Evidence map›Paper›PMID 23565326›Full record

ArticleJournal of oral microbiology2013

Porphyromonas gingivalis: keeping the pathos out of the biont.

Carla Cugini, Vanja Klepac-Ceraj, Elze Rackaityte, James E Riggs, Mary E Davey

Abstract read
In one paragraph

Article in Journal of oral microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. The relationship betweenEpidemiology and infection · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. More Than Just a Periodontal Pathogen -the Research Progress onFrontiers in cellular and infection microbiology · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Frequencies ofPathology oncology research : POR · 2021
    Article
  20. Microorganisms · 2020
    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

5 authors.

Carla CuginiDepartment of Microbiology, The Forsyth Institute, Cambridge, MA, USA ; Department of Oral Medicine Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA.
Vanja Klepac-Ceraj
Elze Rackaityte
James E Riggs
Mary E Davey

Funding

Regulatory Mechanisms Controlling Expression of P. gingivalis Surface StructuresR01DE019117 · NIDCR · UNIVERSITY OF FLORIDA · PI DAVEY, MARY ELLEN · 2009 to 2019
$4.5M
Macrophage Density Regulates T CellsR15CA136901 · NCI · RIDER UNIVERSITY · PI RIGGS, JAMES EDWARD · 2009 to 2009
$199k
Inhibition of P. gingivalis Biofilm Formation by a Streptococcal Effector ProteinF32DE022484 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI CUGINI, CARLA · 2012 to 2013
$104k
NCI NIH HHS R15 CA136901NIDCR NIH HHS F32 DE022484NIDCR NIH HHS R01 DE019117
6 · The paper itself

Abstract

The primary goal of the human microbiome initiative has been to increase our understanding of the structure and function of our indigenous microbiota and their effects on human health and predisposition to disease. Because of its clinical importance and accessibility for in vivo study, the oral biofilm is one of the best-understood microbial communities associated with the human body. Studies have shown that there is a succession of select microbial interactions that directs the maturation of a defined community structure, generating the formation of dental plaque. Although the initiating factors that lead to disease development are not clearly defined, in many individuals there is a fundamental shift from a health-associated biofilm community to one that is pathogenic in nature and a central player in the pathogenic potential of this community is the presence of Porphyromonas gingivalis. This anaerobic bacterium is a natural member of the oral microbiome, yet it can become highly destructive (termed pathobiont) and proliferate to high cell numbers in periodontal lesions, which is attributed to its arsenal of specialized virulence factors. Hence, this organism is regarded as a primary etiologic agent of periodontal disease progression. In this review, we summarize some of the latest information regarding what is known about its role in periodontitis, including pathogenic potential as well as ecological and nutritional parameters that may shift this commensal to a virulent state. We also discuss parallels between the development of pathogenic biofilms and the human cellular communities that lead to cancer, specifically we frame our viewpoint in the context of 'wounds that fail to heal'.

Indexed as

biofilmimmunoediting hypothesispathobiontP. gingivalistumor

Identifiers

PMID23565326
PMCPMC3617648

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.