Platelet-Rich Fibrin

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

Proliferative phase occurs within a few days of injury in which cells that were involved in the battle need to tend to their wounds and the regenerate to restore itself to its formal glory as best as possible. The body’s way of restoring itself is through use of angiogenesis, granulation tissue formation, wound contraction and epithelialization. This combination acts of getting new blood vessels to the damage area, aid in the formation of cells to fill in the area which leads to scar tissue, allow the skin to flexible in the repair process and finally resurface the wound with new epithelial

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

In an article published in JACC: Cardiovascular Interventions, Doctors Madan, Halvorsen, Di Mario, Tan, Westerhout, Cantor, Le May, and Borgia explored whether patients experienced greater risk of undergoing angiography after the administration of fibrinolytic therapy. They concluded that there was not a serious risk of bleeding or death if they receive angiography within four hours of undergoing fibrinolytic therapy (Madan et al., 2015). They also suggest that the patient be moved a center that can perform PCI within 2 hours after fibrinolysis. This article suggests that although fibrinolysis can be success a patient should receive PCI treatment.

This organ system has a number of functions namely, to keep a constant body temperature as well as to ensure coagulation occurs specifically at the site of injury, as well as to ensure no added blood loss occurs to cause life-threatening effects. This process of blood coagulation is explained in three interconnected phases. In the first phase, the enzyme thrombokinase is activated due to the damage of tissue and the breaking down of platelets. Prothrombin is converted into thrombin by the disintegration of the thrombocytes, electrically charged calcium ions and other coagulation factors, as well as the blood activator and tissue activator which become involved in the coagulation process. The second phase includes production of the thrombin that transforms fibrinogen in the blood plasma into fibrin. The thrombus (or blood clotting) is formed by a fibrilliform mesh that encloses the blood cells. Lastly, the third phase, which takes place as retraction occurs of the fibres of the fibrin mesh. Solidification of the fibrous mesh takes place which closes the defect in the vascular wall. Coagulation is then followed by fibrinolysis (re-dissolution of the clot).

Massive hemorrhage is a leading cause of preventable death amongst both civilian and military populations (Abramovich et al., 2013). Pre-hospital care for trauma patients with massive hemorrhage mainly focuses on bleeding control and rapid transport (Hafen, Karren, & Mistovich 2013), but recent studies on the use of tranexamic acid (TXA) as an “anti-clot buster” have sparked interest in development of protocols allowing pre-hospital administration of the drug by EMS agencies in treatment for traumatic hemorrhage (Fox 2016). As an antifibrinolytic drug, TXA works to inhibit the breakdown of clots and reduce blood loss in trauma patients to fight the onset of hemorrhagic shock (Dubose et al., 2012). Following massive trauma, the body’s coagulative response works to promote normal clotting but this process is highly influenced by fibrin breakdown, which works to break down the clots formed as products of coagulation. In patients with hyperfibrinolysis, increased clot breakdown can lead to fatal bleeding and organ failure (Fox 2016). Use of TXA in such patients can potentially work to enhance clot formation and reverse this enhanced fibrinolytic process but studies are being done to prove its benefits in trauma patients with normal fibrinolytic responses as well. Although it was first approved by the FDA in 1986 for treating hemophiliac patients during oral surgery and has been used for decades in cardiovascular surgery to reduce blood loss (Fox 2016), the use of TXA in

After the occurrence of a wound the inflammatory process immediately begins and can last up to 3 days ("Wound Healing" 2016), the initial injury causes the small vessels around the wound site to be disturbed resulting in bleeding, the body’s first response is a haemodynamic one in that it restricts these vessels in order to prevent blood loss. There then comes a rapid release of preformed inflammatory mediators from the cells surrounding the injury, the first thing this causes is the aggregation of platelets, these platelets adhere to extracellular surface structures which are exposed, such as collagen and basement membranes, this in turn causes serotonin from platelet stores to be stimulated. (Kirk, Phillips and Murray 2001)

Tissue plasminogen activator is a fibrinolytic drug which is used to treat thromboembolic disorders, such as ischaemic strokes. These agents initiate secondary fibrinolysis to occur; altering the haemostatic capability. The primary purpose of this agent is to clear occluded blood vessels within the systemic circulation (Bryant & Knights 2011, pp.534-536).

