Evidence map›Paper›PMID 34583558›Full record

ArticleJDR clinical and translational research2022

Transcriptome-wide Gene Expression Analysis in Peri-implantitis Reveals Candidate Cellular Pathways.

A Martin, P Zhou, B B Singh, G A Kotsakis

Open access · greenAbstract read
In one paragraph

Article in JDR clinical and translational research, 2022. 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
2.5field-weighted citation impact, top 11% 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, 20 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Peri-Implant Diseases: The Past, the Present, the Future.Journal of periodontal research · 2025
    Article
  8. Review
  9. Review
  10. Observational
  11. Review
  12. Correlation between Inflammasomes and Microbiota in Peri-Implantitis.International journal of molecular sciences · 2024
    Article
  13. Review
  14. Metabolic Conditions and Peri-Implantitis.Antibiotics (Basel, Switzerland) · 2022
    Review
  15. Review
  16. Review
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

4 authors at 1 institution in 1 country.

A MartinTranslational Periodontal Research Lab, Department of Periodontics, School of Dentistry, UT Health San Antonio, San Antonio, TX, USA.
P ZhouTranslational Periodontal Research Lab, Department of Periodontics, School of Dentistry, UT Health San Antonio, San Antonio, TX, USA.
B B SinghSingh Lab, Department of Periodontics, School of Dentistry, UT Health San Antonio, San Antonio, TX, USA.
G A KotsakisTranslational Periodontal Research Lab, Department of Periodontics, School of Dentistry, UT Health San Antonio, San Antonio, TX, USA.
The University of Texas Health Science Center at Houston · US

Funding

Epigenetic regulations in Sjogern's syndromeR01DE022765 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SINGH, BRIJ B · 2017 to 2021
$1.8M
Titanium particle-induced inflammasome activation in the peri-implant mucosal barrierR03DE029872 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KOTSAKIS, GEORGIOS · 2021 to 2022
$426k
NIDCR NIH HHS R01 DE022765NIDCR NIH HHS R03 DE029872
6 · The paper itself

Abstract

objectivePeri-implantitis is a condition resulting in destructive inflammation in the peri-implant soft tissue barrier. Clinically, it demonstrates vast clinical differences to periodontitis that suggest distinct inflammatory mechanisms. Implant-derived titanium particles (i-TiPs) frequently found around diseased implants appear to alter the microenvironment and confer resistance to antibiotic treatments. Studies in orthopedic implants have demonstrated potent inflammatory responses to i-TiPs involving a variety of cell types in aseptic conditions. Nonetheless, the genetic programs of cells surveilling and supporting the peri-implant soft tissue barrier in response to the combined challenges of biomaterial degradation products and oral bacteria are poorly defined. Thus, we studied gene expression specific to oral peri-implant inflammatory disease.

methodsPeri-implant tissues were collected from healthy or diseased implants (

resultsGenes involved in the endosomal-lysosomal pathway, such as actin polymerization, were strongly upregulated in diseased tissues (

conclusionWithin the limitations of this discovery study, expressive upregulation of genes in the endosomal-lysosomal and oxidative stress pathway suggests that inflammation related to receptor-driven responses to extracellular signals, such as i-TiPs and pathogens, may have a crucial role in peri-implantitis. Results warrant external replication in validation cohorts. KNOWLEDGE TRANSFER STATEMENT: Our findings regarding physiologic processes affected by peri-implantitis could advance knowledge of the mechanisms and consequences of the disease. Understanding the cellular programs that partake in peri-implant inflammation has the potential to translate to novel treatment strategies for patients with peri-implantitis.

Indexed as

Dental ImplantsPeri-ImplantitisActinsAnti-Bacterial AgentsBiocompatible MaterialsHumansInflammationRNATitaniumTranscriptomeActinsAnti-Bacterial AgentsBiocompatible MaterialsDental ImplantsRNATitaniumdental implantinflammationoxidative stressperi-implantitisphagocytosistitanium

Identifiers

PMID34583558
PMCPMC9490470
OpenAlexW3204060305

What OpenQuestion holds

Textmetadata
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.