# Overexpression of the IL‐23/IL‐17A Axis and Their Receptors (IL‐23R and IL‐17RA) in Gingival Tissue of Patients With Periodontitis

**Authors:** Sonia I. Vázquez-Jiménez, Ruth Rodríguez-Montaño, Vianeth M. Martínez-Rodríguez, Juan M. Guzmán-Flores, Ana L. Zamora-Perez, Susana del Toro Arreola, Celia Guerrero-Velázquez

PMC · DOI: 10.1155/ijod/8893504 · International Journal of Dentistry · 2026-01-13

## TL;DR

This study shows that proteins IL-23, IL-17A, and their receptors are overexpressed in the gums of periodontitis patients, linking them to disease progression.

## Contribution

The study provides new evidence of the overexpression of the IL-23/IL-17A axis and its receptors in periodontitis-affected gingival tissue.

## Key findings

- IL-23, IL-17A, IL-23R, and IL-17RA protein levels were significantly higher in periodontitis patients compared to healthy individuals.
- Unexpected molecular weight bands were observed for IL-23R and IL-17RA in periodontitis samples.
- Positive correlations were found between cytokine/receptor levels and clinical parameters like bone loss.

## Abstract

Periodontitis is a chronic immunoinflammatory disease involving various components that affect the tissues surrounding the tooth. The host immune response to the presence of periodontopathogenic microorganisms activates several cytokine systems involved in alveolar bone resorption in periodontitis; among them is the receptor activator of nuclear factor‐κB (RANK)/receptor activator of nuclear factor‐κB ligand (RANKL) system, which depends on the interleukin (IL)‐23/IL‐17 axis. There is a tendency toward increased IL‐23, IL‐17, and IL‐17 receptor (IL‐17RA) and a discrepancy in IL‐23 receptor (IL‐23R) in gingival tissue (GT) of patients with periodontitis. Therefore, the aim of this study was to quantify the expression of the IL‐23/IL‐17A axis using the western blotting (WB) technique in GT samples from patients with periodontitis.

This cross‐sectional study included 49 subjects: 25 healthy subjects and 24 subjects with periodontitis. GT samples were collected during periodontal surgery. WB was used to evaluate the levels of IL‐23, IL‐17A, IL‐23R, and IL‐17RA.

We found a significant increase in IL‐23, IL‐17A, IL‐23R, and IL‐17RA protein levels in the periodontitis group compared with the healthy group; we also detected bands with unexpected molecular weights for both receptors. Moreover, we found a significant positive correlation between IL‐23 and IL‐17A with both receptors, while IL‐23, IL‐17A, IL‐23R, and IL‐17RA correlated positively with two periodontal clinical parameters, namely the clinical attachment level and the percentage of radiographic bone loss (%RBL).

In this study, we detected overexpression of IL‐23, IL‐17A, and their receptors in GT of patients with periodontitis, confirming that the IL‐23/IL‐17A axis is involved in periodontal disease.

## Linked entities

- **Proteins:** IL37 (interleukin 37), IL17A (interleukin 17A), IL23R (interleukin 23 receptor), IL17RA (interleukin 17 receptor A)
- **Diseases:** periodontitis (MONDO:0005076)

## Full-text entities

- **Genes:** TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, IL17RA (interleukin 17 receptor A) [NCBI Gene 23765] {aka CANDF5, CD217, CDw217, IL-17RA, IL17R, IMD51}, TNFRSF11A (TNF receptor superfamily member 11a) [NCBI Gene 8792] {aka CD265, FEO, LOH18CR1, ODFR, OFE, OPTB7}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL23R (interleukin 23 receptor) [NCBI Gene 149233] {aka PSORS7}
- **Diseases:** immunoinflammatory disease (MESH:D004194), periodontal disease (MESH:D010510), bone loss (MESH:D001847), Periodontitis (MESH:D010518)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12796852/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12796852/full.md

## References

57 references — full list in the complete paper: https://tomesphere.com/paper/PMC12796852/full.md

---
Source: https://tomesphere.com/paper/PMC12796852