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        <datestamp>2026-10-01T05:43:25Z</datestamp>
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          <dc:title>Table 1_Synovial inflammation and immune-stromal crosstalk in osteoarthritis-related synovial fibroblast research, 2006–2025: a bibliometric analysis.docx</dc:title>
          <dc:creator>Tiange Xia (24382640)</dc:creator>
          <dc:creator>Xiaoyan Sun (28501)</dc:creator>
          <dc:creator>Zhiwei Jiang (139025)</dc:creator>
          <dc:creator>Yijie Zhang (5179454)</dc:creator>
          <dc:creator>Yi Zhou (2723)</dc:creator>
          <dc:creator>Yang Shao (511623)</dc:creator>
          <dc:creator>Shaoshuo Li (11473120)</dc:creator>
          <dc:creator>Jianwei Wang (128689)</dc:creator>
          <dc:subject>Genetic Immunology</dc:subject>
          <dc:subject>bibliometric analysis</dc:subject>
          <dc:subject>fibroblast-like synoviocytes</dc:subject>
          <dc:subject>immune-stromal crosstalk</dc:subject>
          <dc:subject>osteoarthritis</dc:subject>
          <dc:subject>science mapping</dc:subject>
          <dc:subject>single-cell analysis</dc:subject>
          <dc:subject>synovial fibroblasts</dc:subject>
          <dc:subject>synovitis</dc:subject>
          <dc:description>Background&lt;p&gt;Osteoarthritis (OA) is increasingly understood as a whole-joint organ disease involving cartilage, synovium, subchondral bone, and the local immune-stromal microenvironment. Synovial fibroblasts and fibroblast-like synoviocytes (FLS) participate in synovitis, matrix remodeling, cartilage-synovium crosstalk, pain-associated microenvironments, and disease heterogeneity. However, the knowledge structure, main knowledge sources, and frontier evolution of OA-related synovial fibroblast research remain incompletely mapped.&lt;/p&gt;Methods&lt;p&gt;We retrieved publications on OA-related synovial fibroblasts/fibroblast-like synoviocytes (OA-FLS) published from 2006 to 2025 from the Web of Science Core Collection (WOSCC) and Scopus. After integration and deduplication, Bibliometrix, CiteSpace, VOSviewer, and Python were used to analyze annual publication trends, national and institutional contributions, author and journal distributions, collaboration networks, global and local citation structures, keyword co-occurrence, trend topics, and thematic evolution.&lt;/p&gt;Results&lt;p&gt;A total of 1,881 publications were included, comprising 1,642 articles and 239 reviews. Annual output increased from 53 publications in 2006 to 142 in 2025, with an annual growth rate of 5.32%. China contributed the largest number of publications, whereas international collaboration remained relatively limited. Keyword and citation structures indicated a strong influence of RA-FLS-related knowledge sources. Recent hotspots increasingly involved synovitis, immune-stromal interaction, extracellular vesicle-mediated communication, fibrosis, pain-associated fibroblast states, and single-cell/spatially related studies.&lt;/p&gt;Conclusion&lt;p&gt;OA-FLS research has expanded from early studies of inflammatory mediators and catabolic pathways toward questions about fibroblast states, tissue location, immune-stromal interaction, and clinical phenotype association. These findings suggest a gradual movement from RA-derived conceptual borrowing toward more OA-contextualized interpretation, although this pattern should be understood as a bibliometric inference rather than direct mechanistic proof. Future studies need to clarify which OA-FLS states have stable, reproducible, and pathologically meaningful disease associations through standardized sampling, multicenter validation, spatial localization, functional experiments, and integration with clinical phenotypes.&lt;/p&gt;</dc:description>
          <dc:date>2026-10-01T05:43:25Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fimmu.2026.1898740.s001</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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