Fibrin and Wound Healing

Abstract

Although hemostasis is the major role of fibrin in wound repair, once the clot is present the wound cells must deal with it. The invasion and clearing of fibrin by these cells involves multiple complex processes that may go array XXX and delay wound repair. A good example, of the latter is leg ulcers. These chronic wounds contain a plethora of proteases that digest fibronectin and growth factors in the fibrin clot resulting in a corrupt provisional matrix that no longer supports reepithelialization or granulation tissue formation. Every good wound care provider knows that these wounds will not heal unless the corrupt matrix is removed by vigorous debridement that stimulates the accumulation of a competent provisional matrix.