantly elevated levels of these viruses were found in oral specimens taken from people with periodontal diseases . Since that time there have been many reports of associations between eukaryotic viruses and various clinical forms of periodontitis . Strong arguments can be made that direct viral attacks on cellular components of periodontal tissues (ie, epithelial cells, fibroblasts) and cells of innate immunity (eg, neutrophils) are part of the ecological dysbiosis leading to periodontitis .…”

“…In addition, there are several reports of eukaryotic viruses affecting the virulence properties of putative periodontal pathogens . The growing number of reports linking the presence of elevated levels of eukaryotic viruses to the development of peri‐implantitis suggests that periodontitis and peri‐implantitis share some important pathogenic features …”

“…[96][97][98][99][100] In addition to the role played by bacteria in the development of periodontal diseases, there is a growing body of evidence demonstrating that viruses which prey on host cells (ie, eukaryotic viruses) are part of the etiological story. [101][102][103][104][105] However, currently there is no defined group of bacteria, viruses, or bacteria-virus combinations that can be said to be stand-alone causes of periodontal disease. The microbial communities leading to periodontal disease are much more complicated than was believed even a few years ago.…”