Keloid, also known as keloid disorder and keloidal scar, is the formation of a type of scar which, depending on its maturity, is composed mainly of either type III (early) or type I (late) collagen.It is a result of an overgrowth of granulation tissue (collagen type 3) at the site of a healed skin injury which is then slowly replaced by collagen type 1. May 22, 2019 - Learn what granulation tissue is, why it forms and how to treat it if you notice it around your child's stoma.
Abstract
Hypergranulation tissue (or also known as overgranulation) may negatively influence burn wound healing time and contribute to recurrence of contractures in burn wounds and grafts. Subsequently, the treatment of hypergranulation tissue remains controversial and problematic. In this case series, we aimed to examine the feasibility and document the use of topical hydrocortisone in the treatment of hypergranulation tissue formation resulting from burn wounds. We report five cases where hypergranulation tissue developed following deep dermal/full-thickness burns. Initial burn wound treatment included necrotic tissue debridement, wound cleansing, and Flaminal®. All five cases underwent surgical debridement and split-skin grafting. Upon identification of hypergranulation tissue, hydrocortisone acetate 0.25% was applied topically as usual care for the treatment of hypergranulation tissue. All five patients had deep dermal/full-thickness burns with a total body surface area ranging from 22% to 61% and were aged from 3–41 years. All five cases developed hypergranulation tissue during their admission after debridement and split-thickness skin grafts. All patients showed an improvement in the treated areas with a complete regression of hypergranulation tissue and closure of the burn wounds. No clinically apparent local or systemic side effects of the treatment were observed. Topical hydrocortisone can be utilized as an effective, inexpensive, and noninvasive practical option in the treatment of hypergranulation tissue resulting from burn wounds.
Introduction
Hypergranulation tissue, often referred to as overgranulation or proud flesh, can be defined as an excess of granulation tissue that fills the wound bed to a greater extent than what is required and goes beyond the height of the surface of the wound resulting in a raised tissue mass., Clinically, it is identified as a red friable, shiny tissue with a soft appearance above the level of the surrounding skin.3 Hypergranulation occurs in an array of wounds including burns and venous and pressure ulcers. This tissue prevents migration of epithelial cells across the surface of the wound bed and impedes wound healing.,5 However, the etiology behind the development of hypergranulation tissue is not well understood. Predisposing factors that have been suggested include healing by secondary intention, excessive moisture, prolonged inflammation related to infection or residue dressing fibers, external friction, and the repeated use of occlusive dressings. Furthermore, a prolonged stimulation of fibroplasia and angiogenesis may result in the formation of hypergranulation tissue that is problematic for wound healing.5,9
We estimate that 10%–15% of burn patients admitted to our Unit at the Sheba Medical Center, Tel Hashomer, develop hypergranulation tissue that impedes wound healing. Jewell et al report a similar figure of 17% (nine of 52) in their burns study population that developed hypergranulation tissue. Subsequently, those who developed hypergranulation tissue at the site of graft loss experienced a statistically significant increased healing time. Furthermore, the presence of hypergranulation tissue was a significant independent predictor of time to complete wound healing (R2=0.27; P=0.0131) with a median of 45 days for complete wound healing.
Treatment of hypergranulation tissue includes such methods as dressings that are less occlusive, surgical excision, chemical cautery with silver nitrate, hypertonic saline,9 and laser ablation. However, these treatments are often not considered uniformly successful.9 Topical corticosteroids have been reported to suppress the inflammatory response that contributes to the growth of this tissue.,9, Other mechanisms of action are the suppression of angiogenesis,9 and the reduction of edema related to stabilization of cell membranes.9 However, much of the literature focuses on the treatment of keloid and hypertrophic scars because of the ability of steroids to reduce the excessive fibrous tissue.
To our knowledge, there is limited literature that reports the treatment for hypergranulation tissue formation in burn wounds. Hypergranulation tissue that develops in deep partial and full-thickness burns impedes epithelialization.9 Topical steroid application for the treatment of hypergranulation tissue in burn wounds is standard care in our Burn Center in the Sheba Medical Center, Tel Hashomer, Israel. Here, we present the use of topical hydrocortisone in the treatment of hypergranulation tissue formation resulting from burn wounds.
