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DOI: 10.1055/s-0045-1806931
Salivary Biomarkers of Inflammasome Activation in Unstable Periodontitis: A Case–Control Study

Abstract
Objectives
The objective of this study was to investigate the complex network of inflammasome-related biomarkers (NOD-like receptor thermal protein domain associated protein 3 [NLRP3], caspase-1, interleukin [IL]-1β, IL-18, and IL-37) in unstable periodontitis by examining the salivary concentrations of these specific biomarkers and correlating them with periodontal parameters.
Materials and Methods
The design of this study was an observational case–control study. A salivary sample was collected from periodontally healthy patients (n = 40) and unstable periodontitis patients (n = 40). Full-mouth clinical periodontal parameters were recorded (plaque index, bleeding on probing, periodontal pocket depth, and clinical attachment loss). Enzyme-linked immunosorbent assay analyzed NLRP3, caspase-1, IL-1β, IL-18, and IL-37 salivary levels.
Statistical Analysis
The normality of the data was tested using the Shapiro–Wilk test. Mean, standard deviation, and percentages were used for data description. An independent sample t-test, Mann–Whitney U test, and chi-square test were used to compare the two groups with a p-value of < 0.05. Spearman's correlation analysis was conducted to examine the relationships between variables.
Results
In saliva samples, NLRP3, caspase-1, IL-1β, and IL-18 were the highest in the periodontitis group (p < 0.005), while IL-37 was highest in the healthy group (p < 0.005). There was significant (p < 0.012) negative weak correlation (−0.395) between IL-37 and IL-1β, and significant (p < 0.003) negative moderate correlation (−0.455) between IL-37 and IL-18 in the healthy group. A significant (0.031) positive weak correlation (0.342) was found between the salivary IL-37 and NLRP3, and a significant (p < 0.001) negative moderate correlation (−0.508) was found between salivary IL-37 and IL-1β, in the periodontitis group.
Conclusion
The NLRP3 inflammasomes and their cytokines (caspase-1, IL-1β, and IL-18) significantly promote periodontal inflammation and tissue destruction. In contrast, IL-37 acts as an anti-inflammatory cytokine, inhibiting the activity of the NLRP3 inflammasome and reducing excessive inflammation. This interplay highlights the potential of targeting NLRP3 and enhancing IL-37 as a therapeutic approach for the treatment of periodontal disease.
Publikationsverlauf
Artikel online veröffentlicht:
23. April 2025
© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
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