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Background: Obesity represents the second preventable mortality cause worldwide, and is very often associated with type 2 Diabetes Mellitus (T2DM). The first line treatment is lifestyle modification to weight-loss, but for those who fail to achieve the goal or have difficulty in maintaining achieved results, pharmacological treatment is needed. Few drugs are available today, because of their side effects., Objective: We aim to review actual pharmacological management of obese patients, highlighting differences between Food and Drug Administration - and European Medicine Agency-approved molecules, and pointing out self-medications readily obtainable and widely distributed., Methods: Papers on obesity, weight loss, pharmacotherapy, self- medication and diet-aid products were selected using Medline. Research articles, systematic reviews, clinical trials and meta-analyses were screened., Results: Anti-obesity drugs with central mechanisms, such as phentermine and lorcaserin, are available in USA, but not in Europe. Phentermine/topiramate and naltrexone/bupropion combinations are now available, even though the former is still under investigation from EMA. Orlistat, with peripheral mechanisms, represents the only drug approved for weight reduction in adolescents. Liraglutide has been approved at higher dose for obesity. Anti-obesity drugs, readily obtainable from the internet, include crude-drug products and supplements for which there is often a lack of compliance to national regulatory standards., Conclusions: Mechanisms of weight loss drugs include the reduction of energy intake or the increase in energy expenditure and sense of satiety as well as the decrease of hunger or the reduction in calories absorption. Few drugs are approved, and differences exist between USA and Europe. Moreover, herbal medicines and supplements often sold on the internet and widely used by obese patients, present a risk of adverse effects., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Vascular remodeling is an alteration in the structure of vessels in response to injury or hemodynamic changes. Disturbance of the structural and functional integrity of the endothelial cell layer can be observed in vascular remodeling associated with inflammation. Chemokines have been implicated in a wide range of diseases with prominent inflammatory components, and also in vascular remodeling. Among them, CC-chemokines are of great interest. They act through conventional CC-chemokine receptors (CCRs), widely expressed by leucocytes which are attracted to sites of chronic inflammation. However, many experimental data show that CCRs are expressed by vascular cells, suggesting a direct, leukocyte-independent effect on vascular remodeling., Objective: Here, we discuss the role of CC-chemokines in atherosclerosis, angiogenesis, restenosis and renal dysfunction through direct activation of endothelial cells, endothelial progenitors, vascular smooth muscle cells, platelets, erythrocytes, mesangial cells and fibroblasts., Results: The pathophysiological role of CC-chemokines has become more interesting since the discovery of the atypical chemokine receptor (ACKR) subfamily, that does not couple with G proteins and fails to transmit conventional intracellular signals. It has been demonstrated to be a chemokine scavenger or decoy receptor with a role in the regulation of acute inflammatory responses., Conclusion: At the vascular level, ACKRs are expressed by endothelial cells and endothelial lymphatic cells that seem to regulate angio- and lymph-angiogenesis. Pleiotropic effects of CC-chemokines on vascular wall cells and leukocytes increase their importance in vascular remodeling and suggest new drugs to counteract vascular dysfunction., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Background: Endothelial dysfunction (ED) is a pathophysiological mechanism present in patients affected by type 2 diabetes (T2DM) supporting the development of cardiovascular disease. Among immune- and inflammatory cells accelerating atherosclerosis, dendritic cells (DC) play a pivotal role, however their pathogenetic mechanism has not been fully clarified, at present. The aim of our review is to explore the relationship between ED, DCs and cardiovascular events., Methods: We analysed the literature in Medline database under ''endothelial function OR dysfunction OR vasodilatation'', AND ''dendritic cells" OR "innate immunity" OR "adaptive immunity" AND "diabetes" AND "cardiovascular disease" OR "atherosclerosis". Research articles, systematic reviews and clinical trials have been screened., Results: Both conventional DCs (cDCs) and plasmacytoid cells (pDCs) have been found in the atherosclerotic lesions, together with other pro-inflammatory cells, leading to increase local inflammation. This inflammatory state drives DC interaction with dysfunctional endothelium activating vascular smooth muscle cells. Clinical studies have reported a dysregulation in circulating DC number and function in T2DM patients, especially in those with macrovascular complications, and a significant correlation between reduction in pDCs, TNF-α production and poor glycemic control has been reported., Conclusion: Several studies have proven the prognostic significance of endothelial function and the accumulation of cDCs and pDCs in the arterial intima, thus suggesting their pathogenetic role in atherogenesis. A lack of clinical results is evident, since most observations on human studies are based on circulating measurements despite the fact that different DCs, residing in different tissues, were not detectable in peripheral blood samples. Further preclinical and clinical studies are needed, which should include the measurement of both circulating and tissueresiding DCs simultaneously., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Endothelial dysfunction (ED) is the initial step in the development of atherosclerosis, leading to cardiovascular disease (CVD). It has been suggested that periodontal disease (PD) could be associated to pathogenesis of atherosclerosis, since it is able to trigger a host response with systemic inflammation. Although a number of epidemiological studies have shown that periodontitis could be associated with ED, it is still unclear whether periodontal treatment could improve ED and therefore cardiovascular outcomes. In this narrative review we analysed the literature in the databases of Medline under ''endothelial function OR dysfunction OR vasodilatation'', AND ''periodontal disease" OR periodontal treatment" AND "cardiovascular disease" OR atherosclerosis AND "endothelial biomarker". Research articles, systematic reviews and clinical trials were screened. ED could be related to periodontitis as well as to CVD. Periodontal treatment reduces the risk of teeth loss and may improve ED and the risk of CVD. Since controversial results exist, there is an urgent need for well-designed clinical trials to find and validate novel biomarkers of endothelial function, such as circulating endothelial progenitors, which may be crucial for further investigation of the association of PD with endothelial function and CVD.