Talk:Wound healing

Sorry

Sorry I made this page so rediculously long; it's most of the contents of a paper I wrote for a wound healing tutorial for school. If you want to make new pages ou$<!--Insertformulahere-->=='''Headlinetext'''==$t of each section or something, that would be cool. Though I'd say this page still needs little blurbs about each phase and links to the pages in that case. Also, the proliferation phase is too long in this page and the maturation phase is too short. You can help by expanding the maturation phase and cutting parts you think are unnecessary from proliferation. Also, if you want to take the time to turn all the text's references into footnote links so the text is smaller and easier to read, that would be great. And if you want to find links for all of the references and eliminate ones you think are unnecessary, also great. Matterafact, do whatever you want to it. --Delldot 01:17, 18 October 2005 (UTC)

You have nothing to apologise for. I think this is excellent, interesting and very well supported. Things that might improve it would be internal Wikipedia links and illustrations. --Mylesclough 06:33, 20 October 2005 (UTC)

I'm trying to change the Harvard refs to footnote style to make it shorter and more readable, but I can't get the numbers to correspond to the numbers in the footnotes; they just go up in order they're put in the article, even if the same thing is cited twice. Anyone know how to fix this? If you do, let me know or do it yourself. Thanks. --Delldot 14:50, 20 October 2005 (UTC)

I was recently released from prison. While there, I became fascinated by the whole process of tissue repair through a brief mention in James Gills' "Darwin under the Microscope." I'm by no means ANY kind of an expert on the subject, but yours is the first I've read so specifically tuned to the mechanics of the process. Just want to thank you for feeding a hungry mind! —Preceding unsigned comment added by 158.80.64.2 (talk) 17:07, 23 March 2010 (UTC) Insert non-formatted text here You know maybe it is always a good idea when it is long it will give good answer's.

wow

Thanks for this straight forward explanation of what is often seen as an overwhelming process. I know what you mean about writing too much. I had to cut out most of process in the report I'm writing. But such is the work of editing, right? Thanks again. this is just fantastic.

great work! so interesting...

A lot of this article was removed at the end of May 2006. I'm wondering why it was all removed.

maggots?

Why are there links to sites about maggots when this not discussed in the text? The final link is also inaccesiblem Mike 12:02, 10 October 2006 (UTC)

Major edit in progress

A great deal of material was blanked in may and I didn't notice till now. I'm in the process of restoring it and many of the refs that were removed. I'm also making some changes, and this may take a couple hours. I'd appreciate it if, as a favor to me, you could wait to make any edits until after I remove the notice. If that's not possible, let me know and I can add your edits into the version I'm working on. Thanks much, delldot | talk 04:00, 27 December 2006 (UTC)

I'm about half done converting the refs and have removed the in use template. I'll have to put it up again when I finish replacing the refs. Thanks everyone! delldot | talk 06:34, 27 December 2006 (UTC)

I've stuck the tag back up so I can finish the other half of converting the refs. Let me know if anything comes up. delldot | talk 04:07, 31 December 2006 (UTC)

OK, changes done, tag removed. delldot | talk 05:19, 31 December 2006 (UTC)

scarring

I added a little on scarring, and was going to add two recent reviews, but for some reason it won't work, can someone post to the tutorial on adding references, I can't seem to get the right combination of links. The reference are Eur J Surg. 2002;168(10):523-34. and Wound Repair Regen. 2005 Jan-Feb;13(1):7-12. I plan to extend the scarring section slightly and improve the links to pathological scarringGasboy 23:26, 25 January 2007 (UTC)

Suggested refinement: proliferation phase

Overall quite good, however I think the section on proliferation could use some work on flow --the tie between collagen/angiogenesis/epithelialization and granular tissue was a bit confusing. I'm by no means an expert on this and I don't feel comfortable making the changes myself. --Bobak 23:01, 19 February 2007 (UTC)

Note on scar tissue

Impressive discussion. When I worked on the early topical hyperbaric driven tissue regeneration program with Sandia Nat Lab/UCLA/VA, it was noticed that scar tissues did not form. We were able to fill deep ulcers with healthy tissue in just a few weeks. The only other example of this was working with embryonic tissues. You may thus want to go back and review some of the work of Madalene Heng to get this mechanism. Dr. E. McGowan 68.6.94.22 (talk) 09:44, 9 August 2009 (UTC)

