China
Africa
Explore chapters and articles related to this topic
Microneedling
Published in Rubina Alves, Ramon Grimalt, Techniques in the Evaluation and Management of Hair Diseases, 2021
Rachita S. Dhurat, Sanober Burzin Daruwalla
Tissue remodeling continues for 6–24 months after the initial injury. This involves vascular regression and granulation tissue remodeling, in addition to new formation of ECM components. During remodeling, type III collagen is replaced with newly synthesized type I collagen [13]. ECM formation begins with replacement of granulation tissue collagens and continues with production of newly synthesized collagens. PDGF and TGF-β1, are responsible for the production of key ECM components, such as collagens and fibronectin. TGF-b1 inhibits the synthesis of MMPs and results in greater accumulation of collagen fibers. EGF released by macrophages and platelets stimulates MMP secretion by fibroblasts, mainly during the remodeling phase.
Altered Regulation of Fibrinolysis in Scleroderma and Potential for Thrombolytic Therapy
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Marvin J. Fritzler, David A. Hart
The mechanisms associated with the disease process in the idiopathic form are not well understood. As discussed above, a number of agents have been implicated as the inciting stimulus. After the initial injury, normal repair mechanisms may intervene to effect tissue remodeling and repair (Figure 1). However, in scleroderma, either through persistence of tissue injury or impaired regulation of the fibrotic response, the pathological process supervenes, as evidenced by abnormalities in fibrinolysis (Figure 1). The inflammatory component of the disease process is marked by the release of inflammatory mediators such as interleukin-1 (discussed in References 4 and 47). Evidence for accelerated fibrinogen turnover, fibrin deposition, and altered regulation of plasma fibrinolysis has been obtained from a number of laboratories (reviewed in Reference 4).
Skin Needling in Acne Scars
Published in Antonella Tosti, Maria Pia De Padova, Gabriella Fabbrocini, Kenneth R. Beer, Acne Scars, 2018
Gabriella Fabbrocini, Marianna Donnarumma, Maria Vastarella
Tissue remodeling that is mainly regulated by fibroblasts continues for months after the injury. The remodeling phase starts and continues for several months: Collagen type III is laid down in the upper dermis, just below the basal layer of the epidermis, and is gradually replaced by collagen type I. The matrix metalloproteinases (MMPs 1, 2, and 3) are essential in this process.
Inflammation resolution and specialized pro-resolving lipid mediators in chronic rhinosinusitis
Published in Expert Review of Clinical Immunology, 2023
Peyton Z. Robinson, Daniel N. Frank, Vijay R. Ramakrishnan
Tissue remodeling reflects the severity and chronicity of inflammation, and may further exacerbate the disease. Basement membrane thickening, fibrosis, and stromal edema are associated with highly eosinophilic environments and worse surgical outcomes [20]. These associations suggest that intentional resolution of tissue inflammation may restore local immune homeostasis and integrity of the mucosal barrier. It has been postulated that the conclusion of successful CRS management should result in restoration of normal innate and adaptive immune programs such as mucociliary clearance, healthy host-microbial interactions, and balance of immune activation versus immune tolerance. Reserve epithelial basal cells are airway-specific stem cells capable of restoring normal epithelial cellular composition once relieved of inflammatory conditions, although a recent publication suggests that airway basal cells may be reprogrammed to retain some degree of sensitivity to repeated allergic stimulus [21].
Chronic rhinosinusitis with nasal polyps: insights into mechanisms of disease from emerging biological therapies
Published in Expert Review of Clinical Immunology, 2019
In Caucasian populations, CRSwNP is predominantly a Th2 cell (Figure 1(c)) dominant disease in a milieu of excess interleukin (IL)-4, IL-5, and IL-13 [18]. Local tissue mucosal immunoglobulin E (IgE) levels are in excess and high eosinophil numbers are present. Such inflammation is simply termed T2. Tissue remodeling is extensive [19]. Early studies were merely descriptive of the immunopathology present and did not provide any mechanistic insight into disease pathogenesis and progression. Confirmation of upper airway CRSwNP driven T2 inflammation was helpful, as it not only confirmed the ‘one airway concept’ of almost identical inflammatory programs to the lower airway in asthma but also was the start of reclassifying disease in terms of endotyping. Recent cluster analysis confirms distinct endotype-specific groups and the clinical findings support that these endotypes are associated with phenotypes of disease, with variable response to treatment and altered clinical outcomes [7].
Chronic rhinosinusitis: pathogenesis, therapy options, and more
Published in Expert Opinion on Pharmacotherapy, 2018
Umut Can Kucuksezer, Cevdet Ozdemir, Mubeccel Akdis, Cezmi A. Akdis
The term ‘remodeling’ is used to describe structural tissue changes, which can occur both in diseases and as a part of the normal tissue repair process following wound infliction. Inflammation and mechanical injury can trigger tissue remodeling for the maintenance of normal tissue architecture. However, there may be pathologic consequences in disease settings. Airway remodeling is known to occur both in lower airway diseases, as observed in asthma, and upper airway diseases, including CRS and allergic rhinitis (AR). CRS physiopathology includes the degradation and deposition of the matrix, epithelial hyperplasia, and concentration of plasma proteins [15]. Studies have reported an association between CRS and asthma, which may be the result of common genetic predispositions and mechanistic pathways [16-18]. The immune pathogenesis of CRSwNP has a T helper (Th) 2 cell-driven inflammatory pattern [19]. According to the strength of eosinophilic inflammation, CRSwNP can further be grouped into the eosinophilic and non-eosinophilic subtypes, especially in Asian patients [13]. CRSsNP arises as a result of a distinct inflammatory pattern – a Th1 biased cytokine profile associated with the upregulated production of interferon (IFN)-γ and neutrophilic inflammation [20].