how does granulation tissue start

n) The noun GRANULATION TISSUE has 1 sense:1. new connective tissue and tiny blood vessels that form on the surfaces of a wound during the healing process Familiarity information: GRANULATION TISSUE used as a noun is very rare.

GRANULATION TISSUE

"Audio English.org » Dictionary » G » Grandiosity ... Grapelike GRANULATION TISSUEPronunciation (US): Dictionary entry overview: What does granulation tissue mean?• GRANULATION TISSUE (nou

Dictionary entry details• GRANULATION TISSUE (noun)Sense 1 granulation tissue [BACK TO TOP]Meaning: New connective tissue and tiny blood vessels that form on the surfaces of a wound during the healing process Classified under: Nouns denoting stable states of affairs Synonyms:granulation; granulation tissue Hypernyms (""granulation tissue"" is a kind of...):connective tissue (tissue of mesodermal origin consisting of e.g.

collagen fibroblasts and fatty cells; supports organs and fills spaces between them and forms tendons and ligaments)Hyponyms (each of the following is a kind of ""granulation tissue""):proud flesh (the swollen tissue around a healing wound or ulcer)Learn English with... Proverbs of the week""Beauty may open doors but only virtue enters.""

(English proverb) ""You cannot hunt with a tied dog."" (Albanian proverb) ""An unshod mocks a shoe."" (Arabic proverb) ""Forbidden fruit tastes best."" (Czech proverb)GRANULARGRANULAR PEARLITEGRANULARITYGRANULATEGRANULATEDGRANULATED SUGARGRANULATIONGRANULATION TISSUEGRANULEGRANULIFEROUSEnglish learning courses About Practical English About Telephone English About Accounting English Learn English Free English Language Dictionary British and American English pronunciation Other popular searches:» definition of cheeky » prokaryotic » what does bipartisan mean » quasar » what does eau de toilette mean Page delivered in 0.0745 seconds "

1-newly formed blood vessels (mainly capillaries) 2-proliferative fibroblasts 3- residual inflammatory cells 4-endothelial cells and im sure u know that granulation tissue forms due to an injury, and it's main function is anti infection and to form protection of the wound..

The 4 major components of granulation tissue?

Flag The 4 major components of granulation tissue? Answered by The Wiki Answers ®Community Answers.com ® is making the world better one answer at a time.hiya bro granulation tissue is highly vascularized connective tissue which mainly composed of:

i hope that helped thanks12 people found this useful Was this answer useful? Yes Somewhat No

it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase. Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur.

Wound healing

"From Wikipedia, the free encyclopedianavigation search Hand abrasion Approximate days since injury0 3 17 30Wound healing is an intricate process in which the skin repairs itself after injury.

[1] In this article, wound healing is depicted in a discrete timeline of physical attributes (phases) constituting the post-trauma repairing process. In undamaged skin, the epidermis (surface layer) and dermis (deeper layer) form a protective barrier against the external environment.

When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. [1] [2] This process is divided into predictable phases: blood clotting ( hemostasis ), inflammation, tissue growth (proliferation), and tissue remodeling (maturation).

Blood clotting may be considered to be part of the inflammation stage instead of a separate stage. [3]Deep wound on shin with stitches healing over five weeks Hemostasis (blood clotting): Within the first few minutes of injury, platelets in the blood begin to stick to the injured site.

This activates the platelets, causing a few things to happen. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting. This results in the activation of fibrin, which forms a mesh and acts as ""glue"" to bind platelets to each other.

This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding. [4] [5]Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. This happens through the process of phagocytosis, where white blood cells ""eat"" debris by engulfing

[6] In angiogenesis, vascular endothelial cells form new blood vessels. [7] In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin. [6] Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue. [8] In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells.

When the cells' roles are close to complete, unneeded cells undergo apoptosis. [6]Maturation (remodeling): During maturation and remodeling, collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.

The wound healing process is not only complex but also fragile, and it is susceptible to interruption or failure leading to the formation of non-healing chronic wounds. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease, infection, and metabolic deficiencies of old age. [9]Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection.

Depending on each patient's needs, it can range from the simplest first aid to entire nursing specialties such as wound, ostomy, and continence nursing and burn center care. Approximate times of the different phases of wound healing, [10] with faded intervals marking substantial variation, depending mainly on wound size and healing conditions, but image does not include major impairments that cause chronic wounds.

Contents [ hide ]1 Timing and reepithelialization2 Early vs cellular phase3 Inflammatory phase3.1 Clotting cascade3.2 Vasoconstriction and vasodilation3.3 Polymorphonuclear neutrophils3.4 Macrophages3.5 Decline of inflammatory phase4 Proliferative phase4.1 Angiogenesis4.2 Fibroplasia and granulation tissue formation4.2.1 Collagen deposition4.3 Epithelialization4.4 Contraction5 Maturation and remodeling6 Factors affecting wound healing6.1 Local factors6.2 Systemic factors7 Research and development7.1 Stem cells and cellular plasticity7.2 Wound repair versus regeneration7.3 Scarless wound healing8 Simulating wound healing from a growth perspective9 Wound closure intentions9.1 Primary intention9.2 Secondary intention9.3 Tertiary intention10 Overview of involved growth factors11 Complications of wound healing12 Biologics, skin substitutes, biomembranes and scaffolds13 See also14 Notes and references15 External links Timing and reepithelialization [ edit]Timing is important to wound healing.

Critically, the timing of wound reepithelialization can decide the outcome of the healing. [11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months; [12] [13] If the epithelization of a wounded area is fast, the healing will result in regeneration.

[13]Early vs cellular phase [ edit]A fluorescence micrograph of cells in Drosophila larvae healing after a puncture wound. The arrow points to cells that have fused to form syncytia, and the arrowheads point to cells that are oriented to face the wound.

[14]Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described [1] where the many elements of wound healing are more clearly delineated.

The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase: [1]The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation.

The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. [1] Subdivisions of the cellular phase are: [1] Macrophages and inflammatory components (within 1–2 days), [2] Epithelial - mesenchymal interaction: re-epithelialization ( phenotype change within hours, migration begins on day 1 or 2), [3] Fibroblasts and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14), [4] Endothelial cells and angiogenesis (begins on day 4), [5] Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size).

[1]Inflammatory phase [ edit]Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.

Clotting cascade [ edit]Main article: Coagulation When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. [15] Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass.

[6]Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss. [16] This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited.

[6] Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. [6] The clot is eventually lysed and replaced with granulation tissue and then later with collagen. Platelets, the cells present in the highest numbers shortly after a wound occurs, release mediators into the blood, including cytokines and growth factors.

[15] Growth factors stimulate cells to speed their rate of division. Platelets release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine, [3] which serve several purposes, including increasing cell proliferation and migration to the area and causing blood vessels to become dilated and porous.

In many ways, extravasated platelets in trauma perform a similar function to tissue macrophages and mast cells exposed to microbial molecular signatures in infection: they become activated, and secrete molecular mediators – vasoactive amines, eicosanoids, and cytokines – that initiate the inflammatory process.

Vasoconstriction and vasodilation [ edit]Immediately after a blood vessel is breached, ruptured cell membranes release inflammatory factors like thromboxanes and prostaglandins that cause the vessel to spasm to prevent blood loss and to collect inflammatory cells and factors in the area.

[3] This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at about 20 minutes post-wounding. [3] Vasodilation is the end result of factors released by platelets and other cells. The main factor involved in causing vasodilation is histamine.

[3] [15] Histamine also causes blood vessels to become porous, allowing the tissue to become edematous because proteins from the bloodstream leak into the extravascular space, which increases its osmolar load and draws water into the area. [3] Increased porosity of blood vessels also facilitates the entry of inflammatory cells like leukocytes into the wound site from the bloodstream.

[17] [18]Polymorphonuclear neutrophils [ edit]Within an hour of wounding, polymorphonuclear neutrophils (PMNs) arrive at the wound site and become the predominant cells in the wound for the first two days after the injury occurs, with especially high numbers on the second day. [19] They are attracted to the site by fibronectin, growth factors, and substances such as kinins.

Neutrophils phagocytise debris and kill bacteria by releasing free radicals in what is called a ' respiratory burst. [20] [21] They also cleanse the wound by secreting proteases that break down damaged tissue. Functional neutrophils at the wound site only have life-spans of around 2 days, so they usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages. [22]Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability.

[17] [23] T cells also increase the activity of macrophages. [17]Macrophages [ edit]One of the macrophage's roles is to phagocytize other expended phagocytes, [24] bacteria and damaged tissue, [19] and they also debride damaged tissue by releasing proteases.

[25]Macrophages function in regeneration [26] [27] and are essential for wound healing. [19] They are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis [20] and they also stimulate cells that reepithelialize the wound, create granulation tissue, and lay down a new extracellular matrix. [28] [29] By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury. [24]The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue. [30] [31] Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls.

[32] Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. [23] Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days.

These factors attract cells involved in the proliferation stage of healing to the area. [15]In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility. [33] Macrophages may restrain the contraction phase. [27] Scientists have reported that removing the macrophages from a salamander resulted in failure of a typical regeneration response (limb regeneration), instead bringing on a repair (scarring) response.

[34] [35]Decline of inflammatory phase [ edit]As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. [19] These changes indicate that the inflammatory phase is ending and the proliferative phase is underway. [19] In vitro evidence, obtained using the dermal equivalent model, suggests that the presence of macrophages actually delays wound contraction and thus the disappearance of macrophages from the wound may be essential for subsequent phases to occur.

[27]Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. However, inflammation can lead to tissue damage if it lasts too long. [6] Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus, if the individual's immune system is compromised and is unable to clear the debris from the wound and/or if excessive detritus, devitalized tissue, or microbial biofilm is present in the wound, these factors may cause a prolonged inflammatory phase and prevent the wound from properly commencing the proliferation phase of healing.

This can lead to a chronic wound. Proliferative phase [ edit]About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended. [36] As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time. Angiogenesis [ edit]Further information: Angiogenesis Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound.

[37] Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration.

The tissue in which angiogenesis has occurred typically looks red (is erythematous) due to the presence of capillaries. [37]Angiogenesis occurs in overlapping phases in response to inflammation: Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area. Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix. Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells.

Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli. Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.

Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venules can divide and migrate chemotactically towards the wound, laying down new vessels in the process.

Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment, as hypoxia stimulates the endothelial transcription factor, hypoxia inducible factor (HIF) to transactivate angiogenic genes such as VEGF and GLUT1. Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks. Vascular maturation: the endothelium of vessels mature by laying down new endothelial extracellular matrix, followed by basal lamina formation.

Lastly the vessel establishes a pericyte layer. Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels. [20]Endothelial cells are attracted to the wound area by fibronectin found on the fibrin scab and chemotactically by angiogenic factors released by other cells, [38] e.g.

from macrophages and platelets when in a low-oxygen environment. Endothelial growth and proliferation is also directly stimulated by hypoxia, and presence of lactic acid in the wound. [36] For example, hypoxia stimulates the endothelial transcription factor, hypoxia-inducible factor (HIF) to transactivate a set of proliferative genes including vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1).

To migrate, endothelial cells need collagenases and plasminogen activator to degrade the clot and part of the ECM. [3] [19]Zinc -dependent metalloproteinases digest basement membrane and ECM to allow cell migration, proliferation and angiogenesis. [39]When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. [20] Thus, when tissue is adequately perfused, migration and proliferation of endothelial cells is reduced. Eventually blood vessels that are no longer needed die by apoptosis. [38]Fibroplasia and granulation tissue formation [ edit]Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site.

Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding.

[19] By the end of the first week, fibroblasts are the main cells in the wound. [3] Fibroplasia ends two to four weeks after wounding. As a model the mechanism of fibroplasia may be conceptualised as an analogous process to angiogenesis (see above) - only the cell type involved is fibroblasts rather than endothelial cells.

Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound.

The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia. The deposited fibroblastic connective tissue matures by secreting ECM into the extracellular space, forming granulation tissue (see below).

Lastly collagen is deposited into the ECM. In the first two or three days after injury, fibroblasts mainly migrate and proliferate, while later, they are the main cells that lay down the collagen matrix in the wound site.

[3] Origins of these fibroblasts are thought to be from the adjacent uninjured cutaneous tissue (although new evidence suggests that some are derived from blood-borne, circulating adult stem cells/precursors).

[40] Initially fibroblasts utilize the fibrin cross-linking fibers (well-formed by the end of the inflammatory phase) to migrate across the wound, subsequently adhering to fibronectin. [38] Fibroblasts then deposit ground substance into the wound bed, and later collagen, which they can adhere to for migration. [15]Granulation tissue functions as rudimentary tissue, and begins to appear in the wound already during the inflammatory phase, two to five days post wounding, and continues growing until the wound bed is covered.

Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional extracellular matrix (ECM). The provisional ECM is different in composition from the ECM in normal tissue and its components originate from fibroblasts. [28] Such components include fibronectin, collagen, glycosaminoglycans, elastin, glycoproteins and proteoglycans.

