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Scar
Other namesCicatrix
Scar tissue on an arm
SpecialtyDermatology, plastic surgery

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, 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.

Types

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Man with visible facial scars

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

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Main article: Hypertrophic scars

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 for lighter pigmented skin and the form of dark brown for darker pigmented 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

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Main article: Keloid

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, cuts, 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 exacerbate the condition and worsening of the keloid.

Atrophic

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Atrophic "cigarette paper" scar in Ehlers–Danlos patient

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

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Main article: 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 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

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Humans and other placental mammals have an umbilical scar (commonly referred to as a belly button or 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

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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 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 more severe the initial damage is, the more significant 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 more significantly than wounds from primary closure.[8]

Collagen synthesis

[edit]

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 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 a scar. Over time, the wounded body tissue 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.[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

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

Mechanical stress

[edit]

Wounds under 2 millimeters 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][35] In 2021, it was found that using chemicals to manipulate fibroblasts to not sense mechanical stress brought scar-free healing.[36] The scar-free healing also occurred when mechanical stress was placed onto a wound.[36]

Treatment

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Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows.[37] In 2004, no prescription drugs for the treatment or prevention of scars were available.[38]

Chemical peels

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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.[39] 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.[40]

Filler injections

[edit]

Filler injections of collagen can be used to raise atrophic scars to the level of surrounding skin.[41] Risks vary based upon the filler used, and can include further disfigurement and allergic reaction.[42]

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.[43] There is tentative evidence for burn scars that they improve the appearance.[44][45]

Ablative lasers such as the carbon dioxide laser (CO2) or Er:YAG offer the best results for atrophic and acne scars.[46] Like dermabrasion, ablative lasers work by removing the epidermis.[47][48] 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.[43]

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.[49]

Dressings and topical silicone

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Silicone scar treatments are commonly used in preventing scar formation and improving existing scar appearance.[50] A meta-study by the Cochrane collaboration found weak evidence that silicone gel sheeting helps prevent scarring.[51] However, the studies examining it were of poor quality and susceptible to bias.[51]

Pressure dressings are commonly used in managing burn and hypertrophic scars, although supporting evidence is lacking.[52] Care providers commonly report improvements, however, and pressure therapy has been effective in treating ear keloids.[52] The general acceptance of the treatment as effective may prevent it from being further studied in clinical trials.[52]

Verapamil-containing silicone gel

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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.[53]: 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.[53]: 647–656 

Steroids

[edit]

A long-term course of corticosteroid injections into the scar may help flatten and soften the appearance of keloid or hypertrophic scars.[54]

Topical steroids are ineffective.[55] However, clobetasol propionate can be used as an alternative treatment for keloid scars.[56]

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

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Scarring caused by acne (left), and photo one day after scar revision surgery: The area around sutures is still swollen from 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 primary intention, instead of secondary intention. Deeper cuts need a multilayered closure to heal optimally, otherwise depressed or dented scars can result.[57]

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.[58]

Vitamins

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Research shows the use of vitamin E and onion extract (sold as Mederma) as treatments for scars is ineffective.[52] 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,[55] but Vitamin C and some of its esters fade the dark pigment associated with some scars.[59]

Other

[edit]
  • Cosmetics; Medical makeup can temporarily conceal scars.[60] 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.
  • A 2012 literature review found weak evidence that massage was efficacious in scar management. Any beneficial effect appeared to be greater in wounds created by surgical incision than for traumatic or burn wounds.[61] A 2022 scoping review covering twenty-five studies of 1515 participants reported that all studies reviewed reported favorable outcomes for scar massage, but that "while there may be benefits to scar massage in reducing pain, increasing movement and improving scar characteristics", there was a lack of "consistent research methods, intervention protocols and outcome measures".[62]
  • Microneedling[63]

Society and culture

[edit]

Intentional scarring

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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 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 French escharre, from Late Latin eschara,[64] 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",[65][66] and Middle English skar ("cut, crack, incision"), which is from Old Norse skarð ("notch, gap").[66] The conflation helped to form the English meaning. Compare the place name Scarborough for evolution of skarð to scar.