Patients and methods
Five cases of hypergranulation tissue development in wounds following deep dermal/full-thickness burns were admitted to the Sheba Israel National Burn Center, Tel Hashomer, Israel. All patients identified with the development of hypergranulation emanating from a burn wound over a 3-month period were included in the case series.
In all patients, as per departmental protocol, initial primary burn wound treatment included necrotic tissue debridement, wound cleansing, and Flaminal® (Flen Pharma, Kontich, Belgium). All five of the cases required surgical debridement and split-skin grafting. As soon as hypergranulation tissue was identified, we applied a hydrocortisone acetate 0.25% lotion diluted in a ratio of 125–250 mL to 1 L of sterile water. The solution was not applied directly to the hypergranulation tissue but via gauze pads soaked into the solution, and then sterile bandages were applied to cover the wounds. The application of 125 mL/L of solution was used initially, and in the case where there was no significant improvement, a higher concentration solution was applied up to a maximum of 250 mL/L. After 12 hours, an additional application of the solution was applied utilizing the existing dressings. The dressing was then removed after 12 hours and the whole procedure repeated after wound assessment and cleansing with sterile water and antibacterial solution (chlorhexidine gluconate or iodine solution). During the dressing changes, routine digital photographs were taken with the signed consent of the patient/guardian for the purposes of treatment, teaching and use in academic publications. As this was a retrospective case series report and the procedure described is a well-established standard of care in our Burns Unit at the Sheba Medical Center, the ethics committee of Sheba Medical Center Helsinki Committee, Tel Hashomer, Israel does not require ethics approval to be sought for this case series.
It must be noted that to minimize the systemic effects of steroids absorbed through damaged skin, we intentionally treated one affected area at a time to avoid widespread usage of topical steroids on multiple or extensive burn sites. In addition, we limited the use of topical steroids to a maximum of 4 consecutive days after which we reinitiated standard wound care. The rationale for the 4 consecutive days of topical steroids was based on an internal expert review, our long-term common praxis and experience addressing the hyperinflammatory process, and the fact that the duration is short enough to avoid systemic side effects. If after 4 additional days there was still significant hypergranulation tissue, another course of topical steroids was initiated for up to 4 days. In cases where clinical local infection is suspected, 5% mafenide acetate suspension is combined with the aforementioned treatment as part of our standard care. However, no burn wound infections were noted in the five reported cases. We believe that the steroids reduce the inflammatory process and allow for wound closure. This is supported by the studies of Guo and DiPietro and Hofman et al who state that although systemic corticosteroids inhibit wound healing, low-dosage topical application for the treatment of chronic wounds has been found to accelerate wound healing, reduce pain and wound exudate, and suppress the formation of hypergranulation tissue. However, careful monitoring of the wound must ensue to prevent the risk of infection with prolonged use.
Results
Five cases of hypergranulation tissue in patients with deep dermal/full-thickness burns were treated with topical hydrocortisone acetate 0.25% solution. The age of the patients ranged from 3 to 41 years, and they had a total body surface area (TBSA) range of 22%–70% burned, of which two cases were greater than 50% TBSA. All cases had no significant or relevant medical history. Of the five cases reported, four were male and one was female. The area treated with topical hydrocortisone acetate 0.25% solution ranged from 0.5% to 5% TBSA. Two cases had only one 4-day treatment, one case had the treatment repeated twice, one case had the treatment repeated three times, and the final case had four cycles of the treatment (Table 1).
Table 1
Patient/case | Age, years | Sex | Burn cause | % TBSA | Burn depth | % of treated surface area | Number of 4-day treatments |
---|---|---|---|---|---|---|---|
1 | 41 | M | Electrical burn | 30 | Deep dermal/fullthickness | 0.5 | Once |
2 | 24 | F | Gas explosion | 33 | Deep dermal/fullthickness | 0.5 | Once |
3 | 23 | M | Turpentine burn | 22 | Deep dermal/full thickness | 1 | Repeated twice |
4 | 32 | M | Gas-pipe explosion | 61 | Deep dermal/fullthickness | 5 | Repeated three times |
5 | 3 | M | Molotov cocktail | 70 | Deep dermal/fullthickness | 5 | Repeated four times |
Abbreviations: F, female; M, male; TBSA, total body surface area.