[38] Its main components are fibronectin and hyaluronan, which create a very hydrated matrix and facilitate cell migration. [32] Later this provisional matrix is replaced with an ECM that more closely resembles that found in non-injured tissue. Growth factors ( PDGF, TGF-β) and fibronectin encourage proliferation, migration to the wound bed, and production of ECM molecules by fibroblasts.

Fibroblasts also secrete growth factors that attract epithelial cells to the wound site. Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring. Collagen deposition [ edit]One of fibroblasts' most important duties is the production of collagen.

[37]Collagen deposition is important because it increases the strength of the wound; before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot, which does not provide much resistance to traumatic injury. [20] Also, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts. [41]Type III collagen and fibronectin generally begin to be produced in appreciable amounts at somewhere between approximately 10 hours [42] and 3 days, [38] depending mainly on wound size.

Their deposition peaks at one to three weeks. [28] They are the predominating tensile substances until the later phase of maturation, in which they are replaced by the stronger type I collagen. Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain.

[20] This homeostasis signals the onset of the later maturation phase. Granulation gradually ceases and fibroblasts decrease in number in the wound once their work is done. [43] At the end of the granulation phase, fibroblasts begin to commit apoptosis, converting granulation tissue from an environment rich in cells to one that consists mainly of collagen.

[3]Epithelialization [ edit]The formation of granulation tissue into an open wound allows the reepithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment.

[38] Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebacious (oil) glands are the main cells responsible for the epithelialization phase of wound healing. [43] They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle.

In healing that results in a scar, sweat glands, hair follicles [44] [45] and nerves do not form. With the lack of hair follicles, nerves and sweat glands, the wound, and the resulting healing scar, provide a challenge to the body with regards to temperature control. [45]Keratinocytes migrate without first proliferating. [46] Migration can begin as early as a few hours after wounding.

However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue. [47] Thus the time of onset of migration is variable and may occur about one day after wounding. [48] Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration.

[28]If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. [38] However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes.

[28] If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges. [47]Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide.

[49] Before they begin to migrate, cells must dissolve their desmosomes and hemidesmosomes, which normally anchor the cells by intermediate filaments in their cytoskeleton to other cells and to the ECM. [23] Transmembrane receptor proteins called integrins, which are made of glycoproteins and normally anchor the cell to the basement membrane by its cytoskeleton, are released from the cell's intermediate filaments and relocate to actin filaments to serve as attachments to the ECM for pseudopodia during migration.

[23] Thus keratinocytes detach from the basement membrane and are able to enter the wound bed. [36]Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles.

[32] Actin filaments and pseudopodia form. [36] During migration, integrins on the pseudopod attach to the ECM, and the actin filaments in the projection pull the cell along. [23] The interaction with molecules in the ECM through integrins further promotes the formation of actin filaments, lamellipodia, and filopodia. [23]Epithelial cells climb over one another in order to migrate. [43] This growing sheet of epithelial cells is often called the epithelial tongue.

[46] The first cells to attach to the basement membrane form the stratum basale. These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well. [46] The more quickly this migration occurs, the less of a scar there will be. [50]Fibrin, collagen, and fibronectin in the ECM may further signal cells to divide and migrate.

Like fibroblasts, migrating keratinocytes use the fibronectin cross-linked with fibrin that was deposited in inflammation as an attachment site to crawl across. [25] [32] [43]A scab covering a healing wound As keratinocytes migrate, they move over granulation tissue but stay underneath the scab, thereby separating the scab from the underlying tissue.

[43] [48] Scabs are formed on locations that are exposed to harmful UVR and the main biological function of human wound scabs is to inhibit the exposure to UVR, thus protecting otherwise exposed cells in a wound from UVR-induced DNA damage.

[51] [ unreliable medical source?] Epithelial cells have the ability to phagocytize debris such as dead tissue and bacterial matter that would otherwise obstruct their path. Because they must dissolve any scab that forms, keratinocyte migration is best enhanced by a moist environment, since a dry one leads to formation of a bigger, tougher scab. [25] [38] [43] [52] To make their way along the tissue, keratinocytes must dissolve the clot, debris, and parts of the ECM in order to get through.

[48] [53] They secrete plasminogen activator, which activates plasminogen, turning it into plasmin to dissolve the scab. Cells can only migrate over living tissue, [43] so they must excrete collagenases and proteases like matrix metalloproteinases (MMPs) to dissolve damaged parts of the ECM in their way, particularly at the front of the migrating sheet. [48] Keratinocytes also dissolve the basement membrane, using instead the new ECM laid down by fibroblasts to crawl across. [23]As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more cells for the advancing sheet.

[25] Proliferation behind migrating keratinocytes normally begins a few days after wounding [47] and occurs at a rate that is 17 times higher in this stage of epithelialization than in normal tissues.

[25] Until the entire wound area is resurfaced, the only epithelial cells to proliferate are at the wound edges. [46]Growth factors, stimulated by integrins and MMPs, cause cells to proliferate at the wound edges. Keratinocytes themselves also produce and secrete factors, including growth factors and basement membrane proteins, which aid both in epithelialization and in other phases of healing.

[54] Growth factors are also important for the innate immune defense of skin wounds by stimulation of the production of antimicrobial peptides and neutrophil chemotactic cytokines in keratinocytes. Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating.

[32] When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane. [32] Cells reverse the morphological changes they underwent in order to begin migrating; they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane.

[23]Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin. [32]Contraction [ edit]Contraction is a key phase of wound healing with repair. If contraction continues for too long, it can lead to disfigurement and loss of function.

[33] Thus there is a great interest in understanding the biology of wound contraction, which can be modelled in vitro using the collagen gel contraction assay or the dermal equivalent model. [27] [55]Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts.

[56] In full thickness wounds, contraction peaks at 5 to 15 days post wounding. [38] Contraction can last for several weeks [47] and continues even after the wound is completely reepithelialized. [3] A large wound can become 40 to 80% smaller after contraction. [32] [43] Wounds can contract at a speed of up to 0.75 mm per day, depending on how loose the tissue in the wounded area is.

[38] Contraction usually does not occur symmetrically; rather most wounds have an 'axis of contraction' which allows for greater organization and alignment of cells with collagen. [56]At first, contraction occurs without myofibroblast involvement. [57] Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction. [57] Myofibroblasts contain the same kind of actin as that found in smooth muscle cells. [33]Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges.

[25] They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen. [57] Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size.

[33] In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part. [57]As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. [3] The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis.

[33] The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating.

[19] These events signal the onset of the maturation stage of wound healing. Maturation and remodeling [ edit]When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun. [20] During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen.

[17] Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. [32] The onset of the maturation phase may vary extensively, depending on the size of the wound and whether it was initially closed or left open, [28] ranging from approximately 3 days [42] to 3 weeks. [58] The maturation phase can last for a year or longer, similarly depending on wound type. [28]As the phase progresses, the tensile strength of the wound increases.

[28] Collagen will reach approximately 20% of its tensile strength after 3 weeks, increasing to 80% by 12th week.

The maximum scar strength is 80% of that of unwounded skin. [59] Since activity at the wound site is reduced, the scar loses its red appearance as blood vessels that are no longer needed are removed by apoptosis. [20]The phases of wound healing normally progress in a predictable, timely manner; if they do not, healing may progress inappropriately to either a chronic wound [6] such as a venous ulcer or pathological scarring such as a keloid scar.

[60] [61]Factors affecting wound healing [ edit]Many factors controlling the efficacy, speed, and manner of wound healing fall under two types: local and systemic factors.

[2]Local factors [ edit]Moisture; keeping a wound moist rather than dry makes wound healing more rapid and with less pain and less scarring [62]Mechanical factors Edema Ionizing radiation Faculty technique of wound closure Ischemia and necrosis Foreign bodies.

Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, ""frequently, an innocent skin wound disguises the extensive nature of the injuries beneath"".

[63] First-degree nerve injury requires a few hours to a few weeks to recover. [64] If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry.

A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection. Low oxygen tension Perfusion Systemic factors [ edit]Inflammation Diabetes – Individuals with diabetes demonstrate reduced capability in the healing of acute wounds.

Additionally, diabetic individuals are susceptible to developing chronic diabetic foot ulcers, a serious complication of diabetes which affects 15% of people with diabetes and accounts for 84% of all diabetes-related lower leg amputations.

[65] The impaired healing abilities of diabetics with diabetic foot ulcers and/or acute wounds involves multiple pathophysiological mechanisms. [66] This impaired healing involves hypoxia, fibroblast and epidermal cell dysfunction, impaired angiogenesis and neovascularization, high levels of metalloproteases, damage from reactive oxygen species and AGEs (advanced glycation end-products), decreased host immune resistance, and neuropathy. [66]Nutrients – Malnutrition or nutritional deficiencies have a recognizable impact on wound healing post trauma or surgical intervention.

[67] Nutrients including proteins, carbohydrates, arginine, glutamine, polyunsaturated fatty acids, vitamin A, vitamin C, vitamin E, magnesium, copper, zinc and iron all play significant roles in wound healing.

[66] Fats and carbohydrates provide the majority of energy required for wound healing. Glucose is the most prominent source of fuel and it is used to create cellular ATP, providing energy for angiogenesis and the deposition of new tissues. [68] As the nutritional needs of each patient and their associated wound are complex, it is suggested that tailored nutritional support would benefit both acute and chronic wound healing.

[66]Metabolic diseases Immunosuppression Connective tissue disorders Smoking Smoking causes a delay in the speed of wound repair notably in the proliferative and inflammatory phases.

It also increases the likelihood of certain complications such as wound rupture, wound and flap necrosis, decrease in wound tensile strength and infection. [68]Age – Increased age (over 60 years) is a risk factor for impaired wound healing. [66] It is recognized that, in older adults of otherwise overall good health, the effects of aging causes a temporal delay in healing, but no major impairment with regard to the quality of healing.

[69] Delayed wound healing in patients of increasing age is associated with altered inflammatory response; for example delayed T-cell infiltration of the wound with alterations in the production of chemokines, and reduced macrophage phagocytic capacity. [70]Alcohol – Alcohol consumption impairs wound healing and also increases the chances of infection.

Alcohol affects the proliferative phase of healing. A single unit of alcohol causes a negative effect on re-epithelialization, wound closure, collagen production and angiogenesis. [68]Research and development [ edit]Up until a decade ago, [ when?] the classic paradigm of wound healing, involving stem cells restricted to organ-specific lineages, had never been seriously challenged.

Since then, [ when?] the notion of adult stem cells having cellular plasticity or the ability to differentiate into non-lineage cells has emerged as an alternative explanation.

[1] To be more specific, hematopoietic progenitor cells (that give rise to mature cells in the blood) may have the ability de-differentiate back into hematopoietic stem cells and/or transdifferentiate into non-lineage cells, such as fibroblasts. [40]Stem cells and cellular plasticity [ edit]Multipotent adult stem cells have the capacity to be self-renewing and give rise to different cell types. Stem cells give rise to progenitor cells, which are cells that are not self-renewing, but can generate several types of cells.

The extent of stem cell involvement in cutaneous (skin) wound healing is complex and not fully understood.

It is thought that the epidermis and dermis are reconstituted by mitotically active stem cells that reside at the apex of rete ridges (basal stem cells or BSC), the bulge of hair follicles (hair follicular stem cell or HFSC), and the papillary dermis (dermal stem cells). [1] Moreover, bone marrow may also contain stem cells that play a major role in cutaneous wound healing.

[40]In rare circumstances, such as extensive cutaneous injury, self-renewal subpopulations in the bone marrow are induced to participate in the healing process, whereby they give rise to collagen-secreting cells that seem to play a role during wound repair. [1] These two self-renewal subpopulations are (1) bone marrow-derived mesenchymal stem cells (MSC) and (2) hematopoietic stem cells (HSC).

Bone marrow also harbors a progenitor subpopulation ( endothelial progenitor cells or EPC) that, in the same type of setting, are mobilized to aid in the reconstruction of blood vessels. [40] Moreover, it thought that, extensive injury to skin also promotes the early trafficking of a unique subclass of leukocytes (circulating fibrocytes) to the injured region, where they perform various functions related to wound healing.

[1]Wound repair versus regeneration [ edit]An injury is an interruption of morphology and/or functionality of a given tissue. After injury, structural tissue heals with incomplete or complete regeneration. [71] [72] Whereas, tissue without an interruption to the morphology almost always completely regenerates. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin.

[73] Non-injured skin has a continued replacement and regeneration of cells which always results in complete regeneration. [73]There is a subtle distinction between 'repair' and 'regeneration'. [1] [71] [72] Repair means incomplete regeneration. [71] Repair or incomplete regeneration, refers to the physiologic adaptation of an organ after injury in an effort to re-establish continuity without regards to exact replacement of lost/damaged tissue.

[71] True tissue regeneration or complete regeneration, [72] refers to the replacement of lost/damaged tissue with an ‘exact’ copy, such that both morphology and functionality are completely restored. [72] Though after injury mammals can completely regenerate spontaneously, they usually do not completely regenerate.

An example of a tissue regenerating completely after an interruption of morphology is the endometrium; the endometrium after the process of breakdown via the menstruation cycle heals with complete regeneration.

