Evidence map›Paper›PMID 36159185›Full record

ReviewThe Japanese dental science review2022

Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.

Saif S Saliem, Salwan Y Bede, Paul R Cooper, Ali A Abdulkareem, Michael R Milward, Bashar H Abdullah

Abstract readReview
In one paragraph

Review in The Japanese dental science review, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Article
  2. Article
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  5. Review
  6. Article
  7. Article
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  9. Review
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  11. Article
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  13. Review
  14. Annexin A2 Contributes to Release of Extracellular Vimentin in Response to Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Pharmaceutical biology · 2024
    Article
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

6 authors.

Saif S SaliemCollege of Dentistry, University of Baghdad, P.O. Box 1417, Bab Al Mudam, Baghdad, Iraq.
Salwan Y BedeCollege of Dentistry, University of Baghdad, P.O. Box 1417, Bab Al Mudam, Baghdad, Iraq.
Paul R CooperFaculty of Dentistry, Sir John Walsh Research Institute, University of Otago, P.O. Box 56, Dunedin 9054, New Zealand.
Ali A AbdulkareemCollege of Dentistry, University of Baghdad, P.O. Box 1417, Bab Al Mudam, Baghdad, Iraq.
Michael R MilwardŌSchool of Dentistry, University of Birmingham, 5 Mill Pool Way, B5 7EG Birmingham, UK.
Bashar H AbdullahCollege of Dentistry, University of Baghdad, P.O. Box 1417, Bab Al Mudam, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial mesenchymal transition (EMT) is a process comprising cellular and molecular events which result in cells shifting from an epithelial to a mesenchymal phenotype. Periodontitis is a destructive chronic disease of the periodontium initiated in response to a dysbiotic microbiome, and dominated by Gram-negative bacteria in the subgingival niches accompanied by an aberrant immune response in susceptible subjects. Both EMT and periodontitis share common risk factors and drivers, including Gram-negative bacteria, excess inflammatory cytokine production, smoking, oxidative stress and diabetes mellitus. In addition, periodontitis is characterized by down-regulation of key epithelial markers such as E-cadherin together with up-regulation of transcriptional factors and mesenchymal proteins, including Snail1, vimentin and N-cadherin, which also occur in the EMT program. Clinically, these phenotypic changes may be reflected by increases in microulceration of the pocket epithelial lining, granulation tissue formation, and fibrosis. Both in vitro and in vivo data now support the potential involvement of EMT as a pathogenic mechanism in periodontal diseases which may facilitate bacterial invasion into the underlying gingival tissues and propagation of inflammation. This review surveys the available literature and provides evidence linking EMT to periodontitis pathogenesis.

Indexed as

Cell adhesionEpithelial mesenchymal transitionGrowth factorPeriodontal pathogenPeriodontitisTranscription factor

Identifiers

PMID36159185
PMCPMC9489739

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.