Association between Interleukin-1 Polymorphisms and Susceptibility to Dental Peri-Implant Disease: A Meta-Analysis

Background and objective: Interleukins (ILs), as important biochemical mediators, control the host response to inflammation and are associated with bone resorption. In the present meta-analysis, we investigated the association between IL−1 polymorphisms and susceptibility to dental peri-implant disease (PID). Materials and methods: We searched Web of Science, Cochrane Library, Scopus, and PubMed/Medline databases for studies published until 9 September2021, without any restrictions. We calculated the crude OR and 95% confidence intervals (CI) to estimate the associations between IL−1 polymorphisms and PID risk in the five genetic models. We further performed the subgroup analysis, sensitivity analysis, meta-regression, trial sequential analysis, and calculated the publication bias. Results: Out of 212 retrieved records, sixteen articles were used in the meta-analysis. There was no association between IL−1A (–889), IL−1B (−511), IL−1B (+3953), and IL−1RN (VNTR) polymorphisms and the risk of dental PIDs, but there was an increased risk of IL−1B (+3954) in the patients with PIDs. In addition, an association of the composite genotype of IL−1A (−889)/IL−1B (+3953) was observed with the risk of PIDs, but not for the composite genotype of IL−1A (−889)/IL−1B (+3954). The publication year, the ethnicity, sample size, and the outcome were significantly influenced pooled estimates of some genetic models. Trial sequential analysis showed the lack of sufficient sample sizes in the studies. Conclusions: Among IL−1 polymorphisms evaluated in the meta-analysis, the composite genotype of IL−1A (−889)/IL−1B (+3953) and IL−1B (+3954) were the only polymorphisms associated with the risk of PID. The T allele and CT genotype of IL−1B (+3954) polymorphism were also associated with an elevated risk of PID.

The Association between a MAOB Variable Number Tandem Repeat Polymorphism and Cocaine and Opiate Addictions in Polyconsumers

Genetic analysis of the association between alcohol, cocaine, and opiate addiction and variable number tandem repeat (VNTR) polymorphisms in monoamine oxidase B (MAOB) and serotonergic 5-hydroxytryptamine (serotonin) receptor 1B and 2C (HTR1B 21 and HTR2C) pathway genes was performed in a sample of 302 polyconsumers. Our genetic association analysis revealed a significant association between a 184 base pair (bp) VNTR polymorphism in the MAOB gene and addiction to cocaine and opiates. This work highlights new genetic marker associations in cocaine and opiate polyconsumer addictions. These data help to clarify and quantify the complex role of genetics in addictive disorders, as well as their future contribution to the prevention (genetic counselling), diagnosis (genetic diagnosis of vulnerability), and treatment (pharmacogenomics) of these disorders.

ROLE OF VNTR POLYMORPHIMS OF THE GENES ANTAGONIST OF RECEPTOR OF INTERLEIKINE 1 (IL1RN) AND INTERLEIKINE 4 (IL4) IN CARIES DEVELOPMENT IN CHILDREN

Association of VNTR polymorphisms of two cytokine genes – antagonist of receptor of interleikine 1 (IL1RN) rs2234663 and interleikine 4 (IL4) rs8179190 with dental caries was studied in three groups of chidren with DFC (decompensated form of caries) with average age 10.19±0.54, with SFC (subcompensated form of caries) (11.66±0.46) and with CFC (compensated form of caries) and healthy (12.08±0.38). The genotypes with two “long” alleles L/L by IL1RN were demonstrated mediating resistance to highly active form of caries, and genotypes: A1/A2 P2/P2 and A2/A2 P2/P2 - susceptibility.

Association Between 3'APOB-VNTR Polymorphism and Plasma Lipid Profiles in Type 2 Diabetes Patients

Objective: Apolipoprotein B (APOB) plays an important role in the metabolism of cholesterol and impairment in its function can lead to cholesterol accumulation in the pancreatic islets. It can then reduce insulin secretion and lead to Type 2 diabetes (T2DM). The purpose of this study was to investigate the association of 3chr('39')APOB-VNTR polymorphism with plasma lipid profiles in T2DM individuals in Khorasan Razavi province, Iran. Materials and Methods: In this case-control study, 204 patients with T2DM and 207 non-diabetic volunteers were examined as a control group. All samples were analyzed for plasma lipid profiles. Genotypes were determined by PCR and electrophoresis. Differences in lipid variables between genotypes were assessed using one-way analysis of variance (ANOVA) with SPSS 20.0. Results: We found 18 different alleles of the APOB gene 3chr('39')VNTR comprising from 26 to 45 hypervariable elements (HVEs) in the control groups and 21 alleles ranging from 30 to 51 repeats in the T2DM patients. Short alleles (26 to 29 HVEs) were only in controls and large alleles (46 to 51 HVEs) were only in T2DM patients. Our results showed that in people with long HVE polymorphism, HDL-C levels decreased, but LDL-C increased. Therefore, longer alleles for T2DM are considered risk factors. It was also observed that the TC / HDL-C ratio was significantly lower in shorter genotypes than the longer genotypes in T2DM patients. Conclusion: It is concluded that 3chr('39')APOB-VNTR polymorphisms, especially longer alleles, affect plasma lipid levels in individuals with T2DM and are risk factors for this disease.

Lack of association between ACE I/D, NOS3 VNTR polymorphisms and drug toxicity of tacrolimus treated post-renal transplantation patients

Introduction: Tacrolimus is the most commonly used calcineurin inhibitor for renal transplant individuals. Genetic factors play a major role in allografts by affecting blood pressure regulation, vascular proliferation and inflammatory responses. Objectives: The aim of this study was to evaluate a possible role of the ACE I/D and NOS3 VNTR polymorphisms in kidney transplantation patients treated with tacrolimus in the south Indian population. Patients and Methods: This study included 50 kidney transplant individuals and 100 unrelated healthy individuals from the general population as control. The genotyping was performed by polymerase chain reaction and electrophoresis. Genotypes were compared among cases and controls applying χ2 test. The difference in C/D ratios was compared using Mann–Whitney U test or Kruskal-Wallis test. Results: The ACE ID polymorphisms in different models [genetic (P=0.723), dominant (P=0.148) and recessive (P=0.652)] or allele model (P=0.455) did not differ significantly between the groups. Similarly, there was no significant difference for the NOS3 VNTR genotypes in genetic model (bb vs ba P=0.118; bb vs aa P=0.446), dominant model (bb vs ba+aa P=0.099) and allelic model (b vs a P=0.103). No significant difference was observed for ACE ID and NOS3 VNTR genotypes between the toxicity and non-toxicity groups. Furthermore, no significant association was observed for daily dose and concentration dose ratio for the studied polymorphisms. Conclusion: The present study revealed no significant association between cases and controls as well as toxicity and non-toxicity groups. Furthermore, there was no association between genotypes and daily dose and dose concentration.