[73]In some instances, after a tissue breakdown, such as in skin, a regeneration closer to complete regeneration may be induced by the use of biodegradable ( collagen - glycoaminoglycan) scaffolds. These scaffolds are structurally analogous to extracellular matrix (ECM) found in normal/un-injured dermis.

[74] Interestingly, fundamental conditions required for tissue regeneration often oppose conditions that favor efficient wound repair, including inhibition of (1) platelet activation, (2) inflammatory response, and (3) wound contraction. [1] In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway.

Pharmaceutical agents have been investigated which may be able to turn off myofibroblast differentiation. [75]A new way of thinking derived from the notion that heparan sulfates are key player in tissue homeostasis: the process that makes the tissue replace dead cells by identical cells.

In wound areas, tissue homeostasis is lost as the heparan sulfates are degraded preventing the replacement of dead cells by identical cells. Heparan sulfate analogues cannot be degraded by all know heparanases and glycanases and bind to the free heparin sulfate binding spots on the ECM, therefore preserving the normal tissue homeostasis and preventing scarring. [76] [77] [78]Repair or regeneration with regards to hypoxia-inducible factor 1-alpha (HIF-1a). In normal circumstances after injury HIF-1a is degraded by prolyl hydroxylases (PHDs).

Scientists found that the simple up-regulation of HIF-1a via PHD inhibitors regenerates lost or damaged tissue in mammals that have a repair response; and the continued down-regulation of Hif-1a results in healing with a scarring response in mammals with a previous regenerative response to the loss of tissue.

The act of regulating HIF-1a can either turn off, or turn on the key process of mammalian regeneration.

[79] [80]Scarless wound healing [ edit]Scarless wound healing is a concept based on the healing or repair of the skin (or other tissue/organs) after injury with the aim of healing with subjectively and relatively less scar tissue than normally expected. Scarless healing is sometimes mixed up with the concept of scar free healing, which is wound healing which results in absolutely no scar ( free of scarring). However they are different concepts. A reverse to scarless wound healing is scarification (wound healing to scar more).

Historically, certain cultures consider scarification attractive; [81] however, this is generally not the case in the modern western society, in which many patients are turning to plastic surgery clinics with unrealistic expectations. Depending on scar type, treatment may be invasive (intralesional steroid injections, surgery) and/or conservative ( compression therapy, topical silicone gel, brachytherapy, photodynamic therapy ).

[82] Clinical judgment is necessary to successfully balance the potential benefits of the various treatments available against the likelihood of a poor response and possible complications resulting from these treatments. Many of these treatments may only have a placebo effect, and the evidence base for the use of many current treatments is poor. [83]Since the 1960s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology.

[84] Currently, the principal goals in wound management are to achieve rapid wound closure with a functional tissue that has minimal aesthetic scarring. [85] However, the ultimate goal of wound healing biology is to induce a more perfect reconstruction of the wound area.

Scarless wound healing only occurs in mammalian foetal tissues [86] and complete regeneration is limited to lower vertebrates, such as salamanders, and invertebrates. [87] In adult humans, injured tissue are repaired by collagen deposition, collagen remodelling and eventual scar formation, where fetal wound healing is believed to be more of a regenerative process with minimal or no scar formation.

[86] Therefore, foetal wound healing can be used to provide an accessible mammalian model of an optimal healing response in adult human tissues.

Clues as to how this might be achieved come from studies of wound healing in embryos, where repair is fast and efficient and results in essentially perfect regeneration of any lost tissue. The etymology of the term scarless wound healing has a long history. [88] [89] [90] In print the antiquated concept of scarless healing was brought up the early 20th century and appeared in a paper published in the London Lancet.

This process involved cutting in a surgical slant, instead of a right angle…; it was described in various Newspapers.

[88] [89] [90]Simulating wound healing from a growth perspective [ edit]Considerable effort has been devoted to understanding the physical relationships governing wound healing and subsequent scarring, with mathematical models and simulations developed to elucidate these relationships. [91] The growth of tissue around the wound site is a result of the migration of cells and collagen deposition by these cells. The alignment of collagen describes the degree of scarring; basket-weave orientation of collagen is characteristic of normal skin, whereas aligned collagen fibers lead to significant scarring.

[92] It has been shown that the growth of tissue and extent of scar formation can be controlled by modulating the stress at a wound site. [93]The growth of tissue can be simulated using the aforementioned relationships from a biochemical and biomechanical point of view.

The biologically active chemicals that play an important role in wound healing are modeled with Fickian diffusion to generate concentration profiles. The balance equation for open systems when modeling wound healing incorporates mass growth due to cell migration and proliferation.

Here the following equation is used: D t ρ 0 = Div (R) + R 0,where ρ represents mass density, R represents a mass flux (from cell migration), and R 0 represents a mass source (from cell proliferation, division, or enlargement). [94]Wound closure intentions [ edit]Successful wound healing is dependent on various cell types, molecular mediators and structural elements. [95]Primary intention [ edit]Primary intention is the healing of a clean wound without tissue loss. [95] In this process, wound edges are brought together, so that they are adjacent to each other (re-approximated).

Wound closure is performed with sutures (stitches), staples, or adhesive tape or glue. Primary intention can only be implemented when the wound is precise and there is minimal disruption to the local tissue and the epithelial basement membrane, e.g.

surgical incisions. [96]This process is faster than healing by secondary intention. [95] There is also less scarring associated with primary intention, as there are no large tissue losses to be filled with granulation tissue. [95] (Primary intention does require some granulation tissue to form. )Examples of primary intention include: well-repaired lacerations, well reduced bone fractures, healing after flap surgery.

Secondary intention [ edit]Secondary intention is implemented when primary intention is not possible. This is due to wounds being created by major trauma in which there has been a significant loss in tissue or tissue damage.

[96]The wound is allowed to granulate. Surgeon may pack the wound with a gauze or use a drainage system. Granulation results in a broader scar. Healing process can be slow due to presence of drainage from infection.

Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation. Using antibiotics or antiseptics for the surgical wound healing by secondary intention is controversial. [97]Examples: gingivectomy, gingivoplasty, tooth extraction sockets, poorly reduced fractures, burns, severe lacerations, pressure ulcers.

Tertiary intention [ edit] (Delayed primary closure or secondary suture): The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure. The wound is purposely left open. Examples: healing of wounds by use of tissue grafts. If the wound edges are not reapproximated immediately, delayed primary wound healing transpires.

This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization, collagen deposition, and maturation are occurring. Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas.

Usually the wound is closed surgically at this juncture, and if the ""cleansing"" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

Overview of involved growth factors [ edit]Following are the main growth factors involved in wound healing: Growth factor Abbreviation Main origins Effects Epidermal growth factor EGFActivated macrophages Salivary glands Keratinocytes Keratinocyte and fibroblast mitogen Keratinocyte migration Granulation tissue formation Transforming growth factor-αTGF-αActivated macrophages T-lymphocytes Keratinocytes Hepatocyte and epithelial cell proliferation Expression of antimicrobial peptides Expression of chemotactic cytokines Hepatocyte growth factor HGFMesenchymal cells Epithelial and endothelial cell proliferation Hepatocyte motility Vascular endothelial growth factor VEGFMesenchymal cells Vascular permeability Endothelial cell proliferation Platelet derived growth factor PDGFPlatelets Macrophages Endothelial cells Smooth muscle cells Keratinocytes Granulocyte, macrophage, fibroblast and smooth muscle cell chemotaxis Granulocyte, macrophage and fibroblast activation Fibroblast, endothelial cell and smooth muscle cell proliferation Matrix metalloproteinase, fibronectin and hyaluronan production Angiogenesis Wound remodeling Integrin expression regulation Fibroblast growth factor 1 and 2 FGF-1, −2Macrophages Mast cells T-lymphocytes Endothelial cells Fibroblasts Fibroblast chemotaxis Fibroblast and keratinocyte proliferation Keratinocyte migration Angiogenesis Wound contraction Matrix (collagen fibers) deposition Transforming growth factor-βTGF-βPlatelets T-lymphocytes Macrophages Endothelial cells Keratinocytes Smooth muscle cells Fibroblasts Granulocyte, macrophage, lymphocyte, fibroblast and smooth muscle cell chemotaxis TIMP synthesis Angiogenesis Fibroplasia Matrix metalloproteinase production inhibition Keratinocyte proliferation Keratinocyte growth factor KGFKeratinocytes Keratinocyte migration, proliferation and differentiation Unless else specified in boxes, then reference is: [98]Complications of wound healing [ edit]This section may require cleanup to meet Wikipedia's quality standards.

No cleanup reason has been specified. Please help improve this section if you can. (April 2012) ( Learn how and when to remove this template message)The major complications are many: Deficient scar formation: Results in wound dehiscence or rupture of the wound due to inadequate formation of granulation tissue. Excessive scar formation: Hypertrophic scar, keloid, desmoid. Exuberant granulation ( proud flesh ).

Deficient contraction (in skin grafts) or excessive contraction (in burns). Others: Dystrophic calcification, pigmentary changes, painful scars, incisional hernia Marjolin's ulcer Infection Biologics, skin substitutes, biomembranes and scaffolds [ edit]Advancements in the clinical understanding of wounds and their pathophysiology have commanded significant biomedical innovations in the treatment of acute, chronic, and other types of wounds. Many biologics, skin substitutes, biomembranes and scaffolds have been developed to facilitate wound healing through various mechanisms.

[99] This includes a number of products under the trade names such as Epicel, Laserskin, Transcyte, Dermagraft, Allo Derm/Strattice, Biobrane, Integra, Apligraf, Or Cel, Graft Jacket and Perma Derm. [100]See also [ edit]Collective cell migration Dressing (medical)History of wound care Regeneration in humans Wound bed preparation Wound licking Scar free healing Notes and references [ edit]^ a b c d e f g h i j k l Nguyen, DT; Orgill, DP; Murphy, GT (2009).

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Journal of dermatological science. 41 (2): 97–108. doi: 10.1016/j.jdermsci.2005.09.002. PMID 16226016.^ a b c d Mirastschijski, U.; Haaksma, C. J.; Tomasek, J. J.; Ågren, M. S. (2004). ""Matrix metalloproteinase inhibitor GM 6001 attenuates keratinocyte migration, contraction and myofibroblast formation in skin wounds"". Experimental Cell Research. 299 (2): 465–475. doi: 10.1016/j.yexcr.2004.06.007. PMID 15350544.^ worldwidewounds.com > Figure 3 – The time relationship between the different processes of wound healing.

by Gregory S Schultz, Glenn Ladwig and Annette Wysocki – in turn adapted from Asmussen PD, Sollner B. Mechanism of wound healing. In: Wound Care. Tutorial Medical Series. Stuttgart: Hippokrates Verlag, 1993.^ Morton, Laurel M.; Phillips, Tania J. (April 2016). ""Wound healing and treating wounds: Differential diagnosis and evaluation of chronic wounds"". Journal of the American Academy of Dermatology. 74 (4): 589–605. doi: 10.1016/j.jaad.2015.08.068.

PMID 26979352.^ O'Leary, R; Wood, EJ; Guillou, PJ (2002). ""Pathological scarring: Strategic interventions"". The European journal of surgery. 168 (10): 523–34. PMID 12666691.^ Desmoulière, Alexis; Chaponnier, Christine; Gabbiani, Giulio (2005). ""Tissue repair, contraction, and the myofibroblast"". Wound Repair and Regeneration. 13 (1): 7–12. doi: 10.1111/j.1067-1927.2005.130102.x. PMID 15659031.^ Metzger S (2004). ""Clinical and financial advantages of moist wound management"". Home Healthc Nurse. 22 (9): 586–90. doi: 10.1097/00004045-200409000-00003. PMID 15359168.^ Iconomou TG, Zuker RM, Michelow BJ (1993).

""Management of major penetrating glass injuries to the upper extremities in children and adolescents"". Microsurgery. 14 (2): 91–96. doi: 10.1002/micr.1920140202. PMID 8469109.^ ""Nerve injury"". Johns Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System. Retrieved 2 October 2016.^ Brem, H.; Tomic-Canic, M. (2007).

""Cellular and molecular basis of wound healing in diabetes"". The Journal of Clinical Investigation. 117 (5): 1219–1222. doi: 10.1172/jci32169. PMC 1857239. PMID 17476353.^ a b c d e Guo, S.; Di Pietro, LA. (2010). ""Factors Affecting Wound Healing"". Journal of Dental Research. 89 (3): 219–229. doi: 10.1177/0022034509359125. PMC 2903966. PMID 20139336.^ Arnold, M.; Barbul, A. (2006). ""Nutrition and wound healing"". Plastic and Reconstructive Surgery. 117 (7): 42–58. doi: 10.1097/01.prs.0000225432.17501.6c. PMID 16799374.^ a b c Guo, S.; Di Pietro, L. A.