Minor changes

Great article, I have made some minor changes to the introduction and will look at the rest when I can. If you don't like them - just delete! Thanks. (I spend all day 9-5 looking at wounds so might have something useful to say). —Preceding unsigned comment added by Mark3k (talk • contribs) 23:13, 28 November 2007 (UTC)

timeline

please add a timeline. ex. number of days until this phase... etc etc.Tkjazzer (talk) 01:27, 11 February 2008 (UTC)

Ooh, that's an awesome idea. We could maybe even make an image, that would be very cool. I'll add this to my embarrassingly vast to do list, but if others want to get to this before the end of the next century... delldot talk 10:47, 12 February 2008 (UTC)

Less technical section for non-medical readers?

It would be great if you guys could add a 'wound healing for dummies' section for the non-medical folks. —Preceding unsigned comment added by 84.45.218.135 (talk) 18:49, 25 April 2008 (UTC)

Sounds like a great idea, I can work on getting rid of the too technical language. If you notice something in particular, definitely bring it up here, or have a go at it yourself! delldot on a public computer talk 06:49, 8 May 2008 (UTC)

Section Addition Idea(s)

As a general reader coming here for information, I was disappointed there was no information regarding nutrition to support wound healing. Maybe a section would be helpful on what nutrients are essential for wound healing? Like protein, etc. --142.46.14.98 (talk) 17:36, 25 August 2008 (UTC)

I agree - I think the article is a great start, but could use some additions and improvements. In particular, I think a section about "common problems encountered during the wound healing process" would be very relevant. At the same time, I think many of the terms in use would be much more understandable in ENGLISH instead of Greek and/or Latin. To cite one example I changed, I don't see the sense in using words like "erythematous" when simply "red" is meant. --Can-we-be-sure —Preceding undated comment added 15:31, 18 April 2009 (UTC).

Re: nutrition and common problems---------smoking, high blood sugar, and high fat diets all impact the healing process. If you are concerned about pressure ulcers, then how the capillary pressures are affected and hence blood flow will play out in the progression or recession of the problem. It does not take much to shut down capillary flow, consequently people who can not move will see tissue destruction. The impact of fat on the flow of blood through capillaries and the impacts on the endothelial cell response will affect microthrombi, hence perfusion, hence repair. At blood sugar levels much above 126, the repair process is adversely affected, the level of reduced glutathione GSH)is low in diabetics and this impacts endothelial cell behaviour. You can go to Google scholar or PubMed and read on these things.----------McGowan 68.6.94.22 (talk) 10:10, 9 August 2009 (UTC)

Links?

Does this link really provide more info? "BioTherapeutics Education and Research Foundation." --Abbaroodle (talk) 13:44, 27 July 2009 (UTC)

No, so I have removed it. JamesBWatson (talk) 20:08, 27 July 2009 (UTC)

Pathology

Wound healing is a complex but orderly phenomenon involving a number of processes: i) coagulation ii) induction of an acute inflammatory process by the initial injury iii) regeneration of parenchymal cells iv) migration and proliferation of both parenchymal and connective tissue cells v) synthesis of ECM proteins vi) remodeling of connective tissue and parenchymal components vii) collagenization and acquisition of wound strength

Coagulation: Coagulation is the process by which prothrombin is converted into the proteolytic enzyme thrombin, which in turn cleaves the fibrinogen molecule to form insoluble fibrin in order to stabilize and add to the platelet plug. Coagulation consists of a series of zymogen activation stages in which circulating proenzymes are converted in sequence to activated proteases. The traditional concept of the clotting system evolved from test tube analysis and follows two pathways: the intrinsic pathway involves components normally present in blood, and the extrinsic pathway is initiated by the tissue lipoprotein. The clotting system and inflammation are intimately connected processes. Injury causes hemorrhage from damaged vessels and lymphatics. Vasoconstriction occurs almost immediately as a result of release of catecholamines. Various other vasoactive compounds, such as bradykinin, serotonin and histamine are released from tissue mast cells. They initiate the process of diapedesis, a passage of intravascular cells through vessel walls and into the extravascular space of the wound. Platelets derived from the hemorrhage form a haemostatic clot. The platelets release clotting factors to produce fibrin, which is haemostatic and which forms a mesh for the further migration of inflammatory cells and fibroblasts. Fibrin is produced from fibrinogen, which is formed by the action of thrombin in the presence of thromboplastin. If the fibrin mesh is eliminated, the wounds ultimate strength is diminished. Fibrin serves as the frame work on which fibroblasts and endothelial cells to develop along. Platelets are also extremely important because they are the first cells to produce several essential cytokines, which modulate most of the subsequent wound healing events. These cytokines include PDGF, EGF, TGF-β.

