Understanding Wound Fluid and the Phases of Healing

Problems often arise in the chemical wound healing cascade with chronic nonhealing wounds. Research has established that nonhealing wounds of various etiologies demonstrate elevated levels of pro-inflammatory cytokines, increased protease activity, and diminished growth factor activity. An oxidized regenerated cellulose-collagen dressing significantly reduced exudates, increased granulation, and enhanced epithelialization, thus promoting advanced healing rate. Wounds were advanced from chronic proliferation phase to remodeling/epithelialization phase of the wound healing cascade. One may conclude that accelerated wound healing was achieved with ORC/collagen via its binding protease activity, and facilitating growth factor activity, resulting in progressive angiogenesis and accelerated

[1]  T. Phillips,et al.  Chronic wound fluid suppresses proliferation of dermal fibroblasts through a Ras-mediated signaling pathway. , 2005, The Journal of investigative dermatology.

[2]  K. Harding,et al.  Comparison of oxidative stress biomarker profiles between acute and chronic wound environments , 2004, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[3]  J. Varani,et al.  All-trans-retinoic acid suppresses matrix metalloproteinase activity and increases collagen synthesis in diabetic human skin in organ culture. , 2004, The American journal of pathology.

[4]  A. Schmidtchen,et al.  Heparin binding protein is increased in chronic leg ulcer fluid and released from granulocytes by secreted products of Pseudomonas aeruginosa , 2004, Thrombosis and Haemostasis.

[5]  R. Waddington,et al.  Extracellular matrix metabolites as potential biomarkers of disease activity in wound fluid: lessons learned from other inflammatory diseases? , 2004, The British journal of dermatology.

[6]  G. Clough,et al.  Microdialysis—A Model for Studying Chronic Wounds , 2003, The international journal of lower extremity wounds.

[7]  L. Dubertret,et al.  Randomized trial and local biological effect of autologous platelets used as adjuvant therapy for chronic venous leg ulcers. , 2003, Journal of vascular surgery.

[8]  M. Stacey,et al.  Iron and 8-isoprostane levels in acute and chronic wounds. , 2003, The Journal of investigative dermatology.

[9]  Cathy Thomas Hess,et al.  Orchestrating wound healing: assessing and preparing the wound bed. , 2003, Advances in skin & wound care.

[10]  T. K. Hunt,et al.  Comparison of inflammatory and systemic sources of growth factors in acute and chronic human wounds , 2003, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[11]  K. Burnand,et al.  What Can Wound Fluids Tell Us About the Venous Ulcer Microenvironment? , 2002, The international journal of lower extremity wounds.

[12]  G. Embery,et al.  Comparison of the antioxidant properties of HYAFF-11p75, AQUACEL and hyaluronan towards reactive oxygen species in vitro. , 2002, Biomaterials.

[13]  L. Iversen,et al.  Heparin-binding protein (HBP/CAP37): A missing link in neutrophil-evoked alteration of vascular permeability , 2001, Nature Medicine.

[14]  M. Stacey,et al.  Mitogenic activity and cytokine levels in non‐healing and healing chronic leg ulcers , 2001, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[15]  D. Lowy,et al.  Function and regulation of ras. , 1993, Annual review of biochemistry.