After treatment of the hypergranulation tissue with the described protocol using hydrocortisone acetate 0.25% solution, all cases showed a regression of hypergranulation tissue. Figures 11–3(A) clearly demonstrate hypergranulation tissue prior to treatment. Figures 11–3(B) taken after initial treatment show the hypergranulation tissue resolving or resolved. In all cases, none of the patients needed to be regrafted after topical treatment and no areas treated developed clinical signs of infection at the granulation site, showing complete healing of graft sites. Furthermore, no local or systemic side effects were observed from the use of the topical hydrocortisone.
Case 5.
Notes: (A) Hypergranulation tissue to occipital/parietal region prior to treatment with topical hydrocortisone; (B) 5 weeks after treatment regime with topical hydrocortisone acetate 0.25% solution.
Case 4.
Notes: (A) Hypergranulation tissue to the right iliac region prior to treatment with topical hydrocortisone; (B) 1 week after treatment regime with topical hydrocortisone acetate 0.25% solution.
Case 1.
Notes: (A) Hypergranulation tissue to the left dorsum prior to treatment with topical hydrocortisone; (B) 3 weeks after treatment regime with topical hydrocortisone acetate 0.25% solution.
Discussion
In this case series, we aimed to examine the feasibility and document the use of topical hydrocortisone in the treatment of hypergranulation tissue formation resulting from burn wounds. The use of topical steroids to treat hypergranulation tissue has been reported in the nonburn literature, demonstrating improved wound healing rates., Topical steroids have been reported to reduce the inflammatory process that is thought to contribute to the development of problematic hypergranulation tissue., However, limited data currently exist concerning the application of topical steroids to wounds displaying a chronic inflammatory response. Furthermore, we could only find one small study that focused on the use of topical steroids for the treatment of hypergranulation tissue in burns.9 Consequently, clinicians remain reluctant to use topical corticosteroids on wounds despite the reduction in pain experienced and stimulation of the wound healing trajectory. This reluctance has been related to concerns around impairment of wound healing and infection.
For a wound displaying a prolonged inflammation as described in this case series, the use of a topical steroid would be a valid method for the treatment of hypergranulation evident in burn wounds. Shalom and Wong9 who used 1% hydrocortisone twice a day on burns/plastic surgery patients with hypergranulation tissue unresponsive to standard treatment, achieved complete epithelialization of treated areas within 2–4 weeks. Hofman et al also found the use of topical steroids (Dermovate, London, UK) effective when applied onto hypergranulated tissue over a 2-week period that resulted in a rapid reduction of wound size and immediate pain relief. McShame and Bellet reported, similar to a patient in our case series (case 5), hypergranulated tissue to the parietal scalp of a child. After the application of a topical steroid (fluocinonide 0.05% ointment) twice daily for a 2-week period, significant improvements were noted and the treatment discontinued. Examination at 2 months showed complete resolution of the hypergranulated tissue. It is also interesting to note that the scalp surgical wounds appear to have a propensity for the development of hypergranulation tissue., This concurs with our experience suggesting that the scalp may be particularly predisposed to excessive granulation tissue.
In this case series, we describe a noninvasive, inexpensive technique for the management of hypergranulative tissue that was well tolerated by the patients presented. However, this case series is not without its limitations concerning both the design and sample size of five participants. Nonetheless, the aim of this case series was to report and demonstrate our Burn Centre’s usual practice in the treatment of hypergranulation tissue. Therefore, we believe that further investigation of the use of topical steroids in the treatment of hypergranulation in burns is warranted.
