Viruses in Periodontitis: Evidence, Mechanisms, Diagnosis and Therapeutic Implications

Authors

Dr. Nikita Verma

MDS(pursuing) - Department of Periodontology, Faculty of Dental Sciences, King George's Medical University, Lucknow, Uttar Pradesh (India)

Prof. (Dr.) Anjani Kumar Pathak

MDS, FAOI, FISDR, FPFA - Department of Periodontology, Faculty of Dental Sciences, King George's Medical University, Lucknow, Uttar Pradesh (India)

Prof. (Dr.) Nand Lal

MDS, FADI, FICD, FPFA, AFILD - Department of Periodontology, Faculty of Dental Sciences, King George's Medical University, Lucknow, Uttar Pradesh (India)

Prof. (Dr.) Shalini Kaushal

MDS, FPFA, FICD - Department of Periodontology, Faculty of Dental Sciences, King George's Medical University, Lucknow, Uttar Pradesh (India)

Prof. (Dr.) Pavitra Rastogi

MDS, MNAMS, FICD, FPFA, AFILD - Department of Periodontology, Faculty of Dental Sciences, King George's Medical University, Lucknow, Uttar Pradesh (India)

(Dr). Neetu Rani

Dr. Neetu Rani, MDS (Periodontology), Assistant Professor, King George’s Medical University (KGMU), Lucknow, Uttar Pradesh, India. (India)

Article Information

DOI: 10.51244/IJRSI.2026.1308000352

Subject Category: Medicine

Volume/Issue: 13/8 | Page No: 5448-5457

Publication Timeline

Submitted: 2026-09-07

Accepted: 2026-09-12

Published: 2026-09-26

Abstract

Periodontitis is a biofilm-associated, host-mediated inflammatory disease, but bacterial dysbiosis alone does not fully explain its episodic activity and variable response to treatment. This narrative review evaluates evidence for human herpesviruses and bacteriophages as modifiers of periodontal ecology. Targeted searches of PubMed, PubMed Central and publisher databases were conducted through 31 July 2026. Epstein-Barr virus and human cytomegalovirus are detected more frequently in many deep or active periodontal sites than in healthy sites, although findings vary with population, specimen type and assay. Mechanistic studies support viral effects on cytokine signalling, immune surveillance, epithelial integrity, osteoclastogenesis and viral-bacterial cooperation. Metagenomic studies also identify disease-associated changes in bacteriophage communities. Quantitative polymerase chain reaction is useful for estimating viral burden, but DNA detection alone cannot distinguish latent carriage from active infection. RNA-based assays, tissue localisation and longitudinal sampling are required for stronger causal inference. Mechanical periodontal therapy may reduce viral burden indirectly, whereas evidence for adjunctive antiviral treatment is limited. Current findings support a context-dependent model in which viruses act as ecological or immunological cofactors rather than universal causes of periodontitis. Routine viral testing or antiviral therapy is therefore not justified outside research or carefully selected refractory cases.

Keywords

periodontitis; oral virome; Epstein-Barr virus; cytomegalovirus; bacteriophage; quantitative PCR; antiviral therapy

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