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Introduction
Wound healing is an elaborate and cautious course where the skin and body tissue resurfaces after damage. In the humans usual skin, the outer cover, which is called the epidermis, and the internal one called the dermis, prevent the wound from infections. The wound healing process is vulnerable to interruption and may lead to the formation of chronic wounds. The early phase commences immediately following skin damage while the subsequent phase referred to as the cellular phase entails various cells working together to build inflammatory components. It is possible to predict the progress of wound healing, but occasionally, variations should be expected depending on the magnitude of damage. Even though the different components of wound repair happen progressively and analogously, it is essential to break the entire process into three stages for analysis purposes. The three stages are inflammatory, proliferative, and maturation.
Inflammatory phase
The inflammatory phase commences immediately after skin damage and may last for 24 to 48 hours depending on the magnitude of damage or the cellular process (Eichler & Carlson, 2006). Inflammation occurs immediately after the clotting is initiated. Clotting is the cessation of blood loss from an injured vessel, followed by repair. This repair leads to a state referred to as hemostasis or coalescing of a fibrin clot. This stage starts with hemostasis whereby platelets induce the initial thrombus release repair factors that remove debris and bacteria from the injured skin (Martin & Leibovich, 2005). In a bid to achieve inflammation, several processes are involved and include clotting cascade, vasoconstriction, polymorph nuclear neutrophils, and macrophages.
The clotting cascade is the initial process when the tissue is injured. When blood makes contact with collagen, or the structural protein connecting tissues, blood platelets start producing inflammatory components (Martin & Leibovich, 2005). These blood platelets are essential in generating glycoproteins that have adhesive forces needed to build a mass on the wound surface. The fibrous proteins also known as fibrin and fibronectin join to form a hook that collects the proteins thus preventing bleeding. The formed fibrin-fibronectin plug serves as the principal skeletal anchorage for the wound to allow the deposition of collagen. Granulation tissue followed by collagen mount to replace the clot. Granulation tissue is the newly formed connective tissue that builds on the surfaces of injured skin during hemostasis. Growth factors such as cytokines and hormones trigger cells to increase their rate of cell proliferation and migration to the wounded area (Martin & Leibovich, 2005).
Vasoconstriction and vasodilation are the processes involving the muscular walls of the blood vessels. Vasoconstriction is the contraction of the blood passages while vasodilation is the expansion of the blood passages due to contraction and relaxation of the muscular wall of the vessels (Eichler & Carlson, 2006). The constriction of blood vessels minimizes blood loss and lasts for about ten minutes. Within about 20 minutes of injury, the broadening of the blood passage occurs. This expansion facilitates the permeability of blood vessels to enable the passage of inflammatory cells into the injured area from the bloodstream.
Polymorphonuclear neutrophils (PMNs) are the dominant cells that form at the wound surface within an hour of healing. They last for two days upon the injury. They are attracted to the wound surface by growth factors to kill bacteria and cleanse the wound by producing proteins that restore damaged tissue. On the other hand, macrophages are a type of white blood cell that kills bacteria and digests damaged cells (Eichler & Carlson, 2006). Within two days, macrophages become the predominant cells in the wound site. Macrophages produce growth factors during the third day of healing to attract cells that trigger the proliferation stage of healing to the wound site. Consequently, scar contraction begins, and it depends on the skins surface flexibility. Eventually, a decline of the inflammatory phase begins with the breakdown of the inflammatory factors. The number of PMNs and macrophages decline to signal that the inflammatory phase is closing, and the proliferative phase is advancing. However, a short inflammation time is necessary to avoid tissue damage and the possibility of chronic wounds.
Proliferative phase
The proliferative stage starts to establish during the third day of wounding. At the beginning of the second week of healing, the fibroblasts take control of the wound site. Processes in this phase do not happen in a given format but rather lightly overlap in time. At this stage, cells and growth factors are rapidly growing to speed the process of healing. Besides, Angiogenesis occurs to ensure the supply of oxygen, which is required by epithelial cells (Gilliver, Ashworth, & Ashcroft, 2007). New bloodstreams are formed through angiogenesis to replace the injured vessels. The fibroblasts also produce collagen that assists in strengthening the wound surface.