At the time this case series was reported, there was only one other small study describing the management of hypergranulation tissue in burn patients within the literature.9 We strongly believe that the use of topical hydrocortisone is a viable option to achieve hypergranulation regression and wound closure by reducing the granulation tissue in both the burn wound and within the graft. However, qualitative and nonquantitative end points were defined, and further studies are required to validate our findings and to quantify its effect. Importantly, the method reported in this case series needs to be compared to other current treatment modalities in terms of efficacy, toxicity, and cost-effectiveness in the management of hypergranulating burn wounds.
Footnotes
Disclosure
The authors report no conflicts of interest in this work.
References
Scar | |
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Scar tissue on an arm | |
Specialty | Dermatology, plastic surgery |
A scar is an area of fibrous tissue that replaces normal skin after an injury. Scars result from the biological process of wound repair in the skin, as well as in other organs and tissues of the body. Thus, scarring is a natural part of the healing process. With the exception of very minor lesions, every wound (e.g., after accident, disease, or surgery) results in some degree of scarring. An exception to this are animals with complete regeneration, which regrow tissue without scar formation.
Scar tissue is composed of the same protein (collagen) as the tissue that it replaces, but the fiber composition of the protein is different; instead of a random basketweave formation of the collagen fibers found in normal tissue, in fibrosis the collagen cross-links and forms a pronounced alignment in a single direction.[1] This collagen scar tissue alignment is usually of inferior functional quality to the normal collagen randomised alignment. For example, scars in the skin are less resistant to ultraviolet radiation, and sweat glands and hair follicles do not grow back within scar tissues.[2] A myocardial infarction, commonly known as a heart attack, causes scar formation in the heart muscle, which leads to loss of muscular power and possibly heart failure. However, there are some tissues (e.g. bone) that can heal without any structural or functional deterioration.
- 1Types
- 2Pathophysiology
- 2.1Collagen synthesis
- 2.1.1Fibroblasts
- 2.1Collagen synthesis
- 3Treatment
- 4Society and culture
Types[edit]
All scarring is composed of the same collagen as the tissue it has replaced, but the composition of the scar tissue, compared to the normal tissue, is different.[1] Scar tissue also lacks elasticity[3] unlike normal tissue which distributes fiber elasticity. Scars differ in the amounts of collagen overexpressed. Labels have been applied to the differences in overexpression. Two of the most common types are hypertrophic and keloid scarring,[4] both of which experience excessive stiff collagen bundled growth overextending the tissue, blocking off regeneration of tissues. Another form is atrophic scarring (sunken scarring), which also has an overexpression of collagen blocking regeneration. This scar type is sunken, because the collagen bundles do not overextend the tissue. Stretch marks (striae) are regarded as scars by some.
High melanin levels and either African or Asian ancestry may make adverse scarring more noticeable.[5]
Hypertrophic[edit]
Hypertrophic scars occur when the body overproduces collagen, which causes the scar to be raised above the surrounding skin. Hypertrophic scars take the form of a red raised lump on the skin. They usually occur within 4 to 8 weeks following wound infection or wound closure with excess tension and/or other traumatic skin injuries.[4]
Keloid[edit]
Keloid scars are a more serious form of excessive scarring, because they can grow indefinitely into large, tumorous (although benign) neoplasms.[4]
Hypertrophic scars are often distinguished from keloid scars by their lack of growth outside the original wound area, but this commonly taught distinction can lead to confusion.[6]
Keloid scars can occur on anyone, but they are most common in dark-skinned people.[7] They can be caused by surgery, accident, acne or, sometimes, body piercings. In some people, keloid scars form spontaneously. Although they can be a cosmetic problem, keloid scars are only inert masses of collagen and therefore completely harmless and not cancerous. However, they can be itchy or painful in some individuals. They tend to be most common on the shoulders and chest. Hypertrophic scars and keloids tend to be more common in wounds closed by secondary intention.[8] Surgical removal of keloid is risky and may excerbate the condition and worsening of the keloid.
