Evidence map›Paper›PMID 28000855›Full record

ArticleMolecular medicine reports2017

Involvement of interleukin‑23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis.

Nan Ma, Di Yang, Hirohiko Okamura, Jumpei Teramachi, Tomokazu Hasegawa, Lihong Qiu, Tatsuji Haneji

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 2 institutions in 2 countries.

Nan MaDepartment of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
Di YangDepartment of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
Hirohiko OkamuraDepartment of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
Jumpei TeramachiDepartment of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
Tomokazu HasegawaDepartment of Pediatric Dentistry, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
Lihong QiuDepartment of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
Tatsuji HanejiDepartment of Histology and Oral Histology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770‑8504, Japan.
Tokushima University · JPChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periapical lesions are characterized by the destruction of periapical bone, and occur as a result of local inflammatory responses to root canal infection by microorganisms including Porphyromonas endodontalis (P. endodontalis). P. endodontalis and its primary virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical lesions and alveolar bone loss. Interleukin‑23 (IL‑23) is critical in the initiation and progression of periodontal disease via effects on peripheral bone metabolism. The present study investigated the expression of IL‑23 in tissue where a periapical lesion was present, and the effect of P. endodontalis LPS on the expression of IL‑23 in periodontal ligament (PDL) cells. Reverse transcription‑ quantitative polymerase chain reaction and immunohistochemistry revealed increased levels of IL‑23 expression in tissue with periapical lesions compared with healthy PDL tissue. Treatment with P. endodontalis LPS increased the expression of IL‑23 in the SH‑9 human PDL cell line. BAY11‑7082, a nuclear factor κB inhibitor, suppressed P. endodontalis LPS‑induced IL‑23 expression in SH‑9 cells. Treatment of RAW264.7 cells with conditioned medium from P. endodontalis LPS‑treated SH‑9 cells promoted osteoclastogenesis. By contrast, RAW264.7 cells treated with conditioned medium from IL‑23‑knockdown SH‑9 cells underwent reduced levels of osteoclastogenesis. The results of the present study indicated that the expression of IL‑23 in PDL cells induced by P. endodontalis LPS treatment may be involved in the progression of periapical lesions via stimulation of the osteoclastogenesis process.

Indexed as

AnimalsChromonesHumansImmunohistochemistryInterleukin-23LipopolysaccharidesMiceMorpholinesNFATC Transcription FactorsNF-kappa BNitrilesOsteoblastsOsteogenesisPeriodontitisPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitors2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one3-(4-methylphenylsulfonyl)-2-propenenitrileChromonesInterleukin-23LipopolysaccharidesMorpholinesNfatc1 protein, mouseNFATC Transcription FactorsNF-kappa BNitrilesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-fosRANK LigandRNA, Small InterferingSulfones

Identifiers

PMID28000855
PMCPMC5364876
OpenAlexW2564702059

What OpenQuestion 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 OpenQuestion graph.