Acute Inflammatory Process: Acute inflammation is the immediate and early response to an injurious agent. It is complex reaction the vascularized connective tissue. There are three major components: i) alterations in vascular caliber that lead to an increase in blood flow, ii) structural changes in the microvasculature that permit the plasma proteins and leukocytes to leave the circulation and iii) emigration of the leukocytes from the microcirculation and their accumulation in the focus of injury. Inflammation is a vascular and cellular response that serves to clean dead tissue and foreign bodies from the wound. During this phase, the microcirculatory response is promoted with aggregation of blood cells, kinins, and products favouring haemostasis, and isolation and neutralization of tissue irritants. With this, cleaning of the damaged tissue allows tissue repair. This phase lasts from three to ten days. Macrophages move into the inflammatory environment and are important constituents of granulation tissue, responsible for clearing extracellular debris, fibrin, and other foreign material at the site of repair.

Regeneration of parenchymal cells: Regeneration denotes replacement of injured cells by cells of the same type, sometimes leaving no residual trace of the previous injury. With injury, cell replication is stimulated which is controlled by a complex interplay of growth factors, growth factor receptors, transduction mechanisms and transcription factors. The entry and progression of cells through the cell cycle are controlled by changes in the levels and activities of cyclins.

Fibrosis: Tissue destruction of both parenchymal and stromal tissue cannot be repaired solely by regeneration. Repairing tissue damage then occurs by replacement of nonregenerated parenchymal cells by connective tissue. This involves: i) formation of new blood vessels ii) migration and proliferation of fibroblasts iii) deposition of extracellular matrix (ECM) iv) maturation and organization of the fibrous tissue

Formation of fibrous tissue occurs by formation of granulation tissue which consists of new small blood vessels and proliferation of fibroblasts. Formation of new blood vessels first involves degradation of the basement membrane of parent vessels, to allow formation of a capillary sprout and subsequent cell migration. This is followed by migration of endothelial cells toward the angiogenic stimulus, vascular endothelial growth factor (VEGF) and fibroblast growth factors (bFGF). There is proliferation of endothelial cells behind the leading front of migrating cells. Maturation of endothelial cells then occurs which includes inhibition of growth and remodeling into capillary tubes which is controlled by the angiopoietins and their receptors. Recruitment of periendothelial cells to provide support for the endothelial tubes is the final step in maturation.

Migration of fibroblasts to the site of injury and their subsequent proliferation are triggered by multiple growth factors, including TGF-β, PDGF, EGF, FGF, and the so called fibrogenic cytokines, interleukin-1 and TNF-α. These growth factors are derived from platelets and a variety of inflammatory cells as well as activated endothelium. These inflammatory cells also elaborate TGF-β, PDGF, and bFGF and therefore promote fibroblast migration and proliferation. If the appropriate chemotactic stimuli are present, mast cells, eosinophils, and lymphocytes may be increased in number. Each of these can contribute directly or indirectly to fibroblast migration and proliferation. Of the growth factors involved in inflammatory fibrosis, TGF-β appears to be the most important because of the multitude of effects that favor fibrous tissue deposition. As repair progresses, the number of proliferating endothelial and fibroblast cells decreases. Fibroblasts progressively become more synthetic and deposit increased amounts of ECM. Fibrillar collagens (collagens I, II, III) form a major portion of the connective tissue in repair sites and are important for the development of strength in healing wounds. Collagen synthesis by fibroblasts develops as early as days 3 to 5 and continues for several weeks depending on the size of the wound. Ultimately, the granulation tissue scaffolding is converted into a scar composed of spindle-shaped fibroblasts, dense collagen, fragments of elastic tissue and other ECM components. As the scar matures, vascular regression continues, eventually transforming the richly vascularized granulation tissue into a pale, avascular scar.

