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. 2022 Oct;8(5):1011-1020.
doi: 10.1002/cre2.584. Epub 2022 May 17.

Does periodontitis influence the risk of COVID-19? A scoping review

Arunibha Ghosh  1 , Betsy Joseph  2 , Sukumaran Anil  3   4
Affiliations

Does periodontitis influence the risk of COVID-19? A scoping review

Arunibha Ghosh et al. Clin Exp Dent Res. 2022 Oct.

Abstract

Objective: Research has shown that the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly influences the oral microbiome to expedite systemic diseases by invading harmful oral pathogens near and distant organs. To identify, explore, and map the possible mechanisms underlying periodontitis in severe coronavirus disease 2019 (COVID-19) cases.

Material and methods: Relevant articles published from December 2019 to February 2022 were identified and screened using keywords and inclusion criteria from various databases.

Results: This review sheds light on multiple pathways of periodontitis, the spread of periodontal infection and microbial metabolites to the lungs, and the dysregulated immune system with elevated cytokines, reactive oxygen species generation, nuclear DNA damage, and senescence, which have the potential to promote stronger viral attachment to host cells and the onset of COVID-19 manifestation with increased severity and risk of mortality. In addition, the cytokine connection to SARS-CoV-2, T-cell responses against periodontitis, its connection with COVID-19, the role of host factors, and periodontal therapy have been discussed.

Conclusions: The relationship between COVID-19 and periodontitis needs further investigation along with the development of alternative therapies to prevent periodontitis for better management and control of COVID-19.

Keywords: SARS-CoV-2; cytokines; oral-lung axis; periodontopathogens.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Multiple pathways of periodontitis contribute to cellular senescence in the lungs epithelium and influencing the risk of SARS‐CoV‐2 infection to host cells. ACE2, angiotensin‐converting enzyme‐2; IFN, interferon; IL, interleukin; LPS, lipopolysaccharide; MAPK, mitogen‐activated protein kinase; MCP, monocyte chemoattractant protein; NF, nuclear factor; OLAA, oral–lung aspiration axis; ROS, reactive oxygen species; SARS‐COV‐2, severe acute respiratory syndrome coronavirus‐2; TNF, tumor necrosis factor; T‐regs, regulatory T cells.
See this image and copyright information in PMC

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