Four Phases of NORMAL Skin Wound Healing

Acute wounds normally heal in an orderly and efficient manner and progress smoothly through the four distinct but overlapping phases of woundhealing: hemostasis, inflammation, repair, and remodeling (Figure 1). The process of wound healing is complex and involves a variety of specialized cells, such as macrophages, fibroblasts,and epithelial and endothelial cells. These cells interact with each other and with the extracellular matrix. In addition to the various cellular interactions, healing is also influenced by the action of proteins and glycoproteins, such as cytokines, chemokines, growth factors, inhibitors, and their receptors. Each stage of woundhealing has certain milestones that must occur in order for normal healing to progress.

In the following sections, we first review the key molecular and cellular regulators of the four distinct phases of normal acute wound healing. We then present data that show that most acute wounds fail to progress through the four phases of healing and become “stuck” in a chronic inflammatory phase that is due to the presence of a persistent bioburden of both planktonic bac-teria and especially biofilm bacteria. We explain that bacteria present in the biofilm phenotype are highly tolerant to the antibodies and phagocytic inflammatory cells (neutrophils and macro-phages) of the patient’s immune system, as well as antibiotics and many antiseptics. We emphasize the “down-stream” consequence of the chronic inflammatory status is the presence of elevated levels of proteases (especially matrix metallopro-teases, MMPs) and reactive oxygen species (ROS)that degrade proteins that are essential for healing and lead to impaired healing. Finally, we discuss the concepts of wound bed preparation and emphasize techniques and new therapies that correct the molecular abnormalities in chronic wounds that are barriers to healing.

1. Hemostasis Phase- Fibrin clotting cascade is activated, preventing hemorrhage, and platelets trapped in the fibrin clot release multiple cytokines and growth factors that stimulate the initial chemotactic migration of inflam-matory cells into the wound bed.
   
   
2. Inflammation Phase- Neutrophils migrate into the wound, followed by macrophages, which engulf contaminating bacteria and generate reactive oxygen species (ROS) that kill bacteria in phagosomes. Inflammatory cells also secrete proteases (matrix metalloproteases [MMPs] and neutrophil elastase)that break down damaged extracellular matrix molecules (ECM). Inflamma-tion spontaneously resolves in the absence of continued bioburden.
   
   
3. Repair Phase– Quiescent fibroblasts adjacent to the injury proliferate and migrate into the provisional fibrin matrix, where they synthesize new colla-gen and other ECM components that constitute the initial scar. Some fibro-blasts differentiate into myofibroblasts that contract the developing newscar tissue. Vascular endothelial cells also proliferate and migrate into the provisional fibrin matrix generating new capillaries (granulation tissue). Epithelial stem cells in hair follicles proliferate and migrate over the initial scarmatrix, completing the initial healing of the wound.
   
   
4. Remodeling Phase– During the next 6 to12 months, the initial scar matrix is slowly remodeled by the controlled action of secreted proteases (MMPs)that remove the irregular ECM, which is replaced by more normally orga-nized collagen fibers and other ECM molecules. The density of cells in the scar tissue decreases through controlled apoptosis
   
   

Acute wounds can convert into chronic wounds when the inflammatory phase becomes excessively prolonged, usually due to persistently elevated levels of bacterial bioburden, including biofilms, that lead to chronically elevated levels of proteases and ROS that destroy proteins essential for healing. Wound bed preparation is a process that removes the major barriers to healing and restores the correct balance of bioburden, proteases, growth factors, cyto-kines, and ECM components that allows healing to proceed.

TEXTBOOK OF CHRONIC WOUND CARE:
Read this entire chapter in the “Textbook of Chronic Wound Care, An Evidence Based Approach to Diagnosis and Treatment” Chapter 2 Physiology and Biochemistry of Wound Healing by Gregory S. Schultz, PhDDaniel J. Gibson, PhD.
Published by Best Publishing Company, 2018.

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Are you interested in learning more about wound care? Our sister company, Wound Care Education Partners offers Wound Care Certification Prep Course and Refresher Training which is an online & one day livestream course totalling 25.5 CME/CEU hours. It includes 10.5 hours with Michael White, MD, UHM, MMM, CWS, 15 hours study guide-based online pre-course, 30 lessons (Chapters), each followed by a short quiz. Debridement-specific workshop + hands on practicum & packet, Textbook: Wound Care Certification Study Guide, 2nd Edition, and your access to the study guide precourse content never expires.
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