Research

[edit]
Further information: Scar free healing

Research, before 2009, focused on scar improvements with research into molecular mechanisms. Treatments involving molecular mechanisms including avotermin,[67][68] ribosomal s6 kinase (RSK),[69] and osteopontin[70][71] were investigated at the time. After successful phase I/II trials,[67] human recombinant TGF-β3 (avotermin, planned trade name Juvista) failed in Phase III trials.[72] In 2011, the scientific literature highlighted stress shielding a fresh wound through the wound healing process, brings significant scar improvement and smaller scars.[18][35]

By 2016, skin had been regenerated in vivo and in vitro. and scar-free healing had been operationalized and induced by four main regeneration techniques: by instrument, by materials, by drugs, and 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.[73] By 2021, more people were paying attention to the possibility of scar revision and new technologies.[74]

In 2021, researchers found that, verteporfin, an FDA-approved drug for eye disease, could enable scar-free healing in mice. According to the study, the drug works by blocking mechanical stress signals in fibroblast cells.[75][76][77]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Scar

View on Grokipedia
from Grokipedia
A scar is an area of fibrous tissue that replaces normal after an . It results from the of repair in the skin and other tissues of the body. Scars form when the —a deep layer of —is damaged, leading to the production of by fibroblasts to repair the . While most scars fade over time, taking up to two years or more, they cannot be completely removed and may cause physical or psychological effects depending on their size, location, and type. Common types include hypertrophic, , atrophic, and scars, each with distinct characteristics.

Definition and Formation

Definition

A scar is an area of fibrous that replaces normal following , , or , serving as the body's mechanism to repair damaged tissue. This tissue primarily consists of , a structural protein that forms the , along with fibroblasts and other cells, but it lacks the full complement of such as follicles and sweat glands found in uninjured . Compared to normal , scar tissue exhibits reduced elasticity due to lower levels of and disorganized alignment, resulting in a stiffer, less flexible structure. Normal scars are distinguished from abnormal variants like hypertrophic scars and keloids, which involve excessive deposition leading to raised, thickened tissue. While normal scars remain confined to the boundaries of the original wound and typically flatten over time, hypertrophic scars are elevated but limited to the injury site, and keloids extend beyond it, often continuing to grow. These distinctions highlight that standard scar formation represents a balanced repair process, whereas the abnormal forms reflect dysregulated healing. From an evolutionary perspective, scar tissue evolved to provide rapid protection for underlying tissues and vital organs after injury, prioritizing speed of repair over perfect regeneration to enhance survival in ancestral environments. This fibrotic response, while efficient for immediate wound closure, often results in functional and aesthetic compromises compared to regenerative healing observed in some lower organisms.