Tissue remodeling: The replacement of granulation tissue with a scar involves transitions in the composition of the ECM. This change in ECM composition is brought about by changing balances of synthesis and degradation. Degradation of collagen and other ECM proteins is achieved by a family of matrix metalloproteinases, which are dependent on zinc ions for their activity. Metalloproteinases consist of interstitial collagenases(cleave the fibrillar collagen), gelatinases(cleaves type IV collagen), stromelysins (acts on a variety of ECM proteins including proteoglycans, fibronectin, laminin and amorphous collagens) and membrane bound matrix metalloproteinases. Matrix metalloproteinases are inhibited by a family of specific tissue inhibitors of metalloproteinases which are produced by most mesenchymal cells. Different tissues will have varying modifications to their remodeling process, e.g. bone will have deposition of calcium hydroxyapatite.

Wound strength: For skin, when sutures are removed, usually at the end of the first week, wound strength is approximately 10% of the strength of unwounded skin, but it increases rapidly over the next 4 weeks. At three months, the tensile strength of the wound is about 70 to 80% of unwounded skin.

Local and systemic factors that influence wound healing: Systemic factors which influence wound healing include: i) Nutrition has profound effects on wound healing. Protein deficiency, for example, and particularly vitamin C deficiency inhibit collagen synthesis and retard wound healing. ii) Metabolic status can change wound healing. As exemplified by diabetes mellitus which can slow wound healing. iii) Circulatory status as inadequate blood supply and impaired venous drainage impair wound healing iv) Hormones such as glucocorticoids have anti-inflammatory effects that influence various components of inflammation and fibroplasia and also inhibit collagen synthesis

Local factors which influence healing include the following: i) Infection is the single most important cause of delay in healing ii) Mechanical factors such as early motion of wounds also delay healing iii) Foreign bodies such as sutures and debris constitutes impediments to healing iv) Size, location and type of wound also influence wound healing. Wounds to the face and other well vascularized areas heal more quickly than poorly vascularized wounds

Pathological aspects of wound healing: Inadequate formation of granulation tissue or assembly of a scar can lead to wound dehiscence or ulceration. Dehiscence or rupture of a wound is most common after abdominal surgery and is due to increased abdominal pressure. This mechanical stress on the abdominal wound can be generated by vomiting, coughing or ileus. Wounds can ulcerate because of inadequate vascularization during healing. For example, lower extremity wounds in individuals with atherosclerotic, peripheral vascular disease typically ulcerate. Non healing wounds also form in areas devoid of sensation, neuropathic ulcers, as seen in diabetic peripheral neuropathy. Excessive formation of the components of the repair process can also complicate wound healing. Aberrations of growth may occur even in what may begin initially as normal wound healing. The accumulation of excessive amounts of collagen may give rise to a raised tumorous scar, either a keloid or hypertrophic scar. Keloid scars are more common in blacks. Exuberant granulation tissue may interfere with epithelialization and should be removed. Contraction in the size of a wound is an important part of the normal healing process. An exaggeration of this process is called a contracture and results in deformities of the wound and the surrounding tissues. Contractures are particularly prone to develop on the palms, soles and the anterior aspect of the thorax. These are commonly seen after serious burns and may compromise joint movement. —Preceding unsigned comment added by 65.183.8.194 (talk) 19:09, 9 March 2010 (UTC)

This article should cross-reference WP articles on Wound dressing and wound care.

This article should cross-reference WP articles on Wound dressing and wound care, development and current status of moist bandaging technique as facilitating and speeding healing process while protecting from infection. —Preceding unsigned comment added by Ocdnctx (talk • contribs) 15:03, 15 May 2011 (UTC)

Moist wound healing

According to a British pharmacy company, skin wounds heal more effectively if they are not allowed to dry out and form a hard scab. Is this true, and if it is, what studies have shown evidence for it? Can someone add a section on it to the article, and also anything about the effectiveness of hydrocolloid plasters making wounds heal better? Wsmss (talk) 10:23, 30 April 2012 (UTC)

From a lay-mans point of view, I would think that a wound (scab) left to dry would be natural and add that protective barrier to the environment. Washing the area is good and with this it does help create openings for secretion of blood and pus during times of inflammation and infection. I have this nickle size wound on my leg I been watching for two weeks now and seems to be coming along well. Very low fluid draining. I think to "pick" the scab and or moisten it, you run the risk of it releasing prematurely in turn not getting the proper tissue replaced or repaired.