Impact of Periodontitis on Glycemic Control and Metabolic Status in Diabetes Patients: Current Knowledge on Early Disease Markers and Therapeutic Perspectives

Abstract

Diabetes mellitus and periodontitis are two of the most common chronic diseases affecting the world's population, and they are intimately linked. For several years, in fact, it has been known that there is an interdependent relationship between the two diseases: Diabetes promotes the destruction of periodontal tissues, and periodontal disease negatively affects glycemic control. In relation to the control of dental plaque and oral dysbiosis responsible for periodontal disease, both nonsurgical and surgical therapy associated with proper home hygiene procedures have emerged as essential for good glycemic control. Moreover, several evidences suggest the essential role played by the control of periodontal disease in preventing the onset of the most common complications of diabetes: cardiovascular diseases, retinopathies, and other systemic diseases. The aim of this study is to update the current knowledge on the bi-univocal relationship between diabetes and periodontitis and the impact of therapy in the optimal management of these two disorders. From the information found in the literature, it has emerged that the correct treatment of periodontal disease in diabetic patients represents one of the main mechanisms and means currently established and valid to control periodontal disease and glucose metabolism and prevent the onset or development of diabetic complications.

Figure 1

Impact of diabetes on periodontal health. Hyperglycemia in diabetic subjects favors different pro-inflammatory responses that affect the systemic health and the periodontal tissues. The incremented adipokine production (especially in obese adults) induces the release of different pro-inflammatory mediators such as leptin, IL-6, and TNF-α. Furthermore, AGEs deposition in the different human tissues further stimulates cytokine release and inflammation. Another mechanism of periodontal tissue destruction is the altered neutrophil polymorphonucleates' (PMN) function characterized by enhanced respiratory burst and delayed apoptosis. MMP is the acronym of metalloproteinases. All these factors combined to genetic predisposition and pathological subgingival biofilm lead to the increased risk of severe periodontitis development.

Figure 2

Diabetes enhances inflammation in the periodontium leading to changes in bacterial composition. Diabetes results in more inflammation mirrored by increased leukocytes and cytokine expression, as well as a change in bacterial composition that improves the overall pathogenicity of the microbiota [42].

Figure 3

An explanatory graph of the different molecular pathways referring mainly to the blockade of the insulin receptor ISR-1 by inflammatory mediators (TNF-alpha).