Wound Healing Process

The process is a complex, dynamic sequence of events that restores tissue integrity following , typically resulting in scar formation as a functional but structurally altered endpoint. In normal , this process unfolds through four overlapping phases: , , proliferation, and remodeling. These phases are orchestrated by cellular interactions, cytokines, and growth factors to minimize risk and promote tissue repair while limiting excessive . The phase begins immediately upon injury and lasts from minutes to several hours, primarily involving the formation of a blood clot to stop bleeding and provide a provisional matrix for subsequent repair. Platelets aggregate at the site, releasing fibrinogen and other clotting factors to form a clot, which also traps red blood cells and serves as a scaffold. This phase sets the stage for by sealing the and initiating signaling cascades. Following , the inflammation phase occurs over approximately 1 to 4 days, where immune cells clear , pathogens, and damaged tissue to prevent . Neutrophils arrive first within hours, followed by monocytes that differentiate into macrophages, which phagocytose and release pro-inflammatory mediators. This phase is crucial for transitioning to repair but must resolve promptly to avoid prolonged damage. Growth factors such as transforming growth factor-beta (TGF-β) begin to emerge here, modulating the inflammatory response and promoting of repair cells. The proliferation phase, spanning roughly days 4 to 21, focuses on rebuilding the site through the formation of , which consists of new capillaries, , and components. supplies nutrients via new blood vessel growth, while epithelial cells migrate to cover the surface, achieving reepithelialization. deposit to strengthen the tissue, and TGF-β plays a pivotal role by stimulating fibroblast proliferation, synthesis, and overall tissue regeneration during this stage. This phase overlaps with and lays the foundation for scar maturation. The final remodeling or maturation phase extends from about day 21 up to 2 years, involving the reorganization and strengthening of the matrix to enhance tensile strength and functionality. Type III collagen from earlier phases is gradually replaced by stronger through enzymatic cross-linking and degradation of excess matrix by matrix metalloproteinases. TGF-β continues to influence this remodeling by regulating deposition and balancing synthesis with degradation. During the early maturation phase, a reddish or pink appearance in new skin on a healed scar (including burn scars) is normal due to increased blood vessels (capillaries) supplying the healing tissue. The scar is considered healed when the wound has closed with no open areas, and absence of pain is expected at this stage. This redness typically fades over 12–18 months or up to 2 years as the scar matures, becoming flatter and paler. In normal , this results in a mature scar that is avascular, flatter, and only 70-80% as strong as uninjured tissue, with minimal visibility and preserved function, though deviations can lead to abnormal scarring.

Abnormal Scar Formation

Abnormal scar formation arises from disruptions in the cascade, particularly when the proliferative and remodeling phases fail to resolve appropriately, resulting in excessive and disorganized deposition. In normal healing, the process culminates in a flat, avascular scar that integrates with surrounding tissue; however, dysregulation leads to pathological , where scars become raised and persistent. This transition often stems from a failure in the remodeling phase, where fibers fail to realign properly, instead forming dense, haphazard bundles that impair tissue function. Key triggers of this dysregulation include prolonged , which extends the inflammatory phase and perpetuates immune cell infiltration, thereby stimulating sustained proliferation and matrix synthesis. Excessive activity, frequently amplified by profibrotic signals such as transforming growth factor-beta (TGF-β), drives overproduction of types I and III, contributing to scar . Additionally, an imbalance between matrix metalloproteinases (MMPs)—enzymes that degrade —and their inhibitors (TIMPs) favors net matrix accumulation, as elevated TIMP levels hinder MMP-mediated breakdown during remodeling. Common initiating factors encompass deep dermal , which disrupt adnexal structures and prolong healing; infections, that intensify inflammatory responses through bacterial products; and mechanical tension across the site, which activates mechanotransduction pathways in fibroblasts, promoting fibrotic . Unlike normal scars, which are thin, pale, and minimally fibrotic with restored over time, abnormal scars exhibit increased thickness due to excess, reduced leading to , and heightened that resists remodeling. These mechanisms underlie specific pathologies such as hypertrophic scars, though detailed manifestations vary.

Types

Hypertrophic Scars

Hypertrophic scars are defined as elevated, reddish, and firm scars that develop as an exaggerated response to and remain strictly confined to the boundaries of the original site. These scars typically appear within weeks to months after the initial trauma and can cause significant discomfort, including pruritus and , which may affect the patient's . Unlike scars, which exhibit invasive growth into surrounding tissue, hypertrophic scars are non-invasive and limited to the area. Histologically, hypertrophic scars are characterized by dense nodules of , primarily type III, arranged in a parallel orientation to the epidermal surface with randomly organized bundles and an abundance of myofibroblasts, without any extension beyond the margins. These nodular structures contribute to the scar's raised and rigid appearance. Hypertrophic scars most commonly form in areas of high tension, such as the shoulders, chest, and upper arms, following injuries like burns, , or deep cuts. In many cases, these scars exhibit a potential for spontaneous resolution, often flattening and fading over a period of 1 to 2 years without intervention.