Materials and methods This study was conducted on 30 subjects: 15 with diabetic foot ulcers and 15 with varicose vein ulcers as a comparison group. The study protocol was done according to the local ethics committee of the Menoufia University. Informed consents were taken from the subjects before the start of the study. For all subjects, the followings were done: history taking and clinical examination, clinical evaluation of the ulcers, complete blood count, preparation of platelet rich plasma (PRP) and quantification of Platelet count in it, preparation& application of PRP gel on ulcers, quantification of platelet derived growth factor (PDGF-AB) in PRP prepared before and after activation ,using CaCl2, by sandwich-based enzyme-linked immune-sorbent assay (ELISA) (Ray Biotech – USA)

Neutrophils start with the critical task of destroying and removing bacteria, foreign particles and any remaining damaged tissue. This phagocytic activity is crucial as bacterial imbalance within acute wounds causes the wound to stop healing. Neutrophils are attracted to the site of injury within 24 – 36 hours by pro-inflammatory cytokines including TGF- β. Neutrophils are one of the most abundant cells of the immune system and they are extremely active during the repair of cutaneous wounds. In general, the antimicrobial

Platelets are small fragments of cells. Platelets process coagulation. This is done by them gathering at the site of an injury and in turn sticking to the lining of the injured blood vessel. This is a platform on which blood coagulations occur, resulting in the formation of a fibrin clot. This covers the wound and prevents blood from leaking out. Fibrin also forms the initial building blocks from which new tissue are formed, in- turn promoting the healing process. If there is an imbalance, for example to high of a number of platelets may result in clotting not necessary in the body that can lead to health risks or a lower than normal counts can lead to extensive bleeding. So they protect us by clotting and aiding in healing by producing

APCs are hemocomponents prepared by centrifugation of a blood sample of the patient. The basic concept of this technology is to collect the most active components of the blood sample (eg, platelets, fibrin, and in certain cases leukocytes). This process produces a very high-concentration gradient of platelets whose granules are rich with many substances fundamental to promote the healing process including adhesive proteins; procoagulant factors; cytokines and chemokines; antimicrobial proteins; and a number of mitogenic growth factors , which may trigger angiogenesis and improve tissue

It is amazing to see how this simple protein can have such a large positive impact on the general population; especially to those who have diabetes. This is entire new to me; that is people who are diabetics have a hard time to the heal wounds. My answer to the question is that I believe there are other factors that plays a role in blood clotting. Hsp60 protein may be an important factor, but those that lack Hsp60, I assume can still clot blood, just in the matter of time. I thought this article is relevant to me because my great grandmother suffered from diabetes and my mom is also diabetic, however, it does not seem as if they are having trouble with any wound healing problem. That’s why I hypothesized that there are other factors that plays

TransCyte is a temporary, bioactive synthetic covering with a similar structure to Biobrane, with an addition of fibroblasts. Like Biobrane, it is also used as covering for burn patients before autografting or for patients with partial thickness burns who do not require autografts[11][12]. TransCyte consists of two layers, a silicone outer layer and an inner nylon mesh seeded with fibroblasts. The outer silicone layer is a semipermeable membrane, containing a series of laser-punched holes that allow excess fluids to be drained[13]. The inner nylon mesh membrane is coated with porcine collagen peptides, creating the base onto where the neonatal fibroblasts can be cultured, since collagen is a main component of the skin. In order to seed the fibroblasts within the nylon mesh, the entire membrane, silicone outer layer included, was placed inside a specially designed bioreactor. This bioreactor provided a continuous, constant flow of fibroblasts at a rate of about

royed • Lysosome fuses with phagosome to form phagolysosome • Foreign materials trapped within phagolysosme is digested by enzymes Adaptive immunity • Initiate immune response →present antigens after digestion of foreign material • Antigen (protein on the surface of a pathogen) stimulates T lymphocytes • Antigen on macrophage’s membrane displayed with attachment of MHC II → not recognized as pathogen • Stimulates production of antibodies that attach to pathogen’s antigens →easier for macrophage to attach with cell membrane and undergo phagocytosis Wound Healing • Two days after wound injury polymorphonuclear neutrophils replaced • Platelets and other cells releasing growth factors attract macrophage to wound • Monocytes (matures to become macrophages) passes through blood vessel walls to arrive at wound • Phagocytose foreign material • Repair tissue by producing →platelet derived growth factor →fibroblast growth factor →transforming growth factor beta • Vascular endothelial growth factor stimulated and produced →endothelial cell growth →create granulation tissue →new extracellular matrix generated Macrophage activities • M1 (classically activated)→”killer” →inhibit cell proliferation and damage tissue →activated by natural killer cells and interferon gamma • M2 (alternatively activated)→ “repair” →wound healing and tissue repair →activated by eosinophils and basophils Summary • Effector cell →