(1 March 2010). ""Factors Affecting Wound Healing"". Journal of Dental Research. 89 (3): 219–229. doi: 10.1177/0022034509359125. PMC 2903966. PMID 20139336.^ Gosian, A.; Di Pietro, LA. (2004). ""Aging and wound healing"". World Journal of Surgery. 28 (3): 321–326. doi: 10.1007/s00268-003-7397-6. PMID 14961191.^ Swift, M. E.; Burns, A. L.; Gray, K. L.; Di Pietro, L. A. (2001). ""Age-related alterations in the inflammatory response to dermal injury"". Journal of Investigative Dermatology.

117 (5): 1027–1035. doi: 10.1046/j.0022-202x.2001.01539.x. PMID 11710909.^ a b c d Min, Su; Wang, Song W.; Orr, William (2006). ""Graphic general pathology: 2.3 Incomplete regeneration:"". Pathology. pathol.med.stu.edu.cn. Retrieved 2012-12-07.

The new tissue is not the same as the tissue that was lost. After the repair process has been completed, there is a loss in the structure or function of the injured tissue. In this type of repair, it is common that granulation tissue (stromal connective tissue) proliferates to fill the defect created by the necrotic cells.

The necrotic cells are then replaced by scar tissue.^ a b c d Min, Su; Wang, Song W.; Orr, William (2006). ""Graphic general pathology: 2.2 complete regeneration:"". Pathology. pathol.med.stu.edu.cn. Retrieved 2012-12-07.

(1) Complete regeneration: The new tissue is the same as the tissue that was lost. After the repair process has been completed, the structure and function of the injured tissue are completely normal^ a b c Min, Su; Wang, Song W.; Orr, William (2006). ""Graphic general pathology: 2.2 complete regeneration:"". Pathology. pathol.med.stu.edu.cn. Retrieved 2013-11-10. After the repair process has been completed, the structure and function of the injured tissue are completely normal.

This type of regeneration is common in physiological situations. Examples of physiological regeneration are the continual replacement of cells of the skin and repair of the endometrium after menstruation. Complete regeneration can occur in pathological situations in tissues that have good regenerative capacity.^ Yannas, I. V.; Lee, E; Orgill, DP; Skrabut, EM; Murphy, GF (1989). ""Synthesis and Characterization of a Model Extracellular Matrix that Induces Partial Regeneration of Adult Mammalian Skin"". Proceedings of the National Academy of Sciences. 86 (3): 933–7. Bibcode: 1989PNAS...86..933Y. doi: 10.1073/pnas.86.3.933.

JSTOR 33315. PMC 286593. PMID 2915988.^ O'Leary, R.; Ponnambalam, S.; Wood, E. J. (2003). ""Pioglitazone-induced myofibroblast cell death: Implications for cutaneous scarring"". British Journal of Dermatology. 149 (3): 665–7. doi: 10.1046/j.1365-2133.2003.05501.x. PMID 14511015.^ Tong, Miao; Tuk, Bastiaan; Hekking, Ineke M.; Vermeij, Marcel; Barritault, Denis; Van Neck, Johan W. (2009).

""Stimulated neovascularization, inflammation resolution and collagen maturation in healing rat cutaneous wounds by a heparan sulfate glycosaminoglycan mimetic, OTR4120"". Wound Repair and Regeneration. 17 (6): 840–52. doi: 10.1111/j.1524-475X.2009.00548.x. PMID 19903305.^ Barritault, D.; Caruelle, J.-P. (2006). ""Les agents de régénération (ou RGTAs) : Une nouvelle approche thérapeutique"" [Regenerating agents (RGTAs): a new therapeutic approach]. Annales Pharmaceutiques Françaises (in French). 64 (2): 135–44. doi: 10.1016/S0003-4509 (06)75306-8. PMID 16568015.^ Van Neck et al, Heparan sulfate proteoglycan mimetics thrive tissue regeneration: an overview.

In Intech book under the working title ""Tissue Regeneration"", ISBN 978-953-307-876-2 is scheduled for on line publication on Nov 26, 2011"" [ page needed]^ eurekalert.org staff (3 June 2015). ""Scientist at LIMR leads study demonstrating drug-induced tissue regeneration"". eurekalert.org. Lankenau Institute for Medical Research (LIMR),. Retrieved 3 July 2015.^ Zhang Y, Strehin I, Bedelbaeva K, Gourevitch D, Clark L, Leferovich J, Messersmith PB, Heber-Katz E. Drug-induced regeneration in adult mice. Sci Transl Med. 2015;290.^ Rush, J. (2005). Spiritual tattoo: a cultural history of tattooing, piercing, scarification, branding, and implants, Frog Ltd.^ Brown BC, Mc Kenna SP, Siddhi K, Mc Grouther DA, Bayat A (September 2008). ""The hidden cost of skin scars: quality of life after skin scarring"". Journal of Plastic, Reconstructive & Aesthetic Surgery. 61 (9): 1049–58. doi: 10.1016/j.bjps.2008.03.020. PMID 18617450.^ Bayat A, Mc Grouther DA, Ferguson MW (January 2003). ""Skin scarring"". BMJ. 326 (7380): 88–92. doi: 10.1136/bmj.326.7380.88. PMC 1125033. PMID 12521975.^ Clark, R. (1996). The molecular and cellular biology of wound repair, Springer Us.^ Tonnesen MG, Feng X, Clark RA (December 2000). ""Angiogenesis in wound healing"". The Journal of Investigative Dermatology. 5 (1): 40–6. doi: 10.1046/j.1087-0024.2000.00014.x. PMID 11147674.^ a b Ferguson MW, Whitby DJ, Shah M, Armstrong J, Siebert JW, Longaker MT (April 1996). ""Scar formation: the spectral nature of fetal and adult wound repair"". Plastic and Reconstructive Surgery. 97 (4): 854–60. doi: 10.1097/00006534-199604000-00029. PMID 8628785.^ Brockes JP, Kumar A, Velloso CP (2001). ""Regeneration as an evolutionary variable"". Journal of Anatomy. 199 (Pt 1–2): 3–11. doi: 10.1046/j.1469-7580.2001.19910003.x. PMC 1594962. PMID 11523827.^ a b ""Scarless Healing"". Star. Christchurch, New Zealand: Star. 1906-07-07. pp. Page 4. Retrieved 2013-07-02.^ a b ""Scarless Healing"". Marlborough Express, Volume XXXIX, Issue 160,. paperspast.natlib.govt.nz. 1906-07-12. pp. Page 1. Retrieved 2013-07-02.^ a b ""A Wonderful New Surgery"". Reading Eagle. 1906-07-06. pp. Page 6. Retrieved 2013-07-02.^ Cumming, B. D.; Mc Elwain, D. L. S.; Upton, Z. (2009). ""A mathematical model of wound healing and subsequent scarring"". Journal of the Royal Society Interface. 7 (42): 19–34. doi: 10.1098/rsif.2008.0536. PMC 2839370. PMID 19324672.^ Gurtner, Geoffrey C.; Werner, Sabine; Barrandon, Yann; Longaker, Michael T. (2008). ""Wound repair and regeneration"". Nature. 453 (7193): 314–21. Bibcode: 2008Natur.453..314G. doi: 10.1038/nature07039. PMID 18480812.^ Gurtner, Geoffrey C.; Dauskardt, Reinhold H.; Wong, Victor W.; Bhatt, Kirit A.; Wu, Kenneth; Vial, Ivan N.; Padois, Karine; Korman, Joshua M.; Longaker, Michael T. (2011). ""Improving Cutaneous Scar Formation by Controlling the Mechanical Environment"". Annals of Surgery. 254 (2): 217–25. doi: 10.1097/SLA.0b013e318220b159. PMID 21606834.^ Kuhl, E.; Steinmann, P. (2004). ""Computational modeling of healing: An application of the material force method"". Biomechanics and Modeling in Mechanobiology. 2 (4): 187–203. doi: 10.1007/s10237-003-0034-3. PMID 14872320.^ a b c d Velnar, T.; Bailey, T.; Smrkolj, V. (2009-10-01). ""The Wound Healing Process: An Overview of the Cellular and Molecular Mechanisms"". Journal of International Medical Research. 37 (5): 1528–1542. doi: 10.1177/147323000903700531. ISSN 0300-0605. PMID 19930861.^ a b Armitage, Jon; Lockwood, Sonia (2011-10-01). ""Skin incisions and wound closure"". Surgery (Oxford). Wound Management. 29 (10): 496–501. doi: 10.1016/j.mpsur.2011.06.022.^ Norman, G; Dumville, JC; Mohapatra, DP; Owens, GL; Crosbie, EJ (29 March 2016). ""Antibiotics and antiseptics for surgical wounds healing by secondary intention"". The Cochrane Database of Systematic Reviews. 3: CD011712. doi: 10.1002/14651858. CD011712.pub2. PMID 27021482.^ Table 3-1 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.^ Stejskalová, Anna; Almquist, Benjamin D. (2017-07-26). ""Using biomaterials to rewire the process of wound repair"". Biomater. Sci. 5 (8): 1421–1434. doi: 10.1039/c7bm00295e. ISSN 2047-4849.^ Vyas KS, Vasconez HC. Wound Healing: Biologics, Skin Substitutes, Biomembranes and Scaffolds. Healthcare. 2014; 2 (3):356-400. External links [ edit]Wikimedia Commons has media related to Wound healing. This article's use of external links may not follow Wikipedia's policies or guidelines. Please improve this article by removing excessive or inappropriate external links, and converting useful links where appropriate into footnote references. (February 2013) ( Learn how and when to remove this template message)Wound Repair and Regeneration The official publication of the Wound Healing Society and the European Tissue Repair Society. Journal of Burns and Wounds Fibrogenesis & Tissue Repair, an online open access journal about chronic wound healing and fibrogenesis. EWMA Journal, Journal of the European Wound Management Association Ostomy Wound Management The official journal of the Association for the Advancement of Wound Care. [ show]v t e Pathology [ show]v t e Wound healing [ show]v t e Trauma Categories: Healing Skin physiology Physiology Trauma surgery "

Granulation tissue is an example of fibrovascular proliferation. Granulation tissue contains new small blood vessels, fibroblasts, and mononuclear cells in an edematous extracellular matrix; formation of granulation tissue is part of the repair response. A granuloma is a form of chronic inflammation.

Chronic Inflammation 1-2

"31 terms purplecherry PLUSChronic Inflammation 1-2Learn Flashcards Write Spell Test Match Gravity Advertisement Upgrade to remove ads Like this study set?

Create a free account to save it. Create a free account Maybe later Sort What triggers chronic inflammation? Presistent infection Presence of foreign bodies Autoimmunity Granulation tissue formation is only an end stage of chronic inflammation correct? Incorrect What is the gross appearance of chronic inflammation? 1. Ulceration 2. Thickening of the wall of hollow organ 3.

Changes in tissue texture o Necrosis o Fibrosis What is the difference between the microscopic appearance of chronic and acute inflammation? Chronic-granulatomous, giant cells, lymphocytes, Non-granulatomous-plasma cells lymphocytes, macrophages, fibroblasts and blood vessels Acute-lots of neutrophils, dilation and congestion, of blood vessels, exudate What is the difference between the gross appearance of acute and chronic inflammation?

Acute-warm red swollen Chronic-thickened, ulcerated What are the key cells of chronic inflammation? -Lymphocytes T cells B cells - Macrophages -Fibroblasts What is the definition of chronic inflammation?

inflammation in which the cell population is especially lymphocytes plasma cells macrophages damage, (necrosis), loss of function healing and repair granulation tissue scarring and fibrosis What are the clinical presentations? Low grade fever Loss of weight Loss of appetite loss of function of specific organs When does chronic inflammation follow acute inflammation?

large volume of damage inability to remove debris fails to resolve Can chronic infection happen without acute phase? Yes What is the purpose of granulation tissue? patches tissue defects replaces dead or necrotic tissue What is granulation tissue? Granulation tissue is new connective tissue and tiny blood vessels that form on the surfaces of a wound during the healing process What is the difference between granulomas and granulation tissue?

It consists of a circumscribed collection of epithelioid cells, usually surrounded by lymphocytes. When is granulotomous tissue common? During primary What causes de novo chronic inflammation? material resistant to digestion exogenous substances-no immune response eg glass etc endogenous substances- necrotic tissue, keratin, hair What cytokines have antiviral effects and attract and stimulate other cells?

