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Updated: Apr 28, 2026
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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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Neutrophil S100a9 Deficiency Protects against Periodontal Bone Loss
Y Y Wei1, J Q Zheng1, Y L Zhou1
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Journal of Dental Research
|February 24, 2026
Summary
S100A9 protein deficiency in periodontitis impairs neutrophil extracellular trap (NET) formation, reducing bone resorption. Restoring autophagy or inhibiting S100A9 mitigates periodontitis-induced bone loss.
Area of Science:
- Immunology
- Oral Biology
- Pathology
Background:
- Periodontitis involves microbial dysbiosis, immune dysregulation, and alveolar bone loss.
- S100A8/A9 protein levels are elevated in human periodontitis, but their role in osteoimmunology is unclear.
Purpose of the Study:
- To elucidate the mechanism by which S100A9 regulates osteoimmunological homeostasis in periodontitis.
- To investigate the impact of S100A9 deficiency on neutrophil extracellular trap (NET) formation and bone resorption.
Main Methods:
- Ligature-induced periodontitis model in S100a9 knockout mice.
- Assessment of NET formation, autophagy, osteoclast differentiation, and bone resorption.
- Pharmacological intervention using rapamycin and a S100A9 inhibitor (tasquinimod).
Main Results:
- S100a9 knockout mice showed reduced NET formation and bone resorption.
- S100A9 deficiency inhibited neutrophil autophagy, leading to decreased NETosis and suppressed osteoclast differentiation.
- Autophagy restoration and S100A9 inhibition reversed these effects, mitigating bone loss.
Conclusions:
- S100A9 plays a critical role in regulating osteoclast differentiation through NETosis in periodontitis.
- Targeting S100A9 or enhancing autophagy presents potential therapeutic strategies for periodontitis-associated bone loss.
