Title: Periodontitis and pulmonary fibrosis: A systematic review of the oral lung axis mediated by porphyromonas gingivalis
Abstract:
Background: Idiopathic pulmonary fibrosis (IPF) is a lethal interstitial lung disease. It is defined by progressive alveolar destruction and a median survival of only 2-3 years. While the triggers remain difficult to find, periodontitis (PD)- a chronic inflammatory disease driven by oral dysbiosis. This has emerged as an independent risk factor. This review evaluates the role of the pathogen Porphyromonas gingivalis (Pg) in the oral-lung axis and its contribution to pulmonary fibrosis. This review assesses the role of the pathogen Porphyromonas gingivalis (Pg) in the oral-lung axis and its contribution to pulmonary.
Methods: Following PRISMA guidelines, a systematic search was conducted in PubMed and Web of Science for primary research (2010-2016) examining the PD-PF link. We synthesized evidence from murine models, human cohort data, and in vitro airway epithelial studies.
Results: Evidence suggests that PD aggravates PF by promoting the ectopic colonization of Pg in lung tissue. As confirmed by 16S rRNA sequencing FISH. This translocation triggers a massive infiltration of neutrophils and Th17 cells. Mechanistically, Pg-derived products (gingipains) activate Protease-Activated Receptor 2 (PAR-2) on airway epithelial cells, including CCL20-CCR6-mediated immune remodeling. Neutrophil extracellular traps (NETs) further drive myofibroblast differentiation via TLR9/RAGE signaling. Stress-induced ³2-Adrenergic signaling acts as a tunable node, where canonical pathways (activated by terbutaline) amplify Th17 responses. While biased signaling (nebivolol) suppresses them and reverses T-cell exhaustion.
Conclusion: Pg is a systemic driver of PF through a synergistic Th-17- neutrophil- NET inflammatory loop. Targeting the oral-lung axis and adrenergic signaling bias presents a novel therapeutic strategy for fibrotic lung disease.
