Periodontitis as a potential contributor to lung cancer: Epidemiological evidence, proposed mechanisms, and clinical implications
Abstract
Periodontitis has been proposed as a potential contributor to lung cancer (LC), but the epidemiological, mechanistic, and clinical evidence remains heterogeneous. This structured narrative review evaluates the association between periodontitis and LC, the directness of proposed biological mechanisms, and the implications for risk assessment and supportive care. Observational studies generally report positive associations, although effect estimates vary according to periodontal ascertainment, study population, and adjustment for smoking. Clinically assessed periodontitis, self-reported or administrative diagnoses, tooth loss, periodontal-associated microbial markers, and general oral microbiome profiles represent distinct exposure domains and should not be interpreted interchangeably. The absence of a clear association among lifelong never smokers and the lack of supportive Mendelian randomization evidence further limit causal inference. Human studies demonstrate oral-lower airway microbial overlap, while experimental LC models support microbiota-related inflammatory and oncogenic signaling; however, periodontal origin, directional microbial transmission, and a continuous causal pathway from periodontitis to LC have not been established. Clinically, periodontitis should not modify current eligibility for low-dose computed tomography (LDCT) screening, and oral or respiratory microbiome biomarkers remain investigational. Perioperative oral care has comparatively stronger evidence for reducing postoperative pulmonary infectious complications, but this benefit should not be extrapolated to tumor recurrence or survival. Overall, current evidence supports an observational association and biological plausibility, whereas independent causality and an oncologic benefit of periodontal treatment remain unproven.
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BibTeX
@article{dong2026periodontitis,
title = {{Periodontitis as a potential contributor to lung cancer: Epidemiological evidence, proposed mechanisms, and clinical implications}},
author = {Hanchi Dong and Hua Xin},
journal = {iScience},
year = {2026},
month = oct,
doi = {10.1016/j.isci.2026.117985},
url = {https://www.cell.com/iscience/fulltext/S2589-0042(26)03368-7},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Periodontitis as a potential contributor to lung cancer: Epidemiological evidence, proposed mechanisms, and clinical implications
AU - Hanchi Dong
AU - Hua Xin
PY - 2026
DA - 2026/10/23
JO - iScience
DO - 10.1016/j.isci.2026.117985
UR - https://www.cell.com/iscience/fulltext/S2589-0042(26)03368-7
AB - Periodontitis has been proposed as a potential contributor to lung cancer (LC), but the epidemiological, mechanistic, and clinical evidence remains heterogeneous. This structured narrative review evaluates the association between periodontitis and LC, the directness of proposed biological mechanisms, and the implications for risk assessment and supportive care. Observational studies generally report positive associations, although effect estimates vary according to periodontal ascertainment, study population, and adjustment for smoking. Clinically assessed periodontitis, self-reported or administrative diagnoses, tooth loss, periodontal-associated microbial markers, and general oral microbiome profiles represent distinct exposure domains and should not be interpreted interchangeably. The absence of a clear association among lifelong never smokers and the lack of supportive Mendelian randomization evidence further limit causal inference. Human studies demonstrate oral-lower airway microbial overlap, while experimental LC models support microbiota-related inflammatory and oncogenic signaling; however, periodontal origin, directional microbial transmission, and a continuous causal pathway from periodontitis to LC have not been established. Clinically, periodontitis should not modify current eligibility for low-dose computed tomography (LDCT) screening, and oral or respiratory microbiome biomarkers remain investigational. Perioperative oral care has comparatively stronger evidence for reducing postoperative pulmonary infectious complications, but this benefit should not be extrapolated to tumor recurrence or survival. Overall, current evidence supports an observational association and biological plausibility, whereas independent causality and an oncologic benefit of periodontal treatment remain unproven.
SN - 2589-0042
ER -