Keloid Scars

Keloid scars are characterized by an overgrowth of fibrous tissue that extends beyond the boundaries of the original , forming firm, rubbery, tumor-like nodules that can invade surrounding healthy skin. Unlike hypertrophic scars, which remain confined to the site, keloids exhibit aggressive, invasive growth that does not regress spontaneously and may continue to expand over time. These scars often present with symptoms such as intense pruritus, pain, or tenderness, contributing to significant physical and psychological distress. Epidemiologically, keloid formation is more prevalent in individuals with darker tones, including those of African, Asian, , and Mediterranean descent, where incidence rates can reach 4.5% to 16%. The condition predominantly affects people aged 10 to 30 years, with a higher occurrence during and , and shows familial clustering indicative of genetic predispositions. Histologically, feature thick, hyalinized bundles arranged in whorls, with increased deposition of and glycosaminoglycans (including components), alongside elevated cellularity marked by numerous active fibroblasts. This structure includes "tongue-like" advancing edges that facilitate the invasive proliferation beyond the original injury site. Keloids have high recurrence rates, up to 100% following surgical excision alone, attributed to persistent fibroblastic hyperactivity and incomplete resolution of the underlying fibroproliferative process even after various treatments.

Atrophic Scars

Atrophic scars, also known as depressed or sunken scars, form indentations in the skin due to the destruction or insufficient production of underlying , fat, or other supportive tissues during the process, resulting in a loss of volume and a pitted or depressed appearance relative to the surrounding . This contrasts with raised scars such as hypertrophic or scars, where excess tissue buildup creates elevation above the surface. These scars commonly arise from conditions or events that cause significant dermal damage and , including severe acne vulgaris, varicella () infections, and certain surgical interventions where tissue loss occurs without adequate regeneration. Acne-related atrophic scars, in particular, represent the most prevalent form, often developing after inflammatory lesions destroy sebaceous glands and surrounding . Atrophic scars are typically subclassified based on their morphology, especially in contexts: ice pick scars are narrow, deep, and V-shaped pits less than 2 mm wide that extend into the ; boxcar scars feature broader, rectangular depressions with defined, sharp vertical edges and widths of 1.5–4 mm; and rolling scars present as shallow, wavy indentations with sloped edges that give the skin an undulating texture due to fibrous bands tethering the to . These subtypes highlight the varied degrees of tissue loss and healing impairment. In terms of appearance, atrophic scars often manifest as pale or hypopigmented areas with thinned and , exhibiting irregular textures such as visible pits, troughs, or softened contours that disrupt the skin's smooth surface. The skin in these regions may appear translucent or shiny due to the reduced thickness and loss of normal dermal architecture.

Striae Distensae

Striae distensae, commonly known as , are linear atrophic scars resulting from mechanical stretching of the skin beyond its elastic capacity, leading to dermal tears and subsequent . They manifest as reddish-purple lines in their early phase, termed striae rubra, which evolve into pale, white lines known as striae alba as the inflammation subsides. These marks represent a subtype of atrophic scars characterized by widespread linear patterns due to sustained tension rather than focal depressions from . Striae distensae commonly appear on the , thighs, breasts, hips, , lower back, and shoulders, areas prone to expansion during physiological changes. They frequently develop in contexts of rapid skin distension, such as (affecting 43% to 88% of cases), (6% to 86%), and (up to 43%). Additional risk arises in conditions like , where excess weakens dermal integrity, promoting violaceous striae on the , thighs, and breasts. Histologically, striae distensae feature a thinned epidermis with flattening and loss of rete ridges, alongside dermal changes including fragmented and horizontally oriented collagen bundles that are sparse and parallel to the skin surface. Elastin fibers in the dermis are diminished, clumped, and disorganized, contributing to the loss of skin resilience. The progression of striae distensae begins with an inflammatory phase, where striae rubra appear raised, erythematous, and edematous due to inflammatory infiltrate and vascular dilation. Over 6 to 12 months, these fade through reduced inflammation and collagen remodeling, maturing into permanent, hypopigmented striae alba that are atrophic and scar-like, with no further spontaneous resolution.

