Abstract
Fibrosis is a condition that affects the connective tissue in an organ or tissue in the restorative or responsive phase as a result of injury. The consequences of excessive fibrotic tissue growth may lead to various physiological complications of deformity and impairment due to hypertrophic scars, keloids, and tendon adhesion without understating the psychological impact on the patient. However, no method accurately quantifies the rate and pattern of subcutaneous induced hypertrophic fibrosis. We, therefore, devised a rodent excisional model to evaluate the extent of fibrosis with talc. Tissue specimens were set on formalin, and paraffin sections for histological, immunohistochemical, and molecular analysis talc was used to induce the fibroproliferative mechanism typical of hypertrophic scars. This pathway is relevant to the activation of inflammatory and fibrotic agents to stimulate human hypertrophic scarring. This model reproduces morpho-functional features of human hypertrophic scars to investigate scar formation and assess potential anti-scarring therapies.
Highlights
Keloids, tendon adhesion and other diseases resulting from excessive connective tissue formation to a pathological degree are challenging undertakings for plastic and orthopedic surgeons who are not able to guarantee satisfactory outcomes.Fibrosis is a condition that occurs in connective tissue and tissue as a typical physiological consequence of the reparative mechanism that follows injury
We propose to redesign the pathological mechanism that underpin hypertrophic scarring with the use of talc
Besides, significant levels of growth factor transcripts, such as the fibroblast growth factor (FGF) 7, FGF10, transforming growth factor (TNF) A, and vascular endothelial growth factor (VEGF)
Summary
Fibrosis is a condition that occurs in connective tissue and tissue as a typical physiological consequence of the reparative mechanism that follows injury. Hypertrophic fibrosis increases the tissue volume due to an anomalous propagation of fibroblast cells and aggregation of extracellular elements such as collagen. The healing process of a tissue injury is characterized by three concurring mechanisms: inflammation, proliferation and remodeling (Reinke and Sorg, 2012). These phases occur at onset of the lesion with hematoma, movement of cells from the surrounding tissue and the activation of inflammatory mediators. New blood vessels form from pre-existing vessels followed by the deposition of extracellular
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