Rafail et al. examine the role effects of the complement system, a division of the immune system, on the wound healing process in miceexcisional cutaneou. The study focused focuses on the third (C3) and fifth (C5) main components of the complement system believed to mediate the inflammatory responsetwo., C3 and C , The experimenters induceThe C3-/- mice, lacking the third component of the complement system, exhibited smaller wound surface areas compared to C3 +/+ mice. The authors suggest the decreased inflammatory response and the increased presence of mast cells and α-SMA+ vessels indicate the development of new vasculature and account for the improved wound healing rates in C3-/- mice. Mice lacking C5 similarly exhibited increased …show more content…
The differential healing rates among three mice in a group may result from individual variation within each mouse. For example, the immune system of one mouse, that accounts for 2 data points, may promote faster healing for an unexamined reason. With a single mouse’s wounds constituting one-third of the data, individual variability easily obscures the true cause for accelerated healing and prevents generalization of the results to conclude the differences are due to C3 inhibition.
In addition to the concerns regarding C3 mice sample size, Rafail et al. extrapolate the mechanism of delayed wound healing in the C3 +/+ group, attributing the results to C5a signaling. The authors use data to support the difference in wound healing rates and composition between both the C3 groups and the C5 groups; however, they stretch the results to connect the C3 and C5 components with an unexamined mechanism. The study never explores C3 mediation by C5a, yet suggests C5a as a mediator along the C3 pathway. Data limit the logical conclusions that follow from a study; without supporting evidence, a mechanism to describe C5a as a mediator in the C3 pathway is a conjecture.
Despite the challenges with sample size ambiguity and extrapolation of a C5a mediation mechanism, the study methodically demonstrates the effects of the C3 component through reconstitution studies. After initial results suggested C3 deficiency improves wound healing, reconstitution of C3-/- mice with C3
This paper will be a research critique on the article “Frequent Application of the New Gelatin-Collagen Nonwoven Accelerates Wound Healing”, by Schiefer, J.L. and Rath, R, and each section will be examined using our textbook “Understanding Evidence-Based Practice”. The article’s main focus was on determining the effect of healing when using multiple collagen nonwoven applications to chronic wounds. Twelve mini-pigs where used to test this technique and the findings indicated that this method was promising, because the wounds had a faster healing rate when multiple application of gelatin-collagen nonwoven was used as treatment. Analyzing the articles components, we can see that although it does contain preliminary
The main outcome measures were the percent area of the wound compared to baseline area of the wound. As the wound decreased in size it is theoretically assumed that the wound is healing. The central concepts of the study were based on ultraviolet-C positive effects on wound healing in vitro. In vitro studies effects include; modification of growth factors, fibronectin release from fibroblast, epidermal cell proliferation, killing of pathogens, accelerated DNA synthesis, and antibiotic-resistant organisms.
The inflammation reaction to a skin cut is beneficial. When we have a skin cut or a trauma to the skin. Inflammation is a mechanism of defense; the body will release chemicals like histamine to promote capillary permeability and will increase the number of white blood cells to fight pathogens. This process will lead to healing the wound.
Skin repair is an important physiological process which is essential for homeostasis, restoring barrier function and preventing infection (Martin, 2009; Boateng and Catanzano, 2015). Wound healing is defined as a complex, dynamic and the specific biological process associated with the phenomena of tissue regeneration and growth (Mazumder et al., 2016). Regeneration can be defined as a tissue that significantly damaged either completely or partially removed and tissue's original function and cell types must be functional and structurally restored (Mazumder et al., 2016). The process of healing comprises a cytokine, blood cells, extracellular matrix and growth factor (Joao De Masi et al., 2016). The growth factor is a protein that activates and
The main function of neutrophils is to clear the wound region from being exposed to microorganisms and remove the debris near the wound area, although they end up producing some proteases and reactive oxygen species which causes some minor damages. Monocytes appear in the wound after this and differentiate into macrophages. These macrophages produce cytokines which recruit and activate specific leukocytes that promote inflammatory response. Macrophages along with neutrophils help in removing the apoptotic cells. During this process the macrophages undergo phenotypic transition to stimulate keratinocytes, fibroblasts, and angiogenesis to promote tissue regeneration, thereby promoting the transition from inflammation to proliferative phase of healing. The next event in inflammation is T-lymphocytes migrating to the wound site. Although their role is not yet clearly understood, studies using mice models have revealed that delayed T-lymphocyte infiltration and decrease in concentration of these cells may lead to impaired wound healing. Specifically the dendritic epidermal-cells (DETC), due to their unique dendritic morphology, transform keratinocytes and produce fibroblast growth factor 7 (FGF-7), keratinocytes growth factors, and insulin-like growth factor-1, to support keratinocyte proliferation and cell survival.
