出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/13 04:23:04」(JST)
| Scar | |
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A minor scar from a cut to the forearm, approx. one year since the wound.
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| Classification and external resources | |
| Specialty | Dermatology, plastic surgery |
| ICD-10 | L90.5 |
| MeSH | D002921 |
Scars are areas of fibrous tissue (fibrosis) that replace normal skin after injury. A scar results from the biological process of wound repair in the skin and other 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.
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] Scars differ from other scars 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,[3] 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.[4]
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.[3]
Keloid scars are a more serious form of excessive scarring, because they can grow indefinitely into large, tumorous (although benign) neoplasms.[3]
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.[3]
Keloid scars can occur on anyone, but they are most common in dark-skinned people.[5] 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.[6]
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,[7][8] chickenpox, other diseases [especially Staphylococcus (or MRSA) infection], surgery, or accidents.
Stretch marks (technically called striae) are also a form of scarring. These are caused when the skin is stretched rapidly (for instance during pregnancy,[9] significant weight gain, or adolescent growth spurts),[10] 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.[9]
Elevated corticosteroid levels are implicated in striae development.[11]
| This section may be too technical for most readers to understand. Please help improve this section to make it understandable to non-experts, without removing the technical details. The talk page may contain suggestions. (January 2012) |
If a wound becomes covered with epithelial tissue within two weeks, minimal collagen will be deposited and no scar will form.[12] Generally, if a wound takes longer than three to four weeks to become covered, a scar will form.[12] 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.[13]
The endometrium 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.[14] All other adult tissues, upon rapid shedding or injury, can scar.
The scar is a result of the body's repair mechanism after injury in many tissues.
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[15] 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.
The scarring is created by fibroblast proliferation,[15] a process that begins with a reaction to the clot.[16]
To mend the damage, fibroblasts slowly form the collagen scar. The fibroblast proliferation is circular[17] and cyclically, the fibroblast proliferation lays down thick, whitish collagen[15] inside the provisional and collagen matrix, resulting in the abundant production of packed collagen on the fibers[15][16][18] 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.[19] This fibroblast proliferation also contracts the tissue.[17][20] In unwounded tissue, these fibers are not overexpressed with thick collagen and do not contract.
The fibroblast involved in scarring and contraction is the myofibroblast,[21] which is a specialized contractile fibroblast.[22] These cells express a-smooth muscle actin (a-SMA).[23]
The myofibroblasts are absent in the first trimester in the embryonic stage; damage then heals scar free;[24] small incisional or excision wounds less than 2 mm also heal without scarring;[24] 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.[22]
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,[21] and is responsible for fibrosis on tissue.[25] Generally, the myofibroblasts disappear from the wound within 30 days,[26] but can stay around in pathological cases in hypertrophy, such as keloids.[22][26]
Prolonged inflammation, as well as the fibroblast proliferation[15] 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.[6]
Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows.[27] As of 2014[update] no prescription drugs for the treatment or prevention of scars were available.[28]
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.[29] 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.[30]
Filler injections of collagen can be used to raise atrophic scars to the level of surrounding skin.[31] Risks vary based upon the filler used, and can include further disfigurement and allergic reaction.[32]
Dermabrasion involves the removal of the surface of the skin with special equipment, and usually involves a local anaesthetic.
Nonablative lasers, such as the Starlux Non-ablative FDA approved laser by Palomar, 585 nm pulsed dye laser, 1064 nm and 1320 nm Nd:YAG, or the 1540 nm Er:Glass are used as the standard laser therapy for hypertrophic scars and keloids.[33] This therapy smooths the epidermis via contact cooling. Multiple sessions are usually required for a significant reduction in redness and improvement in the texture and pliability of hypertrophic scars and keloids.
