ArticleResearch square2026
Periodontitis Primes the Oral Microenvironment for PS-Dependent Non-Canonical Entry Pathways Linked to SARS-CoV-2 Susceptibility.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
11 authors.
Funding
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Abstract
SARS-CoV-2 infection extends beyond the respiratory tract, with the oral cavity emerging as a critical site of viral activity shaped by epithelial receptor expression, microbial interactions, and inflammatory status. Periodontal disease (PD), a chronic dysbiotic condition, may heighten susceptibility to SARS-CoV-2 through inflammation-driven upregulation of non-canonical viral entry pathways. In this study, we investigated genes in the phosphatidylserine (PS)-dependent pathway, including ADAM17, ATP11c, TIM1, TIM3, and TIM4, in gingival tissue, saliva, and oral keratinocytes to define how PD and SARS-CoV-2 coordinately modulate oral viral entry mechanisms. Prepandemic gingival biopsies revealed significant upregulation of all non-canonical receptors in inflamed tissue, indicating that PD alone establishes a permissive molecular environment for PS-mediated microbial entry. In a post-vaccination cohort, salivary expression of these receptors was markedly elevated in COVID-19-positive individuals with PD, accompanied by significantly increased salivary PS levels, suggesting synergistic effects of viral exposure and periodontal inflammation.
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