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Updated: Jan 20, 2026

Murine Model of Advanced Periodontitis Induced by Nylon Ligature in the Second Upper Molar
Published on: May 30, 2025
T and B Cells in Periodontal Disease: New Functions in A Complex Scenario
C M Figueredo1,2, R Lira-Junior3, R M Love4
1School of Dentistry and Oral Health, Griffith University, Queensland 4222, Australia. c.dasilvafigueredo@griffith.edu.au.
Periodontal disease involves T and B cells. Specific subsets and their cytokines, like IL-17 and SOFAT, are key in controlling inflammation and bone loss, influencing disease progression.
Area of Science:
- Immunology
- Periodontology
- Oral Medicine
Background:
- Periodontal disease involves chronic inflammation and immune cell infiltration.
- T and B lymphocytes play critical roles in regulating inflammatory responses and tissue homeostasis.
- Understanding immune cell subsets and their functions is vital for managing periodontal disease progression.
Purpose of the Study:
- To review recent findings on the role of T and B cell subsets in periodontal disease pathogenesis.
- To highlight the significance of cytokine expression by immune cells in disease development.
- To explore the impact of specific immune cell activities on bone metabolism in periodontitis.
Main Methods:
- Narrative review of current literature.
- Analysis of T and B cell subsets, including T regulatory (Treg), CD8+, γδ T, and mucosal-associated invariant T (MAIT) cells.
- Examination of cytokine profiles (e.g., IL-17, IFN-γ, TNF-α) and their relation to osteoclastogenesis via RANKL activation.
Main Results:
- Treg, CD8+, and γδ T cells are crucial for maintaining gingival homeostasis.
- Activated T cells secreting IL-17 and SOFAT induce osteoclastogenesis through RANKL.
- MAIT cells may play a significant role in disease pathogenesis due to their cytokine production.
- B cells can influence alveolar bone loss in a RANKL-dependent manner.
Conclusions:
- New functions for Tregs, SOFAT, MAIT cells, and B cells in RANKL activation have been identified.
- The interplay between distinct T and B cell subtypes determines disease outcome, from gingivitis to periodontitis.
- Immune cell dynamics are central to the transition between stable gingivitis and destructive periodontitis.
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