Periodontal disease and diabetes mellitus: discussion, conclusions, and recommendations.

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including monocytes and endothelial cells. RAGE interaction with specific ligands leads to cellular perturbation and dysfunction that may partially explain the periodontal manifestations of diabetes mellitus.3 When AGEs (the major ligands of RAGE) bind to endothelial cells, permeability and expression of vascular cell adhesion molecule-1 (VCAM-1) increase.4,5 When AGEs bind to monocytes, chemotaxis increases, and these cells produce increased levels of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α).6,7 Binding of RAGE on fibroblast cell surfaces impairs production of both type 1 procollagen mRNA and type 1 collagen in culture.8 These findings suggest that engagement of RAGE leads to a persistent inflammatory response and a reduced repair capacity. Of particular importance, the mechanism to account for increased periodontal disease in diabetes mellitus is consistent with mechanisms involved in other complications of diabetes mellitus (e.g., accelerated atherosclerosis and impaired wound healing).9,10 Dr. Iacopino reviewed the literature that links diabetes, elevated levels of serum lipids, and periodontitis.11 The proposed mechanism is related to the combined effects of hyperglycemia and hyperlipidemia. Hyperlipidemia is seen as elevations of certain freefatty acids, low-density lipoproteins, and triglycerides. The result of this perturbation is altered cell membrane function. Hyperglycemia promotes a hyperinflammatory state. Periodontitis may contribute to this process by promoting a chronic low-level systemic exposure to Gram-negative microorganisms. There are preliminary studies to support the association of infection and hyperlipidemia.12,13 He emphasized the need to consider serum lipid levels when evaluating periodontal disease as a complication of diabetes. Dr. Donahue discussed pathogenic mechanisms involving hyperinsulinemia/insulin resistance and periodontitis.14 The association of increased circulating levels of insulin with an inflammatory response, specifically levels of TNF-α, may be part of a cycle as TNFα can modify cell surface insulin receptors and promote insulin resistance. The reports that addressed the mechanisms underThe association between periodontal disease and diabetes mellitus has been recognized in the dental literature for several decades. The recent accumulating evidence of a relationship between periodontal infections and certain systemic diseases has renewed interest in this association. In addition to the recognized increased occurrence and severity of periodontal disease in patients with diabetes, studies have examined the converse relationship: how does periodontal disease modify glycemic control and can periodontal therapy improve glycemic control? The presentations in this section of the symposium addressed this bidirectional relationship. This discussion of the section on periodontal infections and diabetes mellitus will be divided into 3 parts: 1. Review of the mechanisms linking these disorders; 2. Summary of the studies that evaluate periodontal disease as a complication of diabetes, and the effect of treatment of periodontal disease on glycemic control. Included here is a review of 2 important longitudinal, multicenter randomized clinical trials that examined the effect of glycemic control on complications of diabetes mellitus; and 3. General conclusions for the session and recommendations for the future.