| Epidemiological and clinical studies investigating the association between periodontal disease (PD) and cardiovascular disease (CVD) often implicate the potential role of elevated serum inflammatory markers (IM). However, the relationship between PD and elevated oral and systemic IM is not clearly understood. Objectives. The purpose of this prospective, longitudinal human cohort study was to assess the impact of oral health status and dental treatment on baseline levels and longitudinal changes in oral and systemic IM in adults. Methods. 30 persons aged 29--74 years (55 +/- 11 yrs; mean +/- SD) with terminal dentition (TD; i.e., severe periodontal disease requiring full mouth extraction of at least 8 teeth) and 26 persons aged 31--83 years (54 +/- 13 yrs) who were periodontally healthy (PH; no probing depths >4mm) were recruited at the UNC School of Dentistry. Serum and gingival crevicular fluid (GCF) were collected at baseline, and 2-, 6-, 13-, 26-, and 52-weeks post-baseline for assessment of inflammatory and associated systemic markers including serum C-reactive protein, interleukin-6, lipid panel, complete blood count, and others. Student's t-test was used to test group and visit differences. Additional linear regression and mixed model analysis evaluated several variables individually with the group and visit effects. These variables included age, gender, race/ethnicity, body mass index, smoking status, and other systemic risk factors. Results: Baseline mean GCF Interleukin-1beta and PGE 2, and serum Interleukin-6 were significantly elevated in the TD compared to PH group. This relationship was unchanged following bivariate adjustment for known risk factors. A trend was observed for elevated baseline median CRP in the TD group. Mean IL-6 was consistently significantly lower and apolipoprotein A was consistently significantly higher than at baseline following extractions. Conclusions: These results suggest that TD status and treatment may be associated with a difference and subsequent change in some oral and systemic inflammatory markers independent of known risk factors. However, larger studies are needed to adequately test this hypothesis. This study was supported by National Institutes of Health, National Institute of Dental and Craniofacial Research grants DE00427 and DE013079. |