Contracture Scars

Contracture scars are a type of pathological scar characterized by the tightening and shortening of that pulls on the surrounding , resulting in distortion of nearby structures and restriction of movement. This contraction arises during the process, particularly in the remodeling phase, where excessive fibrotic tissue formation leads to functional impairment. These scars commonly develop following deep dermal or extensive wounds that involve significant tissue loss, often occurring across or near joints in areas such as the , , or limbs, where they can severely limit mobility and posture. For instance, in injuries affecting the upper extremities or face, scars frequently cause flexion deformities that hinder daily activities. Histologically, contracture scars feature densely packed collagen fibers that become aligned parallel to the skin surface during the remodeling stage, contrasting with the basket-weave pattern of normal collagen; this alignment contributes to progressive tissue shrinkage and stiffness. Myofibroblasts, differentiated fibroblasts with contractile properties, drive this process by exerting tension on the , facilitating the reorganization and contraction of . The severity of scars is typically assessed by the degree of loss in at affected joints, with reductions exceeding 50% in severe cases leading to significant functional deficits. Without early intervention, these scars can progressively worsen over months to years as ongoing remodeling amplifies the contractile forces, potentially requiring multidisciplinary management to restore function.

Pathophysiology

Collagen Dynamics

In scar tissue, collagen dynamics are characterized by dysregulated production and remodeling, leading to excessive deposition compared to the balanced composition in normal . Normal predominantly consists of (approximately 80-90%), which provides tensile strength, with type III collagen comprising about 8-11% and contributing to flexibility. In contrast, scars exhibit elevated levels of both type I and type III collagens, with type III often disproportionately increased during formation, resulting in a less organized matrix that impairs functional recovery. This predominance of types I and III in scars, rather than the more diverse profile in uninjured , underlies the structural rigidity and aesthetic alterations observed. The synthesis of collagen in scars begins intracellularly within fibroblasts, where procollagen chains—precursors to mature collagen—are assembled into a triple-helical structure. These procollagen molecules, primarily types I and III, are synthesized on ribosomes and undergo post-translational modifications, including hydroxylation of proline and lysine residues, before folding and secretion into the extracellular space. Upon secretion, N- and C-terminal propeptides are cleaved by proteases, allowing the collagen molecules to polymerize into fibrils. Stabilization occurs through enzymatic cross-linking mediated by lysyl oxidase, which oxidizes lysine and hydroxylysine residues to form covalent bonds, enhancing fibril durability but contributing to the persistent stiffness in scars when overactive. Remodeling imbalances in further perpetuate accumulation, driven by heightened transforming growth factor-β (TGF-β) signaling that upregulates synthesis genes in fibroblasts. Elevated TGF-β, particularly isoform TGF-β1, activates Smad pathways to promote procollagen transcription, leading to net matrix gain and . Concurrently, reduced activity of matrix metalloproteinases (MMPs), such as MMP-1 and MMP-2, diminishes degradation; in hypertrophic scars, MMP downregulation—often due to increased tissue inhibitors of metalloproteinases (TIMPs)—prolongs deposition and hinders the transition to a mature . This imbalance contrasts with normal healing, where MMPs actively remodel the matrix for resolution. During scar maturation, the collagen composition undergoes a dynamic shift: early proliferative scars feature approximately 30-40% type III collagen, forming thin, disorganized that support rapid repair but lack strength. Over months, this evolves to about 80% , with bundles aligning into parallel, denser structures that improve tensile properties, though pathological scars may retain elevated type III proportions. Fibroblasts drive this transition through regulated synthesis, though dysregulation can arrest remodeling.

