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- Title
High expression of aryl hydrocarbon receptor (AhR) plays an important role in the formation of fibrous epulis.
- Authors
Zeng, Xuwen; Xia, Siying; Yan, Xiangzhen; Hu, Congjiao; An, Kangkang; Luo, Lijun
- Abstract
Objectives: Epulis is considered to be a massive reactive lesion rather than a true neoplasia. AhR is thought to be associated with inflammation and development of neoplasms. Here, we aimed to observe the expression of AhR in fibrous epulis and explore its role and possible mechanism in the pathogenesis of epulis. Materials and Methods: Epulis and normal gingival tissues were collected, and AhR expression was detected at the mRNA and protein levels by quantitative polymerase chain reaction (qPCR) and immunohistochemistry, respectively. The expression levels of proinflammatory cytokines and apoptosis‐related factor genes in human periodontal ligament cells (hPDLCs) and human gingival fibroblasts (hGFs) transfected with AhR short interfering RNA (siRNA) or negative control siRNA, upon stimulation with lipopolysaccharide of Porphyromonas gingivalis (Pg‐LPS), were then examined. Finally, the expression levels of the proinflammatory cytokines and apoptosis‐related factor genes in the epulis tissues were observed by qPCR. Results: AhR expression in fibrous epulis was significantly increased at both the mRNA and protein levels. The expression of proinflammatory cytokines and apoptosis‐related factor genes in hPDLCs transfected with AhR siRNA was significantly decreased when stimulated with Pg‐LPS. The same trends were observed for hGFs. The opposite trend was detected in the epulis tissues. Conclusion: AhR may be a key factor in fibrous epulis pathogenesis that acts by regulating the expression of BCL2 family genes and inflammatory factor‐related genes.
- Subjects
PROTEINS; CYTOKINES; LIPOPOLYSACCHARIDES; CELL culture; IMMUNOHISTOCHEMISTRY; CELL receptors; APOPTOSIS; PERIODONTAL disease; GENE expression; GINGIVAL hyperplasia; MESSENGER RNA; POLYMERASE chain reaction; PERIODONTAL ligament
- Publication
Oral Diseases, 2022, Vol 28, Issue 8, p2258
- ISSN
1354-523X
- Publication type
Article
- DOI
10.1111/odi.13940