Patients with poor glycemic control have an average higher blood sugar as opposed to patients without diabetes. One result of increased blood sugar over time is a nonemzymatic glycation of many proteins throughout the body, known as Advanced Glycation Endproducts, or AGE’s. AGEs occur at an increased rate when patients are hyperglycemic, and have direct effects on both pro-inflammatory mediators as well as bone metabolism.67,68 They have been shown to increase pro-inflammatory cytokines through their interaction with the receptor for AGE (RAGE).69,70 Furthermore, AGE levels locally in periodontal tissues71 and in the systemic circulation72 have been linked to an increased periodontal inflammatory state and more advanced periodontitis in patients with type 2 diabetes.73 Therefore, it is clear that AGE-RAGE interactions are important in the pathogenesis of periodontal disease in patients with diabetes. RAGE activation leads to an exaggerated inflammatory response and increased tissue destruction that is typical of periodontitis in diabetic patients.78 This interaction may also account for the relationship between glycemic control and periodontal destruction observed in epidemiologic studies.
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