Interferons produced by T cells What are macrophages and what do they do? removes debris role in immune system - antigen presenting cell motile phagocyte move from blood long lived take over from neutrophils contain enzymes eg lysozyme produce interferons and other chemicals destroy, influence process What do B cells do?

differentiate to plasma cells antibodies facilitate immune response act with macrophages antigen presenting capacity immune memory What do T cell cytokines do? cytokines attract and hold macrophages activate macrophages and other cells eg lymphocytes permeability What are the functions of T cells? T-cells produce cytokines T-cells produce interferons Some are cytoxic What are fibriblasts? motile cells metabolically active make and assemble structural proteins collagens various types What are the outcomes of chronic inflammation?

ongoing tissue damage and destruction insidious loss of function cellular and stromal response granulation tissue, angiogenesis scarring and fibrosis granuloma formation What are granulomas? aggregates of epithelioid macrophages in tissue may contain giant cells may surround dead material may be surrounded by lymphocytes contain neutrophils, eosinophils response to indigestible antigen many are type IV hypersensitivity reactions What are giant cells? epithelioid histioytes (macrophages)? fusion of macrophages to form larger cells large cytoplasm; multiple nuclei several types not always granuloma for giant cells to be present What are the different types of giant cells? Langerhahns (often seen in TB), Foreign body granulomas (often associated with pyogenic bacteria), Warthin-Finkeldy type (often seen in measles)What are the three most important infectious granulotomous diseases?

tuberculosis - Mycobacterium tuberculosis leprosy - Mycobacterium leprae syphilis - Treponema pallidum What is caseous necrosis? it is a pattern of necrosis that is associated with a unique inflammatory reaction - the granuloma. you get amorphous, granular debris in the center of granulomatous cell reaction - necrotic tissue gets soft, white and friable.

grossly looks like cheese. seen in TB. What is the granulomatous lesion seen in syphyllys? Primary chancre ; syphilitic gumma What are examples of non-infective inflammatory diseases? rheumatoid disease - tissue specific auto-immune disease, sarcoidosis - classical clinical picture Crohn's disease - chronic inflammatory bowel disease What is sarcoidosis?

Sarcoidosis (from sarc meaning ""flesh"", -oid, ""like"", and osis, ""diseased or abnormal condition abnormal collections of chronic inflammatory cells (granulomas) that can form as nodules in multiple organs most often located in the lungs or the lymph nodes, but any organ can be affected.

Onset is usually gradual. Sarcoidosis may be asymptomatic or chronic What is involved in wound healing? phase of acute inflammation granulation tissue formation local angiogenesis - new vessels grow fibrosis and scar formation Advertisement Upgrade to remove ads Features Quizlet Live Quizlet Learn Diagrams Flashcards Mobile Help Sign up Help Center Honor Code Community Guidelines Students Teachers About Company Press Jobs Privacy Terms Follow us Language© 2018 Quizlet Inc. "

. (See also healing and keloid .) Beneath the skin is a fibrous connectivetissue known as subcutaneous tissue, composed of cells called fibroblasts, which after injury arestimulated to grow into granulation tissue, knitting the wound together. Scar tissue is formed by dense masses of granulation tissue.

scar

scar (redirected from scarring) Also found in: Dictionary, Thesaurus, Legal, Encyclopedia, Wikipedia. Related to scarring: scarring alopeciascar [ skar] a mark remaining after the healing of a wound, such as one caused by injury, illness, smallpoxvaccination, or surgery

Called also cicatrix. Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.scar ( skar ), Fibrous tissue replacing normal tissues destroyed by injury or disease or divided after an incision. [G. eschara, scab]Farlex Partner Medical Dictionary © Farlex 2012scar ( skahr) cicatrix; a mark remaining after the healing of a wound or other morbid process.

By extension, any visible manifestation of an earlier event. Dorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.scar (skär)n. A mark left on the skin after a surface injury or wound has healed.v.1. To mark with a scar or become marked with a scar.2. To form a scar. The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company.

Published by Houghton Mifflin Company. All rights reserved.scar See cicatrix. Mosby's Medical Dictionary, 9th edition. © 2009, Elsevier.scar Vox populi Fibrous tissue that fills in defects in skin and other tissues that remain afterinjury.

See Icepick scar, Railroad track scar, Trapdoor scar, U-shaped scar. Mc Graw-Hill Concise Dictionary of Modern Medicine. © 2002 by The Mc Graw-Hill Companies, Inc.scar ( skahr) The fibrous tissue replacing normal tissues destroyed by injury or disease.

Sometimes calledcicatrix. [G. eschara, scab]Medical Dictionary for the Health Professions and Nursing © Farlex 2012scaravascular fibrous tissue overlain by thin epidermis; characteristic of healing by secondaryintention, e.g. at site of surgical incision, healed ulcer or other traumatic episode affectingskin/deeper tissues Illustrated Dictionary of Podiatry and Foot Science by Jean Mooney © 2009 Elsevier Limited. All rights reserved.scar ( skahr) Fibrous tissue replacing normal tissues destroyed by injury or disease or divided after an incision.

[G. eschara, scab]Medical Dictionary for the Dental Professions © Farlex 2012scar,n See cicatrix.scar, apical, n the end product of wound repair. A radiolucent area characterized histologically by dense fibrous connective tissue. It is commonly noted in areas of tooth extraction.

Mosby's Dental Dictionary, 2nd edition. © 2008 Elsevier, Inc. All rights reserved.scarcicatrix; a mark remaining after the healing of a wound, such as one caused by injury, illness or surgery.constricting scarcontraction of scar tissue causing constriction of vascular channel or hollow viscus.honorable scarin judging dogs, scars resulting from injuries suffered as a result of work are permissibleand do not detract from the dog's features.hypertrophic scaran overabundance of connective tissue in a wound, identified by history of traumatizedwound, infection and histological examination reveals hairs, foreign body, pockets of infection.scar tissuea dense mass of granulation tissue.

Saunders Comprehensive Veterinary Dictionary, 3 ed. © 2007 Elsevier, Inc. All rights reserved Patient discussion about scar Q. except for for the scars, are there any more consequence to burns?

10 years ago i wasburned in my face and right hand from boiling water. i was hospitalized and was treated with skingrafts from my thighs. In the last four weeks I feel a strange feeling in my scar. Its hard to describethe exact feeling but it kind of a painful lump inside my flesh.

10 years After that accident can it be that my body is still not over this injury? A. burn scars have 3 optional ways of evolving.

a) nothing happens - shouldn't hurt at all (this is by far the most common situation) b) nerve trapping (which happened to me. Its usually begins months after the burn and not years.and you dont have a lump) c) skin cancer from the scar.

this is a rare syndrome but you must go to your GP do exclude it.its called marjolin ulcer. Q. what should i do if i got burned from boiling water? how should i take care of my self?will i get a scar? A. oooo OOOooo! i hope you are asking a hypothetic question... a friend wife of mine still gotscars from a boiling water accident a few years back.

anyway, here is a site that givesinstructions on how to react after burns. boiling water is probably second degree burns:http://familydoctor.org/online/famdocen/home/healthy/firstaid/after-injury/638.html More discussions about scar This content is provided by i Medix and is subject to i Medix Terms. The Questions and Answers are not endorsed or recommended and are made available by patients, not doctors. Want to thank TFD for its existence? Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content . Link to this page: Facebook Twitter

Granulation tissue is composed of capillaries, fibroblasts, macrophages (to clean up debris), and collagen, fibronectin, and proteoglycans. Neovascularization - Within days, angiogenesisi begins and new capillaries form and supply nutrients in addition to providing some initial bridging of the wound.

Wound Healing

page sectionsintroductioninflammationproliferationmaturationfactors affecting wound healingresources and referencestopic development Wound Healinglast authored: Dec 2009, David La Pierre last reviewed: Introduction Wound Retraction - Although not considered part of the healing process, the first immediate change in the wound is usually enlargement through contraction of the surrounding musculature and an increase in resting tissue tension.

This may give the illusion of tissue loss when there actually is not any. Coagulation and Clot Formation - This begins to occur within minutes of the injury.

Hemostasis describes cessation of blood flow and formation of a clot. The blood clot which forms will eventually dehydrate and contract, forming a scab and providing some degree of protection for the delicate healing tissue beneath. Platelet aggregation results in the release of mediators which increase capillary permeability and activate the inflammatory response.

Fibrin plugs form in lymphatics and help prevent bacterial spread.return to top Inflammation (reactive)Inflammation begins within minutes to hours, and can be caused by physical injury, antigen-antibody reactions, or infection.

Increased capillary permeability and chemotaxis result in the presence of polymorphonuclear leukocytes and macrophages which rid the wound of bacteria and debris. In addition, they activate tissue fibroblasts and stimulate them to lay down collagen. Thrombus releases factors such as PDGF, recruiting inflammatory cells. Neutrophils almost immediately, closely followed by macrophages. Fibroblasts arrive within a few days.late inflammation 48-72 hours.>72hours: lymphocytes, peaking at day 7Macrophages debride and remove dead tissue, recruit fibroblasts via secretion of IL-1, TNF-a, and TGF-beta. Wounds depleted of macrophages are slow to heal.return to top Proliferation (regenerative)This phase begins within 2-3 days and lasts 2-4 weeks. Fibroblasts migrate inwards following chemoattractant signals from macrophages. They secrete collagen, elastin, and proteoglycans. Overgrowth of scar tissue as inflammation resolves.

Collagen formation: begins day 5-7, increases in linear fashion; increase in ratio of I: III. Collagen provides tensile strength to tissues. fibroblasts will produce immature collagen - the precursor to scar tissue. Early collagen is a jelly like substance with little tensile strength.

Fibroblasts will continue to produce new collagen for several weeks. In addition, they begin the process of collagen alignment and cross linking which is required for tensile strength in scar tissue Epithelialization: detachment, migration, proliferation, differentiation, and stratification Epithelial cells at the wound edge flatten, detach, and migrate across the open wound. Proliferation begins again once the wound surface is covered. Stratified squamous epithelium again begins to form as cells differentiate.

Within two days injury, a sutured wound will be completely covered with new epithelium. This process will take considerably longer in gaping wounds which are allowed to heal secondarily (not sutured - fill in on their own).return to top Maturation (remodeling)3 weeks until 1 year post-injuryequilibrium between collagen synthesis and degradation The capillary network supporting proliferation begins to regress, and collagen becomes organized along lines of skin tension.

Wound Contraction - Independent of collagen formation, wounds which are left open will begin to contract in size by 4 - 5 days. This process is less important in sutured wounds. Scar Maturation - Collagen remodeling continues for up to a year following injury. This results in ongoing changes in size and bulk of scar tissue.return to top Factors Affecting Wound Healing Given time, most wounds will heal without suturing.

The process will take longer and there may be a less cosmetic result, however there are some advantages which will be discussed later. Inflammation is a necessary part of wound healing and should not be confused with infection. A narrow margin of erythema (typically less than 1 - 2 cm) is usually indicative of a normal inflammatory response.

Wider margins of erythema or erythematous streaking proximal to the injury often indicates infection. Although a wound may seem ‘stuck together’ soon after the injury, it has little tensile strength. The initial adhesion is caused by a combination of clot adhesion and neovascularisation.

These wounds may reopen if placed under tension. Wounds do not begin to gain tensile strength from collagen until 5 - 7 days. Although collagen formation is complete within three weeks, a wound has only achieved ~ 20 % of its final strength by this time and ~ 60 % by four months.

Scar tissue continues to remodel for at least 6 - 12 months after an injury. Patients may be distressed by the initial appearance of a scar, however decisions to revise an ‘ugly scar’ should be put off for at least a year.

Delayed Wound Healing The following factors may predispose to delayed wound healing: Infection Poor Blood Supply - locally in the wound or systemically i.e. peripheral vascular disease. Malnutrition - Vitamin C Deficiency (scurvy) is the classic example.

Chronic Illness - Diabetes, Chronic Renal Failure. High Wound Tension - i.e. wounds over extensor surfaces of joints. Drugs - i.e. systemic corticosteroids. Some of these factors may be modified i.e. proper wound cleaning to prevent infection, improved patient nutrition, closure techniques which reduce skin tension.

Delayed presentation - wounds greater than 6 - 8 hours old are at increased risk. Contaminated wounds - organic material i.e. wood or feces are more likely to cause infection than are inert/inorganic materials such as glass or metal.

Anatomic Site - areas with poor blood supply such as the distal extremities are higher risk than vascular areas such as the scalp or face. Devitalized Tissue - crushed or avascular tissue promotes bacterial proliferation Bite Wounds - saliva has large numbers of pathogenic bacteria.

Use of Local Anaesthesia with Epinephrine - causes local vasospasm and decreases blood flow. Presence of Subcutaneous Sutures - buried sutures provide a nidus for infection.

Impaired Host Defenses - Immune suppressed or chronically ill patients are at highest risk. Nutritionprotein, zinc, ironvitamins A, C, EMetabolic statusdiabetes - likely neuropathy moreso that ischemiaobesity Circulatory statusatherosclerosis, cardiac failurewound tensionsmoking - nicotine is a vascoconstrictor and CO prevents oxygen release, both decreasing tissue perfusion Drugssteroids - decrease inflammation and healing NSAIDs - decrease collagen synthesischemotherapy Agedecreased rates of mitosisdecreased tensile strength Radiationdamages endothelium, fibroblasts, and lymphatics Infectioneven subclinical infection can retard wound healingno healing with >10 5 bacteria/gram, or any beta-hemolytic strepblood supplydecreased perfusion impairs fibroblasts and ECM deposition, angiogenesis, and epithelializations Mechanical movement Foreign bodywound size (smaller, faster)wound locationtype of wound (cleancongenital diseases Pseudoxanthoma elasticum Ehlers-Danlos syndromecutis laxaprogeria (immature aging)Werner syndrome Epidermolysis bullosa A partial-thickness wound heals via epithelialization, derived from the edges, hair follicles, and sweat glands.

There is minimal matrix deposition and wound contraction. Granulation tissue is small, red granular foci which bleed easily and are commonly seen in freshly healing tissue.