Atrophic[edit]
An atrophic scar takes the form of a sunken recess in the skin, which has a pitted appearance. These are caused when underlying structures supporting the skin, such as fat or muscle, are lost. This type of scarring is often associated with acne,[9][10]chickenpox, other diseases (especially Staphylococcus infection), surgery, certain insect and spider bites, or accidents. It can also be caused by a genetic connective tissue disorder, such as Ehlers–Danlos syndrome.[11]
Stretch marks[edit]
Stretch marks (technically called striae) are also a form of scarring. These are caused when the skin is stretched rapidly (for instance during pregnancy,[12] significant weight gain, or adolescent growth spurts),[13] or when skin is put under tension during the healing process, (usually near joints). This type of scar usually improves in appearance after a few years.[12]
Elevated corticosteroid levels are implicated in striae development.[14]
Umbilical[edit]
Humans and other placental mammals have an umbilical scar (commonly referred to as to a navel) which starts to heal when the umbilical cord is cut after birth. Egg-laying animals have an umbilical scar which, depending on the species, may remain visible for life or disappear within a few days after birth.[15][16]
Pathophysiology[edit]
A scar is the product of the body's repair mechanism after tissue injury. If a wound heals quickly within two weeks with new formation of skin, minimal collagen will be deposited and no scar will form.[17] When the extracellular matrix senses elevated mechanical stress loading, tissue will scar,[18] and scars can be limited by stress shielding wounds.[18] Small full thickness wounds under 2mm reepithilize fast and heal scar free.[19][20] Deep second-degree burns heal with scarring and hair loss.[2] Sweat glands do not form in scar tissue, which impairs the regulation of body temperature.[21] Elastic fibers are generally not detected in scar tissue younger than 3 months old.[22] In scars rete pegs are lost;[23] through a lack of rete pegs scars tend to shear easier than normal tissue.[23]
The endometrium, the inner lining of the uterus, is the only adult tissue to undergo rapid cyclic shedding and regeneration without scarring; shedding and restoring roughly inside a 7-day window on a monthly basis.[24] All other adult tissues, upon rapid shedding or injury, can scar.
Prolonged inflammation, as well as the fibroblast proliferation[25] can occur. Redness that often follows an injury to the skin is not a scar, and is generally not permanent (see wound healing). The time it takes for this redness to dissipate may, however, range from a few days to, in some serious and rare cases, a few years.[citation needed]
Scars form differently based on the location of the injury on the body and the age of the person who was injured.[citation needed]
The worse the initial damage is, the worse the scar will generally be.[citation needed]
Skin scars occur when the dermis (the deep, thick layer of skin) is damaged. Most skin scars are flat and leave a trace of the original injury that caused them.[citation needed]
Wounds allowed to heal secondarily tend to scar worse than wounds from primary closure.[8]
Collagen synthesis[edit]
Any injury does not become a scar until the wound has completely healed; this can take many months, or years in the worst pathological cases, such as keloids. To begin to patch the damage, a clot is created; the clot is the beginning process that results in a provisional matrix. In the process, the first layer is a provisional matrix and is not scar. Over time, the wounded body tissue then overexpresses collagen inside the provisional matrix to create a collagen matrix. This collagen overexpression continues and crosslinks the fiber arrangement inside the collagen matrix, making the collagen dense. This densely packed collagen, morphing into an inelastic whitish collagen[25] scar wall, blocks off cell communication and regeneration; as a result, the new tissue generated will have a different texture and quality than the surrounding unwounded tissue. This prolonged collagen-producing process results in a fortuna scar.
Fibroblasts[edit]
The scarring is created by fibroblast proliferation,[25] a process that begins with a reaction to the clot.[26]
To mend the damage, fibroblasts slowly form the collagen scar. The fibroblast proliferation is circular[26] and cyclically, the fibroblast proliferation lays down thick, whitish collagen[25] inside the provisional and collagen matrix, resulting in the abundant production of packed collagen on the fibers[25][26] giving scars their uneven texture. Over time, the fibroblasts continue to crawl around the matrix, adjusting more fibers and, in the process, the scarring settles and becomes stiff.[26] This fibroblast proliferation also contracts the tissue.[26] In unwounded tissue, these fibers are not overexpressed with thick collagen and do not contract.
