{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:11:24Z","timestamp":1787015484386,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,11,21]],"date-time":"2012-11-21T00:00:00Z","timestamp":1353456000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clinic Periodontology"],"published-print":{"date-parts":[[2013,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>Lipopolysaccharide is a bacterial virulence factor implicated in chronic periodontitis, which may penetrate the junctional epithelial barrier and basement membrane to insult underlying stroma. We sought to identify lipopolysaccharide\u2010induced global gene expression changes responsible for signalling between stroma and epithelium during disease onset.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>Using a rat lipopolysaccharide periodontitis model, junctional epithelium and underlying stromal tissue were separately collected from healthy and diseased animals by laser\u2010capture microdissection and subject to gene expression microarray analysis. Key gene products identified were validated in gingival epithelial and fibroblast cell cultures.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Global gene expression patterns distinguishing health\n                      <jats:italic>versus<\/jats:italic>\n                      disease were found in and between both tissue types. In stroma, the most significantly altered gene ontology function group (\n                      <jats:italic>Z<\/jats:italic>\n                      \u00a0\u2265\u00a04.00) was cytokines, containing most significantly (\u00b12\u2010fold;\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.05) upregulated genes amphiregulin, IL1\u2010\u03b2 and Fas ligand, all positive, diffusible modulators of the epithelial growth factor receptor pathway. In epithelium, the most significant changes were in downregulated\n                      <jats:styled-content style=\"fixed-case\">FOS<\/jats:styled-content>\n                      \u2010related antigen\u20101 gene, somatostatin receptor\u20102 gene and mucin\u20104 gene, all negative modulators of the epithelial growth factor receptor pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results establish a periodontitis model for studying gene product interactions and suggests that the onset of junctional epithelial disease hyperproliferation involves a concerted stromal\u2013epithelial signalling axis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jcpe.12023","type":"journal-article","created":{"date-parts":[[2012,9,24]],"date-time":"2012-09-24T21:35:31Z","timestamp":1348522531000},"page":"8-17","source":"Crossref","is-referenced-by-count":15,"title":["Lipopolysaccharide induces a stromal\u2013epithelial signalling axis in a rat model of chronic periodontitis"],"prefix":"10.1111","volume":"40","author":[{"given":"James D.","family":"Firth","sequence":"first","affiliation":[{"name":"Department of Oral Biological &amp; Medical Sciences Faculty of Dentistry, University of British Columbia Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisuke","family":"Ekuni","sequence":"additional","affiliation":[{"name":"Department of Preventive Dentistry Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kita\u2010ku Okayama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichiro","family":"Irie","sequence":"additional","affiliation":[{"name":"Department of Preventive Dentistry Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kita\u2010ku Okayama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takaaki","family":"Tomofuji","sequence":"additional","affiliation":[{"name":"Department of Preventive Dentistry Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kita\u2010ku Okayama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manabu","family":"Morita","sequence":"additional","affiliation":[{"name":"Department of Preventive Dentistry Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kita\u2010ku Okayama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward E.","family":"Putnins","sequence":"additional","affiliation":[{"name":"Department of Oral Biological &amp; 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