This is caused by fragile, newly formed capillaries which proliferate and invade damaged tissue along with fibroblasts. Slough is the accumulation of dead cellular debris on the wound surface. It tends to be yellow due to the presence of leukocytes.

A scab, or crust, seal a wound but prevent new cells from crossing the wound, instead forcing them to burrow downwards. When the scab comes off, there will be a more noticable depression. For this reason, scabs should be avoided. Unless you like scars. Wound contractionimportant in healing wounds due to interaction between ECM and fibroblast, leading to fibroblast stimulation and differention into myofibroblast. Contractures are pathological shortening of scar tissuereturn to top Resources and Referencesreturn to top Topic Developmentauthors:reviewers:return to top Sharing In Health is for training in careers with inherent risks; consult with a health care professional before making any decision. We cannot be held responsible for adverse events of any kind. Please forgive and contact us regarding errors. Feel free to use and share this material as widely as possible, according to our Creative Commons license.

g? 1. collagen fills the wound bed, new blood vessels develop, and granulation tissue is formed by fibroblasts, giving the wound a bright red granular appearance 2. wound closes by epithelialization a process in which epithelial cells grow to cover the wound bed

Wound Healing-Theroy

"79 terms byeazel Wound Healing-Theroy Learn Flashcards Write Spell Test Match Gravity Advertisement Upgrade to remove ads Like this study set? Create a free account to save it. Create a free account Maybe later Sort What is an abrasion? It is a mechanical injury resulting from scraping away of skin or mucous membrane What does debridement mean?

The removal of dirt, foreign matter, and dead or devitalized tissue from a wound What does dehiscence mean? Partial or total separation of the edges of a wound What does epithelialization mean? Movement of epithelial cells to the wound bed What is eschar?

Thick, leathery, necrotic, devitalized tissue What does evisceration mean? Protrusion of internal organs through an incision What does exudate mean? Fluid and cells that have escaped from blood vessels during the inflammatory response and are left in surrounding tissues What is a fistula? An abnormal passage between two internal organs or between internal organs and the external skin surface What is granulation tissue?

Any soft pink fleshy projections that form during the healing process in a wound that does not heal by primary intention, it consists of capillaries surrounded by fibrous collagen What is a hematoma?

An accumulation of bloody fluid beneath tissue What is a hemorrhage? Bleeding from a wound bed or site What is maceration? A softening of the epidermis caused by prolonged contact with moisture, such as a wet sheet or diaper What is a pressure ulcer?

Any lesion caused by ischemia from unrelieved pressure that leads to damage of the skin and underlying tissues What is a primary lesion? The first lesion to appear on the skin in response to a causative agent, usually has a recognizable structure What is a secondary lesion? A change in a primary lesion in the epidermal layer caused by any of several factors, including scratching, rubbing, medications, and the client's medical condition or disease process What is slough?

Necrotic tissue that is moist, stringy and yellow in color. It must be cleansed and removed to allow the wound to heal What is the definition of wound?

A disruption of the normal anatomical structure and function that results from pathological processes that arise internally or externally to the involved organ (s)Petechiae- small purplish hemorrhagic spots on the skin.

Often appear in clients with platelet deficiencies. Keloid Who is at risk? -is a scar that forms at the site of an injury or incision and spreads beyond the borders of the original lesion. (over healed) Greek: kele means tumor and eidos means shape Psoriasis- A chronic skin disorder in which red, scaly plaques with sharply defined borders appear on the body surface Greek: an itching Ecchymosis= bruise , superficial bleeding under the skin What causes cellulitis?

Bacteria enters skin via a cut or break and results in an infection of connective tissue with severe inflammation of dermal and subcutaneous layers Who are at risk for a venous stasis ulcer?

• People w/poor circulation • Cardiac patients • Obese patients What is the treatment for cellulitis? • resting the affected area (wiki) • cutting away dead tissue (wiki) • antibiotics (lecture notes and wiki) • anti-inflammatory medication (lecture notes)How are wounds classified? Can you use more than 1 classification? • Cause (intentional/unintentional) • Severity (superficial/deep) • Cleanliness (risk for infection) • Color (chronic) YESWhat is the difference between intentional and unintentional?

Intentional wounds are caused by surgical incisions, whereas unintentional result from accidental injury or trauma, animal bites, violence, or adverse effects of health care What is the difference between superficial (partial-thickness and deep (full-thickness)? Partial-thickness wounds extend through the first layer of skin (epidermis) and into, but not through, the second layer of skin (dermis).

Full-thickness wounds extend through both the epidermis and the dermis and may involve subcutaneous tissue, muscle, and possibly bone What type of wound is more at risk for infection?

Wounds resulting from trauma are created under ""dirty"" or ""clean"" conditions, tissue damage is variable, wound edges may not be easily approximated, and scarring is more likely. What type of wound is less of a risk for infection? A surgical incision is created under sterile conditions, tissue damage is minimized, and healthy wound edges are approximated so that new tissue can grow and connect the tissue with minimal scarring.

Is a surgical wound an acute or chronic wound? Acute What is a chronic wound? Chronic wounds are those that have an insidious onset, a prolonged healing process, and fail to progress through a normal, orderly, and timely sequence of repair What does approximated mean in wound care?

to draw two tissue surfaces close together as in the repair of a wound Open wound DESCRIPTION and POSSIBLE CAUSE Description Disruption or break in skin Possible Cause Penetration by sharp object or instrument (such as knife, scalpel, bullet)Closed wound DESCRIPTION and POSSIBLE CAUSE Description No disruption or break in skin Possible cause Trauma caused by blow with blunt object Clean wound DESCRIPTION and POSSIBLE CAUSE Description Wound free of infectious organisms Possible Cause Surgical incision not entering or affected by secretions from respiratory, GI, or GU tracts Contaminated wound DESCRIPTION and POSSIBLE CAUSE Description Wound with microorganisms Possible Cause Penetration of skin by dirt, bacteria Penetrating wound DESCRIPTION and POSSIBLE CAUSE Description Wound with break through epidermis, dermis, and underlying tissues.

May enter organs Possible Cause Penetration by object or instrument (usually accidental)Abrasion wound DESCRIPTION and POSSIBLE CAUSE Description Superficial injury caused by rubbing or scraping of skin against another surface Possible Cause Friction injury resulting from fall or rubbing against bed linens Laceration wound DESCRIPTION and POSSIBLE CAUSE Description Open wound with jagged edges Possible Cause Penetration of skin by sharp object Contusion wound DESCRIPTION and POSSIBLE CAUSE Description Closed wound, may be swollen, discolored and painful Possible Cause Blunt trauma, such as being hit by object What is hemostasis?

The control of bleeding, is the process by which injured blood vessels constrict and platelets accumulate. How long before hemostasis begins? Occurs within minutes of the initial injury unless there are underlying clotting disorders What are the 3 phases of wound healing and how long do they last on average?

1. Inflammatory (includes hemostasis) 3-4 days 2. Proliferative (reconstruction) 4-21 days 3. Maturation (remodeling )3-4 weeks What happens during the 1st phase of wound healing? 1. Histamine is secreted by mast cells and damaged tissues, leading to capillary dilation 2. migration of cells, complement, and antibodies 3. leukocytes (neutrophils) migrate into the wound and begin to ingest bacteria 4. monocytes migrate, change into macrophages and, through phagocytosis, clean the wound bed of bacteria and cellular debris (prepare the wound bed for healing) 5.

Lymphocytes migrate last and are thought to stimulate angiogenesis (the development of new blood vessels) 6. Macrophages stimulate biological regulators (cytokines) and the formation of fibroblasts (connective tissue-producing cells) 7. fibrin network forms to provide a structure to aid the formation of fibrous bridges as well as epithelial cells that move inward from the wound edges to create an epithelial layer. What happens during the 2nd phase of wound healin

g? 1. collagen fills the wound bed, new blood vessels develop, and granulation tissue is formed by fibroblasts, giving the wound a bright red granular appearance 2. wound closes by epithelialization a process in which epithelial cells grow to cover the wound bed

3. day 5, the wound has filled with highly vascular fibroblastic connective tissue 4. day 7, the surface epithelium has a normal thickness and the subepithelial layers are bridged 5. Progressive collagen accumulation during the second week results in the basic structure of the scar, which is initially bright red but later fades What happens during the 3rd phase of wound healing?

• This phase is characterized by reorganization of the collagen fibers, wound remodeling, and maturation of the tissues to approximate the skin's original strength • Although the wound is considered fully healed, the tissue will always be at risk for breakdown because the wound's tensile strength never exceeds 80% of its pre-injury strength How long does it take for a scar to achieve its maximum strength of 80%?

2 years What are the types of wound healing? • Primary intention • Secondary intention • Tertiary intention Explain primary intention healing?

• Clinician approximates (aligns) the wound edges or margins and secures them using sutures, staples, or Steri-Strips • occurs in the first 14 days after injury • Wounds that heal by primary intention have a lower risk of infection, little tissue loss, and minimal scarring. Healing by primary intention takes a predictable course through the stages of hemostasis, inflammation, proliferation, and maturation Explain secondary intention healing?

• healing by secondary intention is prolonged • When the skin or wound edges cannot be approximated, as in a pressure ulcer or a wound that is large or infected, all dead (necrotic) and infectious tissue must be removed and the wound must fill with granulation tissue, some tissue regeneration (epithelialization) proceeds from the margins • Wound contraction plays a greater role • generally involves greater tissue loss, higher risk for infection, prolonged healing, and a large scar Explain tertiary intention healing (delayed primary closure)?

• Occurs in wounds that may be contaminated, infected, or draining exudate • These wounds may be left open intentionally for 3 to 5 days to let healing begin by allowing the contaminated or infected matter or exudate to drain out • Once the infection clears, and granulation has begun, the wound is closed with sutures, staples, or Steri-Strips.

What are some lifestyle factors that impair wound healing? • personal hygiene • nutrition and fluid status • activity and exercise level • smoking and substance abuse What are some other factors that influence/impair wound healing? • Old age • Immunosuppression • Incontinence • Hypoxemia • Diabetes • Infections • neurological impairments • medical-surgical procedures • medications What is a pressure ulcer?

A pressure ulcer is any lesion caused by ischemia from unrelieved pressure that leads to necrosis of underlying tissues How does a pressure ulcer develop? When soft tissue is compressed between a bony prominence (such as the hip) and an external surface (such as a mattress).

With prolonged pressure, the blood supply to the tissue's capillary network is disrupted, causing impeded blood flow to the surrounding tissues leading to local tissue ischemia, edema, inflammation, and cell death Describe stage I pressure ulcer: An observable, pressure-related alteration of intact skin whose indicators, as compared with the adjacent or opposite area on the body, may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy), and sensation (pain, itching)Describe stage II pressure ulcer: Partial-thickness skin loss involving the epidermis, dermis, or both.

The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater Describe stage III pressure ulcer: Full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend to, but not through, the underlying fascia.

The ulcer presents clinically as a deep crater with or without undermining of adjacent tissues. Describe stage IV pressure ulcer: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (such as tendon, joint capsule).

What is friction? A superficial injury to layers of the skin where the epidermal layer is rubbed off. What does shear mean? A mechanical force that acts on a skin area in a direction parallel to the body's surface (client sliding down in bed)Braden Scale: How many areas are assessed?

1. Sensory perception-ability to respond meaningfully to pressure related discomfort 2. Moisture-degree to which skin is exposed to moisture 3. Activity-degree of physical activity 4. Mobility-ability to change and control body movement 5. Nutrition-usual food intake 6.

Friction and shear Braden Scale: What does the score mean? • Client's total score can range from 6-23 • Lower the score higher the risk EXPECTED OUTCOMES FOR THE CLIENT WITH IMPAIRED SKIN INTEGRITY • Maintains a normal temperature or baseline vital signs • Maintains nutritional intake to support wound healing • Maintains adequate fluid intake • Performs activities of daily living • Performs wound care and dressing changes as instructed • States the signs and symptoms of infection • Verbalizes discharge instructions for wound care Roles in Wound Healing: carbohydrates, fats and calories Energy for wound regeneration and repair Roles in Wound Healing: copper Cross-linking of collagen fibers Roles in Wound Healing: Iron Oxygen transport Roles in Wound Healing: protein Collagen synthesis, epidermal proliferation & immune response Roles in Wound Healing: Vitamin A Collagen synthesis, epidermal proliferation & immune response Roles in Wound Healing: Vitamin B complex Protein synthesis & Cross-linking of collagen fibers Roles in Wound Healing: Vitamin C Collagen synthesis and capillary wall integrity Roles in Wound Healing: Zinc Collagen synthesis and immune response What does a red would mean?

Healing with clean, healthy granulation (protect)What does a yellow wound mean? Contains slough (clean)What does a black wound mean?