Myofibroblast[edit]
Mammalian wounds that involve the dermis of the skin heal by repair not regeneration (except in 1st trimester inter-uterine wounds and in the regeneration of deer antlers). Full thickness wounds heal by a combination of wound contracture and edge re-epitheliasation. Partial thickness wounds heal by edge re-epithelialisation and epidermal migration from adnexal structures (hair follicles, sweat glands and sebaceous glands. The site of keratinocyte stem cells remains unknown but stem cells are likely to reside in the basal layer of the epidermis and below the bulge area of hair follicles.
The fibroblast involved in scarring and contraction is the myofibroblast,[27] which is a specialized contractile fibroblast.[28] These cells express α-smooth muscle actin (α-SMA).[19]
The myofibroblasts are absent in the first trimester in the embryonic stage where damage heals scar free;[19] in small incisional or excision wounds less than 2 mm that also heal without scarring;[19] and in adult unwounded tissues where the fibroblast in itself is arrested; however, the myofibroblast is found in massive numbers in adult wound healing which heals with a scar.[28]
The myofibroblasts make up a high proportion of the fibroblasts proliferating in the postembryonic wound at the onset of healing. In the rat model, for instance, myofibroblasts can constitute up to 70% of the fibroblasts,[27] and is responsible for fibrosis on tissue.[29]
Generally, the myofibroblasts disappear from the wound within 30 days,[30] but can stay around in pathological cases in hypertrophy, such as keloids.[28][30] Myofibroblasts have plasticity and in mice can be transformed into fat cells, instead of scar tissue, via the regeneration of hair follicles.[31][32]
Treatment[edit]
Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows.[33] As of 2014 no prescription drugs for the treatment or prevention of scars were available.[34]
Chemical peels[edit]
Chemical peels are chemicals which destroy the epidermis in a controlled manner, leading to exfoliation and the alleviation of certain skin conditions, including superficial acne scars.[35] Various chemicals can be used depending upon the depth of the peel, and caution should be used, particularly for dark-skinned individuals and those individuals susceptible to keloid formation or with active infections.[36]
Filler injections[edit]
Filler injections of collagen can be used to raise atrophic scars to the level of surrounding skin.[37] Risks vary based upon the filler used, and can include further disfigurement and allergic reaction.[38]
Laser treatment[edit]
Nonablative lasers, such as the 585 nm pulsed dye laser, 1064 nm and 1320 nm Nd:YAG, or the 1540 nm Er:Glass are used as laser therapy for hypertrophic scars and keloids.[39] There is tentative evidence for burn scars that they improve the appearance.[40][41]
Ablative lasers such as the carbon dioxide laser (CO2) or Er:YAG offer the best results for atrophic and acne scars.[42] Like dermabrasion, ablative lasers work by destroying the dermis to a certain depth. Healing times for ablative therapy are much longer and the risk profile is greater compared to nonablative therapy; however, nonablative therapy offers only minor improvements in cosmetic appearance of atrophic and acne scars.[39]Combination laser therapy and microneedling may offer superior results to single modality treatment. The biggest recent advance in scar management is the use of fractionated CO2 laser and immediate application of topical steroid (Triamcinolone).
Radiotherapy[edit]
Low-dose, superficial radiotherapy is sometimes used to prevent recurrence of severe keloid and hypertrophic scarring. It is thought to be effective despite a lack of clinical trials, but only used in extreme cases due to the perceived risk of long-term side effects.[43]
Dressings & topical silicone[edit]
Silicone scar treatments are commonly used in preventing scar formation and improving existing scar appearance.[44] A meta-study by the Cochrane collaboration found weak evidence that silicone gel sheeting helps prevent scarring.[45] However, the studies examining it were of poor quality and susceptible to bias.[45]
Pressure dressings are commonly used in managing burn and hypertrophic scars, although supporting evidence is lacking.[46] Care providers commonly report improvements, however, and pressure therapy has been effective in treating ear keloids.[46] The general acceptance of the treatment as effective may prevent it from being further studied in clinical trials.[46]
Steroids[edit]
A long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.[47]
Topical steroids are ineffective.[48] However, clobetasol propionate can be used as an alternative treatment for keloid scars.[49]
Topical steroid applied immediately after fractionated CO2 laser treatment is however very effective (and more efficacious than laser treatment alone) and has shown benefit in numerous clinical studies.