Cellular Mechanisms

Fibroblasts serve as the primary cellular mediators in scar formation, functioning as the main producers of components, including , during the process. Upon injury, these resident dermal cells become activated by pro-inflammatory cytokines such as transforming growth factor-beta (TGF-β), leading to their proliferation, migration into the wound bed, and differentiation into more contractile phenotypes. This activation is essential for tissue repair but becomes dysregulated in excessive scarring, where fibroblasts exhibit heightened responsiveness to growth factors, resulting in sustained proliferation and matrix synthesis. Myofibroblasts, derived primarily from fibroblasts, represent a key differentiated state characterized by the expression of alpha-smooth muscle actin (α-SMA), which enables them to generate contractile forces that facilitate closure. In normal , myofibroblasts transiently appear during the proliferative phase to promote formation and contraction; however, in pathological scars such as hypertrophic scars and keloids, these cells persist beyond the resolution phase, contributing to excessive tissue contraction and . This persistence is linked to continued exposure to TGF-β and other signaling molecules, preventing their reversion to quiescent fibroblasts or elimination through . Macrophages play a central role in orchestrating the inflammatory response that influences scar development, transitioning from pro-inflammatory M1 phenotypes early in healing to pro-fibrotic phenotypes that release growth factors like TGF-β and (PDGF), thereby promoting activation and production. In abnormal scarring, macrophages prolong the inflammatory milieu by sustaining release, which exacerbates recruitment and differentiation. Similarly, s accumulate in the site and degranulate to release , , and additional growth factors such as basic fibroblast growth factor (bFGF), which heighten , stimulate proliferation, and extend the inflammatory phase, fostering an environment conducive to hypertrophic and scar formation. Increased density has been observed during the active growth of these scars, correlating with enhanced fibrotic responses. A critical factor in excessive scar formation is the failure of , or , in key scar-associated cells like fibroblasts and myofibroblasts, leading to their prolonged presence and continued matrix deposition. In normal resolution, reduces cellularity as the scar matures, but in pathological conditions, resistance to apoptotic signals—mediated by anti-apoptotic pathways such as upregulation—results in hypercellular scars with persistent fibrotic activity. This apoptotic dysregulation contributes to the imbalance in cellular turnover, amplifying the overall fibrotic outcome from these cellular interactions.

Mechanical Influences

Mechanical forces play a pivotal role in scar development by influencing cellular behavior and (ECM) organization during . Tension forces, particularly at sites under mechanical stress such as joints or areas of repetitive movement, promote the differentiation and contraction of myofibroblasts, leading to aligned deposition that exacerbates scar formation. This alignment occurs as contractile forces pull fibers into parallel bundles, contributing to the raised and thickened appearance of hypertrophic scars. For instance, studies have shown that mechanical loading early in the proliferative phase inhibits in fibroblasts, sustaining their activity and driving excessive ECM production. Shear forces and further modulate scar severity by altering signaling pathways. These forces engage on the cell surface, triggering intracellular cascades that enhance ECM deposition and fibrotic responses. In regions exposed to shear, such as or pressure-prone sites, fibroblasts exhibit increased expression of profibrotic factors, resulting in denser scar tissue. This mechanosensitive response is evident in clinical observations where wounds under sustained heal with greater density compared to unloaded sites. Recent studies as of 2025 have identified elevated expression of the mechanosensitive Piezo2 in fibroblasts, which amplifies fibrotic signaling in response to mechanical cues, contributing to excessive scar formation. Examples illustrate the impact of mechanical environment on scar outcomes: linear, widened scars commonly develop in high-mobility areas like the knees or elbows due to ongoing tension, whereas wounds in low-tension zones, such as the face, often result in minimal or flat scarring with better cosmetic results. Mechanotransduction underlies these effects, as physical forces are transmitted from the ECM through and the to the nucleus, upregulating genes associated with , including those encoding types I and III. This pathway amplifies scar formation by sustaining a profibrotic cellular state.