Presence of eschar (debride)List some complications of wound healing? • Dehiscence • Evisceration • Fistula • Hemorrhage • Infection • Adhesions What would you assess a wound for? • Infection • Redness (erythema),edema, warmth • Drainage: creamy, yellow, yellow-green, purulent • Odor • Tachypnea • WBCs elevated (usually systemic) • Pain, tenderness at site • Fever, • Elevated Sedimentation rate (Erythrocyte Sedimentation Rate or ESR) non-specific test What do maggots do to a wound? Ingest & digest bacteria & have been used to heal wounds infected with MRSA or that fail to respond to other treatments How does maggot treatment work? Larvae secrete digestive enzymes into wound bed and then crawl around the wound to locate nutrients in dissolving tissue "

In the second wound healing stage, proliferation, the wound begins to be rebuilt with new, healthy granulation tissue. For the granulation tissue to be formed, the blood vessels must receive a sufficient supply of nutrients and oxygen.

Understanding the Healing Stages of Wounds

Understanding the Healing Stages of Wounds August 27, 2014 by Advanced Tissue 0 19

The wound healing stages are made up of three basic phases: inflammation, proliferation and maturation. There are many types of wounds that require different wound care products for proper recovery from an ulcer or laceration, but most go through similar healing stages.

The duration of each healing stage may vary according to factors such as tissue health, management methods and efficiency of the body’s immune system, but the medical community agrees that there are three main phases.

Learn more about these healing stages to be better acquainted with the progress of your wound healing plan.

Inflammation The first phase of healing is inflammation, the body’s natural response to trauma. After the wound has been inflicted, homeostasis begins – the blood vessels constrict and seal themselves off as the platelets create substances that form a clot and halt bleeding.

Once hemostasis is achieved the blood vessels dilate, letting nutrients, white blood cells, antibodies, enzymes and other beneficial elements into the affected area to promote good wound healing and stave off infection. This is when someone would begin to experience the physical effects of inflammation – swelling, pain, heat and redness, according to the Australian Wound Management Association. Proliferation

Healthy granulation tissue is granular and uneven in texture; it does not bleed easily and is pink / red in colour. The colour and condition of the granulation tissue is often an indicator of how the wound is healing. Dark granulation tissue can be indicative of poor perfusion, ischaemia and / or infection.

Phases of Wound Healing

Phases of Wound Healing Whether wounds are closed by primary intention, subject to delayed primary closure or left to heal by secondary intention 1, the wound healing process is a dynamic one which can be divided into three phases.

It is critical to remember that wound healing is not linear and often wounds can progress both forwards and back through the phases depending upon intrinsic and extrinsic forces at work within the patient 2. The phases of wound healing are 2: Inflammatory phase Proliferation phase Maturation phase The inflammatory phase is the body’s natural response to injury.

After initial wounding, the blood vessels in the wound bed contract and a clot is formed. Once haemostasis has been achieved, blood vessels then dilate to allow essential cells; antibodies, white blood cells, growth factors, enzymes and nutrients to reach the wounded area.

This leads to a rise in exudate levels so the surrounding skin needs to be monitored for signs of maceration.

It is at this stage that the characteristic signs of inflammation can be seen; erythema, heat, oedema, pain and functional disturbance. The predominant cells at work here are the phagocytic cells; ‘ neutrophils and macrophages ’; mounting a host response and autolysing any devitalised ‘necrotic / sloughy’ tissu

e. During proliferation, the wound is ‘rebuilt’ with new granulation tissue which is comprised of collagen and extracellular matrix and into which a new network of blood vessels develop, a process known as ‘ angiogenesis ’.

Healthy granulation tissue is dependent upon the fibroblast receiving sufficient levels of oxygen and nutrients supplied by the blood vessels.

By day 3, the acute inflammatory response is replaced by chronic inflammation (macrophages). Also at 3 days, granulation tissue begins forming, courtesy of growth factors secreted by platelets, macrophages and endothelial cells. Growth factors induce regeneration of the basal cells of the epidermis By day 5, granulation tissue has filled the incisional space. During the second week, collagen accumulates. Leukocytes, edema, and increased vascularity begin to disappear.

Tissue Repair

"14 terms J34JTissue Repair Learn Flashcards Write Spell Test Match Gravity Advertisement Upgrade to remove ads Like this study set?

Create a free account to save it. Create a free account Maybe later Sort HY*Three Phases of Cutaneous Wound Healing Inflammation Initial injury has clot formation with platelet adhesion and aggregation HY*Proliferation Formation of granulation tissue: Proliferation of fibroblasts and vascular endothelial cells HY* Re-epithelialization & Maturation ECM deposition, re-modeling, wound contraction in large surface wounds Healing by first intention Wounds with APPROXIMATED opposed edges e.g. healing of a clean, uninfected surgical incision. Incisional space immediately fills with clotted blood Within 24 hours, cellular evidence of acute inflammation (NEUTROPHILS) appear.

By the end of the first month, the connective tissue scar is formed and the epidermis is fully regenerated. Tensile strength plateaus at ~3 months. Healing by second intention Wounds with separated edges More extensive loss of cells and tissue.

nflammation reaction more intense Much larger amount of granulation tissue WOUND CONTRACTION by myofibroblasts Substantial scar formation Formation of blood clot/Acute inflammation NEUTORPHILS Activation of coagulation pathways with blood clot forming on wound surface (dehydratin of surface clot gives scab; also necrotic debris/exudate in large wounds Clot stops bleeding Clot acts as a scaffold for cells migrating into wound Growth factors, cytokines and chemokines are released VEGF: causes edema due to increased vascular permeability Neutrophils Granulation tissue Proliferation of fibroblasts and vascular endothelial cells in first 24 to 72 hours This leads to the formation of granulation tissue, so-called because of its pink, soft, granular appearance on the surface of wounds Amount of granulation tissue formed depends on size of tissue defect and amount of inflammation Granulation tissue is maximal at 5 to 7 days Histology of granulation tissue: blood vessel formation (angiogenesis) and fibroblast proliferation, edema Angiogenesis in granulation tissue Proliferation of newly formed small blood vessels (angiogenesis) New vessels originate, in part, from ""budding"" of pre-existing blood vessels that are within the area of repair New vessels are immature and have leaky interendothelial junctions, allowing an exudate to form --> therefore granulation tissue is edematous Angiogenesis involves several growth factors, particularly VEGF and also FGF --> these factors stimulate endothelial mitosis and migration of the new blood vessels Cell Proliferation and Collagen Deposition: Macrophages Macrophages replace neutrophils in 48HRs Macrophages are a key component of tissue repair: Clear debris, fibrin and other foreign material, promote angiogenesis and ECM deposition Macrophages secrete multiple cytokines and growth factors which trigger migration and subsequent proliferation of fibroblasts Cell Proliferation and Collagen Deposition: Fibroblasts TGF-ß; most important fibrogenic agent: produce by most cells in granulation tissue and causes fibroblast migration and proliferation, increased synthesis of collagen and fibronectin, and decreased degradation of ECM by metalloproteinases.

At first provisional matrix has fibrin, plasma fibronectin and type III collagen Type III is replaced by type I collagen as wound healing progresses Tissue Remodeling Replacement of granulation tissue with scar tissue Involves both synthesis and degradation of ECM components Degradation by matrix metalloproteinases (MMPs) NEEDS ZINC. Scar Formation Weeks to months after onset of injury, granulation tissue is transformed into a mature scar.

Amount of collagen and ECM proteins increases Number of fibroblasts and vascularity decreases Fully mature scar is practically avascular, has very few cells, no dermal appendages (i.e. hair follicles) and has dense collagen Wound Strength When sutures removed (usually at end of first week), wound strength is about 10% that of unwounded skin Wound strength increases rapidly over the next 4 weeks By 3 months, strength plateaus to 70-80% of the tensile strength of unwounded skin (may never regain 100%)Hypertrophic Scars VS keloid hypertrophic DO NOT GO BEYOND THE INITIAL WOUND SITE BUT KELOID DOES WITH TYPE III COLLAGEN "

)Granulation tissue is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process. [1] Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size.

Granulation tissue

"Not to be confused with Granuloma. ""Proud flesh"" redirects here. For other uses, see Proud Flesh (disambiguation).

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Examples of granulation tissue can be seen in pyogenic granulomas and pulp polyps. Contents [ hide ]1 Appearance2 Structure2.1 Extracellular matrix2.2 Immunity2.3 Vascularization3 References Appearance [ edit]Example of granulation tissue from a cut on a finger with ""proud flesh"".

During the migratory phase of wound healing, granulation tissue is:light red or dark pink in color, being perfused with new capillary loops or ""buds"";soft to the touch;moist; andbumpy (granular) in appearance, due to punctate hemorrhagespulseful on palpationpainless when healthy [2]Structure [ edit]Granulation tissue is composed of tissue matrix supporting a variety of cell types, most of which can be associated with one of the following functions:formation of extracellular matrix,operation of the immune system, orvascularisation. An excess of granulation tissue ( caro luxurians) is informally referred to as ""proud flesh."" [3]Extracellular matrix [ edit]Main article: Extracellular matrix The extracellular matrix of granulation tissue is created and modified by fibroblasts.

Initially, it consists of a network of type-III collagen, a weaker form of the structural protein that can be produced rapidly. This is later replaced by the stronger, long-stranded type-I collagen, as evidenced in scar tissue. Immunity [ edit]The main immune cells active in the tissue are macrophages and neutrophils, although other leukocytes are also present.

These work to phagocytize old or damaged tissue, and protect the healing tissue from pathogenic infection. This is necessary both to aid the healing process and to protect against invading pathogens, as the wound often does not have an effective skin barrier to act as a first line of defense.

Vascularization [ edit]It is necessary for a network of blood vessels to be established as soon as possible to provide the growing tissue with nutrients, to take away cellular wastes, and transport new leukocytes to the area. Fibroblasts, the main cells that deposit granulation tissue, depend on oxygen to proliferate and lay down the new extracellular matrix. In vascularisation, also called angiogenesis, endothelial cells quickly grow into the tissue from older, intact blood vessels.

These branch out in a systematic way, forming anastomoses with other vessels. Approximate times of the different phases of wound healing, [4] with substantial variation depending on wound size and healing conditions. Granulation tissue formation is seen in green box at days to weeks. References [ edit]^ ""Granulation Tissue Definition"".

Memidex. Retrieved 25 October 2014.^ Bhat, Sriram (2013). Srb's Manual of Surgery, 4e. Jaypee Brother Medical Pub. p. 18. ISBN 9789350259443.^ Healing and Repair Chapter 9 from an ""Introduction to Pathology"" on a Tuskegee University website^ Reference list is found on image main page. [ hide]v t e Wound healing Blood vessels Angiogenesis Intussusception Vasculogenesis Other Fibrosis Maggot therapy Granulation tissue Growth factor Scar Stem cell "

Within hours of the fracture, the blood from the fracture fragments forms a mesh of clotted blood, which is the first link between the two fragments. The mesh contains special cells called Fibroblasts, which begin to lay down tissue called Granulation tissue between 4 and 10 days after the fracture occurs. The Granulation tissue forms a 'scaffold' between the two fragments, from which the formation of a Soft Callus can begin.

Inflammation Stage

Bone Fracture Healing Explained Inflammation Stage Introduction1 Broken Bones Explained2 Inflammation Stage3 Soft Callus Formation Stage4 Hard Callus Formation Stage5 Bone Remodelling Stage Three to Five Days Following the Fracture The Inflammation Stage begins the moment the bone is broken and lasts for around five days.

As we have described earlier, bone has a very good blood supply due to the channels within its structure. When a fracture occurs there is massive disruption to these channels and a large amount of bleeding from the fracture fragments. This is what causes immediate swelling and bruising in the area of the broken bone. This is known as a Haematoma, which means bleeding within the tissue.

The damaged bone tissue at the edges of the fracture fragments die back and the dead cells release chemicals called Cytokines which initiate the healing process.

Osteoclasts work to remove the dead bone cells. However, Osteoblasts are unable to work to lay down new bone tissue at this stage because of the movement of the fracture fragments which stops Osteoblast activity.

The principle of treatment by a trauma doctor during this immediate stage following a broken bone is to ensure the fracture fragments are returned back into place. This helps to stem the blood flow from the broken bones and substantially reduces the pain.

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ory Wound Repair Proliferation Phase 2 Characterized by Granulation tissue (new blood vessels, fibroblasts, epithelial cells) bright pink to red due to extensive capillaries, grows from wound edge to center fragile

Wound Care Fundamentals Chapter 28

"120 terms bonniecurtis Wound Care Fundamentals Chapter 28Wound Care Fundamentals Chapter 28Learn Flashcards Write Spell Test Match Gravity Advertisement Upgrade to remove ads Sort Wound Definition - Damaged skin or soft tissue Occurs as a result of trauma Cuts, blows, poor circulation, chemicals, excessive hot or cold Wound OPEN - surface of skin or mucous membrane is not intact (could be accidental or Intentional)Wound CLOSED - no opening of skin or mucous membrane (exp blunt trauma pressure)Incision- a clean separation os skin and tissue with smooth even edges Laceration- a separation os skin and tissue in which the edges are torn and separated and irregular Abrasion- a wound in which the surface layers are scraped away Avulsion- stripping away of large areas of skin and underlying tissue, leaving cartilage and bone exposed Ulceration- a shallow crater in which skin or mucous membranes is missing Puncture- an opening of skin, underlying tissue, or mucosus membrane caused by a narrow sharp pointed object Contusion (Closed Wounds)- injury to soft tissue underlying the skin from the force of contact with a hard object, sometimes called a bruise.

