Evidence map›Paper›PMID 35298525›Full record

ArticlePloS one2022

Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis.

Anneke Wilharm, Christoph Binz, Inga Sandrock, Francesca Rampoldi, Stefan Lienenklaus, Eva Blank, Andreas Winkel, Abdi Demera, Avi-Hai Hovav, Meike Stiesch and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. The Role of IL-17 in Periodontitis and Its Systemic Connections.International journal of molecular sciences · 2025
    Review
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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

11 authors at 3 institutions in 2 countries.

Anneke WilharmInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Christoph BinzInstitute of Immunology, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-6789-4967
Inga SandrockInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Francesca RampoldiInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Stefan LienenklausInstitute of Laboratory Animal Science, Hannover Medical School, Hannover, Germany.
Eva BlankDepartment of Prosthetic Dentistry and Biomedical Materials Science, Hannover Medical School, Hannover, Germany.
Andreas WinkelDepartment of Prosthetic Dentistry and Biomedical Materials Science, Hannover Medical School, Hannover, Germany.
Abdi DemeraInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Avi-Hai HovavInstitute of Dental Sciences, Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel.
Meike StieschDepartment of Prosthetic Dentistry and Biomedical Materials Science, Hannover Medical School, Hannover, Germany.
Immo PrinzInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEHebrew University of Jerusalem · ILUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontitis is one of the most common infectious diseases in humans. It is characterized by a chronic inflammation of the tooth-supporting tissue that results in bone loss. However, the role and source of the pro-inflammatory cytokine interleukin-17 (IL-17) and of the cells producing it locally in the gingiva is still controversial. Th17 αβ T cells, CD4+ exFoxP3+ αβ T cells, or IL-17-producing γδ T cells (γδ17 cells) seem to be decisive cellular players in periodontal inflammation. To address these issues in an experimental model for periodontitis, we employed genetic mouse models deficient for either γδ T cells or IL-17 cytokines and assessed the bone loss during experimental periodontal inflammation by stereomicroscopic, histological, and μCT-analysis. Furthermore, we performed flow-cytometric analyses and qPCR-analyses of the gingival tissue. We found no γδ T cell- or IL-17-dependent change in bone loss after four weeks of periodontitis. Apart from that, our data are complementary with earlier studies, which suggested IL-17-dependent aggravation of bone loss in early periodontitis, but a rather bone-protective role for IL-17 in late stages of experimental periodontitis with respect to the osteoclastogenicity defined by the RANKL/OPG ratio.

Indexed as

Alveolar Bone LossPeriodontitisAnimalsCytokinesGingivaInflammationInterleukin-17MiceCytokinesInterleukin-17

Identifiers

PMID35298525
PMCPMC8929577
OpenAlexW4220946758

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.