Ablative lasers such as the carbon dioxide laser or Er:YAG offer the best results for atrophic and acne scars.[34] Like dermabrasion, ablative lasers work by destroying the epidermis 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.[33]
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.[35]
Silicone scar treatments are commonly used in preventing scar formation and improving existing scar appearance.[36] A meta-study by the Cochrane collaboration found weak evidence that silicone gel sheeting helps prevent scarring.[37] But the studies examining it were of poor quality and susceptible to bias.[37]
Pressure dressings are commonly used in managing burn and hypertrophic scars, although supporting evidence is lacking.[38] Care providers commonly report improvements, however, and pressure therapy has been effective in treating ear keloids.[38] The general acceptance of the treatment as effective may prevent it from being further studied in clinical trials.[38]
A long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.[39]
Topical steroids are ineffective.[40]
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.[41]
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.[citation needed]
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]
Research shows the use of vitamin E and onion extract (sold as Mederma) as treatments for scars is ineffective.[38] Vitamin E causes contact dermatitis in up to 33% of users and in some cases it may worsen scar appearance.[40] But Vitamin C and some of its esters fade the dark pigment associated with some scars.[42]
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.
First attested in English in the late 14th century CE, the word scar derives from Old French escharre, from Late Latin eschara,[43] 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".[44][45]
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.[46]
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.[47]
Research has also implicated osteopontin in scarring.[48][49]
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.
Formation of a thick eschar, slow healing (>1month), Obvious scarring, hair loss.
<ref> tag; name "Roseborough2004" defined multiple times with different content (see the help page).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)
|chapter= ignored (help)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
In hypertrophic scar tissue, no sweet gland and hair follicle exist usually because of the dermal and epidermal damage in extensive thermal skin injury, thus impairing regulation of body temperature
Importantly, the endometrium is the only adult tissue to undergo rapid cyclic repair without scarring.
As part of the healing process, specialized cells called fibroblasts in adjacent areas of skin produce a fibrous connective tissue made up of collagen. The bundles formed by these whitish, rather inelastic fibres make up the bulk of the scar tissue...
The body launches a complex rescue operation. Specialized cells called fibroblasts lurking just beneath the surface of the skin jump into action, enter the provisional wound matrix (the clot) and start secreting collagen to close the wound as fast as possible.
In the process, it liberates yet more growth factor that in turn stimulates other fibroblasts to become contractile…
The matrix grows stiffer and, at a certain point, the fibroblasts stop migrating and, like Popeye, change into powerful contractile cells, anchoring themselves to the matrix and pulling the edges of the wound together.
myofibroblasts become differentiated from other cells in the wound within a few days after the onset of healing, and in the rat model can reach a peak where about 70% of the fibroblastic cells present are of the myofibroblast phenotype.
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.
Aside from normal fibroblasts, myofibroblasts, specialized contractile fibroblasts, also can contribute to wound repair. These cells express a-smooth muscle actin (a-SMA) and are characterized using transmission electron microscopy by a well-developed rough endoplasmic reticulum, nuclei with irregular borders, secretory vesicles denoting active collagen synthesis, and organized microfilament bundles.
Studies in sheep have indicated that myofibroblasts are absent in early scarless fetal wounds but are present during healing at later stages when prominent scarring occurs. In addition, incisional or small excisional wounds (2 mm) heal without a scar and do not contain myofibroblasts. In contrast, larger excisional wounds that heal with a scar contain strong a-SMA staining, with the number of myofibroblasts correlating with the size of the wound and amount of scarring.
During tissue repair, specialized cells called myofibroblasts migrate to the wound where they generate the adhesive and tensile forces required for wound closure. Normally, these myofibroblasts then disappear from the wound. But if they persist and continue to make connective tissue, it can become too thick, preventing the organ from functioning properly.
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.
Early and effective acne treatment can prevent severe acne and the scarring that often follows
Deep cuts need multi-layered closure to heal optimally; otherwise, depressed or dented scars can result
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| リンク元 | 「線維増殖症」「線維増殖」 |