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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
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Comprehensive analysis of transcriptome and pathway interactions in periodontitis
Bruno César de Vasconcelos Gurgel1, Nathalia Vilela2, Kaio Henrique Soares3
1Universidade Federal do Rio Grande do Norte, Departamento de Odontologia, Natal, RN, Brasil.
Journal of Applied Oral Science : Revista FOB
|October 22, 2025
Summary
Severe periodontitis involves altered gene expression and molecular pathways. Key pathways like Wnt/β-catenin and IL-17 signaling are dysregulated, impacting immunity and epithelial integrity.
Area of Science:
- Genomics and Molecular Biology
- Oral Health Research
- Immunology
Background:
- Periodontitis is a prevalent inflammatory disease affecting oral tissues.
- Understanding the molecular mechanisms underlying severe periodontitis is crucial for developing effective treatments.
Purpose of the Study:
- To elucidate the transcriptomic profile of severe periodontitis.
- To identify dysregulated molecular pathways involved in periodontitis pathogenesis.
Main Methods:
- RNA sequencing was performed on gingival tissues from severe periodontitis patients and healthy controls.
- Differentially expressed genes (DEGs) were identified and analyzed using Ingenuity Pathway Analysis (IPA).
- Protein expression of selected DEGs was validated using immunohistochemistry (IHC).
Main Results:
- A total of 1651 DEGs were identified, with 909 upregulated and 742 downregulated in periodontitis.
- Upregulated genes included mitochondrial genes, pseudogenes, long non-coding RNAs, and immunoglobulins.
- Downregulated genes included keratin family members, immune modulators (e.g., CD207), and Wnt/β-catenin pathway components; IL-17 signaling was suppressed.
Conclusions:
- Severe periodontitis is characterized by significant transcriptomic alterations.
- Dysregulation of Wnt/β-catenin and IL-17 signaling pathways contributes to periodontitis.
- Altered gene expression impacts cell chemotaxis, innate immunity, and epithelial barrier function in periodontitis.

