This review is to examine the current literatures on the relationship between periodontitis and hypertension as well as to explore the possible biological pathways underlying the linkage between these health conditions. Hypertension is one of the major risk factors for cardiovascular diseases. Oxidative stress and endothelial dysfunction are among the critical components in the development of hypertension. Inflammation has received much attention recently and may contribute to a pivotal role in hypertension. Periodontitis, a chronic low-grade inflammation of gingival tissue, has been linked to endothelial dysfunction, with blood pressure elevation and increased mortality risk in hypertensive patients. Inflammatory biomarkers are increased in hypertensive patients with periodontitis. Over the years, various researches have been performed to evaluate the involvement of periodontitis in the initiation and progression of hypertension. Many cross-sectional studies documented an association between hypertension and periodontitis. However, more well-designed prospective population trials need to be carried out to ascertain the role of periodontitis in hypertension.

Cardiovascular disease (CVD) is one of the leading major causes of morbidity and mortality worldwide. It may result from the interactions between multiple genetic and environmental factors including sedentary lifestyle and dietary habits. The quality of dietary oils and fats has been widely recognised to be inextricably linked to the pathogenesis of CVD. Vegetable oil is one of the essential dietary components in daily food consumption. However, the benefits of vegetable oil can be deteriorated by repeated heating that leads to lipid oxidation. The practice of using repeatedly heated cooking oil is not uncommon as it will reduce the cost of food preparation. Thermal oxidation yields new functional groups which may be potentially hazardous to cardiovascular health. Prolonged consumption of the repeatedly heated oil has been shown to increase blood pressure and total cholesterol, cause vascular inflammation as well as vascular changes which predispose to atherosclerosis. The harmful effect of heated oils is attributed to products generated from lipid oxidation during heating process. In view of the potential hazard of oxidation products, therefore this review article will provide an insight and awareness to the general public on the consumption of repeatedly heated oils which is detrimental to health.

Thermally oxidized oil generates reactive oxygen species that have been implicated in several pathological processes including hypertension. This study was to ascertain the role of inflammation in the blood pressure raising effect of heated soybean oil in rats. Male Sprague-Dawley rats were divided into four groups and were fed with the following diets, respectively, for 6 months: basal diet (control); fresh soybean oil (FSO); five-time-heated soybean oil (5HSO); or 10-time-heated soybean oil (10HSO). Blood pressure was measured at baseline and monthly using tail-cuff method. Plasma prostacyclin (PGI(2) ) and thromboxane A(2) (TXA(2) ) were measured prior to treatment and at the end of the study. After six months, the rats were sacrificed, and the aortic arches were dissected for morphometric and immunohistochemical analyses. Blood pressure was increased significantly in the 5HSO and 10HSO groups. The blood pressure was maintained throughout the study in rats fed FSO. The aortae in the 5HSO and 10HSO groups showed significantly increased aortic wall thickness, area and circumferential wall tension. 5HSO and 10HSO diets significantly increased plasma TXA(2) /PGI(2) ratio. Endothelial VCAM-1 and ICAM-1 were significantly increased in 5HSO, as well as LOX-1 in 10HSO groups. In conclusion, prolonged consumption of repeatedly heated soybean oil causes blood pressure elevation, which may be attributed to inflammation.

Oil thermoxidation during deep frying generates harmful oxidative free radicals that induce inflammation and increase the risk of hypertension. This study aimed to investigate the effect of repeatedly heated palm oil on blood pressure, aortic morphometry, and vascular cell adhesion molecule-1 (VCAM-1) expression in rats. Male Sprague-Dawley rats were divided into five groups: control, fresh palm oil (FPO), one-time-heated palm oil (1HPO), five-time-heated palm oil (5HPO), or ten-time-heated palm oil (10HPO). Feeding duration was six months. Blood pressure was measured at baseline and monthly using tail-cuff method. After six months, the rats were sacrificed and the aortic arches were dissected for morphometric and immunohistochemical analyses. FPO group showed significantly lower blood pressure than all other groups. Blood pressure was increased significantly in 5HPO and 10HPO groups. The aortae of 5HPO and 10HPO groups showed significantly increased thickness and area of intima-media, circumferential wall tension, and VCAM-1 than other groups. Elastic lamellae were disorganised and fragmented in 5HPO- and 10HPO-treated rats. VCAM-1 expression showed a significant positive correlation with blood pressure. In conclusion, prolonged consumption of repeatedly heated palm oil causes blood pressure elevation, adverse remodelling, and increased VCAM-1, which suggests a possible involvement of inflammation.

The retention of low-density lipoprotein (LDL) is a key process in the pathogenesis of atherosclerosis and largely mediated via smooth-muscle cell-derived extracellular proteoglycans including the glycosaminoglycan chains. Macrophages can also internalize lipids via complexes with proteoglycans. However, the role of polarized macrophage-derived proteoglycans in binding LDL is unknown and important to advance our understanding of the pathogenesis of atherosclerosis. We therefore examined the identity of proteoglycans, including the pendent glycosaminoglycans, produced by polarized macrophages to gain insight into the molecular basis for LDL binding. Using the quartz crystal microbalance with dissipation monitoring technique, we established that classically activated macrophage (M1)- and alternatively activated macrophage (M2)-derived proteoglycans bind LDL via both the protein core and heparan sulfate (HS) in vitro . Among the proteoglycans secreted by macrophages, we found perlecan was the major protein core that bound LDL. In addition, we identified perlecan in the necrotic core as well as the fibrous cap of advanced human atherosclerotic lesions in the same regions as HS and colocalized with M2 macrophages, suggesting a functional role in lipid retention in vivo . These findings suggest that macrophages may contribute to LDL retention in the plaque by the production of proteoglycans; however, their contribution likely depends on both their phenotype within the plaque and the presence of enzymes, such as heparanase, that alter the secreted protein structure.