{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T12:46:19Z","timestamp":1790858779839,"version":"4.1.0"},"reference-count":18,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2008,7,4]],"date-time":"2008-07-04T00:00:00Z","timestamp":1215129600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:p><jats:bold>Background and Objectives:\u2002<\/jats:bold> Interleukin\u20104 (IL\u20104), secreted mainly by T\u2010helper\u20032 cells, is a key cytokine for the growth and proliferation of B\u2003lymphocytes. Previous studies have proved that IL\u20104 has an anti\u2010inflammatory effect owing to its efficient inhibition of the production of proinflammatory cytokines such as tumour necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), IL\u20101\u03b1, IL\u20101\u03b2, IL\u20106 and IL\u20108 by monocytes\/macrophages. The aim of the present study was to assess the relation between clinical parameters and concentrations of IL\u20104 within gingival crevicular fluid from inflamed gingiva and periodontitis sites and, subsequently, after treatment of the periodontitis sites.<\/jats:p><jats:p><jats:bold>Material and Methods:\u2002<\/jats:bold> A total of 60\u2003subjects were divided into three groups based on gingival index (GI), pocket probing depth and clinical attachment loss (CAL): healthy (group\u20031), gingivitis (group\u20032) and chronic periodontitis (group\u20033). A fourth group (group\u20034) consisted of 20\u2003subjects from group\u20033, 6\u20138\u2003weeks after treatment (i.e. scaling and root planing). Gingival crevicular fluid samples collected from each patient were quantified for IL\u20104 using the enzymatic immunometric assay.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> The highest mean concentration of IL\u20104 was obtained for group\u20031 (99.39\u2003\u00b1\u200349.33\u2003pg\/mL) and the lowest mean concentration of IL\u20104 was obtained for group\u20033 (15.78\u2003\u00b1\u200321.92\u2003pg\/mL). The mean IL\u20104 concentrations for group\u20032 (64.34\u2003\u00b1\u200339.56\u2003pg\/mL) and group\u20034 (68.92\u2003\u00b1\u200342.85\u2003pg\/mL) were intermediate between the levels in healthy subjects and periodontitis subjects.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> The mean concentration of IL\u20104 decreased from periodontal health to disease. Thus, we suggest that type\u20032 helper T\u2003cell cytokine, as represented by IL\u20104, was associated with the remission or improvement of periodontal disease.<\/jats:p>","DOI":"10.1111\/j.1600-0765.2007.01079.x","type":"journal-article","created":{"date-parts":[[2008,7,6]],"date-time":"2008-07-06T01:15:56Z","timestamp":1215306956000},"page":"712-716","source":"Crossref","is-referenced-by-count":47,"title":["Interleukin\u20104, a T\u2010helper\u20032 cell cytokine, is associated with the remission of periodontal disease"],"prefix":"10.1111","volume":"43","author":[{"given":"A. R.","family":"Pradeep","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Roopa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. P.","family":"Swati","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,11,2]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1177\/00220345840630031801"},{"key":"e_1_2_5_3_2","first-page":"400","article-title":"Cytokines and periodontal disease: immunopathological role of interleukins for B\u2003cell responses in chronic inflamed gingival tissues","volume":"64","author":"Fujihashi K","year":"1993","journal-title":"J Periodontol"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.07.040189.001045"},{"key":"e_1_2_5_5_2","doi-asserted-by":"publisher","DOI":"10.1902\/jop.1998.69.10.1098"},{"key":"e_1_2_5_6_2","first-page":"213","volume-title":"Clinical Periodontology and Implant Dentistry","author":"Kinane DF","year":"1998"},{"key":"e_1_2_5_7_2","doi-asserted-by":"crossref","first-page":"1127","DOI":"10.4049\/jimmunol.139.4.1127","article-title":"High\u2010efficiency purification and chemical characterization of B\u2003cell stimulatory factor\u20101\/interleukin\u20034","volume":"139","author":"Ohara J","year":"1987","journal-title":"J Immunol"},{"key":"e_1_2_5_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.10.3803"},{"key":"e_1_2_5_9_2","doi-asserted-by":"crossref","first-page":"1392","DOI":"10.1182\/blood.V76.7.1392.1392","article-title":"Interleukin\u20104 (IL\u20104) inhibits secretion of IL\u20101\u03b2, tumor necrosis factor\u2010\u03b1 and interleukin\u20106 by human monocytes","volume":"76","author":"Te Velde AA","year":"1990","journal-title":"Blood"},{"key":"e_1_2_5_10_2","doi-asserted-by":"crossref","first-page":"3020","DOI":"10.4049\/jimmunol.143.9.3020","article-title":"IL\u20104 inhibits H2O2 production and antileishmanial capacity of human cultured monocytes mediated by IFN\u2010\u03b3","volume":"143","author":"Lehn M","year":"1989","journal-title":"J Immunol"},{"key":"e_1_2_5_11_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.144.2.625"},{"key":"e_1_2_5_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.55.2.227"},{"key":"e_1_2_5_13_2","doi-asserted-by":"crossref","first-page":"925","DOI":"10.4049\/jimmunol.149.3.925","article-title":"IL\u20104 up\u2010regulates IL\u20101 receptor antagonist gene expression and its production in human blood monocytes","volume":"149","author":"Orino E","year":"1992","journal-title":"J Immunol"},{"key":"e_1_2_5_14_2","first-page":"331","article-title":"Absence of exogenous interleukin\u20104\u2010induced apoptosis of gingival macrophages may contribute to chronic inflammation in periodontal diseases","volume":"148","author":"Yamamoto M","year":"1996","journal-title":"Am J Pathol"},{"key":"e_1_2_5_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/0306-9877(92)90056-I"},{"key":"e_1_2_5_16_2","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-051X.2003.300201.x"},{"key":"e_1_2_5_17_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.1996.tb00295.x"},{"key":"e_1_2_5_18_2","doi-asserted-by":"publisher","DOI":"10.3109\/00016356309011240"},{"key":"e_1_2_5_19_2","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0757.2003.03103.x"}],"container-title":["Journal of Periodontal Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1111%2Fj.1600-0765.2007.01079.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/j.1600-0765.2007.01079.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,15]],"date-time":"2023-10-15T02:18:37Z","timestamp":1697336317000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/j.1600-0765.2007.01079.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2008,11,2]]},"references-count":18,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2008,12]]}},"alternative-id":["10.1111\/j.1600-0765.2007.01079.x"],"URL":"https:\/\/doi.org\/10.1111\/j.1600-0765.2007.01079.x","archive":["Portico"],"relation":{},"ISSN":["0022-3484","1600-0765"],"issn-type":[{"value":"0022-3484","type":"print"},{"value":"1600-0765","type":"electronic"}],"subject":[],"published":{"date-parts":[[2008,11,2]]}}}