Effect of ADSCs-Exos on Pg-LPS-Induced Osteoclastogenesis in an In Vitro Inflammatory Model.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Periodontitis is a chronic inflammatory disorder characterized by tissue degradation and bone loss. Lipopolysaccharide (LPS) accelerates disease progression by host immune activation, inducing localized inflammatory infiltration and osteoclastogenesis, and disrupting bone metabolic homeostasis. Adipose-derived mesenchymal stem cells (ADSCs) exert anti-inflammatory, anti-apoptotic, and regenerative effects via paracrine signaling. Methods 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). ADSC-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 in vitro periodontitis model, PKH26-labeled ADSC-Exos were internalized by cells, as shown by confocal microscopy. Their effects on osteoclastic markers (TRAP, MMP-9, and COX-2) and signaling mediators (RANK and TRAF6) were evaluated using real-time PCR and western blotting. Results ADSCs-Exos suppressed early osteoclast differentiation in Pg-LPS-induced in vitro periodontitis model. Mechanistic studies revealed that ADSCs-Exos mitigated inflammation by modulating the COX-2/TRAF6/RANK signaling axis. Conclusions This study investigated

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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