Inflammation- the physiologic defense immediately after tissue injury, last approximately 2-5 days.

(its purpose is to 1. Limit the local damage 2. Remove injured cells and debris 3. Prepare the wound for healing,Proliferation- Remodeling Wound Repair Inflammation Phase 1 Definition - physiological defense that occurs immediately after tissue injury Purpose Limits the local damage , Removes injured cells and debris, Prepares wound for healing Wound Repair Inflammation Phase 1 The inflammatory response Lasts about 2 Lasts about 2-5 days Wound Repair Inflammatory Response First Stage Local Response Blood Vessels Constrict,Then dilate, Platelets form loose clot to control bleeding, Damaged cells membranes become more permeable Plasma and chemical substances released Signs and symptoms of infection of wound include?

Swelling, Redness, Warmth, Pain, Decreased function Second Wave of Defense inflammation Leukocytes and Macrophages (white blood cells) migrate to site of injury Body produces more to take their place, Leukocytosis confirmed through blood specimen Blood test WBC w/differential, Rise in neutrophils and monocytes suggests inflammatory response or infectious process occurring Neutrophils and monocytes responsible for ?

phagocytosis of pathogens, coagulated blood cellular debris They clean area of wound injury and prepare site for wound healing Wound Repair Proliferation Phase 2- Period during which new cells fill and seal a wound Occurs 2 days to 3 weeks after the inflammat

Granulation tissue (new blood vessels, fibroblasts, epithelial cells) bright pink to red due to extensive capillaries, grows from wound edge to center fragile AND Collagen (protein substance tough and inelastic) adhesive strength of wound increases . Blood vessels begin to shrink, Pink color disappears@ Main substance you will see during the proliferation stage?

Granulation & collagen Integrity of skin is restored by? Resolution, Regeneration and scar formation Resolution - process by which damaged cells recovers and re-establishes their normal function Regeneration - cell duplication Scar formation replacement of damaged cells with fibrous tissue acts as non functioning patch Scar Formation- replacement of damaged cells with a fibrous tissue, act as non functioning patch Wound Repair Remodeling Phase 3 - Period during which the wound undergoes changes and maturation (Lasts 6 months to 2 years Wound contracts Scar shrinks) scar is stronger, but not as strong as original tissue Wound Healing is affected by?

Type of wound injury, Expanse or depth of wound, Quality of circulation, Amount of wound debris, Presence of infection, Status of the patient's health, excessive pulling or tension on edges Wound Healing Speed Depends on? of wound repair takes place..... Extent of scar tissue that forms..... Depends on how the wound heals The key to wound healing is?

Adequate blood flow to the injured tissue Types of Healing? First intention, Second intention, Third intention Evisceration- wound separation with protrusion of organs (these complications most likely within 7-10 days after surgery)dehiscense- separate of wound edges Pressure ulcer- a wound caused by prolonged capillary compression that is sufficient to impair circulation to the skin and underlying tissue First (primary) intention Reparative process wound edges are directly next to one another, Space between wound narrow, small amount of scar tissue forms (EXAMPLE- surgical wound)Second intention- Reparative process wound edges are widely separated , More time consuming and complex Margin of wounds are not in direct contact additional time is needed for granulation tissue to extend across wound, Cautious wound care Third intention- Reparative process when the wound edges are widely separated later brought together with some type of closure material Broad deep scar Deep, contains extensive drainage and tissue debris May use drainage device or absorbent gauze Wound Management Defined Techniques to promote wound healing Goals of wound management Surgical wound reapproximate the tissue to restore its integrity Goals of wound management Pressure ulcer- primary goal is prevention if not prevented then goal primary goal is prevention if not prevented then goal reduce the size of the wound ,restore skin and tissue integrity What is the main goal of wound management of pressure ulcer is?

Is prevention!Dressing- cover over a wound Drains- are tubes that provide a means for removing blood and drainage from a wound Closed drains- tubes that terminate in a receptacle (exp hemovac, Jackson -prat (JP)Hydrocolloid dressings- self adhesive, opaque, air and water- occlusive wound covering, they keeps wounds moist, most wounds heal more quickly because new cells grow rapidly in a wet enviroment.

(if dressing remains intact can be left in place up to 1 week)Wound Management Using a Dressing Purposes- Keep wound clean, Absorbing drainage, Controlling bleeding, Protecting the wound from injury, Holding medication in place, Maintaining a moist environment Wound Management Types of Dressings- Gauze, Transparent Hydrocolloid ,Gauze Dressing Guaze dressing - -Absorbent Obscure wound, interfere with assessment Granulation tissue may adhere Secure with tape, cover fresh wounds likely to bleed Transparent Dressings- exp opsite) allow nurses to assess wound without removing dressing, advantages are less bulky, used to cover IV sites, are not absorbent, and tend to loosen.

Montgomery straps- strips of tape with eyelets (kind of looks like a gurtle, used in patients who are having skin break down during removal of tape)Hydrocolloid Dressings- Self adhesive, opaque, air and water occlusive helps Keep wounds moist Can be Left in place for 1 week Repels other body substances , make sure to Size generously (exp Duoderm)When to Do Dressing Changes?\ When the Wound requires assessment, Dressing is loose or saturated, or if Dr wants to assess Reinforce if MD desires to change it Drains Definition - tubes that provide a means for removing blood and drainage from a wound Types of Drains include?

Open drains and closed drains Open Drains- Flat flexible drains, occurs passively by gravity and capillary action Closed Drains- Tubes that terminate in a receptacle Hemovac, Jackson Pratt Pull fluid by creating vacuum or negative pressure knee or breast surgery Cleansing site of Drain- Insertion site is cleansed in a circular manner,Precut drain gauze place around the base of the drain Sutures - knotted ties that hold incision together Silk or synthetic materials used to hold up to 2 weeks Staples - wide metal clips (In place for 2 days to 2 weeks) After taking out, apply Steri-strips ""butterflies""Bandage - strip or roll of cloth wrapped around a body part ( exp Ace bandage)Binder application single T binder/double Tbinder, used for rectal/vaginal surgery or decure dressing to anuse, perineium or groin Reasons for Use Bandages/Binders - Hold dressing in place - tape not indicated or dressing extremely large ,Supporting area around a wound or injury to reduce pain, Limiting movement in the wound area to promote healing Roller bandage applications 1.

Elevate and support the limb @. Wrap from distal to proximal direction. 3. Avoid gaps between each turn of the bandage 3.

Exert equal, but not excessive tension with each turn 4. Keep the bandage free from wrinkles 5. Secure the end of the roller bandage with metal clips. 6. Check the color and sensation of exposed fingers or toes often. 7. Remove the bandage for hygiene and replace at least twice a day Debridement Definition removal of dead tissue Types of Debridement Sharp - use of scissors or scalpel Enzymatic debridement involves the use of a topically applied chemical substance that breaks down and liquefy wound debris Autolytic debridement - self dissolution, is a painless, natural physiologic process that allows the body's enzymes to soften, liquefy, and release devitalized tissue.

occlusive or semi occlusive dressing Mechanical Debridement- i involves physical removal of debris from a deep wound. One technique is application of Wet to dry dressings, hydrotherapy, irrigation, used on eyes, ears, vagina Hydrotherapy- therapeutic use of water in which the body part of the wound is submerged in a whirlpool tank the agitation of the water which contains an antiseptic, softens the dead tissue.

Loose debris that remains is removed afterward by sharp debridement Irrigation- Technique for flushing debris Structures commonly irrigated include?

Wounds ,Eye, Ear, Vagina Heat and Cold Applications- Ice bag (reduce swelling), Chemical pack (cold), Compress (warm/cool), Aqua thermia (cool/heat pad), soaks (body submerged for 15-20 mins), moist packs Uses for Cold- Reduces fevers, Prevents swelling, Controls bleeding, Relieves pain, Numbs sensation Uses for Heat- Provides warmth, Promotes circulation, Speeds healing, Relieves muscle spasm, Reduces pain Types of Therapeutic Baths ?

Oatmeal, Sitz Therapeutic Baths- those preformed for other than hygiene purposes , help to reduce high fever or apply medicated substances to the skin to treat skin disorders or discomfort. Pressure Ulcer (Decubitus)Usually appear ? over bony prominences Sacrum, Hips, Heels, Elbows, shoulder blades, back of head What Factors Contribute to Pressure Ulcers?

Infrequent movements of body parts, Pressure in local capillaries to less than 32 mm Hg for 1-2 hours without intermittent relief, causes cells die from lack of oxygen and nutrition Stage I Pressure Ulcers intact but reddened skin fails to resume normal color when pressure is relieved (skin is not broken)Stage II Pressure Ulcers- pressure ulcer is red accompanied by blistering or skin tear Stage III Pressure Ulcers- shallow skin crater that extends to the subcutaneous tissue May have serous or purulent drainage Stage IV Pressure Ulcers- life threatening deeply ulcerated tissue, exposing muscle and bone, Infection may spread throughout body Sepsis Preventing Decubitus Ulcer Step 1 Identify Clients at Risk Things help with preventon of Decubitus ulcers include?

Turning every 2 hours, 45 degree angle Clients at Risk for Decubitus Ulcer include? Inactive, Immobile, Malnourished, Emaciation, Diaphoresis, Incontinence, Vascular Disease, Localized Edema, Dehydration, Sedation Prevention of Pressure Ulcers Step 2 - Implement measures to reduce conditions under which pressure ulcer is likely to form Nursing Diagnoses For Decubitus Ulcer?

Acute Pain ,Impaired Skin Integrity, Ineffective Tissue Perfusion, Impaired Tissue Integrity, Risk for Infection Sepsis- potentially fatal systemic infection Massage boney prominences only if?

Skin blanches with pressure relief Shearing force- effect that moves layers of tissue in opposite directions Skin tear- shallow break in the skin Serious drainage leaking plasma serum that is clear Purulent drainage- blue, white greenish fluid caused by would infection thicker with pus, smell Sanguinous Fluid is large amounts of RBC from knee/hip surgery Serosanguineous fluid is clear with blood tinged fluid Two basic wounds are Open and closed Three sequential phases of wound repair inflammation, proliferation, remodeling Undermining means erosion of tissue from underneath intact skin at wound edge Slough means dead tissue on wound surface moist, stringy, yellow, tan, gray or green Necrotic tissue dry, brown, black tissue (dead, no nutrience)Wound complications are Dehiscence, Evisceration (client describes feeling of something giving way)What should you do if something gives way on a surgical wound Position client to put less strain on area, lay down and lift knees if possible, if organs hanging out put moistened sterile dressing over organs and tissues keep area mosit What should the nurse watch for if somthing gives way on a surgical wound Notify DR, alert for s&s of impaired blood flow, swelling, pallor, mottled appearance, coolness of tissue and wound, watch for shock, take vital signs Dehiscense & evisceration caused by Unusual strain on incision site, premature removal of sutures and staples, distention of ab, compromised tissue, insufficient dietary intake protein, vit c, weak tissue Will temp increase due to infection Yes Steri strips butterflies are hold incision together, close superficial lacerations When do you irrigate a wound and why before a dressing is applied and done when granulated tissue has formed on surface debris remove it gently How do you do an eye irrigation flush toxic chemicals/debris from eyes/displace mucus/other drainage accumulated in area, use warm water and direct solution onto conjunctiva How to do an ear irrigation remove debris, contraindicated if tympanic membrane is perforated, inspect for object before, direct warm fluid up toward roof of canal, than place cotton ball Heat is used for warmth, circulation, speeds healing, relieves muscle spasm, reduce pain, increase joint movement Cold is used for reduce fever, prevent swelling, control bleeding, relieves pain, numbs sensation What are the risk factors to develop ulcer inactivity, immobility, malnutrition, emaciation, diaphoresis (sweat), incontinence, sedation, vascular disease, localized edema, dehydration, diabeties When should you do a risk assessment On admission, weekly, yearly and use Brden and Norton scales Braden Scales Has six subscales: sensory perception, moisture, activity, mobility, nutrition and friction & shear, need 23 points and 18 below is risk Norton Scales Has six as well: general physical condition, mental state, activity, mobility, incontinence, medications, need score of 24 below 15 and 16 is risk General Gerontologic considerations Wound healing takes twice as long for an 80 year old, age related changed affect healing like thinning of dermal layer of skin, decreased subcutaneous tisse, inflammation is more subtle, diminised immune response from t-lymph and mobility requires aggressive skin care to prevent ulcers What can interfer with adequate nutrition, wound healing and urinary incontinence Depression, poor appetite, cognitive impairments, physical/economic carriers Conditions that interfer with circulation cardiace, diabetes, circulation - increase older adult susceptibility to delayed wound healing and infections - firsk for thermal skin injury Phagocytosis neutrophils and monocytes are wbc responsible for this...they consume pathogens, coagulated blood and cell debris, clean injured area and prepare for wound healing Moist wounds heal quicker because new cells grow faster "