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. 2026 Sep 22;16:1964724. doi: 10.3389/fcimb.2026.1964724

Figure 2.

Infographic showing how periodontal dysbiosis and alcohol metabolism in the oral cavity generate acetaldehyde, a carcinogen, which travels to the lungs via the bloodstream and microaspiration, promoting pulmonary carcinogenesis through DNA damage, genetic instability, and impaired DNA repair in lung epithelial cells, with smoking further enhancing acetaldehyde production.

Schematic illustration of microbial acetaldehyde metabolism as a genotoxic mechanism linking periodontal disease to lung cancer. Periodontal dysbiosis promotes the overgrowth of acetaldehyde-producing oral microorganisms (e.g., Neisseria spp., S. mitis, R. mucilaginosa) that possess alcohol dehydrogenase (ADH). These bacteria metabolize ethanol to acetaldehyde, a Group 1 carcinogen. Acetaldehyde induces DNA adduct formation, point mutations, genomic instability, and activates oncogenic MAPK/NF-κB signaling while inhibiting DNA repair. Smoking potentiates this pathway by enhancing bacterial acetaldehyde production. Acetaldehyde reaches the lungs via microaspiration or hematogenous routes, causing direct DNA damage in pulmonary epithelial cells and potentially driving lung carcinogenesis. This mechanism operates independently of, and synergistically with, inflammation-driven pathways.