A scar (or scar tissue) 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 and other body organs and tissues. Thus, scarring is a natural part of the healing process, except for minor lesions; every wound (e.g., after an accident, disease, or surgery) results in some scarring. An exception to this is 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. This collagen scar tissue alignment is usually of inferior functional quality to the normal collagen randomized 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. In addition, 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, some tissues (e.g., bone) can heal without 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. Scar tissue also lacks elasticity, unlike normal tissue, which distributes fiber elasticity. As a result, scars differ in the amounts of collagen overexpressed. 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 the regeneration of tissues. Another form is atrophic scarring (sunken scarring), which also overexpresses collagen-blocking renewal. This scar type is hollow because the collagen bundles do not overextend the tissue. Finally, stretch marks (striae) are scars by some.
High melanin levels and either African or Asian ancestry may make adverse scarring more noticeable.
Hypertrophic scars occur when the body overproduces collagen, which causes the spot to rise above the surrounding skin. Hypertrophic scars take the form of a red raised lump on the skin for lighter-pigmented skin and a state of dark brown for darker-pigmented skin. They usually occur within 4 to 8 weeks following wound infection or closure with excess tension and other traumatic skin injuries.
Keloid scars are a more severe form of excessive 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 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 shoulders and chest. Hypertrophic scars and keloids tend to be more common in wounds closed by secondary intention. Surgical removal of the keloid is risky and may exacerbate the condition and worsening of the keloid.
An atrophic scar forms 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 infection), surgery, particular insect and spider bites, or accidents. In addition, atrophic scars are possible by a genetic connective tissue disorder, such as Ehlers–Danlos syndrome.
Stretch marks (technically called striae) are also a form of scarring. Formation happens when the skin is stretched rapidly (for instance, during pregnancy, significant weight gain, or adolescent growth spurts) or when the skin is under tension during the healing process (usually near joints). This type of scar usually improves in appearance after a few years.
Elevated corticosteroid levels implicate striae development.
Humans and other placental mammals have an umbilical scar (commonly called a navel) that starts to heal after cutting the umbilical cord after birth. In addition, egg-laying animals have an umbilical scar that may remain visible for life, depending on the species, or disappear within a few days after birth.
Key processes contributing to the quasi-neoplastic expression of keloid pathobiology.
A scar is the product of the body's repair mechanism after tissue injury. If a wound heals quickly within two weeks with a new formation of skin, minimal collagen will deposit, and no scar will form. When the extracellular matrix senses elevated mechanical stress loading, the tissue will scar, and stress-shielding wounds can limit scars. Minor full-thickness wounds under 2mm epithelize fast and heal scar free. Deep second-degree burns heal with scarring and hair loss. Sweat glands do not form in scar tissue, which impairs body temperature regulation.
Elastic fibers are generally not detected in scar tissue younger than three months old. In scars, rete pegs lose presence; due to the lack of rete pegs, scars tend to shear easier than normal tissue.
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 every month. All other adult tissues, upon rapid shedding or injury, can scar.
Prolonged inflammation, as well as 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). However, the time it takes for this redness to dissipate may range from a few days to a few years in some severe and rare cases.
Scars form differently based on the location of the injury on the body and the injured person's age.
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.
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. In order to patch the damage, a clot is created; this clot is the beginning process that results in a provisional matrix. In the process, the first layer is a provisional matrix and is not scared. 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 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.
Fibroblast proliferation is the process of forming scars, which begins with a reaction to the clot. To mend the damage, fibroblasts slowly form the collagen scar. 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. However, these fibers are not overexpressed with thick collagen in unwounded tissue and do not contract.
EPF and ENF fibroblasts carry a genetic trace with the Engrailed-1 genetic marker. Therefore, EPFs are the primary contributors to all fibrotic outcomes after wounding. EMFs do not contribute to fibrotic outcomes.
Mammalian wounds that involve the skin's dermis heal by repair, not regeneration (except in 1st-trimester inter-uterine wounds and the regeneration of deer antlers). Full-thickness wounds heal by a combination of wound contracture and edge re-epithelialization. Partial thickness wounds heal by edge re-epithelialization 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, a specialized contractile fibroblast. These cells express α-smooth muscle actin (α-SMA). The myofibroblasts are absent in the first trimester in the embryonic stage, where damage heals scar free; in minor incisional or excision wounds less than 2 mm that also heals without scarring; and in adult unwounded tissues where the fibroblast in itself arrest; however, the myofibroblast generate 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 are responsible for fibrosis in tissue. Generally, the myofibroblasts disappear from the wound within 30 days but can stay around in pathological cases of hypertrophy, such as keloids. In addition, myofibroblasts have plasticity and, in mice, can be transformed into fat cells, instead of scar tissue, via the regeneration of hair follicles.
