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Atherosclerosis, a chronic inflammatory and oxidative stress-mediated disease impacting the arterial system, stands as a primary cause of morbidity and mortality worldwide. The complexity of this disease, driven by numerous factors, requires a thorough investigation of its underlying mechanisms. In our study, we explore the complex interplay between cholesterol homeostasis, macrophage dynamics, and atherosclerosis development using a Petri net-based model anchored in credible, peer-reviewed biological and medical research. Our findings underscore the significant role of macrophage colony-stimulating factor (M-CSF) inhibition in reducing atherosclerotic plaque formation by modulating inflammatory responses and lipid accumulation. Furthermore, our model highlights the therapeutic potential of targeting the C-X-C motif ligand 12 (CXCL12)/ C-X-C motif chemokine receptor type 4 (CXCR4) pathway to hinder hematopoietic stem and progenitor cells’ (HSPCs’) mobilization and plaque development. Based on the results obtained, which are in agreement with current studies, additional strategies are also proposed, such as decreasing M1 macrophage polarization for therapeutic gains, opening the door to future research and novel treatment approaches.

Adipolin, neprilysin, and chemerin have pleiotropic properties; therefore, their concentrations may influence health complications associated with obesity. The study aimed to search the relationship between adipokine levels and anthropometric and metabolic parameters as well as blood pressure values, taking into account the influence of gender and age. The study group consisted of 88 people aged 30–60 years. It was found that chemerin concentration is positively correlated with glycaemia in the 120′ OGTT (rs = 0.412; p = 0.030) in obese women. There was a negative correlation between adipolin and LDL-C serum concentration (rs = −0.414; p = 0.044) in obese individuals with normal glucose tolerance and a positive correlation between chemerin concentration and triglyceridemia (rs = 0.333; p = 0.033) in the men. Moreover, high chemerin levels (above median values) were observed 3.79 times more frequently (OR = 3.79; 95% CI: 1.03–13.91; p = 0.040) in the male population characterized by elevated triglyceride levels (above 1.7 mmol/L). In the logistic regression analyses, we found that the frequency of high plasma adipolin concentrations increases with age (p = 0.005) only in people with a BMI < 30 kg/m2. It was also shown that the concentrations of the studied adipokines are interrelated. Adipolin, neprilysin and chemerin concentrations are associated with selected anthropometric and metabolism exponents.

Atherosclerosis is a multifactorial disease that affects large arteries and causes much morbidity and mortality worldwide. Despite ongoing research for several decades, it is still a global health problem that cannot be stopped and cured completely. Furthermore, the development of this disease is contributed to by various processes, primarily disturbances in cholesterol metabolism, local low-grade inflammation, and oxidative stress, resulting in the formation of atherosclerotic plaques. In this work, a stochastic Petri net model was constructed and subsequently analyzed to examine the impact of these factors on the development and progression of atherosclerosis. The use of knockout- and simulation-based analysis allowed for a comprehensive investigation of the studied phenomena. Our research has demonstrated that while cholesterol is a contributing factor in atherosclerosis, blocking its impact alone is insufficient in halting the progression of this disorder. Inhibition of oxidative stress is also important when blocking the impact of phosphoprotein phosphatase inhibitor-1 (PPI-1), microsomal triglyceride transfer protein (MTTP), and 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR), as our model shows that this action reduces the number of foam cells underlying atherosclerosis. The results obtained further support the previous observations that the combined treatment is significantly effective in enhancing therapeutic efficacy against atherosclerosis.

Bruxism is occlusal behaviour that often leads to stomatognathic system overload. Inflammatory markers in the periodontium are detectable in the gingival crevicular fluid (GCF). GCF production fluctuates due to various factors. Our study aimed to assess the effect of tooth clenching or grinding on GCF volume and proinflammatory IL-1β concentration in GCF. This pilot study was carried out on 20 participants aged 21 to 28 with good general health (per 10 people studied and control groups). GCF volume was measured with Periotron 8010 after absorbing for 30 s with PerioPaper strips. Twelve samples were collected from each patient—the buccal and lingual surfaces of teeth 16, 11, 24, 36, 31, and 44 were included. Laboratory examination of IL-1β concentration was performed. In patients with pathological tooth wear, a tendency to increase GCF secretion and IL-1β concentration in GCF was found. GCF volumes were higher in posterior teeth, while IL-1β levels were higher in anterior teeth. Crevices at the molars seem to have a potential predictive value in diagnosing periodontal microinflammation in patients with probable bruxism. Due to occlusal overload, these bruxists are more prone to microinflammatory processes in the periodontium. Further studies in a broader group are required to confirm this correlation.