Interleukin-1 beta (IL-1b) is a key inflammatory mediator in periodontal disease and is of value in evaluating inflammatory status of periodontal tissues.  Objectives:  To assess associations between clinical periodontal status and IL-1b concentration in gingival crevicular fluid (GCF).  Methods:  The sample comprised 5,816 community-dwelling adults aged 52-74 years enrolled in the Atherosclerosis Risk in Communities (ARIC) study at four US study sites:  Forsyth County, NC; Jackson, MS; Minneapolis, MN; and Washington County, MD.  GCF was sampled on blotting paper from up to 16 periodontal pockets, and IL-1b concentration was measured using ELISA.  Clinical measurements at the same periodontal sites were made by calibrated examiners and used to compute summary variables for presence/absence of gingival bleeding (GB), maximum pocket depth (MaxPD) and maximum attachment level (MaxAL). Anthropomorphic measures and questionnaires were used to quantify covariates associated with systemic inflammatory burden and/or periodontal disease:  body mass index, smoking, diabetes, oral hygiene, dental visits, sex, race and ARIC study site. Subject's mean GCF IL-1b concentration was the dependent variable in multivariable ANOVA, with periodontal measures and covariates as explanatory variables.  Results:  In bivariate analysis, GCF IL-1b concentration increased significantly (P<0.05) as MaxPD increased from 0-2mm (mean ± sd =115.0 ± 100.2 mg/L) to 4+mm (160.1 ± 103.7 mg/L) and as MaxAL increased from 0-2mm (130.0 ± 99.9 mg/L) to 4+mm (150.9 ± 107.3 mg/L).  GCF IL-1b concentration was greater among people who had GB (153.6 ± 107.3 mg/L) compared with people did not (113.7 ± 90.7 mg/L).  In multivariate analysis, PD and GB persisted as independent explanatory variables (P<0.05) controlling for all covariates.  However, AL was not a significant variable in the multivariable model.  Conclusions:  GCF IL-1b was positively associated with clinical signs of periodontal disease. This   association was independent of known risk factors for systemic inflammation.  Supported by: NIDCR DE-11551 and NHLBI.