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Updated: Jun 9, 2025
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Apoptotic vesicles from macrophages exacerbate periodontal bone resorption in periodontitis via delivering miR-143-3p
Junhong Xiao1,2, Yifei Deng1, Jirong Xie1
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, 430079, China.
Abstrct:
BACKGROUND: Apoptotic vesicles (ApoVs), which are extracellular vesicles released by apoptotic cells, have been reported to exhibit substantial therapeutic potential for inflammatory diseases and tissue regeneration. While extensive research has been dedicated to mesenchymal stem cells (MSCs), the investigation into immune cell-derived ApoVs remains limited, particularly regarding the function and fate of macrophage-derived ApoVs in the context of periodontitis (PD).
Results:
Our study corroborates the occurrence and contribution of resident macrophage apoptosis in Porphyromonas gingivalis (Pg)-associated PD. The findings unveil the pivotal role played by apoptotic macrophages and their derived ApoVs in orchestrating periodontal bone remodeling. The enrichments of diverse functional miRNAs within these ApoVs are discerned through sequencing techniques. Moreover, our study elucidates that the macrophage-derived ApoVs predominantly deliver miR-143-3p, targeting insulin-like growth factor-binding protein 5 (IGFBP5), thereby disrupting periodontal bone homeostasis.
Conclusions:
Our study reveals that macrophages in Pg-associated PD undergo apoptosis and generate miR-143-3p-enriched ApoVs to silence IGFBP5, resulting in the perturbation of osteogenic-osteoclastic balance and the ensuing periodontal bone destruction. Accordingly, interventions targeting miR-143-3p in macrophages or employment of apoptosis inhibitor Z-VAD hold promise as effective therapeutic strategies for the management of PD.
Insights
Macrophages undergoing apoptosis release vesicles that worsen periodontal disease by delivering miR-143-3p, disrupting bone homeostasis. Targeting these vesicles or apoptosis may treat periodontitis.
Area of Science:
- Immunology
- Extracellular Vesicles
- Periodontal Disease
Background:
- Apoptotic vesicles (ApoVs) show therapeutic potential for inflammation and tissue regeneration.
- Research on immune cell-derived ApoVs, especially from macrophages in periodontitis (PD), is limited.
Purpose of the Study:
- Investigate the role of macrophage apoptosis and their derived ApoVs in Porphyromonas gingivalis (Pg)-associated PD.
- Determine the function and molecular mechanisms of macrophage-derived ApoVs in periodontal bone remodeling.
Main Methods:
- Corroborating macrophage apoptosis in Pg-associated PD.
- Sequencing to identify functional miRNAs within macrophage-derived ApoVs.
- Elucidating the targeting of IGFBP5 by delivered miR-143-3p.
Main Results:
- Macrophage apoptosis contributes to Pg-associated PD.
- Macrophage-derived ApoVs orchestrate periodontal bone remodeling.
- These ApoVs deliver miR-143-3p, targeting IGFBP5 and disrupting bone homeostasis.
Conclusions:
- Macrophages in Pg-associated PD generate miR-143-3p-enriched ApoVs that silence IGFBP5, leading to bone destruction.
- Interventions targeting miR-143-3p or using apoptosis inhibitors like Z-VAD show therapeutic promise for PD.
