In vivo efficacy of BNPs was assessed using a murine model of periodontitis by measuring alveolar bone resorption and gingival IL-17 expression as outcomes of Pg-induced inflammation.
It was observed that miRNA-146a was downregulated but IL-17 and IL-35 were upregulated in the plasma of patients with periodontitis than in healthy controls. miRNA-146a was inversely correlated with IL-17 and IL-35 in patients with periodontitis. miRNA-146a overexpression inhibited proliferation of PDLSCs derived from both periodontitis-affected teeth and healthy teeth. miRNA-146a overexpression led to downregulated IL-17 and IL-35 expression in PDLSCs isolated from periodontitis-affected teeth.
Collectively, these findings indicated that IL‑17A facilitated osteoclast differentiation and bone resorption in vitro and in vivo, which may contribute to the understanding of the molecular basis of IL‑17A in alveolar bone destruction and provide insight on the clinical therapeutic targets for periodontitis.
In parallel, IL-17A-related immune responses were attenuated in berberine-treated OVX-periodontitis rats with a lower serum level of proinflammatory cytokines and reduced IL-17A<sup>+</sup> cells in alveolar bone as compared with vehicle-treated OVX-periodontitis rats.
Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis.
The results suggest that the evolution of gingivitis to periodontitis is related to the accumulation of activated Th1 cells (IFN-γ and TNF-α) associated with the presence of increased IL-17.
Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.
We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-α and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.
The percentages of Th17 significantly increased in the peripheral blood, which was consistent with gingival tissues study that Th17 cells related transcription factor RORγt mRNA and IL-17 increased in the course of periodontitis.
The present study suggests that IL-35 could directly suppress IL-17 expression via ROR<i>α</i> and ROR<i>γ</i>t inhibition and might play an important role in inflammatory diseases such as periodontitis.
This meta-analysis examined the relationship between IL-17A (rs2275913) and IL17F (rs763780 T/C) gene polymorphisms and the risk of inflammatory diseases, including periodontitis, rheumatoid arthritis (RA), and inflammatory bowel disease.
In the field of oral mucosal immunity, through the study of patients with select gene disruptions, the interleukin-17 (IL-17) pathway has emerged as a critical element in oral immune surveillance and susceptibility to inflammatory disease, with disruptions in the IL-17 axis now strongly linked to mucosal fungal susceptibility, whereas overactivation of the same pathways is linked to inflammatory periodontitis.
A case-control study was conducted on patients with chronic periodontitis (CP) and healthy controls with the aim of evaluating possible association between interleukin 17A (IL17A) G197A (rs2275913) and IL17F T7488C (rs763780) polymorphisms and periodontitis.
Oral lichen planus and chronic periodontitis may have interaction in disease pathogenesis, while IL-17 detection in local lesions may be helpful in identifying the disease severity in periodontitis patients with oral lichen planus.
The aim of present study was to evaluate the expression of IL17A and occurrence of the IL17A (rs2275913), IL17F (rs763780) and IL23R (rs11209026) gene polymorphisms in different clinical forms or severity of periodontitis in a sample of Brazilian individuals.