Evidence map›Paper›PMID 25476976›Full record

ArticleJournal of endodontics2015

Analysis of multiple cytokine polymorphisms in individuals with untreated deep carious lesions reveals IL1B (rs1143643) as a susceptibility factor for periapical lesion development.

Alisa Dill, Ariadne Letra, Letícia Chaves de Souza, Mamatha Yadlapati, Claudia Cristina Biguetti, Gustavo Pompermaier Garlet, Alexandre R Vieira, Renato Menezes Silva

Open access · greenAbstract read
In one paragraph

Article in Journal of endodontics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 41 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Alisa DillDepartment of Endodontics, School of Dentistry, University of Texas Health Science Center at Houston, Houston, Texas.
Ariadne LetraDepartment of Endodontics, School of Dentistry, University of Texas Health Science Center at Houston, Houston, Texas.
Letícia Chaves de SouzaDepartment of Endodontics, School of Dentistry, University of Texas Health Science Center at Houston, Houston, Texas.
Mamatha YadlapatiDepartment of Endodontics, School of Dentistry, University of Texas Health Science Center at Houston, Houston, Texas.
Claudia Cristina BiguettiOsteoimmunology Lab, Department of Biological Sciences, School of Dentistry of Bauru, University of Sao Paulo, Brazil.
Gustavo Pompermaier GarletOsteoimmunology Lab, Department of Biological Sciences, School of Dentistry of Bauru, University of Sao Paulo, Brazil.
Alexandre R VieiraDepartment of Oral Biology, University of Pittsburgh, Pittsburgh, Pennsylvania.
Renato Menezes SilvaDepartment of Endodontics, School of Dentistry, University of Texas Health Science Center at Houston, Houston, Texas. Electronic address: Renato.M.Silva@uth.tmc.edu.
The University of Texas Health Science Center at Houston · USUniversidade de São Paulo · BRUniversity of Pittsburgh · US

Funding

Genetics of CariesR01DE018914 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VIEIRA, ALEXANDRE REZENDE · 2009 to 2013
$2.2M
NIDCR NIH HHS R01 DE018914NIDCR NIH HHS R01-DE18914
6 · The paper itself

Abstract

introductionIt has been proposed that individual genetic predisposition may contribute to persistent apical periodontitis. Cytokines are associated with levels of inflammation and are involved in caries, pulpal, and periapical tissue destruction. We hypothesized that polymorphisms in cytokine genes may contribute to an individual's increased susceptibility to apical tissue destruction in response to deep carious lesions.

methodsSubjects with deep carious lesions with or without periapical lesions (≥3 mm) were recruited at the University of Pittsburgh, Pittsburgh, PA, and the University of Texas at Houston, Houston, TX. Genomic DNA samples of 316 patients were sorted into 2 groups: 136 cases with deep carious lesions and periapical lesions (cases) and 180 cases with deep carious lesions but no periapical lesions (controls). Nine single-nucleotide polymorphisms in IL1B, IL6, TNF, RANK, RANKL, and OPG genes were selected for genotyping. Genotypes were generated by end point analysis using TaqMan chemistry (Invitrogen, Carlsbad, CA) in a real-time polymerase chain reaction instrument. Allele and genotype frequencies were compared among cases and controls using the PLINK program (http://pngu.mgh.harvard.edu/purcell/plink/). Ninety-three human periapical granulomas and 24 healthy periodontal ligament tissues collected postoperatively were used for messenger RNA expression analyses of IL1B.

resultsA single-nucleotide polymorphism in IL1B (rs1143643) showed allelic (P = .02) and genotypic (P = .004) association with cases of deep caries and periapical lesions. We also observed altered transmission of IL1B marker haplotypes (P = .02) in these individuals. IL1B was highly expressed in granulomas (P < .001).

conclusionsVariations in IL1B may be associated with periapical lesion formation in individuals with untreated deep carious lesions. Future studies could help predict host susceptibility to developing periapical lesions.

Indexed as

Genetic Association StudiesAdultAgedAllelesDental CariesFemaleGenetic Predisposition to DiseaseGenotypeHumansInterleukin-1betaMaleMiddle AgedPeriapical AbscessPeriapical PeriodontitisPolymorphism, Single NucleotideTooth ApexIL1B protein, humanInterleukin-1betaApical periodontitiscytokinesgenetic polymorphisms

Identifiers

PMID25476976
PMCPMC5682944
OpenAlexW2072691881

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.