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The Role of IL-17 in Periodontitis and Its Systemic Connections
Tobias Bonsmann1, Martyna Mochol1, Ewa Bonsmann1
1Department of Periodontology, Pomeranian Medical University in Szczecin, Powstańców Wlkp 72, 70-111 Szczecin, Poland.
International Journal of Molecular Sciences
|November 27, 2025
Summary
Interleukin 17 (IL-17) is key in periodontitis (PD) and linked to systemic diseases. While IL-17 gene variants show weak PD links, IL-17 levels may serve as biomarkers, and therapies targeting it require careful consideration.
Area of Science:
- Immunology
- Periodontology
- Genetics
Background:
- Interleukin 17 (IL-17) plays a critical role in the interplay between periodontal dysbiosis and host immune responses.
- This review examines the current understanding of IL-17 in periodontitis (PD), its systemic implications, and the influence of IL-17 gene variants.
Purpose of the Study:
- To synthesize evidence on IL-17's role in periodontitis pathogenesis and its association with systemic conditions.
- To evaluate the clinical utility of IL-17 as a biomarker and discuss therapeutic implications of targeting IL-17 in PD.
Main Methods:
- Review of clinical and experimental studies investigating IL-17 in periodontitis.
- Analysis of literature linking IL-17 signaling pathways with systemic inflammatory diseases.
- Examination of genetic association studies concerning IL-17A and IL-17F polymorphisms in PD.
Main Results:
- Elevated IL-17 levels correlate with periodontitis severity, promoting inflammation, neutrophil recruitment, and bone resorption.
- Periodontopathogens like P. gingivalis and A. actinomycetemcomitans activate Th17 responses.
- Converging evidence suggests shared inflammatory pathways involving IL-17 in periodontitis, rheumatoid arthritis, diabetes, and psoriasis.
- IL-17 gene polymorphisms show heterogeneous and modest associations with PD risk.
- IL-17 in crevicular fluid, saliva, or serum shows potential as a monitoring biomarker for PD.
Conclusions:
- IL-17 is a significant mediator in periodontitis, contributing to local tissue destruction and systemic inflammation.
- IL-17-centered signaling highlights a shared inflammatory network across barrier tissues and systemic sites.
- Further research with standardized methodologies and multiomics is needed to clarify IL-17's causal versus compensatory roles in PD.
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