# The Influence of Genetic Polymorphisms of IL33 and IL1RL1 Genes on the Immunopathogenesis of Periodontitis

## TL;DR

This study explores how genetic variations in IL33 and IL1RL1 genes affect the risk and progression of periodontitis, a tooth-supporting tissue disease.

## Contribution

The study identifies specific gene polymorphisms (rs7025417 in IL33 and rs3821204 in IL1RL1) as risk or protective factors for periodontitis.

## Key findings

- The IL33 rs7025417 C/C genotype increases periodontitis risk in nonsmokers.
- The IL1RL1 rs3821204 G/G genotype is protective against periodontitis.
- IL-33 serum levels are elevated in periodontitis patients compared to controls.

## Abstract

Periodontitis (PD) is an inflammatory disease that affects the protective and supporting tissues of teeth. Mutations in cytokines and their receptors may influence the immunopathogenesis of PD, but the role of interleukin-33 (IL-33) and IL1RL1 is not clear. Thus, this study aimed to analyze the polymorphisms in IL33 (rs1929992 and rs7025417) and IL1RL1 (rs11685424 and rs3821204) genes and the IL-33 serum levels in PD patients. A case–control study was performed with 186 PD patients and 189 controls. Genotyping was performed by polymerase chain reaction using sequence-specific primer (PCR-SSP) technique. Serum levels of IL-33 were determined using the immunoenzymatic method. Statistical analyses were performed using SNPStats and OpenEpi. p > 0.05 was considered statistically significant. The IL33 rs7025417 C/C genotype was a risk factor for PD in nonsmokers (p=0.0015) regardless of smoking status and gender. In the general population, the IL1RL1 rs3821204 G/G genotype was protective for PD (p=0.006), regardless of gender. Nevertheless, the IL-33 serum levels were increased in patients compared to controls (p < 0.0001); however, no difference was observed among PD patients. The polymorphisms IL33 rs7025417 and IL1RL1 rs3821204 were associated with risk and protection, respectively, and the production of IL-33 was higher in PD patients than in controls, independent of the extent or severity of the disease.