Systemic Inflammatory Biomarkers and Their Association With Periodontal and Diabetes-Related Factors in the Diabetes and Periodontal Therapy Trial, A Randomized Controlled Trial.

Abstract

The present study evaluates effects of non-surgical periodontal treatment on serum biomarkers in patients with type 2 diabetes mellitus (t2DM) and chronic periodontitis who participated in the Diabetes and Periodontal Therapy Trial (DPTT); and associations among diabetes markers, serum biomarkers, and periodontal measures in these patients. DPTT participants randomized to receive immediate or delayed non-surgical periodontal therapy were evaluated at baseline and 6 months. Serum samples from 475 participants with 6-month data were analyzed for the following biomarkers: 1) high sensitivity C-reactive protein; 2) E-selectin; 3) tumor necrosis factor (TNF)-α; 4) vascular cell adhesion molecule (VCAM); 5) interleukin (IL)-6; 6) IL-8; 7) intercellular adhesion molecule; and 8) IL-10. Changes in biomarker levels from baseline and correlations among biomarker levels and clinical findings were analyzed. No differences between treatment and control groups were observed for any biomarkers at baseline or 6 months (P >0.05 for all variables). VCAM levels increased by an average (standard deviation) of 17.9 (99.5); ng/mL (P = 0.006) and E-selectin decreased by 2.33 (16.08) ng/mL (P = 0.03) in the treatment group after 6 months. E-selectin levels were significantly correlated with DM-related variables (hemoglobin A1c [HbA1c] and fasting glucose) at baseline and with 6-month change in both groups; no significant correlations were found among periodontal clinical parameters and serum biomarkers or DM-related variables. Neither HbA1c or body mass index varied during the study period in either study group. Non-surgical periodontal therapy and periodontal disease severity were not associated with significant changes in serum biomarkers in DPTT participants during the 6-month follow-up. Correlations among changes in E-selectin, IL-6, and DM-related variables suggest that t2DM may be the primary driver of systemic inflammation in these patients.