Narrow Results

Vascular physiology and disease progression, such as atherosclerosis, are mediated by hemodynamic force generated from blood flow. The hemodynamic force exerts on vascular endothelial cells (ECs), which could perceive the mechanical signals and transmit them into cell interior by multiple potential shear sensors, collectively known as mechanotransduction. However, we do not understand completely how these shear-sensitive components orchestrate physiological and atherosclerotic responses to shear stress. In this review, we provide an overview of biomechanical mechanisms underlying vascular physiology and atherosclerotic progression. Additionally, we summarize current evidences to illustrate that atherosclerotic lesions preferentially develop in arterial regions experiencing disturbance in blood flow, during which endothelial dysfunction is the initial event of atherosclerosis, inflammation plays dominant roles in atherosclerotic progression, and angiogenesis emerges as compensatory explanation for atherosclerotic plaque rupture. Especially in the presence of systemic risk factors (e.g., hyperlipidaemia, hypertension and hyperglycemia), the synergy between these systemic risk factors with hemodynamic factors aggravates atherosclerosis by co-stimulating some of these biomechanical events. Given the hemodynamic environment of vasculature, understanding how the rapid shear-mediated signaling, particularly in combination with systemic risk factors, contribute to atherosclerotic progression through endothelial dysfunction, inflammation and angiogenesis helps to elucidate the role for atherogenic shear stress in specifically localizing atherosclerotic lesions in arterial regions with disturbed flow.

This study investigates the feasibility of using high-resolution ultrasound imaging echogenicity to quantitatively diagnose gingival inflammation. Gingival samples were extracted from the study participants during gingivectomy procedures. Ultrasound mechanical scanning of the samples was immediately conducted ex-vivo to render cross-sectional images of high resolution, at different locations. Samples’ histological preparation and analysis was followed after performing ultrasound imaging. Histological sections were then matched with ultrasound images at different sections for each gingival sample. The matched image pairs were used to estimate two quantitative measures; relative inflammation area and ultrasound image echogenicity. These parameters were employed to judge the diagnostic potential of gingival ultrasound imaging. The results show that ultrasound images exhibited low intensity levels at the inflamed gingival regions, while healthy layers showed higher intensity levels. The relative area parameter implied a strong relationship between ultrasound and histological images. Ultrasound echogenicity was found to be statistically significant in differentiating between some inflammation degrees in the studied gingival samples. In summary, ultrasound imaging has the potential to be a noninvasive adjunct diagnostic tool for gingival inflammation, and may help assess the stage of the disease and ultimately limit periodontal disease occurrence; taking into consideration the limits of this study.