Periodontitis is a complex, multifactorial chronic disease traditionally attributed to bacterial biofilms.However, recent advancements in molecular diagnostics have established a significant paradigm shift, identifying viral strains as key contributors to the disease's onset and progression.This paper reviews the active role of viruses-specifically the Herpesviridae family (EBV, HCMV, and HSV-1), HIV, HPV, and SARS-CoV-2-in modulating the periodontal microenvironment. Pathogenesis: Viruses contribute to tissue destruction through the suppression of host immune responses, direct cytopathic effects on fibroblasts and epithelial cells, and a synergistic "tag-team" interaction with periodontal pathogens like Porphyromonas gingivalis. Viral-Bacterial Synergy: Viral infection triggers the upregulation of pro-inflammatory cytokines, specifically - -, which accelerate alveolar bone resorption and impair the osteogenic potential of periodontal ligament stem cells. Clinical Implications: High viral titers are associated with deeper probing depths, greater attachment loss, and refractory disease patterns. Therapeutic Strategies: While conventional scaling and root planing (SRP) reduces microbial loads, it often fails to eliminate intracellular viral reservoirs.Consequently, the integration of adjunctive systemic antivirals and host-modulatory therapies is emerging as a vital component for managing severe or non-responsive cases.This evolving "poly-microbial + viral" model reorients periodontal management toward a more holistic, interdisciplinary approach to enhance long-term clinical stability and reduce systemic inflammatory burdens.
RAJENDRAN et al. (Thu,) studied this question.