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Fibroblasts, healing process

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. [Pg.297]

In the course of healing, miliary tuberculosis or small diffuse disseminated foci give rise to scarred transformation with the morphological picture of tuberculous pseudocirrhosis as a result of vascularization, fibroblasts and histiocytic connective tissue. As a rule, however, no major hepatic dysfunction results from the cicatrization of the healing process, which no longer (or barely) exhibits the specific character of granulation tissue. [Pg.477]

During the healing process, hybrid cells, known as myofibroblasts, appear in the dermis. They have the morphological characteristics of both fibroblasts and smooth muscle cells. They are responsible for tissue contraction-retraction during healing. Their cytoplasm contains networks of myofilaments that are in contact with specialized zones of the plasma membrane and can interact with the adjacent cells or connective tissue. These myofibroblasts appear to be differentiated fibroblasts that have acquired the properties of smooth muscle cells. Controlled stimulation with DMAE, for example, is a good way to achieve a tightening effect on the skin. [Pg.44]

Basic fibroblast growth factor (bFGF) is a potent mitgen that stimulates the proliferation of a wide variety of cells and could play a crucial role in wound healing processes. The therapeutic potential of bFGF has not been fully realized, however, because of its susceptibility to proteolytic inactivation and short duration of retention at the site of action. Sulfated oligosaccharides, including a sodium salt of... [Pg.826]

Davison, J.M. and Broadley, K.N. (1991) Manipulation of the wound-healing process with basic fibroblast growth factor. Ann. N. Y. Acad. Sci. 638 306-315. [Pg.364]

Fibroblasts are the first cells to anchor on the implant s surface during the healing process. Their excessive adhesion and proliferation can lead to... [Pg.387]

Orotic acid stimulates the healing process. In mice with an experimental injury the daily oral administration of potassium orotate fastened the healing process, the differentiation of fibroblasts, and the formation and transfer of RNA from nucleus to cytoplasm [347]. Also the rate of collagen synthesis was higher during the stimulation of the wound healing process by potassium orotate [348]. [Pg.35]

D22 Dudnikova, G. N. and Ryvnyak, V. V. Autoradiographic and electron-microscope study of fibroblasts during stimulation of the healing process. Arkh. Patol., 38, 13-18 (1976) (Russ.)... [Pg.61]


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Healing process

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