Causes and Risk Factors

Genetic Predispositions

Genetic predispositions play a significant role in the propensity for abnormal scar formation, particularly hypertrophic and scars, with evidence from familial clustering and twin studies indicating a strong heritable component. Studies have shown that scarring exhibits a recurrence rate of up to 50% in individuals with a family history, particularly among African populations, underscoring the influence of factors. Twin studies further support this, demonstrating concordance in identical twins and suggesting patterns consistent with autosomal dominant with incomplete . Ethnic variations highlight the genetic basis of scar proneness, with individuals of African, Asian, and descent facing a substantially higher risk of formation—approximately 15 times greater than in Caucasians. This disparity is attributed to population-specific genetic profiles that modulate fibrotic responses during . For instance, genome-wide association studies have identified susceptibility loci more prevalent in these groups, contributing to the elevated incidence observed in darker-skinned populations. Specific genetic variants in key pathways have been implicated in aberrant scarring. Polymorphisms in the TGF-β pathway, such as those in the (e.g., the -509C/T variant), influence keloid susceptibility by altering signaling that regulates production and activity; the T allele, in particular, is linked to reduced risk. Similarly, variants in genes like COL1A1, including the promoter -1997 G/T polymorphism, are associated with increased synthesis in keloid and hypertrophic scars, promoting excessive deposition. These findings from candidate gene studies emphasize the role of heritable alterations in genes. Certain inherited disorders also predispose individuals to atypical scarring. Ehlers-Danlos syndrome (EDS), caused by mutations in -encoding genes such as COL5A1 or COL3A1, leads to poor and characteristic atrophic scars due to impaired collagen fibril formation and tissue fragility. In classic EDS, wounds often result in wide, thin "cigarette paper" scars, reflecting the underlying defect in dermal integrity.

Environmental and Physiological Factors

Infections at sites prolong the inflammatory phase of healing, thereby elevating the risk of formation by sustaining excessive activity and deposition. Delayed closure similarly extends , promoting and increasing the likelihood of abnormal scarring outcomes. Bacterial , as a key environmental trigger, further exacerbates this process by amplifying local immune responses that hinder timely resolution. Nutritional deficiencies play a significant role in modulating scar severity through their impact on tissue repair. deficiency impairs synthesis by disrupting hydroxylation of and residues, leading to weakened scar tissue and prolonged healing times. , meanwhile, compromises immune function by reducing and activity, which delays closure and heightens susceptibility to infections that worsen scarring. Hormonal fluctuations represent another critical physiological influence on scar development. Elevated estrogen levels during contribute to the formation of striae distensae by altering dermal integrity and elasticity, often resulting in linear atrophic scars on the and thighs. Similarly, heightened from impairs by suppressing production and prolonging , thereby increasing the propensity for hypertrophic or scars. Age and underlying comorbidities also shape scarring patterns as non-genetic factors. Children exhibit more prominent hypertrophic scarring due to heightened inflammatory responses and rapid tissue growth, particularly in or surgical wounds. In adults, conditions like delay through hyperglycemia-induced microvascular damage and impaired immune modulation, often leading to chronic wounds with exaggerated fibrotic scarring.

