{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T13:22:13Z","timestamp":1770297733921,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100004799","name":"Australian Dental Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004799","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Disease Markers"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>This study profiled the local and systemic inflammatory responses to experimentally induced gingivitis. Eight females participated in a 21-day experimental gingivitis model followed by a 14-day resolution phase. Bleeding on probing and plaque index scores were assessed before, during, and after resolution of gingival inflammation, and samples of saliva, GCF, and plasma were collected. Samples were assessed for biomarkers of inflammation using the BioPlex platform and ELISA. There were no significant changes in GCF levels of cytokines during the experimental phase; however, individual variability in cytokine profiles was noted. During resolution, mean GCF levels of IL-2, IL-6, and TNF-<jats:italic>\u03b1<\/jats:italic>decreased and were significantly lower than baseline levels (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.003<\/mml:mn><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.025<\/mml:mn><\/mml:math>, and<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.007<\/mml:mn><\/mml:math>, resp.). Furthermore, changes in GCF levels of IL-2, IL-6, and TNF-<jats:italic>\u03b1<\/jats:italic>during resolution correlated with changes in plaque index scores (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mi>r<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.88<\/mml:mn><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.004<\/mml:mn><\/mml:math>;<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:mi>r<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.72<\/mml:mn><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.042<\/mml:mn><\/mml:math>;<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\"><mml:mi>r<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.79<\/mml:mn><\/mml:math>,<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M9\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.019<\/mml:mn><\/mml:math>, resp.). Plasma levels of sICAM-1 increased significantly during the experimental phase (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M10\"><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.002<\/mml:mn><\/mml:math>) and remained elevated and significantly higher than baseline levels during resolution (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M11\"><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:math>). These results support the concept that gingivitis adds to the systemic inflammatory burden of an individual.<\/jats:p>","DOI":"10.1155\/2013\/948569","type":"journal-article","created":{"date-parts":[[2013,10,20]],"date-time":"2013-10-20T17:02:07Z","timestamp":1382288527000},"page":"543-549","source":"Crossref","is-referenced-by-count":22,"title":["Local and Systemic Inflammatory Responses to Experimentally Induced Gingivitis"],"prefix":"10.1155","volume":"35","author":[{"given":"Shaneen J.","family":"Leishman","sequence":"first","affiliation":[{"name":"The University of Queensland, School of Dentistry, Brisbane QLD 4072, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory J.","family":"Seymour","sequence":"additional","affiliation":[{"name":"The University of Queensland, School of Medicine, Herston QLD 4006, Australia"},{"name":"Sir John Walsh Research Institute, University of Otago, Dunedin 9054, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pauline J.","family":"Ford","sequence":"additional","affiliation":[{"name":"The University of Queensland, School of Dentistry, Brisbane QLD 4072, 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