scholarly journals A Systematic Review and Meta-Analysis on Multiple Cytokine Gene Polymorphisms in the Pathogenesis of Periodontitis

2022 ◽  
Vol 12 ◽  
Author(s):  
Xin Liu ◽  
Hui Li

AimPeriodontitis is an inflammatory disease that destroys both soft and hard periodontal tissues. However, a complex periodontal cytokine network remains unclear. This systematic review explored multiple cytokine gene polymorphisms in the pathogenesis of periodontitis.Material and MethodsA systematic search was performed using the databases from previous publications, which indicated the association between cytokine polymorphisms and periodontitis pathogenesis. Meta-analysis was conducted using fixed or randomized models to calculate the significance of multiple cytokine polymorphisms. A total of 147 articles were analyzed with polymorphisms in 12 interleukins [Th1 (IL-2, IFN-γ, and TNF-α), Th2 (IL-4 and IL-13), Th17 (IL-1α, IL-1β, IL-6, and IL-17), and Treg cytokines (IL-10 and TGF-β)]. Doi plot was used to probe the occurrence of publication bias.ResultsThe polymorphisms of IL-2 and TNF-α of Th1 cytokine family may be associated with the pathogenesis or the prevention of periodontitis risk, while the polymorphism of IFN-γ is not related to periodontitis risk. The polymorphisms for IL-4 and IL-13 of Th2 cytokine family are not found to be associated with the pathogenesis of periodontitis. For the polymorphisms of the members of Th17 cytokine family, different IL-1α polymorphisms may have inverse actions in the pathogenesis of periodontitis. IL-1β is a noteworthy cytokine biomarker in periodontitis development and progression. IL-6 may have a protective function in the inflammatory responses of periodontitis, and IL-17 has a weak relationship the inflammatory responses. The polymorphisms for the members of Treg cell cytokines may have a protective function against periodontitis risk. LFK indexes show the major asymmetry due to publication bias.ConclusionIL-1β is a notable cytokine biomarker in periodontitis risk. Treg cytokines favor an anti-inflammatory and protective environment. Further data are needed to confirm the present conclusion due to publication bias.

2012 ◽  
Vol 24 (12) ◽  
pp. 1102-e566 ◽  
Author(s):  
M. Bashashati ◽  
N. Rezaei ◽  
H. Bashashati ◽  
A. Shafieyoun ◽  
N. E. Daryani ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Sasitorn Yongcharoen ◽  
Sasivimol Rattanasiri ◽  
D. Olga McDaniel ◽  
Mark McEvoy ◽  
Chukiat Viwatwongkaseam ◽  
...  

We performed a systematic review and meta-analysis with the aim of assessing the association between cytokine gene polymorphisms and graft rejection in heart transplantation. We identified relevant studies from Medline and Embase using PubMed and Ovid search engines, respectively. Allele frequencies and allele and genotypic effects were pooled. Heterogeneity and publication bias were explored. Four to 5 studies were included in pooling of 3 gene polymorphisms. The prevalences of the minor alleles for TNFα-308, TGFβ1-c10, and TGFβ1-c25 were 0.166 (95% CI: 0.129, 0.203), 0.413 (95% CI: 0.363, 0.462), and 0.082 (95% CI: 0.054, 0.111) in the control groups, respectively. Carrying the A allele for the TNFα-308 had 18% (95% CI of OR: 0.46, 3.01) increased risk, but this was not significant for developing graft rejection than the G allele. Conversely, carrying the minor alleles for both TGFβ1-c10 and c25 had nonsignificantly lower odds of graft rejection than major alleles, with the pooled ORs of 0.87 (95% CI: 0.65, 1.18) and 0.70 (95% CI: 0.40, 1.23), respectively. There was no evidence of publication bias for all poolings. An updated meta-analysis is required when more studies are published to increase the power of detection for the association between these polymorphisms and allograft rejection.


2010 ◽  
Vol 19 (3) ◽  
pp. 762-776 ◽  
Author(s):  
Bárbara Peleteiro ◽  
Nuno Lunet ◽  
Carla Carrilho ◽  
Cecília Durães ◽  
José Carlos Machado ◽  
...  

2013 ◽  
Vol 28 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Sasivimol Rattanasiri ◽  
D. Olga McDaniel ◽  
Mark McEvoy ◽  
Thunyarat Anothaisintawee ◽  
Abhasnee Sobhonslidsuk ◽  
...  

2019 ◽  
Vol 21 (5) ◽  
pp. 552-563
Author(s):  
Sahereh Mirzaei ◽  
Larisa Burke ◽  
Anne G. Rosenfeld ◽  
Susan Dunn ◽  
Jennifer R. Dungan ◽  
...  

The purpose of this study was to determine whether relationships exist among protein cytokines, cytokine gene polymorphisms, and symptoms of potential acute coronary syndrome (ACS). Participants included 438 patients presenting to the emergency department (ED) whose symptoms triggered a cardiac evaluation (206 ruled in and 232 ruled out for ACS). Presence or absence of 13 symptoms was recorded upon arrival. Levels of tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-18 were measured for all patients. A pilot analysis of 85 patients (ACS = 49; non-ACS = 36) genotyped eight single-nucleotide polymorphisms (SNPs; four TNF and four IL6 SNPs). Logistic regression models were tested to determine whether cytokines or SNPs predicted symptoms. Increased levels of TNF-α and IL-6 were associated with a decreased likelihood of chest discomfort for all patients. Increased levels of IL-6 were associated with a lower likelihood of chest discomfort and chest pressure for ACS patients, and an increased likelihood of shoulder and upper back pain for non-ACS patients. Elevated IL-18 was associated with an increased likelihood of sweating in patients with ACS. Of the four TNF SNPs, three were associated with shortness of breath, lightheadedness, unusual fatigue, and arm pain. In all, protein cytokines and TNF polymorphisms were associated with 11 of 13 symptoms assessed. Future studies are needed to determine the predictive ability of cytokines and related SNPs for a diagnosis of ACS or to determine whether biomarkers can identify patients with specific symptom clusters.


2011 ◽  
Vol 39 (5) ◽  
pp. 5187-5194 ◽  
Author(s):  
Wen-jia Peng ◽  
Qian He ◽  
Jin-xia Yang ◽  
Bing-xiang Wang ◽  
Man-man Lu ◽  
...  

2004 ◽  
Vol 11 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Michiel C. Warlé ◽  
Herold J. Metselaar ◽  
Wim C.J. Hop ◽  
Hugo W. Tilanus

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