Dental Plaque is defined as a BioFiolm of Structured Resilient Yellow Greyish substance that adheres to intra oral tooth surface or other hard surface in the oral cavity including removal and fixed restoration.. In a study on 20 thrombosed coronary arteries in our laboratory, the classical lipid-rich morphology was found indeed in 50% of the underlying ruptured plaques, but the other 50% had either a substantial fibrous cap (25% or more of the entire plaque thickness) or were almost completely fibrous in composition, albeit all with surface erosions . Davies
Therefore, although basically protective, in these advanced plaques the inflammatory process has a worse side-effect: destabilization and plaque rupture. C.K. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. In the atherosclerotic plaque these growth factors are produced by ‘injured’ endothelial cells and macrophages or released from thrombus [1, 51]. (A) Coronary plaque of a 67 year old male, containing an eccentric mildly stenosed plaque with complete disruption of the fibrous cap (boxed area), mural thrombus and hemorrhage into the lipid core. New insights into the pathogenesis of atherosclerosis as revealed by PDAY, Carotid bifurcation atherosclerosis: Quantitative correlaton of plaque localization with flow velocity profiles and shear stress, Shear stress influences the release of platelet derived growth factor and basic fibroblast growth factor by arterial smooth muscle cells, Vascular endothelium: An integrator of pathophysiological stimuli in atherogenesis, Expression of ICAM-1 and VCAM-1 and monocyte adherence in arteries exposed to altered shear stress (published erratum appears in Arterioscler Thromb Vasc Biol 1995;15:429), Copyright © 1999, European Society of Cardiology, Approaches to treat pulmonary arterial hypertension by targeting bmpr2 — from cell membrane to nucleus, Co-ordinated mitochondrial degradation by autophagy and heterophagy in cardiac homeostasis, Hydralazine protects the heart against acute ischaemia/reperfusion injury by inhibiting Drp1-mediated mitochondrial fission, Heart regeneration: beyond new muscle and vessels, 3 Instability and stability: a balance between inflammation and repair, 4 The acute ischemic event: a multifactorial process, 5 Classical risk factors and acute plaque complications, https://doi.org/10.1016/S0008-6363(98)00276-4, Receive exclusive offers and updates from Oxford Academic.
A.E. van Suylen
Inflammation is involved in the formation and growth of a stable plaque but also plays an important role in the transformation into the unstable plaque by stimulating metalloproteinase, macrophages and thrombotic activity. Zhou
It is important to note that the culprit plaques of clinically stable patients do not always appear stable histologically. Pickering
(A) Detail of a lipid-rich plaque, showing part of the lipid core, bordered by foam cell macrophages (red cells), and smooth muscle cells (blue cells) in the fibrous cap (anti-CD68/anti-α-actin immunostain). Sukhova
Kovanen et al. Filamentous bacteria (f) appear to be invading cocci microcolonies. J.
Other findings of interest concern the various inflammatory products released by cells in unstable plaques: increased numbers of macrophages producing the proteolytic enzyme gelatinase B (MMP9) [34, 35], the inflammatory cytokine TNF- and tryptase-producing mast cells , vasoactive substances such as angiotensin I  and endothelin , larger amounts of the thrombosis initiator Tissue Factor [38, 39], and increased numbers of Interleukin-2 receptors on T cells (as marker for acute T cell activation in unstable lesions) . Thickening of the intima-media complex implies occult plaque formation, but plaque may, of course, be seen directly with ultrasound when it achieves sufficient size to protrude into the carotid artery lumen. extended this view by using used entire (atherosclerotic) arteries to investigate atherosclerosis associated vascular wall remodeling.
The most important mechanism of acute coronary syndrome (ACS) is plaque rupture and subsequent thrombus formation. Role of Tilianin against Acute Lung Injury in In Vitro LPS-Induced Alveolar Macrophage Cells and an In Vivo C57BL/6 Mice Model. Faites l’expérience d’Adobe Stock avec 10 images offertes. At autopsy, lipid-rich plaques are frequently found underlying coronary thrombosis [3, 14, 15]. In mature human plaques these mechanisms have not been investigated thus far, but a recent study in our laboratory revealed a relationship between the direction of arterial flow and local differences in macrophage and smooth muscle cells densities in entire carotid artery plaques which were taken at autopsy. C.M. Anti-Inflammatory Effect of Mangiferin on an Experimental Model of Allergic Rhinitis through the Inhibition of NF-ÎºB Signaling Pathways.
(B) shows a detail of the erosion underneath the thrombus.
In this paper, we analyze a simplified model of plaque growth to derive physically meaningful results about the growth of plaques. 1, 2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1). Ischemic stroke in the cerebral artery.
et al. We investigated coronary atherectomy specimens of 58 patients with clinically well defined coronary artery diseases, of which 28 had chronic stable angina of more than 2 months duration without progression. A. Ambrose
Expression of adhesion molecules on neovessels in atherosclerotic plaques. Gotlieb
A.E. The pathogenesis of coronary artery disease and the acute coronary syndromes.
The continued recruitment of T-cells and macrophages at sites of ‘dysfunctional endothelium’ appears to be a constant feature of lesion initiation and progression as it accentuates the chronic inflammatory nature of atherosclerosis .
