Evidence map›Paper›PMID 14977979›Full record

ArticleInfection and immunity2004

Porphyromonas gingivalis induces receptor activator of NF-kappaB ligand expression in osteoblasts through the activator protein 1 pathway.

Nobuo Okahashi, Hiroaki Inaba, Ichiro Nakagawa, Taihei Yamamura, Masae Kuboniwa, Koji Nakayama, Shigeyuki Hamada, Atsuo Amano

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Pathogenicity ofFrontiers in cellular and infection microbiology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Molecular mechanisms ofThe Japanese dental science review · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

8 authors at 2 institutions in 1 country.

Nobuo OkahashiDepartment of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Osaka-Suita 565-0871, Japan. okahashi@dent.osaka-u.ac.jp
Hiroaki Inaba
Ichiro Nakagawa
Taihei Yamamura
Masae Kuboniwa
Koji Nakayama
Shigeyuki Hamada
Atsuo Amano
Nagasaki University · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Porphyromonas gingivalis, an important periodontal pathogen, is closely associated with inflammatory alveolar bone resorption, and several components of the organism such as lipopolysaccharides have been reported to stimulate production of cytokines that promote inflammatory bone destruction. We investigated the effect of infection with viable P. gingivalis on cytokine production by osteoblasts. Reverse transcription-PCR and real-time PCR analyses revealed that infection with P. gingivalis induced receptor activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL) mRNA expression in mouse primary osteoblasts. Production of interleukin-6 was also stimulated; however, osteoprotegerin was not. SB20350 (an inhibitor of p38 mitogen-activated protein kinase), PD98059 (an inhibitor of classic mitogen-activated protein kinase kinase, MEK1/2), wortmannin (an inhibitor of phosphatidylinositol 3 kinase), and carbobenzoxyl-leucinyl-leucinyl-leucinal (an inhibitor of NF-kappaB) did not prevent the RANKL expression induced by P. gingivalis. Degradation of inhibitor of NF-kappaB-alpha was not detectable; however, curcumin, an inhibitor of activator protein 1 (AP-1), prevented the RANKL production induced by P. gingivalis infection. Western blot analysis revealed that phosphorylation of c-Jun, a component of AP-1, occurred in the infected cells, and an analysis of c-Fos binding to an oligonucleotide containing an AP-1 consensus site also demonstrated AP-1 activation in infected osteoblasts. Infection with P. gingivalis KDP136, an isogenic deficient mutant of arginine- and lysine-specific cysteine proteinases, did not stimulate RANKL production. These results suggest that P. gingivalis infection induces RANKL expression in osteoblasts through AP-1 signaling pathways and cysteine proteases of the organism are involved in RANKL production.

Indexed as

Adhesins, BacterialAnimalsBacteroidaceae InfectionsBase SequenceCarrier ProteinsCells, CulturedCysteine EndopeptidasesCytokinesDNA, ComplementaryFemaleGene ExpressionGingipain Cysteine EndopeptidasesHemagglutininsHumansJNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsAdhesins, BacterialCarrier ProteinsCysteine EndopeptidasesCytokinesDNA, ComplementaryGingipain Cysteine EndopeptidasesHemagglutininsJNK Mitogen-Activated Protein KinasesMembrane GlycoproteinsMitogen-Activated Protein KinasesRANK LigandReceptor Activator of Nuclear Factor-kappa BRNA, MessengerTNFRSF11A protein, humanTnfrsf11a protein, mouseTNFSF11 protein, humanTnfsf11 protein, mouseTranscription Factor AP-1

Identifiers

PMID14977979
PMCPMC356028
OpenAlexW2140364019

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.