Surgery[edit]
Scar revision is a process of cutting the scar tissue out. After the excision, the new wound is usually closed up to heal by primary intention, instead of secondary intention. Deeper cuts need a multilayered closure to heal optimally, otherwise depressed or dented scars can result.[50]
Surgical excision of hypertrophic or keloid scars is often associated to other methods, such as pressotherapy or silicone gel sheeting. Lone excision of keloid scars, however, shows a recurrence rate close to 45%. A clinical study is currently ongoing to assess the benefits of a treatment combining surgery and laser-assisted healing in hypertrophic or keloid scars.
Subcision is a process used to treat deep rolling scars left behind by acne or other skin diseases. It is also used to lessen the appearance of severe glabella lines, though its effectiveness in this application is debatable. Essentially the process involves separating the skin tissue in the affected area from the deeper scar tissue. This allows the blood to pool under the affected area, eventually causing the deep rolling scar to level off with the rest of the skin area. Once the skin has leveled, treatments such as laser resurfacing, microdermabrasion or chemical peels can be used to smooth out the scarred tissue.[citation needed]
Vitamins[edit]
Research shows the use of vitamin E and onion extract (sold as Mederma) as treatments for scars is ineffective.[46] Vitamin E causes contact dermatitis in up to 33% of users and in some cases it may worsen scar appearance and could cause minor skin irritations,[48] but Vitamin C and some of its esters fade the dark pigment associated with some scars.[51]
Other[edit]
- Cosmetics; Medical makeup can temporarily conceal scars.[52] This is most commonly used for facial scars.
- Dermabrasion involves the removal of the surface of the skin with special equipment, and usually involves a local anaesthetic.
- Massage has weak evidence of efficacy in scar management. Any beneficial effect appears to be greater in wounds created by surgical incision than traumatic wounds or burn wounds.[53]
- Microneedling[54]
Society and culture[edit]
Intentional scarring[edit]
The permanence of scarring has led to its intentional use as a form of body art within some cultures and subcultures. These forms of ritual and non-ritual scarring practices can be found in many groups and cultures around the world.
Etymology[edit]
First attested in English in the late 14th century, the word scar derives from a conflation of Old Frenchescharre, from Late Latineschara,[55] which is the latinisation of the Greek ἐσχάρα (eskhara), meaning 'hearth, fireplace', but in medicine 'scab, eschar on a wound caused by burning or otherwise,[56][57] and Middle Englishskar ('cut, crack, incision'), which is from Old Norseskarð ('notch, gap').[57] The conflation helped to form the English meaning. Compare Scarborough for evolution of skarð to scar.
Research[edit]
An intradermal injection of transforming growth factor beta 3 (TGFβ3) is being tested. The results of three trials already completed were published in the Lancet along with an editorial commentary.[58][59] Another variation under research is a silk-derived sericinhydrogel dressing.[60]
A study implicated the protein ribosomal s6 kinase (RSK) in the formation of scar tissue and found the introduction of a chemical to counteract RSK could halt the formation of cirrhosis. This treatment also has the potential to reduce or even prevent altogether other types of scarring.[61]
Research has also implicated osteopontin in scarring.[62][63]
References[edit]
- ^ abSherratt, Jonathan A. (2010). 'Mathematical Modelling of Scar Tissue Formation'. Department of Mathematics, Heriot-Watt University. Retrieved 20 August 2010.
This is composed of the same main protein (collagen) as normal skin, but with differences in details of composition. Most crucially, the protein fibres in normal tissue have a random (basketweave) appearance, while those in scar tissue have pronounced alignment in a single direction.
