Heridas Y Cicatrizacion

W o u n d H ea l i n g P ri m er
Stephanie R. Goldberg,

MD

a

, Robert F. Diegelmann,

PhD

b,

*

KEYWORDS
 Acute wound  Phases of healing  Healing mechanisms
 Guidelines for healing

Surgeons often care for patients with conditions of abnormal wound healing, which
include conditions of excessive wound healing, such as fibrosis, adhesions, and
contractures, as well asconditions of inadequate wound healing, such as chronic nonhealing ulcers, recurrent hernias, and wound dehiscences. Despite many recent
advances in the field, which have highlighted the importance of adjunct therapies in
maximizing the healing potential, such as optimization of nutrition, growth factor
therapy, advanced wound dressing materials, and bioengineered skin substitutes,
conditionsof abnormal wound healing continue to cause significant cost, morbidity,
and mortality. To understand how conditions of abnormal wound healing can be corrected, it is important to first understand the basic principles of wound healing.
PHASES OF WOUND HEALING

Wound healing consists of a complex but very orderly array of overlapping phases in
which highly specialized cells interact with anextracellular matrix to lay down a new
framework for tissue growth and repair.1 There are 4 distinct but overlapping phases
of wound healing, which include hemostasis, inflammation, proliferation, and remodeling (Fig. 1). These phases are influenced by the various cellular interactions and are
regulated by the local release of chemical signals such as cytokines, chemokines,
growth factors, andinhibitors.2,3
HEMOSTASIS PHASE

Immediately after tissue injury, hemostasis occurs to minimize hemorrhage. While the
blood vessels constrict, platelets are activated by binding to the exposed collagen in
the extracellular matrix. The platelets then release fibronectin, thrombospondin, sphingosine 1 phosphate, and von Willebrand factor, which promote further platelet

a

Department ofSurgery, Virginia Commonwealth University Medical Center, West Hospital,
16th Floor, West Wing, 1200 East Broad Street, Richmond, VA 23298-0645, USA
b
Department of Biochemistry and Molecular Biology, Virginia Commonwealth University
Medical Center, 1101 East Marshall Street, Sanger Hall, Room 2-007, Richmond, VA
23298-0614, USA
* Corresponding author.
E-mail address: rdiegelm@vcu.edu
SurgClin N Am 90 (2010) 1133–1146
doi:10.1016/j.suc.2010.08.003
surgical.theclinics.com
0039-6109/10/$ – see front matter Ó 2010 Elsevier Inc. All rights reserved.

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Goldberg & Diegelmann

Fig. 1. Phases of normal wound healing. Cellular and molecular events during normal
wound healing progress through 4 major integrated phases: hemostasis, inflammation,
proliferation, and remodeling.(From Cohen IK, Diegelmann RF, Lindblad WJ, editors.
Wound healing: biochemical and clinical aspects. Philadelphia: W.B. Saunders; 1993; with
permission.)

activation and aggregation.4 As these activation and other clotting factors are
released, a fibrin matrix is deposited in the wound, which functions as a provisional
matrix to stabilize the wound site. The aggregated platelets then becometrapped in
the fibrin matrix, thus forming a stable clot within the provisional matrix (Fig. 2).5
Several important mediators that are released by platelets are responsible for the
initiation and progression of wounds through the subsequent phases of wound healing. These mediators include platelet-derived growth factor (PDGF) and transforming
growth factor b (TGF-b). TGF-b and PDGF recruitadditional cells, such as neutrophils
and macrophages, to enter the wound. PDGF also recruits fibroblasts to the wound

Fig. 2. Hemostasis phase. At the time of injury, the fibrin clot forms the provisional wound
matrix and platelets release multiple growth factors that initiate the repair process. (From
Greenfield, LJ, editor. Surgery: scientific principles and practice. Philadelphia: J.B....