Nicotine Vaping, Oral Microbiome Dysbiosis, and Periodontal Inflammation in Adolescents: Mechanistic Evidence to Inform U.S. School-Based Prevention Policy and the National Interest — A Narrative Review

Background: Electronic cigarettes remain the most commonly used tobacco product among U.S. middle and high school students, and a substantial share of adolescents who vape do so frequently, with flavored disposable devices. Meta-analyses comparing adult e-cigarette users with smokers and non-smokers report an intermediate and heterogeneous periodontal profile, and often lower bleeding on probing, which has encouraged the perception that vaping is periodontally benign. This review asks whether the mechanistic evidence supports that perception. Materials and Methods: Narrative review of PubMed-indexed literature (2016-2026) on electronic nicotine delivery systems and the oral microbiome, host inflammation and oxidative stress, periodontal cell biology, microvascular function and clinical periodontal outcomes, together with U.S. youth surveillance data and schoolbased prevention evaluations. Three recent mechanistic reviews on oxidative stress, platelet-rich fibrin biology and implant-surface cell biology were used as an interpretive framework. Findings were graded by model (in vitro, animal, human) and by whether adolescents were actually studied. Results: Vaping is consistently associated with a distinct subgingival community that is enriched in inflammationassociated taxa and that, according to the available longitudinal and cross-sectional data, lies between the communities of smokers and non-smokers. Aerosol constituents are metabolized by oral biofilms into dense, exopolysaccharide-rich structures, and the oral mycobiome is also remodelled. In host cells, e-cigarette aerosol and flavorings induce carbonyl and oxidative stress, receptor for advanced glycation end-products (RAGE) upregulation and pro-senescence signalling, which converge on the same AGE-RAGE-NF-κB axis that drives diabetes-associated periodontitis. Nicotine impairs the proliferation, migration and osteogenic differentiation of periodontal ligament stem cells through a miR-1305/RUNX2 mechanism, while e-cigarette aerosol reduces gingival fibroblast function on titanium surfaces. Nicotine vaping acutely increases thrombogenicity and impairs microvascular function, which offers a plausible explanation for the reduced bleeding on probing reported in meta-analyses. Almost no study enrolled adolescents. Conclusion: The mechanistic evidence does not support the view that vaping is periodontally neutral. It suggests instead a pattern of subclinical dysbiosis and inflammation that conventional periodontal indices may underdetect. Because exposure begins in adolescence, school-based prevention, routine screening during dental visits and flavor-access policy are biologically justified. Adolescent-specific longitudinal studies with microbial and inflammatory endpoints are required