Zusammenfassung
Wundheilungsmechanismen können durch unterschiedliche Grunderkrankungen behindert werden und den Zustand einer chronisch schlecht heilenden Wunde entwickeln. Für eine effiziente Therapiestrategie ist es notwendig, die Grunderkrankung zu identifizieren, zu behandeln und die pathologische Wundheilung gezielt zu normalisieren. Hierzu sind detaillierte Kenntnisse über die ablaufenden zellulären und molekularen Mechanismen notwendig. In dieser Übersicht sollen neue Erkenntnisse über die normale und pathologische Wundheilung und die sich daraus ergebenden konservativen Therapieansätze dargestellt werden.
Abstract
Underlying disease may impair normal wound healing, leading to chronic, poorly healing wounds. Efficient treatment strategies require identification and treatment of the underlying disease as well as directed correction of the wound healing defect. A thorough knowledge of tissue repair mechanisms at the cellular and molecular level will help to achieve these goals. This review focuses on new developments in wound healing research and the resulting non-operative therapeutic implications.
Literatur
Armstrong DG, Lavery AL, for the Diabetic Foot Study Consortium (2005) Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet 366: 1704–1710
Badiavas E, Falanga V (2003) Treatment of chronic wounds with bone marrow-derived cells. Arch Dermatol 139: 510–516
Banda MJ, Knighton DR, Hunt TK, Werb Z (1982) Isolation of a nonmitogenic angiogenesis factor from wound fluid. Proc Natl Acad Sci 79: 7773–7777
Barrick B, Campbell EJ, Owen A (1999) Leukocyte proteinases in wound healing: roles in physiologic and pathologic processes. Wound Rep Reg 7: 410–422
Bullard KM, Lund L, Mudgett JS et al. (1999) Impaired wound contraction in stromelysin-1-deficient mice. Ann Surg 230: 260–265
Eming SA, Smola H, Krieg T (2002) The treatment of chronic wounds: current concepts and future aspects. Cells Tissues Organs 172: 105–117
Eming SA, Lauer G, Cole M et al. (2004) Increased levels of the soluble variant of the VEGF receptor VEGFR-1 (sFlt-1) are associated with poor prognosis in wound healing. J Invest Dermatol 123: 799–802
Eming SA, Smola-Hess S, Hirche D et al. (2006) A novel property of Povidon-iodine: inhibition of excessive protease levels in chronic non-healing wounds. J Invest Dermatol 126: 2731–2733
Eming SA, Krieg T, Davidson JM (2007) Inflammation in wound repair: molecular and cellular mechanisms. J Invest Dermatol 127: 514–525, (Perspective Article)
Eming SA, Krieg T, Davidson JM (2007) Gene therapy and wound healing. Clin Dermatol 25: 79–92
Grinnell F, Ho C, Wysocki A (1992) Degradation of fibronectin and vitronectin in chronic wound fluid: analysis by cell blotting, immunoblotting and, cell adhesion assays. J Invest Dermatol 98: 410–416
Grinnell F, Zhu M (1996) Fibronectin degradation in chronic wounds depends on the relative levels of elastase, a1-proteinase inhibitor, and a2-macroglobulin. J Invest Dermatol 106: 335–341
Herouy Y, Hellstern MO, Vanscheidt E et al. (2000) Factor XIII-mediated inhibition of fibrinolysis and venous leg ulcers. Lancet 355: 1970–1971
Hubbell JA (2006) Matrix-bound growth factors in tissue repair. Sw Med Wkly 136: 387–391
auf dem Keller U, Kumin A, Braun S, Werner S (2006) Reactive oxygen species and their detoxification in healing skin wounds. J Invest Dermatol Symp Proc 11: 106–111
Katz MH, Alvarez AF, Kirsner RS et al. (1991) Human wound fluid from acute wounds stimuates fibroblasts and endothelial cell growth. J Am Acad Dermatol 25: 1054–1058
Kjolseth D, Frank JM, Barker JH et al. (1994) Comparison of the effects of commonly used wound agents on epithelialization and neovascularization. J Am Coll Surg 179: 305–312
Körbling M, Estrov Z (2003) Adult stem cells for tissue repair – a new therapeutic concept. N Engl J Med 349: 570–582
Lauer G, Sollberg S, Cole M et al. (2000) Expression and proteolysis of VEGF is increased in chronic wounds. J Invest Dermatol 115: 12–18
Lauer G, Sollberg S, Cole M et al. (2002) Generation of a novel proteolytic resistant VEGF165 variant by a site directed mutation at the plasmin sensitive cleavage site. FEBS Letters 531: 309–313
Loots MA, Lamme EN, Zeegelaar J et al. (1998) Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Deramtol 111: 850–857
Lutolf MP, Hubbell JA (2005) Synthetic biomaterials as instructive extracellular microenvironments for morphogenesis in tissue engineering. Nat Biotechnol 23: 47–55
Martin P (1997) Wound healing – aiming for perfect skin regeneration. Science 276: 75–81
Martin P, Leibovich SJ (2005) Inflammatory cells during wound repair: the good, the bad and the ugly. Trends Cell Biol 15: 599–607
Ono I, Gunji H, Zhang JZ et al. (1995) Studies on cytokines related to wound healing in donor site wound fluid. J Dermatol Sci 10: 241–245
Romer J, Bugge TH, Pyke C et al. (1996) Impaired wound healing in mice with a disrupted plasminogen gene. Nature Med 2: 287–292
Roth D, Piekarek M, Christ H et al. (2006) Plasmin modulates VEGF-A mediated angiogenesis during wound repair. Am J Pathol 168: 670–684
Scharffetter-Kochanek K, Schüller J, Meewes C et al. (2003) Das chronisch venöse Ulcus cruris – Pathogenese und Bedeutung des „aggressiven Mikromilieus“. J Dtsch Dermatol Gesellsch 1: 58–67
Singer AJ, Clark RAF (1999) Cutaneous wound healing. N Engl J Med 341: 738–746
Streit M, Beleznay Z, Braathen LR (2006) Topical application of the TNF-a antibody Infliximab improves healing in chronic wounds. Int Wound J 3: 171–179
Vogt PM, Hauser J, Rossbach O et al. (2001) Polyvinyl pyrrolidone-iodine liposome hydrogel improves epithelialization by combining moisture and antisepis. A new concept in wound therapy. Wound Repair Regen 9: 116–122
Werner S, Grose R (2003) Regulation of wound healing by growth factors and cytokines. Physiol Rev 83: 835–870
Wlaschek M, Scharffetter-Kochanek K (2005) Oxidative stress in chronic venous leg ulcers. Wound Rep Reg 13: 452–461
Wozniak G (2000) Vom Ulcus cruris zum Myokardinfarkt. Med Welt 51: 25–30
Interessenkonflikt
Der korrespondierende Autor weist auf folgende Beziehungen hin: S.A. Eming. T. Krieg Beratertätigkeit bei Bayer Innovation GmbH.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Eming, S., Kaufmann, J., Löhrer, R. et al. Chronische Wunde. Hautarzt 58, 939–944 (2007). https://doi.org/10.1007/s00105-007-1402-1
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00105-007-1402-1