5). J. Davies
Asterisk is in the thrombosed lumen. A.V.
et al. Immunocytochemical analysis of the cellular composition of human atherosclerotic lesions, Atherosclerotic lesions in humans. But, certainly not all the plaques in patients with stable coronary artery disease fulfil these criteria for stability. Moreover, the association between inflamed lipid lesions and local vessel dilation provides another clue why many mildly stenotic lesions do rupture. Frostegard
- Acheter ce vecteur libre de droit et découvrir des vecteurs similaires sur Adobe Stock A vulnerable plaque is a kind of atheromatous plaque – a collection of white blood cells and lipids in the wall of an artery – that is particularly unstable and prone to produce sudden major problems such as a heart attack or stroke. (B) Adjacent section stained with Picro Sirius Red (collagen red, media yellow) shows a decrease in collagen density where the macrophages have accumulated.
New insights have emerged on a possible role for inflammation and repair also in local arterial wall remodeling in terms of dilation and shrinkage, with consequences for the geometry of the entire vessel . (A) High grade stenosing lesion with occlusive thrombosis of a 32 year old male who died instantly of acute myocardial infarction. 2- Dégagez à partir du doc b et c les caractéristiques structurales des roches métamorphiques. Atherectomy specimens obtained from patients with unstable coronary artery disease frequently contain more fragments of extracellular debris than those of patients with stable angina [16–18]. On the left side is a lipid-rich plaque. Plaque biofilm formation at 1 week. vector art, clipart and stock vectors. E.P. A.C.
The preference of inflammatory cells for lipid plaques as alluded to earlier is not coincidental, and presently there are several arguments in support of an intriguing relationship between lipids and inflammation.
Aux limites, c’est-à-dire aux bordures des plaques a lieu une forte activité sismique et volcanique. This is illustrated in Fig. (Abstract). N.
Cell death leads to the spill of lipids and, hence, the enlargement of the soft lipid core . Plaque disruptions may vary greatly in extent from tiny fissures or erosions of the plaque surface to deep intimal tears which extend into the soft lipid core of lesions; in all these instances, at least some degree of thrombus formation occurs [5, 6]. Bentz van de Berg
On the other hand, lipid associated inflammation introduces tissue degrading effects. Baseline patient characteristics of the two groups are shown in Table Table2. Asmaa ROUILLI 2 1- Décrivez la répartition des roches métamorphiques dans la région d’Uzerche. Hemodynamic factors such as local disturbances in flow velocity and alterations in shear stress form another risk factor for plaque initiation and growth . Discontinuity of the endothelium allows a contact between the blood stream and highly thrombogenic plaque materials (collagen fibrils and lipid debris insulated with Tissue Factor), which initiates activation of the coagulation system with at least some degree of thrombus formation 4. Cross-section of an atherosclerotic plaque, which is heavily infiltrated with macrophages (red) and contains only scarce smooth muscle cells (blue) in the fibrous cap (anti-CD68/anti-α-actin immunodouble stain). Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. Maximum accumulation of Plaque takes place in 21 days.
et al. Burke et al. For this reason, large plaques may angiographically be visualized as only mildly stenotic. An adjacent tissue section shows accumulations of macrophages (red cells) at the rupture site. Triposkiadis F(1), Sitafidis G, Kostoulas J, Skoularigis J, Zintzaras E, Fezoulidis I.
Initial plaque formation takes as long as 2 hours to start forming. Zeiher
W.H. In only 15% of these patients, all the plaques causing >50% stenosis were fibrous, while in 13% of patients virtually all plaques had a lipid core.
O.J. van der Wal
Smooth muscle proliferation and matrix synthesis implies a mechanism of slowly progressive growth of plaques; it serves to encapsulate the soft atheroma and organizes episodes of thrombus formation, either spontaneously or artificially induced. Atherosclerosis detailed illustration. Illustration about Stable plaque formation in the human artery.
Plaque near gingival sulcus has fewer coccal forms and more filamentous bacteria (860×). A.C.
The majority of coronary thrombi (∼75%) is caused by plaque rupture.1,2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1).3,4 Other common features include expansive remodelling, large plaque size, plaque haemorrhage, neovascularization, adventitial inflammation, and ‘spotty’ calcifications.4 Thin-cap fibroatheroma caps are usually <65 µm thick.4Figure 2 summarizes factors co… Clarijs
Une plaque lithosphérique est une zone stable délimitée par des zones actives. R.
Sixty percent of these plaques were fibrous, but 40% had a pool of extracellular lipids. E.
(From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. Atherosclerotic plaques are classified into 2 types, stable and vulnerable, the latter having a high risk of rupture. In this respect inflammation is closely related to a process of repair. T. By Tefi. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. These studies also showed the importance of the thickness of a fibrous cap (thickness in millimetres being inversely related to the peak stress in the cap), and the stenosis rate (circumferential stresses in the plaques gradually decreased when stenosis severity increased) ; it gives at least one explanation for the fact that many plaques rupture at a stenosis rate of less than 50%. TGF-β and other growth factors, including platelet derived growth factor (PDGF) and basic fibroblast growth factor (bFGF), play an important role in wound healing and the reparative stage of many chronic inflammatory diseases. Lipid related inflammation in the plaque leads to degradation and weakening of the plaque tissue. Flugelman
Arrow to the right indicates the reparative effects of smooth muscle cells, leading to the formation of a stable fibrous plaque. But they may become vulnerable, there is a risk of rupture and lead to thrombosis.
Fully developed plaques contain highly variable amounts of inflammatory cells, but largest concentrations can be found in lipid-rich lesions where they occupy the attenuated cap, the shoulder parts of the lesions or both [12, 13]. In both sections the same immunodouble staining is applied (anti-CD68/anti-α-actin immunodouble stain). On the other hand, smooth muscle cell proliferations and collagen synthesis exert reparative and stabilizing effects. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and …
Moreover, densities of and interstitial collagen were either low in the entire cap, or decreased at rupture sites compared with the adjacent plaque tissue. Holm
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