Periodontal Health and Disease in the Context of Systemic Diseases

Figure 3

The hyperglycaemic state in diabetic patients induces: (1) the expression of irreversible advanced glycation end products (AGEs) and related receptors (RAGE) and (2) enhancement of oxidative stress and (3) modulation of the RANKL/OPG ratio both directly and indirectly through the AGE/RAGE axis. The result is immune cell dysfunction and cytokine imbalance. All the above, complemented by the effects of subgingival dysbiosis and the circulating adipokines produced due to diabetes-associated adiposity and dyslipidemia, induce a vicious cycle of enhanced periodontal destruction and impaired tissue repair, leading to acceleration and worsening of periodontal disease. Of course, a significant interindividual variation in these processes must be considered (genetics, age, smoking, and stress). Adapted from “A Review of the Evidence for Pathogenic Mechanisms that May Link Periodontitis and Diabetes,” Taylor, J.J. [60], Journal of Clinical Periodontology, 2013, 40: S113-S134, Copyright (2013), reproduced with permission from Wiley.