“The process by which tissue repair takes place is termed wound healing and is comprised of a continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore a semblance of their usual discipline and having done so resume their normal function”. ("The Cellular Biology of Wound Healing" 2016)
Stechmiller, J. K. (2010). Understanding the Role of Nutrition and Wound Healing. Nutrition in Clinical Practice, 25(1), 61-68. doi:10.1177/0884533609358997
Fibroblasts are mesenchymal cells that play an important role in the wound healing process. These cells are responsible for releasing inflammatory agents that recruit white blood cells to areas of damaged tissue. Fibroblasts also respond to these chemicals and differentiate into myofibroblasts. These myofibroblasts are characterized by their up-regulated rate of extracellular matrix component production and their ability to physically manipulate the extracellular matrix. When the wound healing process becomes unregulated, this results in what is referred to as a fibrotic response (Kendall). As a result fibrosis, or the thickening and scarring of connective tissues, occurs. Fibrosis is the excess deposition of ECM components like collagen and
In order for Mr Jones’ wound to heal, his nutritional status would need to be improved as part of his nursing care. An array of authors have noted that protein in particular is essential in wound healing. Lewis and Harding (1993), state that protein is like a building block in the process of constructing the wound bed. They also note that malnourishment of protein prolongs the inflammatory phase of wound
While inflammation is often viewed in a negative connotation, inflammation is actually an essential component of the healing process. Inflammation is commonly associated with pain, swelling, and redness; however, these effects are the body’s natural response to injury as blood and white blood cells move into the tissue and stimulate the repair process.2, 29 Therefore it is important to understand that even though certain molecular signals are traditionally identified as pro-inflammatory molecules, they are also critical molecules to support tissue regeneration through stimulation of reparative cells. Only when inflammation persists, as in chronic wounds, can it lead to tissue damage and prevent progression through the healing process. Therefore,
Inflammation is a normal immune reaction in response to tissue injury or invading exogenous molecules/ pathogens and can be either localized or systemic. The aim of acute inflammation is restoring the tissue homeostatic imbalance by promoting tissue repair and eliminating the causative stimuli through a complex but highly regulated cascade of events (Medzhitov 2008). Under physiological conditions, successful acute inflammation is followed by a resolution phase during which pro-inflammatory processes are suppressed and physiological homeostasis is achieved. However, an ongoing inflammatory event or an impaired resolution phase characterized by continuous pro-inflammatory processes results in chronic inflammation (Maskrey et al. 2011; Fullerton
When the body is inflicted with a penetrating wound, vessels and tissue fibers are ripped and broken. The area is then filled with leaking blood from the surrounding vessels and the outermost blood flow begins to form a scab. The surrounding vessels at that time constrict to minimize the blood leakage in a process known as vasoconstriction. The first step of the body is to clot the blood and achieve hemostasis, or blood clotting to impede blood leakage. The blood also coagulates, forming into a gel-like substance from its liquid state. The area of damage undergoes the coagulation cascade in which a fibrin clot is made. Blood platelets begin to release inflammatory factors and express glycoproteins on the cell membranes, a sticky-like protein, in order to aggregate. The area then forms a fibrin matrix via fibrin and fibronectin fibers, which provide the scaffold for incoming cells. this fibrin clot plays a crucial role in clotting the surrounding area as well as trapping essential proteins and cells. (https://en.wikipedia.org/wiki/Wound_healing)(http://www.nature.com/nature/journal/v453/n7193/full/nature07039.html) The matrix serves as the primary structural support of the wounded area until it is replaced by collagen and later granulation tissues.
Inflammation is the immune system’s response to infection and injury and has been implicated in the pathogeneses of arthritis, cancer and stroke, as well as in neurodegenerative and cardiovascular disease. It is an intrinsically beneficial event that leads to removal of offending factors and restoration of tissue structure and physiological function.
Cutaneous wounds are the result of disruption of skin integrity and healing process is a series of complex cellular events. Wound healing is a natural process of tissue restoration guided by secreted mediators, cytokines and growth factors. Although the wound healing process takes place with its own intrinsic factors, various risk factors such as infection, malnutrition and aging etc. have a serious impact on tissue repair process [8,9]. Microorganisms such as B. subtilis, S. aureus, E. coli, K. pneumoniae and P. aeruginosa are major infecting pathogens found in the open wound [8]. Different Ayurvedic classics of India (Charaka Samhita, Sushruta Samhita, and Ayurveda Siksha), evident the long history of wound management therapy, where approximately 70% medicines are of plant origin. World Health Organization estimated that 80% of the world’s population still rely on plant-based medicines for their primary health care, including skin related disorders specially wounds [10]. Fibroblast cells impart an important role in wound repair process and the main cellular component of granulation tissue which is involved in the synthesis and deposition of collagen fibres, contraction and re-epithelialization of the wound. Fibroblast cells also secrete growth factors, such as platelet derived growth factor (PDGF), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and
Inflammation is a part of our body’s immune system that helps in the healing process of our injury. However, long-term inflammation may cause severe damages to our organs leading to diseases.