Wounds under 2mm generally do not have a scar; more extensive wounds generally scar. In 2011 it was found that mechanical stress can stimulate scarring and that stress shielding can reduce scarring in wounds. In 2021 it was found that using chemicals to manipulate fibroblasts, not to sense mechanical stress brought scar-free healing. The scar-free healing also occurs when mechanical stress takes place on a wound.
Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows. Unfortunately, in 2004, no prescription drugs for treating or preventing scars were available.
Chemical peels are chemicals that 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 collagen injections raise atrophic scars to the level of surrounding skin. Risks vary based on the filler and can include further disfigurement and allergic reactions.
Nonablative lasers, such as the 585 nm pulsed dye laser, 1064 nm, 1320 nm Nd: YAG, or the 1540 nm Er: Glass, are used as laser therapy for hypertrophic scars and keloids. There is tentative evidence that burns scars improve the appearance. Ablative lasers such as the carbon dioxide laser (CO2) or Er: YAG offer the best results for atrophic and acne scars.
Like dermabrasion, ablative lasers work by removing the epidermis. Healing times for ablative therapy are much longer, and the risk profile is more significant compared to nonablative therapy; however, nonablative therapy offers only minor improvements in the cosmetic appearance of atrophic and acne scars.[ Combination laser therapy and micro-needling may offer superior results to single modality treatment. The most significant recent advance in scar management is the use of fractionated CO2 laser and the immediate application of topical steroid Triamcinolone.
Low-dose, superficial radiotherapy prevents the 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.
Dressings and topical silicone
Silicone scar treatments prevent scar formation and improve existing scar appearance. A meta-study by the Cochrane Collaboration found weak evidence that silicone gel sheeting helps prevent scarring. However, the studies examining it were of poor quality and susceptible to bias.
Pressure dressings are commonly used in managing burn and hypertrophic scars, although supporting evidence is lacking. However, care providers commonly report improvements, and pressure therapy has effectively treated ear keloids. Unfortunately, the general acceptance of the treatment as effective may prevent it from being further studied in clinical trials.
Verapamil-containing silicone gel
Verapamil, a type of calcium channel blocker, is a candidate drug for treating 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 existed. In addition, gross morphologic features suggested that the combination of verapamil and silicone improves the overall quality of hypertrophic scars by reducing scar height and redness—evidence with quantifiable histomorphometric parameters. However, Oral verapamil is not a good choice because it lowers blood pressure. Intralesional injection of verapamil is also suboptimal because of the required injection frequency. On the other hand, topical silicone gel combined with verapamil does not lead to systemic hypotension, is convenient to apply, and shows enhanced results.
A long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.
Topical steroids are ineffective. However, clobetasol propionate is an alternative treatment for keloid scars.
A 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.
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 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 with other methods, such as pressotherapy or silicone gel sheeting. Lone excision of keloid scars, however, shows a recurrence rate close to 45%. Therefore, a clinical study is 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 lessens 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 smooth out the scarred tissue.
Research shows that using 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 and cause minor skin irritations. However, Vitamin C and some of its esters fade the dark pigment associated with some scars.
Cosmetics; Medical makeup can temporarily conceal scars. 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 anesthetic.
Massage has weak evidence of efficacy in scar management. Any beneficial effect is more significant in wounds created by surgical incision than traumatic or burns wounds.
Society and culture
Main article: Scarification
The permanence of scarring has led to its intentional use as a form of body art within some cultures and subcultures. These ritual and non-ritual scarring practices can be found in many groups and cultures worldwide.
First attested in English in the late 14th century, the word scar derives from a conflation of Old French eschar, from Late Latin eschar, which is the Latinisation of the Greek ἐσχάρα (Akshara), meaning "hearth, fireplace," but in medicine "scab, eschar on a wound caused by burning or otherwise," and Middle English skar ("cut, crack, incision"), which is from Old Norse skarð ("notch, gap"). The conflation helped to form the English meaning. Compare Scarborough for the evolution of skarð to scar.
Research before 2009 focused on scar improvements with research into molecular mechanisms. Molecular mechanisms such as Juvista, ribosomal s6 kinase (RSK), and osteopontin were studied. In 2011, the scientific literature highlighted that stress shielding a fresh wound through the wound-healing process brings significant scar improvement and more minor scars.
Main article: Regeneration in Human tissue
By 2016, the skin regenration in vivo. In vitro, scar-free healing has 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 prevents scar formation.