{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T21:00:44Z","timestamp":1774558844095,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[1999,11,1]],"date-time":"1999-11-01T00:00:00Z","timestamp":941414400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[1999,11]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Our previous studies in diabetic (DB) rats suggest that hyperlipidemia may cause a dysregulation of the cellular and local cytokine response to periodontitis (AP). The objective of the present study was to determine if diabetes has a similar dysregulatory effect on the gingival response to AP in humans. Methods: Peripheral blood, as well as gingival tissue (GT) and gingival crevicular fluid (GCF), was obtained from a total of 35 patients who were categorized into the following groups based on level of diabetic (type 2) control and presence or absence of adult periodontitis (AP): group 1, systemically and periodontally healthy (n = 6); group 2, systemically healthy with adult periodontitis (n = 7); group 3, wellcontrolled diabetes and periodontally healthy (n = 6); group 4, well\u2010controlled diabetes with adult periodontitis (n = 5); group 5, poorly controlled diabetes and periodontally healthy (n = 5); group 6, poorly controlled diabetes and adult periodontitis (n = 6). All subjects were given a thorough periodontal examination, including probing depths (PD), clinical attachment levels (CAL), gingival index (GI), plaque index PI), and vertical bitewing radiographs. Blood studies included levels of glycated hemoglobin (HbA1c), triglycerides (TG), cholesterol (CHL), low\u2010density lipoproteins (LDL), and high\u2010density lipoproteins (HDL). The levels of interleukin\u20101 beta (IL\u20101\u03b2) in GCF and GT, interleukin\u20106 (IL\u20106), and platelet\u2010derived growth factor AB (PDGF\u2010AB) in GT from patients in each experimental group were analyzed by enzyme\u2010linked immunosorbent assay (ELISA).<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> Our results indicate that all clinical indices except PI were significantly elevated in the poorly controlled and well\u2010controlled diabetics, compared to systemically healthy patients, but only in the subjects without preexisiting AP (Tukey's multiple comparisons, <jats:italic>P<\/jats:italic> &lt;0.05). Pairwise linear regression analysis revealed significant (P &lt;0.01) positive associations between periodontal inflammation (PD, CAL, PI, GI) and levels of GCF IL\u20101\u03b2, GT IL\u20101\u03b2, GT IL\u20106, but not GT PDGF; moreover, GT IL\u20106 levels were significantly associated (<jats:italic>P<\/jats:italic> &lt;0.05) with GT IL\u20101\u03b2. As TG levels increased in the non\u2010AP patients (group 1 &lt; group 3 &lt; group 5), there was a trend, not significant, for increased GCF IL\u20101\u03b2 levels and increased gingival inflammation. Interestingly, periodontitis resulted in increased PDGF\u2010AB levels in the gingiva of systemically healthy and well\u2010controlled diabetes patients, but this increase was obtunded in poorly controlled diabetes patients.<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> This confirms our earlier work in the diabetic rat model. These studies indicate that decreased metabolic control in type 2 diabetics results in increased serum triglycerides and has a negative influence on all clinical measures of periodontal health, particularly in patients without preexisting periodontitis. Levels of the cytokine IL\u20101\u03b2 showed a trend for increasing as diabetic control diminished. In contrast, levels of the growth factor PDGF, which normally increase in periodontitis, decreased in poorly controlled diabetics with periodontitis. These studies suggest a possible dysregulation of the normal cytokine\/growth factor signaling axis in poorly controlled type 2 diabetics that may contribute to periodontal breakdown\/diminished repair. <jats:italic>J Periodontol 1999;70:1313\u20101321<\/jats:italic><\/jats:p>","DOI":"10.1902\/jop.1999.70.11.1313","type":"journal-article","created":{"date-parts":[[2005,2,2]],"date-time":"2005-02-02T06:01:16Z","timestamp":1107324076000},"page":"1313-1321","source":"Crossref","is-referenced-by-count":105,"title":["Heightened Gingival Inflammation and Attachment Loss in Type 2 Diabetics With Hyperlipidemia"],"prefix":"10.1002","volume":"70","author":[{"given":"Christopher W.","family":"Cutler","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert L.","family":"Machen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ravi","family":"Jotwani","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony M.","family":"Iacopino","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1999,11]]},"container-title":["Journal of Periodontology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/aap.onlinelibrary.wiley.com\/doi\/pdf\/10.1902\/jop.1999.70.11.1313","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T14:22:52Z","timestamp":1760883772000},"score":1,"resource":{"primary":{"URL":"https:\/\/aap.onlinelibrary.wiley.com\/doi\/10.1902\/jop.1999.70.11.1313"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1999,11]]},"references-count":0,"journal-issue":{"issue":"11","published-print":{"date-parts":[[1999,11]]}},"alternative-id":["10.1902\/jop.1999.70.11.1313"],"URL":"https:\/\/doi.org\/10.1902\/jop.1999.70.11.1313","archive":["Portico"],"relation":{},"ISSN":["0022-3492","1943-3670"],"issn-type":[{"value":"0022-3492","type":"print"},{"value":"1943-3670","type":"electronic"}],"subject":[],"published":{"date-parts":[[1999,11]]}}}