Advanced Glycation End Products: Possible Link between Metabolic Syndrome and Periodontal Diseases

Abstract

On a planetary scale, Metabolic Syndrome (MetS)is the third cause of inability after malnutrition and nicotinism, even higher than water shortage and sedentariness. In the USA, the prevalence is estimated at over 25 percent of the population; in Italy, it involves approximately 25 percent of men and even 27 percent of women. These are very high figures, corresponding to approximately 14 million affected individuals. The prevalence is alarming and must not be underestimated, particularly in the dental field, where more than one patient out of four sitting in a dentist chair is affected. The etiology of periodontal disease has not yet been clarified, and recently the idea to consider it as a multifactor pathology has been developed. Cofactors such as the formation of free radicals of oxygen (ROS), oxidative stress, lipid peroxidation, and formation of glycation end-products (AGEs) probably play an important role in the onset of periodontal disease. The AGEs are compounds physiologically produced by the cells. However, they accumulate and cause pro-inflammatory conditions, when the cellular clearance fails, or in hyperglycemic and oxidative states. All these conditions can be clinically summarized as Metabolic Syndrome. The purpose of this literature review is to establish a relationship between two pathologies with very high prevalence: Metabolic Syndrome and Periodontal Disorder. The literature seems to have clarified that MetS involves a pro-oxidation status, which induces AGE formation. AGEs play a very important role in the course and severity of periodontal diseases.

Glycation and oxidative stress in the failure of dental implants: a case series

“…One of our recent reviews of literature also supports the hypothesis that glycation and oxidative stress are the possible common link with periodontal diseases in patients with metabolic syndrome, which is an example of systemic proinflammatory condition [8]. Minor pro oxidant conditions, too, like moderate smoking, unbalanced diet, mild hypertension, minor or undiagnosed hyperglycemia, can promote ROS production and irreversible accumulation in genetically predisposed patients [8].…”

“…The AGEs are heterogeneous products, that are constantly formed in physiological conditions, but significantly increase in hyperglycaemia and excessive oxidative stress [8,9]. Recent studies suppose that the AGEs are involved in a large number of systemic diseases, where the oxidative component is strong, such as in diabetes and hypertension [8]. …”

Is There an Association between Periodontitis and Hypertension?

“…In patients with MS, an increased caloric intake can cause an increased production of ROS, inducing insulin resistance and hyperinsulinemia, which can evolve into type 2 diabetes. Oxidation products can increase neutrophil adhesion, chemotaxis and advanced glycation end-products, which could also be implicated in the degeneration and damage of periodontal tissue [64]. Recent systematic review and meta-analysis showed evidence for an association between MS and PD [65].…”

“…Individuals with moderate to severe PD show higher blood pressure levels [66, 67]. Thus, insulin resistance and oxidative stress seem to be common elements present in MS, periodontitis, CVD and hypertension [61-64]. The (Fig.…”

A population-based study on the association between the intake of soft drinks and periodontal disease in Taiwanese adults aged 35–44 years (KCIS no. 33)

“…For instance, glucose-containing carbonated soft drinks increase carbonyl stress burden (3) , which, in turn, may result in a decrease in antioxidant concentration in oral saliva (4) and enhance oxidative nitration in association with the inflammatory reaction (5) . From the biological viewpoint, the inflammatory reaction caused by such oxidative stress is highly associated with systemic diseases, such as metabolic syndrome, diabetes, hypertension, asthma and periodontal disease (PD) (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16) . Oxidative stress (2,3,6,8,9,(13)(14)(15) pertaining to PD may be mediated through advanced glycation end-products that are created through non-enzymatic pathways from monosaccharide substances, dicarbonyls originating from the Maillard reaction, sugar self-oxidation and other molecular pathways (16,17) .…”