{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T22:23:05Z","timestamp":1771539785470,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,2,1]],"date-time":"2009-02-01T00:00:00Z","timestamp":1233446400000},"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":[[2009,2]]},"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> The goal of this study was to assess whether non\u2010smoking patients with type 2 diabetes present with increased levels of local and systemic proinflammatory mediators and, if so, whether such an increase is associated with enhanced clinical gingival inflammation compared to non\u2010smoking patients without diabetes.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> We used a cross\u2010sectional database consisting of 725 self\u2010reported lifelong non\u2010smokers aged 53 to 74 years. Gingival crevicular fluid (GCF) levels of interleukin (IL)\u20101\u03b2 and prostaglandin E<jats:sub>2<\/jats:sub> (PGE<jats:sub>2<\/jats:sub>) and serum levels of IL\u20106 were measured using enzyme\u2010linked immunosorbent assay. No participant had probing depth &gt;3 mm. Participants with bleeding on probing (BOP) in &lt;10% of sites were classified as healthy, whereas those with BOP in \u226510% of sites were defined as having biofilm\u2013gingival interface (BGI) gingivitis.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> Approximately 53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2 diabetes, respectively. The mean age\u2010adjusted level of GCF IL\u20101\u03b2 was significantly elevated in the diabetic group compared to the non\u2010diabetic group (<jats:italic>P<\/jats:italic> = 0.048), but serum IL\u20106 (<jats:italic>P<\/jats:italic> = 0.14) and GCF PGE<jats:sub>2<\/jats:sub> were not (<jats:italic>P<\/jats:italic> = 0.98). The mean GCF IL\u20101\u03b2 and PGE<jats:sub>2<\/jats:sub> levels were significantly elevated in subjects with BGI gingivitis (136.2 \u00b1 112.9 ng\/ml and 277.2 \u00b1 187.2 ng\/ml, respectively) compared to subjects with gingival health (95.9 \u00b1 82.9 ng\/ml and 205.7 \u00b1 149.6 ng\/ml, respectively), regardless of diabetic status (<jats:italic>P<\/jats:italic> &lt;0.001 for both). However, serum IL\u20106 was elevated in subjects with BGI gingivitis compared to subjects with gingival health only among subjects with diabetes (2.9 \u00b1 3.2 pg\/ml versus 1.5 \u00b1 1.4 pg\/ml; <jats:italic>P<\/jats:italic> = 0.008). With the exception of serum IL\u20106 in subjects without diabetes, an increase in the levels of proinflammatory mediators was associated with increased odds of having BGI gingivitis. The associations were stronger in the diabetic group.<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> Type 2 diabetes may increase the host inflammatory response to oral biofilm, which, in turn, may exacerbate preconditions associated with gingivitis in susceptible individuals. Furthermore, systemic inflammation, as demonstrated by the increased level of serum IL\u20106, is associated with BGI gingivitis among non\u2010smoking patients with diabetes.<\/jats:p>","DOI":"10.1902\/jop.2009.080385","type":"journal-article","created":{"date-parts":[[2009,2,2]],"date-time":"2009-02-02T10:22:40Z","timestamp":1233570160000},"page":"307-316","source":"Crossref","is-referenced-by-count":50,"title":["Levels of Serum Interleukin (IL)\u20106 and Gingival Crevicular Fluid of IL\u20101\u03b2 and Prostaglandin E<sub>2<\/sub> Among Non\u2010Smoking Subjects With Gingivitis and Type 2 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