BackgroundSince chronic apical periodontitis (CAP) appears to be a risk factor for coronary heart disease, the aim of the study was to determine the relationship between the size of CAP lesion and inflammatory markers (hsCRP, IL-6, TNF-α), as well as lipids and lipoproteins (LpPLA2, apoAI, apoB level) in blood serum of patients with CAP.MethodsThe patients studied (n = 43) were divided into groups: patients under 50 and over 50 years of age, and a separate subgroup of the oldest age with the largest size of CAP lesions. Apolipoprotein AI (apoAI) above 150 mg/dL and below 150 mg/dL was used as an important criterion for the division of patients into groups. The CAP lesion size was measured using the Kodak digital imaging system software. The control group consisted of clinically healthy volunteers (n = 20) without CAP. Lipids were measured on a Siemens analyzer (Germany), apoAI, apoB, hsCRP levels were determined by immunonephelometric method, using the Health Care Diagnostic Product (Siemens GmbH, Germany), and IL-6, TNF-α and LpPLAG7 assay kits (ELISA, R&D Systems) were used.ResultsThe findings suggested that in patients with CAP and their age increase, the CAP lesion size, the concentration of inflammatory markers and LpPLA2 mass increased. Correlations between the CAP lesion size and LpPLA2 mass and between the CAP lesion size and TG level in patients with apoAI 150 ≤ mg/dL showed increase TG in atherogenic apoB-containing triglyceride-rich lipoprotein and TC in cholesterol-rich lipoprotein. The patients with a low apoAI and high LpPLA2 level can have a higher risk of odontogenic disease and progression of atherosclerosis and coronary heart disease.ConclusionWe have found a positive correlation between apoAI level and the CAP lesion size and a negative correlation between LpPLA2 level and the CAP lesion size. The results suggest that apoAI and LpPLA2 in HDL particles have antiinflammatory action and together can limit the CAP lesion size in patient with a higher apoAI level. The literature data on the distribution of lipoprotein particles in subjects are still insufficient, so this problem requires further studies.

No abstract

The aim of the study was to examine concentrations and relationships between melatonin levels assessed at 0:200 hrs and 0:700 hrs, lipid hydroperoxide (LPO) assessed at 0:200 hrs and 0:700 hrs, and apolipoprotein (apo)AI, apoAII, apoB, high sensitivity C-reactive protein (hsCRP) and NT-proBNP, in 27 patients with chronic heart failure (CHF) (17 patients - with NYHA class II and 10 - with NYHA class III). In the study, Lipoproteins apoAI, apoAII, apoB, high sensitivity C-reactive protein (hsCRP) levels were determined by way of immunonephelometric methods, serum melatonin concentration was measured by using a competitive enzyme immunoassay technique, while serum LPO concentration was measured by using Cayman’s Lipid Hydroperoxide Assay Kit. In the study, CHF patients without acute inflammatory response demonstrated a decreased concentration of high density lipoprotein cholesterol (HDL-C), apoAI, apoAII levels, but an increased concentration of NT-proBNP, hsCRP and LPO at night, and LPO at daytime; however, the concentration of LPO at 0:700 was lower than at 0:200. Pearson’s correlation test and multiple ridge stepwise regression showed that melatonin administered at night exerts an effect on the composition of apoAI and apoAII of HDL particles, and induces decreased LPO at 0:700, but has no effect upon NT-proBNP levels in patients with NYHA class II. However, in patients with NYHA class III, melatonin administered at night induces an increase in the content of apoAII and apoAI, which further decreases hsCRP, and this, together with the administered melatonin, brings about daytime decreases in NT-proBNP and hsCRP levels. The results indicated that the content of apoAII and apoAI in HDL particles and melatonin demonstrate an anti-oxidative and anti-inflammatory effect, and together, have a cardio-protective effect on patients with advanced CHF. Hence, the results support melatonin being a cardio-protective agent. These relationships, however, need to be confirmed in further studies.

No abstract

Disturbances in lipids, and inflammations plays a key role in the pathogenesis of all stages of atherosclerosis. The aim of present study was to investigate concentration of hCRP, lipids (TC, TG, LDL-C, nonHDL-C, HDL-C) and lipid ratios (TC/HDL-C, LDL-C/HDL-C, TG/HDL-C) in patients with moderate dyslipidemia and compared to the healthy subjects, and relation between hCRP and lipids and lipid ratios. We studied 40 patients with moderately dyslipidemia (male and female) at the age between 21-63 years and the reference group. The reference group constituted of 14 subjects chosen from normolipidemic healthy individuals. The patients with moderate dyslipidemia had significantly increased hCRP, TG, LDL-C levels and significantly increased lipid ratios (TG/HDL, LDL-C/HDL-C). The concentration of hCRP was significantly positively correlated with TG, TC, LDL-C, nonHDL-C concentrations and TG/HDL-C, LDL-C/HDL-C ratios. We concluded that chronic inflammation disease can disturb lipids concentration and can accelerate atherosclerosis. However, these results are required further studies.