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Interleukin (IL)-33 is a dual-function protein that may play important roles as both a cytokine and intracellular nuclear factor. It may also function similarly to prototypical alarmin IL-1α, as an endogenous danger signal to alert innate immune system cells to tissue damage during trauma or infection, as it can be released in the extracellular space after endothelial cell damage or mechanical injury. The aim of this study was to determine possible correlations between concentrations of IL-33 and IL-1α in gingival crevicular fluid (GCF) and plasma obtained from healthy patients, those with chronic periodontitis (CP), and those with generalized aggressive periodontitis (GAP) patients. Forty-five patients with an age range of 20-60 years were enrolled and divided into 3 groups: Group H, 30 samples (15 GCF and 15 plasma) from 15 patients with healthy periodontium; Group CP, 30 samples from 15 patients with CP; and Group GAP, 30 samples from 15 patients with GAP. The clinical periodontal parameters investigated in all groups comprised the gingival index score, probing pocket depth, and clinical attachment level. The GCF and plasma levels of IL-33 and IL-1α were quantitated using enzyme linked immunosorbent assay. The mean IL-33 concentrations in GCF and plasma were highest in Group GAP, followed by Group CP, with the lowest in Group H; the difference among them was statistically significant (p&lt;0.05). Concentration of IL-1α followed the same trend as that of IL-33 in GCF, but was lower than detection levels in plasma. The GCF and plasma concentrations of IL-33 correlated with IL-1α concentrations in GCF. Concentrations of IL-33 and IL-1α in GCF varied significantly between healthy patients and those with disease, allowing healthy patients to be distinguished from those with GAP or CP. The results of this study suggest that IL-33 offers a potential inflammatory marker of periodontal disease, similar to IL-1α.

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Correlations between Interleukin-33 and -1α Levels in Gingival Crevicular Fluid and Plasma in Patients with Chronic or Aggressive Periodontitis and Disease-free Subjects