Healing, Scarring, and Contractures
The closure of open wounds resulting from trauma involves the depositing of new connective tissue matrix. The amount required is dictated by the severity of injury in terms of depth and area. This new connective tissue matrix is immature, and in some cases, can undergo modifications, a reduction in size. This reduction is called wound contraction and forces generated by resident fibroblasts are responsible for it. The mechanics for wound contraction require the organization of surrounding connective tissue matrix. This proposed mechanism involves a cooperation between cell generated cytoplasmic muscular forces and collagen fibers. Experimental work shows that resident fibroblasts function as individual units in this reorganization process. Evidence is lacking to support the idea that a specialized cell, the myofibroblast acting as a multicellular contractile unit could be accountable for producing wound contraction. The morphological appearance of stress fibers in resident fibroblasts in healing wounds may in fact signify the termination of that cell’s involvement in the process of wound contraction. Experimental evidence argues for fibroblast locomotion being the mechanism attributed for organization of the connective tissue matrix. Further the control of this cellular force appears linked to the composition of the newly deposited collagen matrix. A matrix rich in type III collagen contracts faster and to a greater degree than one made from type I collagen. It is suggested that granulation tissue that has a type III rich collagen matrix will contract more readily than one with less type III collagen. Evidence presented from in vitro models suggests that fibroblasts generate the forces of contraction, and collagen controls those forces in wound closure by the wound contraction process.
KeywordsFractionation Peri Fibril Rhodamine Lost
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