Systemic inflammatory responses in patients with type 2 diabetes with chronic periodontitis

Objective: The objective of this case-control study was to quantify the immune responsiveness in individuals with type 2 diabetes (T2D) as compared with patients without diabetes (NT2D) diagnosed with periodontitis. Research Design and Methods: Peripheral blood was collected from 20 patients with moderate-to-severe chronic periodontitis (10 T2D, 10 NT2D). Blood samples were stimulated with ultrapure Porphyromonas gingivalis and Escherichia coli lipopolysaccharide (LPS) for 24 hours. 14 cytokines/chemokines were quantified in culture supernatants using multiplex technology. Results: T2D individuals demonstrated higher unstimulated levels of interleukin 6 (IL-6), IL-1 beta, tumor necrosis factor alpha, interferon gamma, IL-10, IL-8, macrophage inflammatory protein 1 alpha (MIP1 alpha), and 1 beta (MIP1 beta), and higher stimulated levels of IL-6, IL-8, IL-10, MIP1 alpha and MIP1 beta, along with lower unstimulated and stimulated levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) when compared with NT2D (p<0.05). Importantly, the LPS-induced levels of IL-6, IL-8, IL-10 and MIP1 alpha strongly correlated with severity of disease, measured by pocket depths (PD), within the T2D group (r(2)>= 0.7, p<0.05), but not within NT2D. Conclusions: Among patients with chronic periodontitis, patients with T2D seem to have an enhanced LPS-induced immune responsiveness than individuals without diabetes, which correlates with periodontal disease severity, concomitant with a less robust GM-CSF response. This data may in part explain the higher predisposition to periodontitis in this population.