Evidence map›Paper›PMID 26620730›Full record

ArticleClinical oral investigations2016

Regulation of p53 under hypoxic and inflammatory conditions in periodontium.

S Memmert, L Gölz, P Pütz, A Jäger, J Deschner, T Appel, G Baumgarten, B Rath-Deschner, S Frede, W Götz

Abstract read
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In one paragraph

Article in Clinical oral investigations, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  4. Observational
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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

10 authors at 1 institution in 1 country.

S MemmertDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany. svenja.memmert@ukb.uni-bonn.de.
L GölzDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany.
P PützDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany.
A JägerDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany.
J DeschnerSection of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Bonn, Germany.
T AppelClinic of Oral and Maxillofacial Surgery, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Bonn, Germany.
G BaumgartenClinic and Polyclinic of Anesthesiology and Intensive Care Medicine, Faculty of Medicine, University of Bonn, Bonn, Germany.
B Rath-DeschnerDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany.
S FredeClinic and Polyclinic of Anesthesiology and Intensive Care Medicine, Faculty of Medicine, University of Bonn, Bonn, Germany.
W GötzDepartment of Orthodontics, Center of Dento-Maxillo-Facial Medicine, Faculty of Medicine, University of Bonn, Welschnonnenstr 17, 53111, Bonn, Germany.
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDifferent studies suggest that inflammation as well as hypoxia leads to an increase of p53 protein levels. However, the implication of p53 during oral inflammatory processes is still unknown. The aim of this study was therefore to investigate the effect of hypoxia and inflammation on p53 regulation in human periodontium in vitro and in vivo. MATERIALS AND

methodsUnder hypoxic and normoxic conditions, human primary periodontal ligament (PDL) fibroblasts (n = 9) were stimulated with lipopolysaccharides (LPS) from Porphyromonas gingivalis (P.g.), a periodontal pathogenic bacterium. After different time points, cell viability was tested; p53 gene expression, protein synthesis, and activation were measured using quantitative RT-PCR, immunoblotting, and immunofluorescence. Moreover, healthy and inflamed periodontal tissues were obtained from 12 donors to analyze p53 protein in oral inflammatory diseases by immunohistochemistry.

resultsLPS-P.g. and hypoxia initially induced a significant upregulation of p53 mRNA expression and p53 protein levels. Nuclear translocation of p53 after inflammatory stimulation supported these findings. Hypoxia first enhanced p53 levels, but after 24 h of incubation, protein levels decreased, which was accompanied by an improvement of PDL cell viability. Immunohistochemistry revealed an elevation of p53 immunoreactivity in accordance to the progression of periodontal inflammation.

conclusionsOur data indicate that p53 plays a pivotal role in PDL cell homeostasis and seems to be upregulated in oral inflammatory diseases. CLINICAL RELEVANCE: Upregulation of p53 may promote the destruction of periodontal integrity. A possible relationship with carcinogenesis may be discussed.

Indexed as

Cell SurvivalFibroblastsFluorescent Antibody TechniqueHumansHypoxiaImmunoblottingImmunohistochemistryInflammationLipopolysaccharidesPeriodontal LigamentPorphyromonas gingivalisReal-Time Polymerase Chain ReactionTumor Suppressor Protein p53LipopolysaccharidesTumor Suppressor Protein p53HypoxiaInflammationp53PDLPeriodontal ligament cellsPeriodontium

Identifiers

PMID26620730
OpenAlexW2189611061

What OpenQuestion holds

Textmetadata
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Registered trials

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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.