In:
PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 3 ( 2022-3-17), p. e0265486-
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.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0265486
DOI:
10.1371/journal.pone.0265486.g001
DOI:
10.1371/journal.pone.0265486.g002
DOI:
10.1371/journal.pone.0265486.g003
DOI:
10.1371/journal.pone.0265486.g004
DOI:
10.1371/journal.pone.0265486.g005
DOI:
10.1371/journal.pone.0265486.s001
DOI:
10.1371/journal.pone.0265486.s002
DOI:
10.1371/journal.pone.0265486.s003
DOI:
10.1371/journal.pone.0265486.s004
DOI:
10.1371/journal.pone.0265486.r001
DOI:
10.1371/journal.pone.0265486.r002
DOI:
10.1371/journal.pone.0265486.r003
DOI:
10.1371/journal.pone.0265486.r004
DOI:
10.1371/journal.pone.0265486.r005
DOI:
10.1371/journal.pone.0265486.r006
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2267670-3
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