The accumulation of the granulation tissue into the wound enables the reepithelialization process to occur. The epithelial cells crawl across the new tissue to create a border between the wound and the external environment. At this point, growth factors secrete antimicrobial peptides to act as an innate immune defense of the wound. Therefore, the contraction process begins when the proliferation cells stop migrating and form a new basement membrane. Contraction begins about eight days after wounding, just after fibroblasts differentiate into myofibroblasts. The myofibroblasts are smooth muscle cells and facilitate contraction. A normal contraction should minimize the size of the wound by approximately 60% concerning the magnitude of the damage (Mosser, & Edwards, 2008). Contraction speed highly depends on the flexibility of the tissue in the wound. During the contraction, the wound edges are pulled to form a closure.
When contraction occurs, there is a probability that scar contracture may manifest. Scar contracture is an unusual sealing of a wound and may result in the excessive stretch of the skin surface. Fibroblasts produce collagen to strengthen the wound during the myofibroblasts contraction. The breakdown of the cells matrix occurs and triggers fibroblasts to stop moving and dividing.
Maturation and Remodeling
Maturation marks the end of wounding since it commences when the wound is sealed. This phase can commence within the second week and can go on for as long as two years. At this stage, collagen secretion and breakdown reach equilibrium causing maturation of tissue repair to begin. During this phase, the type III collagen that is predominant during proliferation gives way to type I collagen. The earlier disoriented collagen fibers are restructured to assume their normal position. Cellular activity minimizes, and the reddish appearance of the wound surface decline. This decline is due to the reduction in the number of blood vessels on the wounded surface. The collagen is aligned along tension points to resist mechanical stress. The collagen is firmly cross-linked into fibers that are strong enough to withstand regular external pressures. Nonetheless, the total strength of the new collagen cannot equal the strength of undamaged collagen. This phase may differ widely due to exogenous factors, malnutrition, or the size of the wound. As the remodeling advances, the wound surface strengthens. Consequently, the scar tissue also toughens to attain about 80% of the strength of the compact tissue (Edwards & Harding, 2004). The activity at the wound site minimizes making the scar tougher. The scar serves as an indicator that the wound has healed.
Factors affecting wound healing
Ultimately, factors that affect wound repair can be divided into systemic and local. Systemic factors are health or disease-oriented and they determine the ability to heal while local factors directly affect the state of the wound. Local factors include oxygenation and infection. Sufficient oxygen supply is important to sustain metabolic activities and cellular activities. On the other hand, wound infection is common due to the presence of microorganisms found at the surface of the skin. However, inflammation may be prolonged and lead to a chronic state. Systemic factors include age, stress, diabetes, and medication among other factors (Edwards & Harding, 2004). These factors derail cellular activity causing a temporal delay in wound repair. Nearly all stages of healing suffer age-related delays thus prolonging the healing process.
Conclusion
Wound repair is an intricate physiological process defined by various cellular activities as discussed above. Various factors can lead to impaired wound repair by derailing one or multiple stages of the process. However, to enhance wound repair, it is necessary to avoid the systemic factors that are human-induced such as malnutrition, alcohol, and smoking.
References
Edwards, R., & Harding, K. (2004). Bacteria and Wound Healing. Current Opinion in Infectious Diseases, 17(2), 91-96.
Eichler, M., & Carlson, M. (2006). Modeling dermal granulation tissue with the linear fibroblast-populated collagen matrix: A comparison with the round matrix model. Journal of Dermatological Science, 41(2), 97-108.
Gilliver, S., Ashworth, J., & Ashcroft, G. (2007). The hormonal regulation of cutaneous wound healing. Clinics in Dermatology, 25(1), 56-62.
Martin, P., & Leibovich, S. (2005). Inflammatory cells during wound repair: the good, the bad and the ugly. Trends in Cell Biology, 15(11), 599-607.
Mosser, D., & Edwards, J. (2008). Exploring the full spectrum of macrophage activation. Nature Reviews, Immunology, 8(12), 958-969.
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