Evidence map›Paper›PMID 23305098›Full record

ArticleBMC microbiology2013

Integrin α5β1-fimbriae binding and actin rearrangement are essential for Porphyromonas gingivalis invasion of osteoblasts and subsequent activation of the JNK pathway.

Wenjian Zhang, Jun Ju, Todd Rigney, Gena Tribble

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Direct cellular contact byScience advances · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Opportunistic pathogeniScience · 2024
    Article
  6. Review
  7. The Japanese dental science review · 2021
    Review
  8. Review
  9. Article
  10. Frontiers in cellular and infection microbiology · 2021
    Article
  11. The Roles of Integrin α5β1 in Human Cancer.OncoTargets and therapy · 2020
    Review
  12. Article
  13. Article
  14. ProbioticFrontiers in microbiology · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Novel inflammatory pathways in periodontitis.Advances in dental research · 2014
    Review
  20. Apoptosis-associated uncoupling of bone formation and resorption in osteomyelitis.Frontiers in cellular and infection microbiology · 2013
    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 2 institutions in 1 country.

Wenjian ZhangDepartment of Diagnostic and Biomedical Sciences, University of Texas School of Dentistry at Houston, 7500 Cambridge Street, Suite 5366, Houston, TX 77054, USA. Wenjian.Zhang@uth.tmc.edu
Jun Ju
Todd Rigney
Gena Tribble
The University of Texas at Austin · USThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic periodontitis is an infectious disease of the periodontium, which includes the gingival epithelium, periodontal ligament and alveolar bone. The signature clinical feature of periodontitis is resorption of alveolar bone and subsequent tooth loss. The Gram-negative oral anaerobe, Porphyromonas gingivalis, is strongly associated with periodontitis, and it has been shown previously that P. gingivalis is capable of invading osteoblasts in a dose- and time-dependent manner resulting in inhibition of osteoblast differentiation and mineralization in vitro. It is not yet clear which receptors and cytoskeletal components mediate the invasive process, nor how the signaling pathways and viability of osteoblasts are affected by bacterial internalization. This study aimed to investigate these issues using an in vitro model system involving the inoculation of P. gingivalis ATCC 33277 into primary osteoblast cultures.

resultsIt was found that binding between P. gingivalis fimbriae and integrin α5β1 on osteoblasts, and subsequent peripheral condensation of actin, are essential for entry of P. gingivalis into osteoblasts. The JNK pathway was activated in invaded osteoblasts, and apoptosis was induced by repeated infections.

conclusionsThese observations indicate that P. gingivalis manipulates osteoblast function to promote its initial intracellular persistence by prolonging the host cell life span prior to its intercellular dissemination via host cell lysis. The identification of molecules critical to the interaction between P. gingivalis and osteoblasts will facilitate the development of new therapeutic strategies for the prevention of periodontal bone loss.

Indexed as

EndocytosisHost-Pathogen InteractionsMAP Kinase Signaling SystemActinsAnimalsApoptosisCells, CulturedFimbriae, BacterialIntegrin alpha5beta1MiceOsteoblastsPorphyromonas gingivalisProtein BindingActinsIntegrin alpha5beta1

Identifiers

PMID23305098
PMCPMC3566952
OpenAlexW1986779093

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.