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Inflammasome-Related Transcriptomic Profiles in Periodontitis and Peri-Implantitis Reveal a Shared Inflammatory
Miguel Padial-Molina1,2, David Herrera-Garcia1, Pablo Galindo-Fernandez3,4
1Department of Oral Surgery and Implant Dentistry, School of Dentistry, University of Granada, Granada, Spain.
Objectives:
To compare clinical, histological, immunohistochemical, and targeted gene-expression features related to inflammasome signaling across healthy tissues, periodontitis, and peri-implantitis.
Materials And Methods:
This exploratory cross-sectional study included supracrestal soft-tissue biopsies from 6 healthy controls, 17 periodontitis, and 18 peri-implantitis lesions. Evaluations included clinical data, histomorphometric collagen quantification, immunohistochemical staining (CD45, NLRP3, AIM2, CASP1, IL-1β), and targeted digital transcriptomic profiling of 20 preselected inflammasome-related genes using the NanoString nCounter platform. Data were analyzed using non-parametric statistics and FDR-corrected correlation matrices.
Results:
Periodontitis and peri-implantitis showed greater clinical inflammation, reduced collagen content, and increased inflammatory infiltrate compared with healthy tissues. Peri-implantitis displayed the more severe clinical phenotype and greater tissue disruption. At the molecular level, disease-associated changes were captured by AIM2, CASP1, IL1B, GBP5, TXNIP, CGAS, STING1, and PANX1 rather than NLRP3 alone. Except for a minor pairwise difference in CGAS (p = 0.031), individual gene expression did not differ between the diseased states. Stratified correlation analyses demonstrated coordinated within-group co-expression networks among priming, sensor, and effector transcripts, reflecting descriptive pathway patterns within each clinical cohort.
Conclusions:
Periodontitis and peri-implantitis share a substantial inflammasome-related host-response framework. Rather than revealing a distinct inflammasome program, peri-implantitis exhibits a largely overlapping molecular profile that occurs within a clinically more severe and structurally more disrupted lesion environment. These findings suggest that the biological distinction between the two diseases may lie less in pathway identity than in the tissue context in which a shared inflammatory machinery is expressed.
