Diabetes and periodontitis both involve significant dysregulation of the immune system. Periodontal tissue breakdown occurs in response to bacterial stimuli as a result of host inflammatory response. Periodontal tissue breakdown seen in disease is mediated by pro-inflammatory cytokines and mediators. There are significant differences in the inflammatory response among individuals, which influences susceptibility to disease as well as severity of disease progression.62 The immunologic dysregulation seen in diabetes is associated with both metabolic and physiologic changes in tissues. The most significant are hyperglycemia leading to the formation of AGEs as well as hyperlipidemia. Furthermore, diabetic subjects have an increased hyperinflammatory state and demonstrate increased serum levels of pro-inflammatory cytokines. As pro-inflammatory cytokines increase, patient’s glycemic control gets worse in a dose-dependent manner.53-65 Common pro-inflammatory biomarkers implicated in both periodontal disease and diabetes mellitus include interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), receptor activator of nuclear factor kappa B ligand (RANKL), and matrix metalloproteinases (MMPs).
Because inflammation is central to the pathophysiology of both periodontitis and diabetes, the role of inflammatory mediators in the interaction is critical and a summary of some of the key mechanisms will be discussed (Figure 3).
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