IL18 Polymorphism and Periodontitis Susceptibility, Regardless of IL12B, MMP9, and Smoking Habits.

Patrícia Yumeko Tsuneto,Joana Maira Valentini Zacarias,Ana Maria Sell,Victor Hugo De Souza,Josiane Bazzo De Alencar,Cléverson O Silva,Jeane Eliete Laguila Visentainer

doi:10.1155/2019/9585964

Patrícia Yumeko Tsuneto, Joana Maira Valentini Zacarias + Show 5 more

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https://doi.org/10.1155/2019/9585964

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Journal: Mediators of Inflammation	Publication Date: Apr 1, 2019
Citations: 11	License type: CC BY 4.0

Affiliation: Universidade Estadual de Maringá

Abstract

Genetic variations contribute to the susceptibility in the development of periodontitis. The aim of this study was to investigate the influence of IL18, IL12, and MMP9 polymorphisms in the chronic periodontitis. This case-control study involved 381 individuals matched by gender and age. Genotyping of IL18 (rs187238 and rs1946518) and IL12B (rs3212227) was performed by PCR-SSP and PCR-RFLP was used for MMP9 (rs3918242). IL-18 and MMP-9 were quantified in the serum by ELISA. SNPStats and OpenEpi software were used for statistical analysis and, in order to eliminate smoking as a confounding factor, the analyses were also performed in nonsmoking subjects. The IL18-137G/C genotype was associated with the risk of chronic periodontitis in nonsmokers (Pc = 0.03; OR = 1.99; overdominant inherence model). In the multivariate analyses, homozygous IL18-137G/G and IL18-607C/C were more frequent in males compared to women with these same genotypes (OR = 2.51 and OR = 3.30, respectively). The serum levels of the IL-18 in patients were higher than those in healthy controls (P = 0.005). IL12B and MMP9 polymorphisms and MMP-9 serum concentration were similar in patients and controls. In this study, IL18 was associated with chronic periodontitis susceptibility. Men had greater risk than women for developing the disease when IL18 polymorphism was considered and the susceptibility was independent of the smoking status.

Highlights

Chronic periodontitis (CP) is a complex and common oral disease of microbial origin, characterized by inflammatory responses that affect the supporting tissue of the tooth, resulting in the formation of a periodontal pocket and alveolar bone resorption [1, 2]
Despite the presence of bacteria, immune response is involved in the pathogenesis of CP and genetic polymorphisms in the mediators of immunity have been associated with the susceptibility and severity of periodontitis [4,5,6]
The participants were divided into two different groups: (i) the chronic periodontitis group (CP) was composed by individuals who had at least 5 sites in different teeth with probing depth (PD) ≥ 5 mm, clinical attachment level (CAL) ≥ 3 mm, and more than 25% of bleeding on probing (BOP); and (ii) the control group was formed by individuals who displayed a PD of less than 4 mm and exhibited less than 25% of BOP

Summary

Introduction

Chronic periodontitis (CP) is a complex and common oral disease of microbial origin, characterized by inflammatory responses that affect the supporting tissue of the tooth, resulting in the formation of a periodontal pocket and alveolar bone resorption [1, 2]. Interleukins (ILs) and matrix metalloproteinases (MMPs) are related to the development of inflammatory response, remodeling of periodontal tissue and bone resorption [7]. Studies have indicated that IL-18 induces the release of matrix metalloproteinase 9 (MMP-9) and IL-1β, both with proinflammatory activity, resulting in tissue degradation [9]. The IL-18, belonging to the IL-1 cytokine superfamily, is involved in a wide variety of inflammatory diseases [10,11,12]. It is mainly produced by Mediators of Inflammation monocytes, active macrophages, and dendritic cells in response to antigenic stimuli such as lipopolysaccharide of Gram-negative bacteria [13]

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