Effect Of Adscs-Exos On Osteoclasis By Lps In Periodontitis
exosomes derived from adipose mesenchymal stem cells to down-regulate the expression of osteoclast genes and protein-related mechanisms. ADSCs were isolated using collagenase digestion and characterized by flow cytometry for surface markers and multilineage differentiation potential (assessed by Oil Red O and Alizarin Red S staining). ADSCs-Exos were isolated via size-exclusion chromatography and ultrafiltration, and characterized by transmission electron microscopy, nanoparticle tracking analysis, and immunoblotting. In a Pg-LPS-induced periodontitis model, PKH26-labeled ADSCs-Exos were internalized by cells, as shown by confocal microscopy. Their effects on osteoclastic markers (TRAP, MMP-9, COX-2) and signaling mediators (RANK, TRAF6) were evaluated using qRT-PCR and immunoblotting. ADSCs-Exos suppressed early osteoclast differentiation in a concentration-dependent manner, downregulating osteoclastogenesis-related genes (TRAP, RANK) and inflammatory mediators (MMP-9, COX-2). Mechanistic studies revealed that ADSCs-Exos mitigated inflammation by modulating the COX-2/TRAF6/RANK signaling axis. This study demonstrates that ADSCs-Exos effectively inhibit osteoclastic activity and inflammation in periodontitis, offering a potential dual-targeted therapeutic strategy against bone resorption. In this study, we utilized exosomes derived from adipose mesenchymal stem cells to down-regulate the expression of osteoclast genes and protein-related mechanisms in an in vitro osteoclast model of chronic periodontitis constructed with Pg-LPS, and elucidated the effects of ADSCs-Exos on osteoclast regulation in periodontal inflammation.
Authors
- Shu Ma
Institutions
- Guiyang University (CN)
- The First People's Hospital of Guiyang (CN)
Publication Details
- Journal
- International Dental Journal
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1016/j.identj.2025.104590
- Primary Topic
- Oral microbiology and periodontitis research
- Type
- article
- Field-Weighted Citation Impact
- 0.00