2017
DOI: 10.1111/jcpe.12743
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The aggravation of arthritis by periodontitis is dependent of IL‐17 receptor A activation

Abstract: The effects of P. gingivalis-induced periodontitis on arthritis are dependent on Th17 expansion and IL-17RA signalling, which lead to increased neutrophil infiltration into the joints.

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Cited by 31 publications
(39 citation statements)
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“…Peri‐implantitis lesions showed a distinct down‐regulation of melan‐A, a melanocytic marker, and TRPM‐1/melastatin, also expressed on melanocytes, consistent with the presence of melanocytes in the periodontal ligament, which is lacking in peri‐implant tissue, and may suggest these cells play a distinct immunologic role in periodontal inflammation. Comparing periodontitis and health, the most up‐regulated GO term was “T‐helper 17 cell lineage commitment,” in agreement with previous studies, these results implied Th17 immune response as having a key role in periodontitis.…”
Section: Discussionsupporting
confidence: 90%
“…Peri‐implantitis lesions showed a distinct down‐regulation of melan‐A, a melanocytic marker, and TRPM‐1/melastatin, also expressed on melanocytes, consistent with the presence of melanocytes in the periodontal ligament, which is lacking in peri‐implant tissue, and may suggest these cells play a distinct immunologic role in periodontal inflammation. Comparing periodontitis and health, the most up‐regulated GO term was “T‐helper 17 cell lineage commitment,” in agreement with previous studies, these results implied Th17 immune response as having a key role in periodontitis.…”
Section: Discussionsupporting
confidence: 90%
“…Moreover, a periodontitis rat model study showed a variable sitespecific TH17/Treg cell ratio in the oral tissues but detected a TH17 cell increase with a relative Treg cell decrease in peripheral blood, which was proposed to potentially impact development of systemic inflammatory diseases [32]. This hypothesis is supported by a recent study that found that P. gingivalis-induced periodontitis exacerbates arthritis in an IL-17RA (receptor A) dependent manner in an antigeninduced arthritis murine model [33]. The balance of TH17 cells relative to Treg cells is a central component to balancing the immune response such that pathogens are appropriately recognized, but inappropriate immune responses to self and harmless antigens are minimized [19].…”
Section: Introductionsupporting
confidence: 71%
“…influence the time needed to be able to observe clinical signs (15,16,22). In this study, we decided to evaluate the effect of an acute infection with P. gingivalis through repeated intraperitoneal injections of P. gingivalis strain 381.…”
Section: Discussionmentioning
confidence: 99%
“…In patients with RA, a correlation between the presence of P. gingivalis and anti-citrullinated protein antibodies has already been observed (12). Its detrimental effect was also confirmed in vivo in several mouse models, in which P. gingivalis infection exacerbated collagen antibody (AB)-induced arthritis through different mechanisms, including modification of the gut microbiota and the associated autoimmune response (13,14), neutrophil activation (15), or induction of bone destruction (16).…”
mentioning
confidence: 91%