- ^ abJohn Kraft; Charles Lynde, MD, FRCPC. 'Giving Burns the First, Second and Third Degree - Classification of burns'. skincareguide.ca. Retrieved 31 January 2012.
Formation of a thick eschar, slow healing (>1month), Obvious scarring, hair loss.
CS1 maint: Multiple names: authors list (link) - ^A. Bernard Ackerman, MD, Almut Böer, MD, Bruce Bennin, MD, Geoffrey J. Gottlieb, MD (January 2005). Histologic Diagnosis of Inflammatory Skin Diseases An Algorithmic Method Based on Pattern Analysis: Embryologic, Histologic, and Anatomic Aspects: Elastic Fibers (Third ed.). Ardor Scribendi. p. 522. ISBN9781893357259.CS1 maint: Multiple names: authors list (link)
- ^ abcGauglitz, Gerd; Korting, Hans (2011). 'Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies'. Molecular Medicine. 17 (1–2): 113–25. doi:10.2119/molmed.2009.00153. PMC3022978. PMID20927486.
- ^Kelly, A. Paul (2009). 'Update on the Management of Keloids'. Seminars in Cutaneous Medicine and Surgery. 28 (2): 71–76. doi:10.1016/j.sder.2009.04.002. PMID19608056.
- ^Roseborough IE, Grevious MA, Lee RC (January 2004). 'Prevention and treatment of excessive dermal scarring'. J Natl Med Assoc. 96 (1): 108–16. PMC2594768. PMID14746360.
- ^Martini, Frederic H. (2006). Fundamentals of Anatomy & Physiology, Seventh Edition, p. 171. Benjamin Cummings, San Francisco.
- ^ ab'Practical Plastic Surgery for Nonsurgeons - Secondary Wound Closure - Scarring'(PDF). Archived from the original(PDF) on 26 August 2016. Retrieved 11 January 2017.
Wounds that are allowed to heal secondarily tend to have larger and more noticeable scars than the scars that results from primary closure. Secondary healing also has a greater tendency for hypertrophic scar/keloid formation. (page 86)
- ^Goodman GJ (2000). 'Postacne scarring: A review of its pathophysiology and treatment'. Dermatologic Surgery. 26 (9): 857–871. doi:10.1046/j.1524-4725.2000.99232.x. PMID10971560.
- ^Fabbrocini G, Annunziata MC, D'Arco V, De Vita V, Lodi G, Mauriello MC, Pastore F, Monfrecola G (2010). 'Acne Scars: Pathogenesis, Classification and Treatment'. Dermatology Research and Practice. 2010: 1–13. doi:10.1155/2010/893080. PMC2958495. PMID20981308.
- ^'Clinical manifestations and diagnosis of Ehlers-Danlos syndromes'. www.uptodate.com. Retrieved 15 June 2017.
- ^ abBrennan, Miriam; Young, Gavin; Devane, Declan (14 November 2012). 'Topical preparations for preventing stretch marks in pregnancy'. The Cochrane Database of Systematic Reviews. 11: CD000066. doi:10.1002/14651858.CD000066.pub2. ISSN1469-493X. PMID23152199.
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Healing in 2 weeks – minimal to no scar; Healing in 3 weeks – minimal to no scar except in high risk scar formers;Healing in 4 weeks or more – hypertrophic in more than 50% of patients
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These cells, which differentiate from the unwounded tissue cell type (fibroblasts), are responsible for laying down scar tissue. Indeed myofibroblasts remain present in hypertrophic scars up to four years after the original wounding event. An in vitro assay was accordingly developed to identify actives which prevent or reduce myofibroblast formation and thus identify actives which are effective in reducing and/or preventing scar tissue formation.
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the number of myofibroblasts present in the forming scar tissue begins to reduce via apoptosis, until by about 30 days no myofibroblasts are obvious within the scar.
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Deep cuts need multi-layered closure to heal optimally; otherwise, depressed or dented scars can result
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![Hypertrophic Granulation Tissue Hypertrophic Granulation Tissue](https://www.dovepress.com/cr_data/article_submission_image/s113000/113182/113182%20revised%20figure%20390.jpg)
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