Scars are areas of fibrous tissue 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 results in some degree of scarring. An exception to this is animals with regeneration, which do not form scars and the tissue will grow back exactly as before.

Scar tissue is the exact same protein (collagen) as the tissue that it replaces, but the fiber composition of the protein is different; instead of a random basket weave formation of the collagen fibers found in normal tissue, in fibrosis the collagen crosslinks and forms a pronounced alignment in a single direction. 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. 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.

If a wound becomes covered with epithelial tissue within two weeks, minimal collagen will be deposited and no scar will form. Generally, if a wound takes longer than three to four weeks to become covered, a scar will form. Deep second-degree burns heal with scarring and hair loss. Sweat glands do not form in scar tissue, which impairs the regulation of body temperature.

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 over expresses collagen inside the provisional matrix to create a collagen matrix. This collagen over expression continues and crosslinks the fiber arrangement inside the collagen matrix, making the collagen dense. This densely packed collagen, morphing into an inelastic whitish collagen 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, a process that begins with a reaction to the clot.

To mend the damage, fibroblasts slowly form the collagen scar. The fibroblast proliferation is circular and cyclically, the fibroblast proliferation lays down thick, whitish collagen inside the provisional and collagen matrix, resulting in the abundant production of packed collagen on the fibers 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. This fibroblast proliferation also contracts the tissue. In unwounded tissue, these fibers are not over expressed with thick collagen and do not contract.

The fibroblast involved in scarring and contraction is the myofibroblast, which is a specialized contractile fibroblast. These cells express a-smooth muscle actin (a-SMA).

The myofibroblasts are absent in the first trimester in the embryonic stage; damage then heals scar free; small incisional or excision wounds less than 2 mm also heal without scarring; 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. 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, and is responsible for fibrosis on tissue. Generally, the myofibroblasts disappear from the wound within 30 days, but can stay around in pathological cases in hypertrophy, such as keloids.

Prolonged inflammation, as well as the fibroblast proliferation 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.

Scars form differently based on the location of the injury on the body and the age of the person who was injured. The worse the initial damage is, the worse the scar will generally be.

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.

Wounds allowed to heal secondarily tend to scar worse than wounds from primary closure.

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. 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, 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.

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.

Keloid scars are a more serious form of hypertrophic scarring, because they can grow indefinitely into large, tumorous (although benign) neoplasms. 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. Keloid scars are all hypertrophic, but “only a small percentage of hypertrophic scars” are keloid.

Keloid scars can occur on anyone, but they are most common in dark-skinned people. 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 shouldersand chest. Hypertrophic scars and its subset keloids tend to be more common in wounds closed by secondary intention.

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, 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, significant weight gain, or adolescent growth spurts), 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.

Elevated corticosteroid levels are implicated in striae development.

Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows. High melanin levels and either African or Asian ancestry may make adverse scarring more noticeable. As of 2004 no prescription drugs for the treatment or prevention of scars were available.

Collagen induction therapy (CIT) is an aesthetic medical procedure that involves repeatedly puncturing the skin with tiny, sterile needles. Typically, this is done with a specialized device called a microneedling device. CIT is often referred to as “microneedling” or “skin needling” in media and literature.

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. 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.

Filler injections of collagen or Artefill can be used to raise atrophic scars to the level of surrounding skin. Risks vary based upon the filler used, and can include temporary improvement, further disfigurement, and allergic reaction.

Dermabrasion involves the removal of the surface of the skin with special equipment, and usually involves a local anaesthetic.

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 the standard laser therapy for hypertrophic scars and keloids. 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. 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.

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.

Silicone scar treatments are commonly used in preventing scar formation and improving existing scar appearance. The effectiveness and safety of silicone sheeting for the treatment and prevention of scars is supported by an abundance of clinical studies.

Semiocclusive, silicone-based ointments are used to speed healing and reduce the appearance of scars, and likely work in a similar manner as silicone scar sheets.

Pressure dressings are commonly used in managing burn and hypertrophic scars, although supporting evidence is lacking. These involve elastic materials or gauze to apply pressure to the area. For large scars and particularly large burns, pressure garments may be worn. They are believed to work by applying constant pressure to surface blood vessels, and eventually causing scars to flatten and become softer. Retrospective and ultrasonic studies since the 1960s have supported their use, but the only randomized clinical trial found no statistically significant difference in wound healing. Care providers commonly report improvements, however, and pressure therapy has been effective in treating ear keloids. The general acceptance of the treatment as effective may prevent it from being further studied in clinical trials.

Under medical supervision, a long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.

The steroid is injected into the scar itself; since very little is absorbed into the blood stream, side effects of this treatment are minor. However, it does cause thinning of the scar tissue so it does carry risks when injected into scars caused by operations into ruptured tendons. This treatment is repeated at four- to six-week intervals.

Topical steroids are ineffective.

Scar revision is a process of cutting the scar tissue out. After the excision, the new wound is usually closed up to heal byprimary intention, instead of secondary intention. Deeper cuts need a multilayered closure to heal optimally, otherwise depressed or dented scars can result.

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.

Research shows the use of vitamin E and onion extract (sold as Mederma) as treatments for scars is ineffective. Vitamin E causes contact dermatitis in up to 33% of users and in some cases it may worsen scar appearance. But Vitamin C and some of its esters fade the dark pigment associated with some scars.

dermatitis [,dɜːmə'taitis] n.皮炎

dissipate ['disipeit] v.消散

exfoliation [eks,fəuli'eiʃən] n.表皮脱落

hypertrophic [,haipə'trɔfk] adj.肥厚的

melanin ['melənin] n.黑色素

neoplasm ['niːə(ʊ)plæz(ə)m] n.肿瘤

nonablative [nʌn'æblətiv] adj.非剥离性

striae [st'raiiː] n.条纹

sunken ['sʌŋkən] adj.凹陷的

allergic reaction 变态反应

atrophic scars 萎缩性瘢痕

collagen matrix 胶原基质

epithelial tissue 上皮组织

hair follicles 毛囊

hypertrophic scars 增生性瘢痕

keloid scars 瘢痕疙瘩

myocardial infarction 心肌梗死

sweat glands 汗腺

sunken scarring 凹陷性瘢痕

ultraviolet radiation 紫外辐射