Inverse behavior of IL-23R and IL-17RA in chronic and aggressive periodontitis
del Carmen Ruiz-Gutierrez Alondra, Rodriguez-Montano Ruth, Pita-Lopez Maria Luisa, Zamora-Perez Ana Lourdes, Guerrero-Velazquez Celia,
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( del Carmen Ruiz-Gutierrez Alondra ) - University of Guadalajara University Center of Health Sciences Department of Integral Dental Clinics
( Rodriguez-Montano Ruth ) - University of Guadalajara University Center of Health Sciences Department of Integral Dental Clinics
( Pita-Lopez Maria Luisa ) - University of Guadalajara Southern University Center Research Center in Molecular Biology of Chronic Diseases
( Zamora-Perez Ana Lourdes ) - University of Guadalajara University Center of Health Sciences Department of Integral Dental Clinics
( Guerrero-Velazquez Celia ) - University of Guadalajara University Center of Health Sciences Department of Integral Dental Clinics
Abstract
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 ¥êB 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.
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Aggressive periodontitis; Chronic periodontitis; Interleukine-17RA; Interleukine-23R
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