Wound Healing
The physiological process of wound healing can be distinguished into three phases: inflammation, tissue formation, and tissue remodeling. Multiple systemic diseases and topical factors can inhibit mechanisms of normal wound repair, which may lead to chron
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12.5
Sabine A. Eming
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The physiological process of wound healing can be distinguished into three phases: inflammation, tissue formation, and tissue remodeling. Multiple systemic diseases and topical factors can inhibit mechanisms of normal wound repair, which may lead to chronic non-healing wounds. Identification of systemic and topical causes of impaired healing is fundamental for the therapy of non-healing wounds and requires an interdisciplinary approach. Non-healing wounds are symptoms of underlying common (ulcus cruris venosum, ulcus arteriosum, diabetes mellitus, decubitus) or rare (pyoderma gangrenosum, vasculitis, connective tissue disease, drugs, neoplasm, infection, vaso-occlusive disease) etiologies. Identification of factors that impede wound healing is based on the patient’s history, aspects of physical examination, laboratory tests, instrumental investigation, and wound histology. Treatment of non-healing wounds should aim to correct underlying systemic and topical causes and is based on an interdisciplinary treatment regime.
S. A. Eming Department of Dermatology University of Cologne Kerpener Str. 62, 50937 Cologne, Germany
12.5.1 Etiology and Pathophysiology Wound healing is a dynamic, interactive response to tissue injury that involves complex interactions of various resident cells and infiltrating leukocyte subtypes, extracellular matrix molecules, and soluble mediators. The immediate goal in repair is to achieve tissue integrity and homeostasis [51, 67]. To achieve this goal the healing process involves three phases that overlap in time and space: inflammation, tissue formation, and tissue remodeling (Fig. 12.5.1). During the inflammatory phase, platelet aggregation is followed by infiltration of leukocytes into the wound site. In tissue formation, epithelialization and newly formed granulation tissue, consisting of endothelial cells, macrophages, and fibroblasts, begin to cover and fill the wound area to restore tissue integrity. Synthesis, remodeling, and deposition of structural extracellular matrix molecules are indispensable for initiating repair and progression into the healing state. Cellular responses to injury involve direct cell–cell and cell–matrix interactions, as well as the indirect crosstalk between different cell populations by soluble mediators. Indeed, complex interactions between the epidermal and dermal compartment are essential. During the past decade, numerous factors have been identified that are engaged in a complex reciprocal dialogue between epidermal and dermal cells to facilitate wound repair [74]. The sensitive balance between stimulating and inhibitory mediators during diverse stages of repair is crucial for achieving tissue homeostasis following injury. Phases of repair must occur in a proper sequence for optimal wound healing. Multiple systemic diseases and local factors can inhibit mechanisms of normal wound repair, which may lead to non-healing wounds (chronic wound = wound, which shows no tendency for healing at
T. Krieg et al.
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