Lack of Association between Interleukin-1βGene Polymorphism (rs16944) and Chronic Periodontitis: From a Case-Control Studies to an Updated Meta-Analysis

Abstract

Background Interleukin-1β (IL-1β) plays an important role as a mediator of various inflammatory responses in chronic periodontitis. Several studies have investigated the potential relationship between IL-1β polymorphism (rs16944) and susceptibility to chronic periodontitis; inflammatory process is involved, but conclusions is still controversial. Objective The aim of this study was to determine whether the IL-1β polymorphism (rs16944) is associated with susceptibility to chronic periodontitis. Material and Methods For the case-control study, 51 patients with chronic periodontitis and 33 healthy control patients were recruited in the study. Genotyping was conducted by direct sequencing. SNPStats and SPSS 18.0 were used for the analysis of genetic data and to evaluate odds ratios, 95% confidence intervals, and P values; logistic regression models were used. And to perform meta-analysis, studies about IL-1β polymorphism (rs16944) and chronic periodontitis were searched in PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases until July 2017. Results In our case-control study, no significant relationship was revealed between IL-1β polymorphism (rs16944) and chronic periodontitis (P > 0.05 in each model). When combined with the previous studies in the meta-analysis, the result was not associated with chronic periodontitis in any of the models (CC vs. CT + TT: OR = 0.97, 95% CI = 0.762–1.246; CC + CT vs. TT: OR = 0.90, 95% CI = 0.658–1.232; and C vs. T: OR = 0.93, 95% CI = 0.774–1.128). The subgroup analysis stratified by ethnicity showed a weak association between the IL-1β polymorphism (rs16944) and chronic periodontitis in the Caucasian population (recessive model, OR = 1.34, 95% CI = 1.017–1.758, P = 0.037). Conclusion Evidences from a case-control study and the meta-analysis suggest that IL-1β polymorphism (rs16944) is not associated with susceptibility to chronic periodontitis.

Adherence to long‐term supportive periodontal therapy in groups with different periodontal risk profiles

“…The effect of the interleukin‐1β‐polymorphism on periodontitis is still controversial. Recent literature states that there is a lack of evidence for an influence of the interleukin‐1β‐polymorphism on the periodontal status (Hong, Kang, Kim, Kim, & Ban, ), but a study conducted in our department showed a significant higher risk for tooth loss during SPT for interleukin‐1β‐polymorphism positive patients (Eickholz et al, ). However, PRA and interval setting were performed in almost all participants without determination of the interleukin‐1β‐polymorphism.…”

Association of polymorphisms in TNF‐α, IL‐1β, GSTM and GSTT genes with apical periodontitis: is there a link with herpesviral infection?

“…These results should however be interpreted with caution due to the high heterogeneity of the included studies. The present study analysed another SNP of the IL‐1β gene (−511 C >T, rs16944), previously investigated in periodontal disease (Nikolopoulos et al 2008, Hong et al 2018). Although the results of meta‐analyses (Nikolopoulos et al 2008, Hong et al 2018) were rather inconsistent, it was demonstrated clearly that this SNP decreases the risk of AP development in a Serbian population.…”

Genetic polymorphisms in the Interleukins IL1B, IL4, and IL6 are associated with concomitant periodontitis and type 2 diabetes mellitus in Brazilian patients

“…In the last decades, some polymorphisms mainly in genes related to the immune response and bone remodeling have been preferentially chosen in many candidate gene studies 12‐14 . Indeed, it is notable in the literature that those genes seemed to be like “classically periodontally investigated polymorphisms,” which can be evidenced by the development of many meta‐analyses 15‐18 in genes such as (a) (−819 C > T) in the IL‐10 gene, which encodes the important anti‐inflammatory cytokine 19 ; (b) (−889 G > A) in the IL1A gene, which encodes the IL1‐1A cytokine facilitating and amplifying the inflammatory response by induction of adhesion molecules to cellular infiltrate and monocyte stimulation with bone resorption 15 ; (c) (+ 3954 G > A) in the IL1B gene which plays an important role as a mediator of various inflammatory responses in periodontitis 20 ; (d) (−590 C > T) in the IL4 gene that encodes a cytokine involved in the process of inflammation 16 ; (e) (−308 G > A) in the Tumor Necrosis Factor Alpha ( TNFA) gene which encodes a pro‐inflammatory cytokine 21 ; (f) (−174 C > G) in the Interleukin‐6 ( IL‐6 ) gene which encodes an important multifunctional cytokine 22 . Bone remodeling results from the balance between osteoblast and osteoclast activity 23 .…”