The Role Of MMPs In Chronic Wound Edema

By Adrianne P.S. Smith, MD, FACEP

Understanding Key Differences Between Acute And Chronic Wound Fluid
Acute and chronic wounds fluid differs in biochemical content and function. Acute edema fluid activates fibrinogen, initiates pericapillary cuffing and prevents further blood loss. Prolonged cuffing starves injured tissue by reducing the delivery of vital oxygen and nutrients. Fibrin plugs formed during coagulation also block lymphatic drainage and localize the inflammatory reaction to support healing. Inflammatory mediators stimulate MMP transcription and activation. Presumably, the inflammatory mediators vary with differing wound types, the type and extent of colonization and the capability of host modulation.

Postoperative surgical wounds provide a source for acute wound fluid. One can obtain chronic wound fluid from a variety of lower extremity ulcers. Growth factors, MMPs, immune factors, and cytokines are measured. Functional assessments include the ability of the fluids to influence the growth of fibroblasts, endothelial cells and keratinocytes.
Acute wound fluid activates growth factors such as platelet-derived growth factor (PDGF) necessary for fibroblast proliferation, collagen secretion and matrix formation. On the other hand, chronic wound fluid activates MMP-8, -2, and -9 with subsequent degradation of growth factor, reduction of ECM, interference with collagen cross-bridging and decreased deposition of vital stromal structures. In chronic wound fluid samples, epidermal growth factor (EGF) degradation is associated with elevated MMP protease activity. On the other hand, degradation of recombinant vascular endothelial growth factor (rVEGF165) stimulated by chronic leg wound fluid is associated with plasmin.


Thanks a lot for publishing the above article. We surprisingly observed a unique effect on chronic wound healing as diabetic non healing ones. The events we observed were as clot formation(fibrin deposites - hemostatic phase) followed by autodebridementation of necrotic lesions compressing rejection of necrotic tisuues from the periphery to the central wound associated with ECM deposit( inflammation phase)follwoed by granulation tissue formation and wound size decrease (proliferation phase) and complete wound healing in a physiological timed manner. The cases were involved with non healing wound types of diabetes related awith and without hemodyalised states and resistant to therapy of more than 10 months up to 20 months. Our group is ready to exchange experiments and introduce our patent remedy as needed. We welcome all aspects of collaboration in mass production and research projects.
Khodaberdi Kalavi Iran, Mobile: 9111773982, Tel(home): +98 171 3351080, fax: +98 171 4423630, 2269210 Email:

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