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, Immo Prinz

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

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.

Original languageAmerican English
Article numbere0265486
JournalPLoS ONE
Volume17
Issue numberMarch
DOIs
StatePublished - Mar 2022

Bibliographical note

Publisher Copyright:
© 2022 Wilharm et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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