{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T17:51:42Z","timestamp":1790790702602,"version":"4.1.0"},"reference-count":147,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Viruses are increasingly recognized as potential modulators of oral biofilm ecology and periodontal inflammation, expanding the traditional bacterial paradigm of periodontitis. Members of the\n                    <jats:italic>Herpesviridae<\/jats:italic>\n                    family, including Epstein\u2013Barr virus (EBV), human cytomegalovirus (HCMV), and herpes simplex virus (HSV), are frequently detected in periodontal tissues and may influence disease activity through latency, reactivation, immune modulation, epithelial barrier disruption, and interactions with bacteria. These processes may contribute to local dysbiosis and sustained periodontal inflammation. The potential systemic relevance of oral viruses is biologically plausible but remains incompletely established. Viral persistence or reactivation in oral niches may contribute to systemic immune activation through hematogenous spread, saliva\u2010mediated dissemination, aspiration, or amplification of inflammatory mediators as IL\u20101\u03b2, IL\u20106, and TNF\u2010\u03b1. Accordingly, viruses may act as disease modifiers within the broader relationship between periodontitis and systemic conditions including cardiovascular, metabolic, respiratory, neurogenerative, pregnancy\u2010related, and cancer\u2010associated outcomes. However, the strength of evidence differs across these conditions. Current data support a model in which oral viruses, bacteriophages, bacteria, and fungi form an interconnected biofilm ecosystem that may influence periodontitis progression and systemic inflammatory burden. Nevertheless, most available evidence is observational, associative, or derived from mechanistic experimental models, and definitive proof that viruses are independent etiopathogenic drivers of periodontitis is lacking. Future longitudinal and interventional studies are needed to determine whether viral detection reflects bystander association, disease amplification, or a true pathogenic role, and whether antiviral or phage\u2010based strategies offer clinical benefit beyond established periodontal therapy.\n                  <\/jats:p>","DOI":"10.1111\/jre.70137","type":"journal-article","created":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T17:15:41Z","timestamp":1782926141000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Viruses, Periodontitis, and Systemic Diseases"],"prefix":"10.1111","author":[{"given":"Kim Natalie","family":"Solte","sequence":"first","affiliation":[{"name":"Department of Periodontology, Oral Medicine, and Oral Surgery Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1330-0654","authenticated-orcid":false,"given":"Yvonne L.","family":"Hernandez\u2010Kapila","sequence":"additional","affiliation":[{"name":"Division of Digestive Diseases, Biosystems and Function, Periodontics, School of Dentistry UCLA, Vatche &amp; Tamar Manoukian David Geffen School of Medicine UCLA  Los Angeles California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1043-2651","authenticated-orcid":false,"given":"Henrik","family":"Dommisch","sequence":"additional","affiliation":[{"name":"Department of Periodontology, Oral Medicine, and Oral Surgery Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,1]]},"reference":[{"issue":"2","key":"e_1_2_12_2_1","doi-asserted-by":"crossref","first-page":"187","DOI":"10.1111\/j.1600-0765.2005.00790.x","article-title":"Periodontitis Lesions Are a Source of Salivary Cytomegalovirus and Epstein\u2010Barr Virus","volume":"40","author":"Saygun I.","year":"2005","journal-title":"Journal of Periodontal Research"},{"issue":"2","key":"e_1_2_12_3_1","doi-asserted-by":"crossref","first-page":"97","DOI":"10.1111\/j.1600-0765.2005.00770.x","article-title":"Real\u2010Time Polymerase Chain Reaction Quantification of Human Cytomegalovirus and Epstein\u2010Barr Virus in Periodontal Pockets and the Adjacent Gingiva of Periodontitis Lesions","volume":"40","author":"Kubar A.","year":"2005","journal-title":"Journal of Periodontal Research"},{"issue":"4","key":"e_1_2_12_4_1","doi-asserted-by":"crossref","first-page":"449","DOI":"10.1177\/00220345241303138","article-title":"Unveiling the Etiopathogenic Role of Epstein\u2010Barr Virus in Periodontitis","volume":"104","author":"Tonoyan L.","year":"2025","journal-title":"Journal of Dental Research"},{"issue":"3","key":"e_1_2_12_5_1","doi-asserted-by":"crossref","first-page":"239","DOI":"10.1002\/path.5679","article-title":"Salivary Glands Are a Target for SARS\u2010CoV\u20102: A Source for Saliva Contamination","volume":"254","author":"Matuck B. 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