Evidence map›Paper›PMID 10995794›Full record

ArticleThe Journal of clinical investigation2000

Functional human T-cell immunity and osteoprotegerin ligand control alveolar bone destruction in periodontal infection.

Y T Teng, H Nguyen, X Gao, Y Y Kong, R M Gorczynski, B Singh, R P Ellen, J M Penninger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 1 pooled it
22.6field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 1 synthesis or guideline pooled it, 494 citations in OpenAlex.

  1. Pooled it
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  11. Distinct cross talk of IL-17 & TGF-β with the immature CD11cImmunity, inflammation and disease · 2024
    Article
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  18. Roles of osteoclasts in alveolar bone remodeling.Genesis (New York, N.Y. : 2000) · 2022
    Review
  19. Review
  20. Article

87 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Y T TengDivisions of Periodontics and Oral Biology, and Department of Microbiology and Immunology, Faculty of Medicine and Dentistry, the University of Western Ontario, London, Ontario, Canada. yateng@julian.uwo.ca
H Nguyen
X Gao
Y Y Kong
R M Gorczynski
B Singh
R P Ellen
J M Penninger
Western University · CAToronto General Hospital · CAAmgen (Canada) · CAOntario Institute for Cancer Research · CAUniversity of Toronto · CA

Funding

IDENTIFY ANTIGENIC DETERMINANTS OF HUMAN PERIODONTITISR03DE012969 · NIDCR · UNIVERSITY OF WESTERN ONTARIO · PI TENG, YEN-TUNG ANDY · 2000 to 2001
$50k
NIDCR NIH HHS DE12969-01A2
6 · The paper itself

Abstract

Periodontitis, a prime cause of tooth loss in humans, is implicated in the increased risk of systemic diseases such as heart failure, stroke, and bacterial pneumonia. The mechanisms by which periodontitis and antibacterial immunity lead to alveolar bone and tooth loss are poorly understood. To study the human immune response to specific periodontal infections, we transplanted human peripheral blood lymphocytes (HuPBLs) from periodontitis patients into NOD/SCID mice. Oral challenge of HuPBL-NOD/SCID mice with Actinobacillus actinomycetemcomitans, a well-known Gram-negative anaerobic microorganism that causes human periodontitis, activates human CD4(+) T cells in the periodontium and triggers local alveolar bone destruction. Human CD4(+) T cells, but not CD8(+) T cells or B cells, are identified as essential mediators of alveolar bone destruction. Stimulation of CD4(+) T cells by A. actinomycetemcomitans induces production of osteoprotegerin ligand (OPG-L), a key modulator of osteoclastogenesis and osteoclast activation. In vivo inhibition of OPG-L function with the decoy receptor OPG diminishes alveolar bone destruction and reduces the number of periodontal osteoclasts after microbial challenge. These data imply that the molecular explanation for alveolar bone destruction observed in periodontal infections is mediated by microorganism-triggered induction of OPG-L expression on CD4(+) T cells and the consequent activation of osteoclasts. Inhibition of OPG-L may thus have therapeutic value to prevent alveolar bone and/or tooth loss in human periodontitis.

Indexed as

Bacterial ProteinsReceptors, Cytoplasmic and NuclearAdultAggregatibacter actinomycetemcomitansAlveolar Bone LossAnimalsCarrier ProteinsCD4-Positive T-LymphocytesDisease Models, AnimalFemaleGlycoproteinsHistocytochemistryHumansLymphocyte ActivationMaleMembrane GlycoproteinsBacterial ProteinsCarrier ProteinsGlycoproteinsMembrane GlycoproteinsMtrB protein, BacteriaOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BReceptors, Cytoplasmic and NuclearReceptors, Tumor Necrosis FactorRNA-Binding ProteinsTNFRSF11A protein, humanTnfrsf11a protein, mouseTNFRSF11B protein, humanTnfrsf11b protein, mouseTNFSF11 protein, humanTnfsf11 protein, mouseTranscription Factors

Identifiers

PMID10995794
PMCPMC3102542
OpenAlexW2055166353

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.