ArticleStem cell research & therapy2025
hPDLSC-ApoEVs attenuate periodontitis and enhance bone regeneration via NF-κB/S100A9-Mediated M2 macrophage polarization.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Synthesis of MPB@ZnPc Nanomaterials and Their Application in the Treatment of Periodontitis.International journal of molecular sciences · 2026Article
- Lung microbiota-derived deoxyinosine alleviates TBI-aggravated sepsis-induced lung injury via the S100A9/RAGE pathway.Journal of neuroinflammation · 2026Article
- Apoptotic extracellular vesicles act as master regulators of the bone healing niche.Journal of nanobiotechnology · 2026Review
- The macrophage polarization-ferroptosis axis as a therapeutically targetable immunometabolic framework in periodontitis.Frontiers in immunology · 2026Review
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14 authors.
Funding
Abstract
backgroundPeriodontitis is the most prevalent oral disease worldwide, leading to inflammation, alveolar bone loss, and tooth loss. Mesenchymal stem cells (MSCs) transplantation has the potential to alleviate periodontitis and restore alveolar bone, but numerous studies have found that transplanted MSCs undergo apoptosis, releasing apoptotic extracellular vesicles (ApoEVs). Human periodontal ligament stem cells (hPDLSCs) ApoEVs have immunomodulatory and tissue regenerative potential. Still, their role in periodontitis treatment and alveolar bone restoration has not been investigated yet.
methodsThe study isolated hPDLSCs-ApoEVs and investigated the modulatory effect on macrophaghe. We explored the specific molecular mechanisms of hPDLSC-ApoEVs in regulating macrophage polarization in vitro through mRNA-seq and inhibitors. Co-culture experiment demonstrated that hPDLSC-ApoEVs promoted hPDLSC osteogenic differentiation by regulating macrophage polarization. Finally, we verified that hPDLSC-ApoEVs inhibited periodontitis-induced periodontal tissue defects and promoted periodontal bone tissue regeneration in vivo.
resultsThis study found that hPDLSCs-ApoEVs regulate M0 to anti-inflammatory M2 macrophage polarization, as indicated by the upregulation of CD163, IL-10, and ARG1. hPDLSCs-ApoEVs activated NF-κB signaling that upregulated S100A9 in macrophages. hPDLSCs-ApoEVs failed M2 macrophage polarization during inhibition of NF-κB or S100A9. Furthermore, hPDLSCs-ApoEVs-treated macrophage-conditioned medium robustly promoted osteogenic differentiation of hPDLSCs in vitro. Finally, we verified these results in the periodontitis model of male C57BL/6 mice. Local injection of hPDLSCs-ApoEVs facilitated macrophage M2 polarization, alleviated periodontitis, and restored alveolar bone.
conclusionIn conclusion, these findings provide new evidence for the clinical application of hPDLSCs-ApoEVs in periodontitis treatment via macrophage immune modulation-mediated alveolar bone restoration.
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