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자료유형
학술저널
저자정보
Alondra del Carmen Ruiz-Gutierrez (Specialty in Periodontology Department of Integral Dental Clinics University Center of Health Scie) Ruth Rodriguez-Montano (Institute of Research in Dentistry Department of Integral Dental Clinics University Center of Heal) Maria Luisa Pita-Lopez (Research Center in Molecular Biology of Chronic Diseases Southern University Center University of) Ana Lourdes Zamora-Perez (Institute of Research in Dentistry Department of Integral Dental Clinics University Center of Heal) Celia Guerrero-Velazquez (Institute of Research in Dentistry Department of Integral Dental Clinics University Center of Heal)
저널정보
대한치주과학회 Journal of Periodontal & Implant Science Journal of Periodontal & Implant Science 제51권 제4호
발행연도
2021.1
수록면
254 - 263 (10page)

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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.

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