Inflammation. 2: Its role in the healing of chronic wounds.

Why do some wounds fail to heal in the expected time? Part two of this article on inflammation discusses the possible causes, which include recurrence of trauma, bacterial and other contamination and perhaps, above all, the ageing process.

[1]  S. Miller,et al.  Bacteriology of chronic leg ulcers. , 1978, Archives of dermatology.

[2]  A. Vaheri,et al.  Proteolytic activity in leg ulcer exudate , 1993, Experimental dermatology.

[3]  A. Bailey,et al.  Prognostic value of markers of collagen remodeling in venous ulcers , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[4]  J. Kere,et al.  Patterns of matrix metalloproteinase and TIMP‐1 expression in chronic and normally healing human cutaneous wounds , 1996, The British journal of dermatology.

[5]  C. Winterbourn,et al.  Human neutrophil collagenase cleaves alpha 1-antitrypsin. , 1990, The Biochemical journal.

[6]  W. Parks,et al.  Collagenase-1 complexes with alpha2-macroglobulin in the acute and chronic wound environments. , 1998, The Journal of investigative dermatology.

[7]  F. Komada,et al.  Improvement in wound healing by epidermal growth factor (EGF) ointment. II. Effect of protease inhibitor, nafamostat, on stabilization and efficacy of EGF in burn. , 1991, Journal of pharmacobio-dynamics.

[8]  R. Clark,et al.  Fibronectin and fibrin provide a provisional matrix for epidermal cell migration during wound reepithelialization. , 1982, The Journal of investigative dermatology.

[9]  T. Roth,et al.  IL-10 and GM-CSF expression and the presence of antigen-presenting cells in chronic venous ulcers. , 1998, The Journal of surgical research.

[10]  C. McCollum,et al.  Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation. , 1997, Laboratory investigation; a journal of technical methods and pathology.

[11]  F. Grinnell,et al.  Wound fluid from chronic leg ulcers contains elevated levels of metalloproteinases MMP-2 and MMP-9. , 1993, The Journal of investigative dermatology.

[12]  C. N. Rao,et al.  Alpha 1-antitrypsin is degraded and non-functional in chronic wounds but intact and functional in acute wounds: the inhibitor protects fibronectin from degradation by chronic wound fluid enzymes. , 1995, The Journal of investigative dermatology.

[13]  M. Horan,et al.  Aging alters the inflammatory and endothelial cell adhesion molecule profiles during human cutaneous wound healing. , 1998, Laboratory investigation; a journal of technical methods and pathology.

[14]  M. Bonnefoy,et al.  Implication of cytokines in the aggravation of malnutrition and hypercatabolism in elderly patients with severe pressure sores. , 1995, Age and ageing.

[15]  R. Diegelmann,et al.  Ability of chronic wound fluids to degrade peptide growth factors is associated with increased levels of elastase activity and diminished levels of proteinase inhibitors , 1997, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[16]  K. Burnand,et al.  Tissue and urokinase plasminogen activators in the environs of venous and ischaemic leg ulcers , 1993, The British journal of surgery.

[17]  T. Krieg,et al.  Expression and proteolysis of vascular endothelial growth factor is increased in chronic wounds. , 2000, The Journal of investigative dermatology.

[18]  F. Grinnell Fibronectin and wound healing , 1984, Journal of cellular biochemistry.

[19]  G. Schultz,et al.  Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[20]  I. K. Cohen,et al.  Modified cotton gauze dressings that selectively absorb neutrophil elastase activity in solution , 2001, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[21]  M. Hallett,et al.  Inappropriate neutrophil activation in venous disease , 1994, The British journal of surgery.

[22]  M. Longaker,et al.  Tissue inhibitor of metalloproteinases-1 is decreased and activated gelatinases are increased in chronic wounds. , 1995, The Journal of investigative dermatology.

[23]  F. Grinnell,et al.  Degradation of Fibronectin and Vitronectin and Vitronectin in Chronic Wound Fluid: Analysis by Cell Blotting, Immunoblotting, and Cell Adhesion Assays , 1992 .

[24]  Y. Itoh,et al.  Preferential Inactivation of Tissue Inhibitor of Metalloproteinases-1 That Is Bound to the Precursor of Matrix Metalloproteinase 9 (Progelatinase B) by Human Neutrophil Elastase (*) , 1995, The Journal of Biological Chemistry.

[25]  I. K. Cohen,et al.  MMP-8 is the predominant collagenase in healing wounds and nonhealing ulcers. , 1999, The Journal of surgical research.

[26]  I. K. Cohen,et al.  Interleukin-1alpha and collagenase activity are elevated in chronic wounds. , 1998, Plastic and reconstructive surgery.

[27]  T. Tuan,et al.  Temporal expression of urokinase plasminogen activator, plasminogen activator inhibitor and gelatinase‐B in chronic wound fluid switches from a chronic to acute wound profile with progression to healing , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[28]  F. Arnold,et al.  Postural vasoregulation and mediators of reperfusion injury in venous ulceration. , 1997, Journal of vascular surgery.

[29]  M. Stacey,et al.  Levels of Tumor Necrosis Factor-α (TNF-α) and Soluble TNF Receptors in Chronic Venous Leg Ulcers – Correlations to Healing Status , 1998 .

[30]  F. Grinnell,et al.  Fibronectin Degradation in Chronic Wounds Depends on the Relative Levels of Elastase, α1-Proteinase Inhibitor, and α2-Macroglobulin , 1996 .

[31]  L. Norgren,et al.  A randomized trial comparing cadexomer iodine and standard treatment in the out‐patient management of chronic venous ulcers , 1983, The British journal of dermatology.

[32]  I. K. Cohen,et al.  Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. , 1996, The Journal of investigative dermatology.

[33]  H. Dvorak,et al.  Role of the clotting system in cell-mediated hypersensitivity. II. Kinetics of fibrinogen/fibrin accumulation and vascular permeability changes in tuberculin and cutaneous basophil hypersensitivity reactions. , 1975, Journal of immunology.

[34]  F. Grinnell,et al.  Fibronectin profiles in normal and chronic wound fluid. , 1990, Laboratory investigation; a journal of technical methods and pathology.

[35]  A. Rogers,et al.  Involvement of proteolytic enzymes—plasminogen activators and matrix metalloproteinases—in the pathophysiology of pressure ulcers , 1995, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.

[36]  T. Fitzgerald,et al.  Fibronectin involvement in granulation tissue and wound healing in rabbits. , 1982, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[37]  J. Raffetto,et al.  The proliferative capacity of neonatal skin fibroblasts is reduced after exposure to venous ulcer wound fluid: A potential mechanism for senescence in venous ulcers. , 1999, Journal of vascular surgery.

[38]  A. Vaheri,et al.  Matrix metalloproteinases, gelatinase and collagenase, in chronic leg ulcers. , 1996, The Journal of investigative dermatology.

[39]  C. Bunker,et al.  Leukocytes: their role in the etiopathogenesis of skin damage in venous disease. , 1993, Journal of vascular surgery.