Purpose Periodontitis is associated with a dysbiosis of periodontopathic bacteria, which stimulate the interleukin (IL)-23/IL-17 axis that plays an essential role in the immunopathogenesis of this disease, leading to alveolar bone destruction through receptor activator of nuclear factor κB ligand (RANKL). IL-23 receptor mRNA (IL-23R) has been identified in periodontitis, and IL-17 receptor A mRNA (IL-17RA) and its protein have not yet been evaluated in patients with periodontitis. In this study was measure IL-23R and IL-17RA in gingival tissue (GT) from patients with generalized chronic periodontitis (GCP) and generalized aggressive periodontitis (GAP) and to explore correlations with clinical parameters. Methods We included 16 healthy subjects (HS), 18 patients with GCP, and 14 with GAP. GT samples were collected during periodontal surgery. Both IL-23R and IL-17RA were detected by enzyme-linked immunosorbent assay . Results The results were analyzed with Mann-Whitney U test and Spearman' rank correlation coefficients using SPSS version 25.0. We found lower IL-23R levels in patients with GCP and GAP than in HS. Contrarily, we observed higher IL-17RA levels in GCP and GAP patients than in HS. Moreover, we found negative correlations between IL-23R in GT and probing depth and clinical attachment loss (CAL). Likewise, a positive correlation of IL-17RA in GT with CAL was found. Conclusions The results of these findings suggest that the reverse behavior between IL-23R and IL-17RA in periodontitis patients may also be involved with the activation of RANKL, which promotes alveolar bone loss.

Background: Periodontitis (P) is a chronic inflammatory disease characterized by the destruction of periodontium support tissue generated by different immuno-inflammatory mechanisms, including the RANK/RANKL/OPG and the IL-23/IL-17 axis. Methods: The study was performed with healthy subjects (HS) and patients with periodontitis. Plasma samples were obtained from peripheral blood and the gingival tissue (GT) during periodontal surgery. The ELISA technique was used to evaluate the levels of IL-23, IL-17A, IL-23R, and IL-17RA. Results: In the plasma, a significant decrease in IL-17A was observed in patients with periodontitis than HS. In the GT, IL-23, IL-17A, and IL-17RA levels were increased in periodontitis patients; on the contrary, IL-23R levels were decreased in periodontitis patients when compared with HS. Finally, several positive correlations were found: soluble IL-17RA (sIL-17RA) levels in plasma between the percentage of radiographic bone loss (RBL%), and IL-23 with IL-17A in gingival tissue. Conclusions: The detection of the IL-23/IL-17A axis in gingival tissue and plasma provides us with more information on the behavior of this axis in a localized way in the periodontal microenvironment, in contrast to the systemic levels evaluated according to the new classification of periodontitis.

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