{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T03:28:17Z","timestamp":1786332497499,"version":"build-2736575974"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T00:00:00Z","timestamp":1783555200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001352","name":"the National University of Singapore","doi-asserted-by":"crossref","award":["A-0002943-00-00"],"award-info":[{"award-number":["A-0002943-00-00"]}],"id":[{"id":"10.13039\/501100001352","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001352","name":"the National University of Singapore","doi-asserted-by":"crossref","award":["A-0002095-00-00"],"award-info":[{"award-number":["A-0002095-00-00"]}],"id":[{"id":"10.13039\/501100001352","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Ministry of Education Singapore","award":["MOE-T2EP30122-0008"],"award-info":[{"award-number":["MOE-T2EP30122-0008"]}]},{"name":"Ministry of Education Singapore","award":["NUHSRO\/2022\/091\/T1\/Seed-Sep\/04"],"award-info":[{"award-number":["NUHSRO\/2022\/091\/T1\/Seed-Sep\/04"]}]},{"name":"Ninth People\u2019s Hospital affiliated to Shanghai Jiao Tong University School of Medicine","award":["JYZZ265"],"award-info":[{"award-number":["JYZZ265"]}]},{"name":"Postdoctoral Scientific Research Foundation","award":["202601052"],"award-info":[{"award-number":["202601052"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Pulpitis compromises dental pulp defense and repair, and current therapies inadequately resolve inflammation. Mesenchymal stem\/stromal cell (MSC)\u2013derived small extracellular vesicles (sEVs) exhibit potent anti-inflammatory properties, yet their protective role in inflamed dental pulp and underlying mechanisms remain unclear. This study aimed to evaluate the therapeutic potential of MSC-sEVs in experimental rat pulpitis, define the contribution of sEV-associated CD73 activity, and elucidate the molecular mechanisms by which MSC-sEVs attenuate lipopolysaccharide (LPS)\u2013induced inflammatory responses in dental pulp cells (DPCs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>sEVs were enriched from human MSC-conditioned medium by size-based fractionation and characterized for particle size, protein concentration, and CD73\/ecto-5\u2032-nucleotidase (NT5E) activity. Rat pulpitis was induced by LPS application to Class I cavities of maxillary molars. In vitro inflammation was modeled using LPS-stimulated DPC spheroids. Inflammatory mediators were quantified by nitric oxide (NO) quantification and enzyme-linked immunosorbent assay (ELISA), while signaling pathways were examined by Western blotting and pharmacological inhibition of CD73, adenosine receptors, AKT, ERK, and p38 MAPK.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>MSC-sEVs significantly alleviated pulpal inflammation and promoted reparative dentin formation in vivo, with efficacy comparable to mineral trioxide aggregate (MTA). In LPS-stimulated DPC spheroids, MSC-sEVs suppressed pro-inflammatory and nociceptive mediator release. Mechanistically, MSC-sEVs reduced NO, IL-6, MMP9, and NGF production through a CD73\u2013adenosine receptor\u2013dependent pathway involving AKT activation and p38 MAPK inhibition, but not ERK signaling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>MSC-sEVs promote dental pulp repair by modulating inflammation through a CD73-mediated adenosine signaling axis, highlighting their potential as a cell-free therapeutic for early pulpitis intervention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/stmcls\/sxag038","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T11:40:02Z","timestamp":1783424402000},"source":"Crossref","is-referenced-by-count":0,"title":["MSC-derived small extracellular vesicles promote dental pulp repair by alleviating inflammation in pulpitis via AKT and p38 MAPK 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