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Subclustering and differential expression analysis revealed that fibroblast (e.g.,\n                      <jats:italic>APOL2<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      \/\n                      <jats:italic>CCN2<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) and progenitor cell (e.g.,\n                      <jats:italic>CDK5R1<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      \/\n                      <jats:italic>CCRL2<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) subclusters exacerbated fibrosis and immune activation, while\n                      <jats:italic>TMPRSS4<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      \/\n                      <jats:italic>CST5<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      fibroblasts were critical for homeostasis. Pro\u2010inflammatory endothelial subclusters (\n                      <jats:italic>IGHG1<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      \/\n                      <jats:italic>CXCL13<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) expanded, while anti\u2010inflammatory subclusters (\n                      <jats:italic>SERPINA5<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      \/\n                      <jats:italic>SERPINA3<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) diminished, may lead to vascular\u2010immune imbalance. Upregulation of immunoglobulin genes and downregulation of\n                      <jats:italic>MBP<\/jats:italic>\n                      disrupted neural function, while inflamed pulp showed increased B cells and macrophages, decreased T cells and monocytes. Inflammatory pathways (PI3K, EGFR, TGF\u03b2, MAPK, Oestrogen, NF\u2010\u03baB) were upregulated, with enhanced TGF\u03b2 signalling in endothelial cells. Intercellular interaction analysis showed altered\n                      <jats:italic>APP<\/jats:italic>\n                      \u2010\n                      <jats:italic>CD74<\/jats:italic>\n                      signalling in endothelial\u2010macrophage interactions and disrupted\n                      <jats:italic>CXCL14<\/jats:italic>\n                      \u2010mediated communication between immune and endothelial cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      For the first time, we have identified nine cell populations in dental pulp with their spatial localization and intercellular crosstalk using spatial transcriptomic sequencing technology, and mapped the inflammatory landscape of dental pulp. Cellular remodelling\u2014driven by\n                      <jats:italic>APP<\/jats:italic>\n                      suppression,\n                      <jats:italic>CXCL14<\/jats:italic>\n                      deficiency and TGF\u03b2 activation\u2014is a central mechanism in pulpitis progression. These findings provide a preliminary spatial transcriptomic foundation that may inform the development of targeted strategies for vital pulp therapy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/iej.70200","type":"journal-article","created":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T13:26:11Z","timestamp":1781529971000},"page":"2180-2200","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Spatial Transcriptomics Delineates the Inflammatory Landscape of Human Dental Pulp: Regional Crosstalk and Therapeutic Implications"],"prefix":"10.1111","volume":"59","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-0018-1772","authenticated-orcid":false,"given":"Fengyuan","family":"Zhang","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Hospital of Stomatology Sun Yat\u2010Sen University  Guangzhou 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