{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T08:46:09Z","timestamp":1791967569470,"version":"4.3.4"},"reference-count":37,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100011033","name":"Agencia Estatal de Investigaci\u00f3n","doi-asserted-by":"publisher","award":["PID2022\u2010137950NB\u2010I00"],"award-info":[{"award-number":["PID2022\u2010137950NB\u2010I00"]}],"id":[{"id":"10.13039\/501100011033","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Oral Implants Res"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To compare clinical, histological, immunohistochemical, and targeted gene\u2010expression features related to inflammasome signaling across healthy tissues, periodontitis, and peri\u2010implantitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>This exploratory cross\u2010sectional study included supracrestal soft\u2010tissue biopsies from 6 healthy controls, 17 periodontitis, and 18 peri\u2010implantitis lesions. Evaluations included clinical data, histomorphometric collagen quantification, immunohistochemical staining (CD45, NLRP3, AIM2, CASP1, IL\u20101\u03b2), and targeted digital transcriptomic profiling of 20 preselected inflammasome\u2010related genes using the NanoString nCounter platform. Data were analyzed using non\u2010parametric statistics and FDR\u2010corrected correlation matrices.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Periodontitis and peri\u2010implantitis showed greater clinical inflammation, reduced collagen content, and increased inflammatory infiltrate compared with healthy tissues. Peri\u2010implantitis displayed the more severe clinical phenotype and greater tissue disruption. At the molecular level, disease\u2010associated changes were captured by\n                      <jats:italic>AIM2<\/jats:italic>\n                      ,\n                      <jats:italic>CASP1<\/jats:italic>\n                      ,\n                      <jats:italic>IL1B<\/jats:italic>\n                      ,\n                      <jats:italic>GBP5<\/jats:italic>\n                      ,\n                      <jats:italic>TXNIP<\/jats:italic>\n                      ,\n                      <jats:italic>CGAS<\/jats:italic>\n                      ,\n                      <jats:italic>STING1<\/jats:italic>\n                      , and\n                      <jats:italic>PANX1<\/jats:italic>\n                      rather than\n                      <jats:italic>NLRP3<\/jats:italic>\n                      alone. Except for a minor pairwise difference in\n                      <jats:italic>CGAS<\/jats:italic>\n                      (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.031), individual gene expression did not differ between the diseased states. Stratified correlation analyses demonstrated coordinated within\u2010group co\u2010expression networks among priming, sensor, and effector transcripts, reflecting descriptive pathway patterns within each clinical cohort.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Periodontitis and peri\u2010implantitis share a substantial inflammasome\u2010related host\u2010response framework. Rather than revealing a distinct inflammasome program, peri\u2010implantitis exhibits a largely overlapping molecular profile that occurs within a clinically more severe and structurally more disrupted lesion environment. These findings suggest that the biological distinction between the two diseases may lie less in pathway identity than in the tissue context in which a shared inflammatory machinery is expressed.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/clr.70190","type":"journal-article","created":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T07:55:00Z","timestamp":1791964500000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Inflammasome\u2010Related Transcriptomic Profiles in Periodontitis and Peri\u2010Implantitis Reveal a Shared Inflammatory Framework: A Cross\u2010Sectional Study"],"prefix":"10.1111","author":[{"given":"Miguel","family":"Padial\u2010Molina","sequence":"first","affiliation":[{"name":"Department of Oral Surgery and Implant Dentistry, School of Dentistry University of Granada  Granada Spain"},{"name":"Instituto de Investigaci\u00f3n Biosanitaria Ibs. 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GRANADA  Granada Spain"},{"name":"Department of Pathology, School of Medicine University of Granada  Granada Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allinson","family":"Olaechea","sequence":"additional","affiliation":[{"name":"Department of Oral Surgery and Implant Dentistry, School of Dentistry University of Granada  Granada Spain"},{"name":"Instituto de Investigaci\u00f3n Biosanitaria Ibs. 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