Gingival Crevicular Fluid Levels of Interleukin‐1β and Glycemic Control in Patients With Chronic Periodontitis and Type 2 Diabetes

Abstract

Background: Patients with diabetes have increased incidence and severity of periodontal disease not accounted for by differences in the subgingival microbial infection. Poor glycemic control has been consistently associated with periodontal disease severity. Also, recent evidence suggests that hyperglycemia may induce inflammatory cytokine production. Few studies, however, have examined local biochemical measures of periodontal inflammation in patients with type 2 diabetes. The aim of this study was to determine whether glycemic control was related to gingival crevicular fluid (GCF) levels of interleukin‐1β (IL‐1β). Methods: GCF samples were collected from 45 patients with type 2 diabetes and untreated chronic periodontitis. Plaque index (PI), bleeding on probing (BOP), probing depth (PD), and attachment level (AL) were recorded at six sites per tooth. IL‐1β levels were determined from individual GCF samples by enzyme‐linked immunoabsorbent assay (ELISA). Individual site and mean patient values were calculated. Glycated hemoglobin (HbA 1c) levels were measured from anticoagulated whole blood using an automated affinity chromatography system. Serum glucose was also determined. Results: Clinical periodontal measures (PD, AL, BOP) and measures of glycemic control (HbA1c, random glucose) were signifi‐ cantly correlated with GCF IL‐1β. Patients with greater than 8% HbA1c had significantly higher mean GCF IL‐1β levels than patients with less than 8% HbA1c. In a multivariate model adjusting for age, gender, PD, AL, BOP, and PI, HbA1c and random glucose were independent predictors of high GCF IL‐1β. Conclusions: Poor glycemic control is associated with elevated GCF IL‐1β. These data are consistent with the hypothesis that hyperglycemia contributes to an heightened inflammatory response, and suggests a mechanism to account for the association between poor glycemic control and periodontal destruction. J Periodontol 2004;75:1203‐1208.