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Updated: Jan 8, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
FOXP3+ T Cells-An Emerging Evidence in Periodontitis Therapeutics
Revan Birke Koca Ünsal1, Akira Hasuike2, Tamer Badawy3,4
1Schulich School of Medicine & Dentistry Western University, London, Canada.
Objective:
To review interaction of FOXP3+ regulatory T cells with Th17 cells in determining the progression of periodontitis.
Material And Methodology:
Literature review pertaining to FOXP3+ regulatory T cells, Th17 cells, and periodontitis was analyzed. Descriptive summary is presented.
Results:
FOXP3+ regulatory T cells (Tregs) play an essential role in maintaining immune homeostasis and modulating inflammatory responses. The balance between Tregs and pro-inflammatory Th17 cells is crucial in determining the progression of periodontitis, a chronic immune-mediated inflammatory disease. While Tregs are responsible for suppressing excessive immune activation and preventing tissue destruction, an imbalance favoring Th17 cells leads to increased osteoclastic activity and alveolar bone loss through IL-17 and RANKL signaling. The inflammatory microenvironment in periodontitis compromises FOXP3+ Treg stability and function, thereby allowing unregulated immune responses that exacerbate periodontal tissue breakdown. Recent studies suggest that strategies aimed at enhancing Treg-mediated immune regulation, such as IL-2 supplementation, all-trans retinoic acid (ATRA), IL-33 administration, and CCL22-mediated recruitment, could mitigate periodontal inflammation and preserve alveolar bone integrity. Furthermore, systemic conditions like diabetes and obesity play a significant role in disrupting Treg function by promoting a pro-inflammatory environment, impairing immune regulation, and exacerbating immune dysregulation. This dysfunction weakens the protective role of Tregs, leading to an intensified inflammatory response that accelerates periodontal tissue destruction and alveolar bone loss.
Conclusion:
Understanding the mechanisms governing FOXP3+ Treg stability and their interaction with pathogenic Th17 responses is essential for developing targeted immunomodulatory therapies. Future research should focus not only on selectively expanding Tregs but also on translational strategies such as adoptive Treg transfer and IL-17 inhibition, while carefully balancing efficacy and the risk of systemic immunosuppression.
