Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point

Abstract

Diabetes and periodontitis are two of the most prevalent diseases worldwide that negatively impact the quality of life of the individual suffering from them. They are part of the chronic inflammatory disease group or, as recently mentioned, non-communicable diseases, with inflammation being the meeting point among them. Inflammation hitherto includes vascular and tissue changes, but new technologies provide data at the intracellular level that could explain how the cells respond to the aggression more clearly. This review aims to emphasize the molecular pathophysiological mechanisms in patients with type 2 diabetes mellitus and periodontitis, which are marked by different impaired central regulators including mitochondrial dysfunction, impaired immune system and autophagy pathways, oxidative stress, and the crosstalk between adenosine monophosphate-activated protein kinase (AMPK) and the renin-angiotensin system (RAS). All of them are the shared background behind both diseases that could explain its relationship. These should be taken in consideration if we would like to improve the treatment outcomes. Currently, the main treatment strategies in diabetes try to reduce glycemia index as the most important aspect, and in periodontitis try to reduce the presence of oral bacteria. We propose to add to the therapeutic guidelines the handling of all the intracellular disorders to try to obtain better treatment success.

Melatonin protects gingival mesenchymal stem cells and promotes differentiation into osteoblasts

“…This may be due to the low number of cells in each well (150 per well). The relevance of the number of stem cells that must be in the niche to be repaired periodontally is critical as this occurs in an ambiance of inflammation and ROS 38,39 . This experiment confirms that the amount of initial GMSCs is critical to achieving regeneration efficiently.…”

“…The relevance of the number of stem cells that must be in the niche to be repaired periodontally is critical as this occurs in an ambiance of inflammation and ROS. 38,39 This experiment confirms that the amount of initial GMSCs is critical to achieving regeneration efficiently. On the other hand, in the wound scratch assay, MEL reversed the damage caused by BSO and GLUT, which reinforces the fact that MEL could be a powerful adjuvant in promoting proper periodontal regeneration.…”

Periodontitis, Metabolic and Gastrointestinal Tract Diseases: Current Perspectives on Possible Pathogenic Connections

“…Systemic diseases, such as diabetes, can interfere with the periodontal condition, making the prognosis of associated diseases unfavorable [ 33 ]. The chronic evolution of inflammatory diseases is possible in complex conditions, because they often involve several causal components that play a simultaneous role and interact with each other, often in an unpredictable way.…”

“…Over the years, diabetes has been linked to nephropathy, retinopathy, neuropathy, cardiovascular disease and periodontitis. Periodontal disease, considered an inflammatory disease, has been shown to have a number of systemic implications, with several studies suggesting the existence of a two-way link between periodontal health and these various pathologies [ 33 , 34 , 35 ]. Over the years, essential evidence has shown that diabetes is a risk factor for impaired periodontal health.…”

Periodontitis exacerbates endothelial dysfunctions partly via endothelial‐mesenchymal transition in streptozotocin‐induced diabetes rats

“…4 The increased pro-inflammation cytokine levels, comprising C-reactive protein (CRP), tumor necrosis factorα (TNFα), interleukin-6 (IL-6), and interleukin 1β (IL-1β), have been studied in diabetes patients with periodontitis and experiment animal models. 5,6 These elevated cytokines may raise the levels of adhesion molecules such as P-selectin, intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular cell adhesion molecule 1 (VCAM-1), exacerbating endothelial dysfunction. 7 Studies suggest that endothelial-mesenchymal transition (EndMT) serves as a connecting link between endothelial impairment and inflammation.…”