Evidence map›Paper›PMID 18719207›Full record

ReviewJournal of dental research2008

A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17.

S L Gaffen, G Hajishengallis

Open access · greenAbstract readReview
In one paragraph

Review in Journal of dental research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 3 pooled it
7.2field-weighted citation impact, top 2% 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

153 citing papers in PubMed, 3 syntheses or guidelines pooled it, 331 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  13. FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics.Clinical and experimental dental research · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Serum cytokines in periodontal diseases.Periodontology 2000 · 2025
    Review
  18. Review
  19. Article
  20. Article

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

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

2 authors at 2 institutions in 2 countries.

S L GaffenDepartment of Oral Biology, School of Dental Medicine, 36 Foster Hall, 3435 Main St., State University of New York, Buffalo, NY 14214, USA. sig65@pitt.edu
G Hajishengallis
University at Buffalo, State University of New York · USUniversity of Dental Medicine · MM

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Oral Immunity and Adjuvant ReceptorsR01DE017138 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2006 to 2014
$3.8M
Structure-Function Relationships in the IL-17 ReceptorR01AR054389 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2008 to 2012
$1.8M
Oral Pathogen Exploitation of Innate Recognition as a Function of AgeR01DE018292 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2007 to 2011
$1.6M
Anti-Apoptotic Signaling by the IL-2/15 ReceptorR01AI049329 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI GAFFEN, SARAH L. · 2002 to 2006
$1.2M
Signaling by a Tyrosine-Deficient IL-2/15 Receptor BetaR21AI049329 · NIAID · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI GAFFEN, SARAH L. · 2001 to 2001
$267k
NIAID NIH HHS AI49329NIAID NIH HHS R01 AI049329NIAID NIH HHS R21 AI049329NIAMS NIH HHS AR054389NIAMS NIH HHS R01 AR054389NIDCR NIH HHS DE015254NIDCR NIH HHS DE017138NIDCR NIH HHS DE018292NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE017138NIDCR NIH HHS R01 DE018292
6 · The paper itself

Abstract

For almost two decades, the Th1/Th2 paradigm has offered a productive conceptual framework for investigating the pathogenesis of periodontitis. However, as with many other inflammatory diseases, the observed role of T-cell-mediated immunity in periodontitis did not readily fit this model. A new subset of CD4+ T-cells was recently discovered that explains many of the discrepancies in the classic Th1/Th2 model, and has been termed "Th17" based on its secretion of the novel pro-inflammatory cytokine IL-17. The identification of Th17 cells as a novel effector T-cell population compels re-examination of periodontitis in the context of the new subset and its signature cytokines. This review aims to offer a clarifying insight into periodontal pathogenesis under the extended Th1/Th2/Th17 paradigm, and is predicated on the principle that periodontal disease activity is determined by a complex interplay between the immune system and periodontal pathogens. The re-examination of existing periodontal literature and further studies in the light of these new discoveries may help explain how the inflammatory response results in damage to the periodontium while generally failing to control the pathogens. This knowledge is essential for the development of immunomodulatory intervention strategies for fine-tuning the host response to maximize the protective and minimize the destructive aspects of the periodontal host response. Moreover, with the advent of anti-cytokine biologic drugs that target the Th1 and Th17 pathways in autoimmunity, the potential consequences to periodontal disease susceptibility in humans need to be understood.

Indexed as

AnimalsHumansImmunity, CellularInterleukin-17InterleukinsModels, ImmunologicalPeriodontitisTh1 CellsTh2 CellsT-Lymphocyte SubsetsInterleukin-17Interleukins

Identifiers

PMID18719207
PMCPMC2692983
OpenAlexW2036608242

What OpenQuestion holds

Textmetadata
LicenceTDM
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.