Scar

Scar
Other names	Cicatrix
Scar tissue on an arm
Specialty	Dermatology, plastic surgery

A scar (or scar tissue) is an area of

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

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.

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

Stretch marks (technically called striae) are also a form of scarring. These are caused when the skin is stretched rapidly (for instance during

Elevated corticosteroid levels are implicated in striae development.^[14]

Umbilical

Humans and other

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 reepithelize 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.^{[26][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

An 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

The scarring is created by fibroblast proliferation,^[25] a process that begins with a reaction to the clot.^[27] To mend the damage, fibroblasts slowly form the collagen scar. The fibroblast proliferation is circular^[27] 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][27] 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.^[27] This fibroblast proliferation also contracts the tissue.^[27] In unwounded tissue, these fibers are not overexpressed with thick collagen and do not contract.

EPF and ENF fibroblasts have been genetically traced with the Engrailed-1 genetic marker.^[28] EPFs are the primary contributors to all fibrotic outcomes after wounding.^[28] ENFs do not contribute to fibrotic outcomes.^[28][29]

Myofibroblast

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,^[30] which is a specialized contractile fibroblast.^[31] 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.^[31]

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,^[30] and is responsible for fibrosis on tissue.^[32] Generally, the myofibroblasts disappear from the wound within 30 days,^[33] but can remain in pathological cases in hypertrophy, such as keloids.^[31][33] Myofibroblasts have plasticity and in mice can be transformed into fat cells, instead of scar tissue, via the regeneration of hair follicles.^[34][35]

Mechanical stress

Wounds under 2mm generally do not scar^[19][20] but larger wounds generally do scar.^[19][20] In 2011 it was found that mechanical stress can stimulate scarring^[18] and that stress shielding can reduce scarring in wounds.^[18][36] In 2021 it was found that using chemicals to manipulate fibroblasts to not sense mechanical stress brought scar-free healing.^[37] The scar-free healing also occurred when mechanical stress was placed onto a wound.^[37]

Treatment

Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows.^[38] In 2004, no prescription drugs for the treatment or prevention of scars were available.^[39]

Chemical peels

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.^[40] 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.^[41]

Filler injections

Filler injections of

Silicone scar treatments are commonly used in preventing scar formation and improving existing scar appearance.[51] A meta-study by the Cochrane collaboration found weak evidence that silicone gel sheeting helps prevent scarring.^[52] However, the studies examining it were of poor quality and susceptible to bias.^[52]

Verapamil, a type of calcium channel blocker, is considered a candidate drug for the treatment of hypertrophic scars. A study conducted by the Catholic University of Korea concluded that verapamil-releasing silicone gel is effective and is a superior alternative to the conventional silicone gel where decreased median SEI, fibroblast count, and collagen density in all verapamil-added treatment groups were observed.^{[54]: 647–656} Gross morphologic features suggested that the combination of verapamil and silicone improves the overall quality of hypertrophic scars by reducing scar height and redness. This was verified with quantifiable histomorphometric parameters; however, oral verapamil is not a good choice because of its effect of lowering blood pressure. Intralesional injection of verapamil is also suboptimal because of the required frequency for injections. Topical silicone gel combined with verapamil does not lead to systemic hypotension, is convenient to apply, and shows enhanced results.^{[54]: 647–656}

Steroids

A long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.^[55]

Topical steroids are ineffective.^[56] However, clobetasol propionate can be used as an alternative treatment for keloid scars.^[57]

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

Scar revision is a process of cutting the scar tissue out. After the excision, the new wound is usually closed up to heal by

• Cosmetics; Medical makeup can temporarily conceal scars.[61] This is most commonly used for facial scars.
• 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.^[62]
• Microneedling^[63]

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

First attested in English in the late 14th century, the word scar derives from a conflation of

Research, before 2009, focused on scar improvements with research in to molecular mechanisms. Molecular mechanisms such as: juvista,[67]^[68] ribosomal s6 kinase (RSK),^[69] and osteopontin^[70][71] were investigated. In 2011, the scientific literature highlighted stress shielding a fresh wound through the wound healing process, brings significant scar improvement and smaller scars.^[18][36]

Prevention

By 2016, skin had been regenerated in vivo, and in vitro and scar free healing had been operationalized and induced by four main techniques: regeneration by instrument; regeneration by materials; regeneration by drugs; and regeneration by in vitro 3-D printing. In 2018, a silk-derived sericin hydrogel dressing was undergoing research, the material was shown to prevent scar formation.^[72] By 2021, more people were paying attention to the possibility of scar revision alongside new technologies.^[73]

References

External links

Wikimedia Commons has media related to Scars.

• WebMd.com: Skin Scars Directory (archived 21 September 2017)
• American Academy of Dermatology: What is a scar? Archived 21 November 2018 at the Wayback Machine