SynthesisDisease markers2018
Contribution of Interleukin-10-592 (-590, -597) C>A Polymorphisms to Periodontitis Susceptibility: An Updated Meta-Analysis Based on 18 Case-Control Studies.
Synthesis in Disease markers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Next-Generation Examination, Diagnosis, and Personalized Medicine in Periodontal Disease.Journal of personalized medicine · 2022Review
- Interleukin-6 and Interleukin-10 Gene Polymorphisms in Patients with Chronic Periodontitis and Response to Treatment after 3 Years.Acta stomatologica Croatica · 2020Article
- Interleukin Gene Variability and Periodontal Bacteria in Patients with Generalized Aggressive Form of Periodontitis.International journal of molecular sciences · 2020Article
- Immunomodulatory factors gene polymorphisms in chronic periodontitis: an overview.BMC oral health · 2019Review
- Evaluation of IL6, IL10 and VDR alleles distribution in an Italian large sample of subjects affected by chronic periodontal disease.International journal of immunopathology and pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe association between interleukin-10- (IL-10-) 592 (-590, -597) C>A polymorphisms and susceptibility to chronic or aggressive periodontitis (CP or AgP) is conflicting. This meta-analysis is aimed at quantitatively estimating the association. MATERIALS AND
methodsPubMed, Embase, Web of Science, and WANFAN were searched for studies performed prior to January 31, 2018, to collect data for our research. Meta-analysis was performed using RevMan 5.3 or STATA 14.0.
resultsIn total, 18 studies that met our criteria were included. Overall or HWE subgroup analysis of individuals with this polymorphism revealed that in terms of CP susceptibility, there was a significant difference between case groups and control groups in the A allele versus C allele model (OR = 1.38, 95% CI = 1.17-1.64 or OR = 1.38, 95% CI = 1.12-1.70), in the AA versus CC+CA model (OR = 1.49, 95% CI =1.06-2.10 or OR = 1.42, 95% CI = 1.13-1.78), and in the CC versus CA+AA model (OR = 0.69, 95% CI = 0.51-0.92 or OR = 0.68, 95% CI = 0.49-0.93); subgroup analysis based on a nonsmoking population also displayed significance in the A allele versus C allele model (OR = 1.43, 95% CI = 1.15-1.79) and CC versus CA+AA model (OR = 0.62, 95% CI = 0.44-0.87). For this polymorphisms and AgP susceptibility, our analyses revealed a significant association in both the A allele versus C allele model (OR = 1.29, 95% CI = 1.01-1.63) and the AA versus CC+CA model (OR = 1.93, 95% CI = 1.30-2.89); subgroup analysis based on Caucasian or nonsmoking populations showed significant differences in the AA versus CC+CA model (OR = 6.29, 95% CI = 1.78-22.21 or OR = 3.24, 95% CI = 1.59-6.61).
conclusionsIL-10-592 (-590, -597) A allele and the associated AA genotype may be risk factors for the onset of CP or AgP-particularly for the AA genotype and the increased risk of AgP in Caucasian or nonsmoking populations. Conversely, the CC genotype may act as a protective factor against the onset of CP.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.