Evidence map›Paper›PMID 19664151›Full record

ArticleClinical and experimental immunology2009

Expression and regulation of the NALP3 inflammasome complex in periodontal diseases.

N Bostanci, G Emingil, B Saygan, O Turkoglu, G Atilla, M A Curtis, G N Belibasakis

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

Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

75 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
  2. Article
  3. The NLRP3 Inflammasome Regulates Orthodontic Tooth Movement.Orthodontics & craniofacial research · 2026
    Article
  4. Inflammasomes in Oral Pathologies: From Periodontal Disease to Oral Cancer.Advances in experimental medicine and biology · 2026
    Review
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15 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

7 authors at 3 institutions in 2 countries.

N BostanciDepartment of Periodontology, University College London Eastman Dental Institute, London WC1X 8LD, UK. n.bostanci@eastman.ucl.ac.uk
G Emingil
B Saygan
O Turkoglu
G Atilla
M A Curtis
G N Belibasakis
Ege University · TREastman Dental Hospital · GBQueen Mary University of London · GB

Funding

Medical Research Council G0501478
6 · The paper itself

Abstract

Periodontitis is an infectious process characterized by inflammation affecting the supporting structures of the teeth. Porphyromonas gingivalis is a major oral bacterial species implicated in the pathogenesis of periodontitis. Processing of interleukin (IL)-1 family cytokines is regulated by an intracellular innate immune response system, known as the NALP3 [nacht domain-, leucine-rich repeat-, and pyrin domain (PYD)-containing protein 3] inflammasome complex. The aim of the present study was to investigate by quantitative real-time polymerase chain reaction (PCR) the mRNA expression of NALP3, its effector molecule apoptosis associated speck-like protein (ASC), its putative antagonist NLRP2 (NLR family, PYD-containing protein 2), IL-1beta and IL-18 (i) in gingival tissues from patients with gingivitis (n = 10), chronic periodontitis (n = 18), generalized aggressive periodontitis (n = 20), as well as in healthy subjects (n = 20), (ii) in vitro in a human monocytic cell line (Mono-Mac-6), in response to P. gingivalis challenge for 6 h. The clinical data indicate that NALP3 and NLRP2, but not ASC, are expressed at significantly higher levels in the three forms of inflammatory periodontal disease compared to health. Furthermore, a positive correlation was revealed between NALP3 and IL-1beta or IL-18 expression levels in these tissues. The in vitro data demonstrate that P. gingivalis deregulates the NALP3 inflammasome complex in Mono-Mac-6 cells by enhancing NALP3 and down-regulating NLRP2 and ASC expression. In conclusion, this study reveals a role for the NALP3 inflammasome complex in inflammatory periodontal disease, and provides a mechanistic insight to the host immune responses involved in the pathogenesis of the disease by demonstrating the modulation of this cytokine-signalling pathway by bacterial challenge.

Indexed as

Gene Expression RegulationAdultAnalysis of VarianceCARD Signaling Adaptor ProteinsCarrier ProteinsCase-Control StudiesCell LineChronic PeriodontitisCytoskeletal ProteinsFemaleGingivaHumansInterleukin-18Interleukin-1betaMaleMiddle AgedCARD Signaling Adaptor ProteinsCarrier ProteinsCytoskeletal ProteinsInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPYCARD protein, humanRNA, Messenger

Identifiers

PMID19664151
PMCPMC2745037
OpenAlexW1911897482

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.