Prevention

Optimal Wound Care

Optimal wound care immediately following plays a crucial role in minimizing scar formation by promoting orderly , reducing risk, and supporting tissue regeneration. Proper initial management focuses on creating an environment that accelerates epithelialization while preventing complications that could lead to excessive deposition and hypertrophic scarring. Cleaning the thoroughly and performing are essential first steps to remove , necrotic tissue, and , thereby reducing the risk of that can exacerbate scarring. Antiseptics such as gluconate are recommended for skin cleansing around the , as they effectively decrease bacterial load without significantly impairing when used appropriately. For instance, applying solution in concentric circles from the edges outward helps prevent surgical site infections, which are linked to poorer scar outcomes. , whether sharp, enzymatic, or autolytic, further lowers rates by eliminating devitalized tissue that serves as a medium for . Maintaining a moist wound environment through occlusive dressings is a cornerstone of modern care, as it facilitates faster reepithelialization and reduces scarring compared to dry healing methods. Occlusive dressings, such as hydrocolloid or semi-permeable films, prevent , preserve growth factors, and promote , leading to wounds that heal with less tensile strength and fewer hypertrophic features. Clinical reviews indicate that this approach can enhance synthesis in a controlled manner while lowering rates by up to 50% relative to traditional dry dressings. Dressings should be changed as needed to manage without disrupting the moist milieu. Protecting immature scars from (UV) exposure is vital, as UV radiation can cause [hyperpigmentation](/page/Hyper pigmentation) and worsen scar appearance during the remodeling phase. A reddish or pink appearance is normal in the early maturation phase of healed scars, particularly in burn scars, resulting from increased blood vessels (capillaries) supplying the healing tissue. This redness typically fades over 12–18 months or up to 2 years as the scar matures, becoming flatter and paler. Immature scars, particularly in the first 6-12 months, are highly susceptible to darkening when exposed to sunlight, leading to persistent discoloration. Guidelines recommend applying broad-spectrum with SPF 30 or higher daily, along with physical barriers like clothing, to shield the area and promote even fading. Regular moisturizing is also recommended to maintain hydration, support scar remodeling, and aid in the fading process. This practice not only prevents overproduction but also supports overall scar maturation without . Gentle techniques, initiated around week 2 post- once the is closed, help break down excessive bundles and improve scar pliability to prevent . Applying firm but gentle pressure in circular or linear motions for 1-2 minutes several times daily can realign fibers, reduce scar height, and alleviate associated symptoms like pruritus. Systematic reviews of in burn and surgical scars demonstrate its efficacy in decreasing and improving texture, particularly when combined with to avoid . Patients should use clean hands or a and discontinue if or breakdown occurs. Application of sheets or gels is a standard preventive measure starting once reepithelialization is complete (typically 2-3 weeks post-injury), as they provide occlusion, hydration, and mild pressure to regulate production and reduce risk. Clinical guidelines support their use for 12-24 hours daily for at least 3 months in high-risk areas, improving scar and pliability.

Surgical and Procedural Strategies

Surgical and procedural strategies during initial injury management play a critical role in preventing excessive scarring, particularly scars, by minimizing mechanical stress on tissues. These approaches aim to optimize closure and orientation to counteract the tensile forces that drive activation and misalignment, as outlined in underlying pathophysiological mechanisms. By intervening promptly and precisely, surgeons can significantly reduce the incidence of hypertrophic or outcomes in high-risk wounds such as deep lacerations or burns. Tension-free closure is a foundational technique that involves undermining the edges to mobilize adjacent tissue, thereby distributing forces evenly and preventing undue stress on the sutured line. This method, often combined with absorbable sutures like polyglactin, allows for precise of margins without excessive pulling, which lowers the of widened or hypertrophic scars. Studies have shown that such closures result in improved scar , with reduced tension correlating to lower rates of pathological scarring in surgical incisions. For instance, undermining facilitates tension redistribution, enabling primary closure in that might otherwise require more invasive options. Z-plasty and W-plasty are geometric revision techniques applied during initial closure to reorient the wound and break up linear tension lines, promoting healing along relaxed skin tension lines (RSTLs). In , triangular flaps are transposed at 60-degree angles to elongate the scar by 75% while redirecting its direction, which is particularly effective for wounds crossing creases prone to . W-plasty, involving serial small triangular excisions, similarly disrupts straight-line scars into irregular patterns that camouflage better and reduce web-like contractures. These procedures have demonstrated superior outcomes in preventing tension-induced deformities, with altering scar vectors to align with natural . For high-risk wounds like full-thickness burns, early excision of necrotic tissue followed by immediate is a proactive strategy to limit the inflammatory response and scar formation. This involves tangential removal of within the acute phase, then covering the defect with autografts or temporary allografts to accelerate re-epithelialization and minimize excess. Clinical evidence indicates that early excision reduces hypertrophic scarring by shortening the healing timeline and preserving viable , with ensuring stable coverage that resists . For burns, pressure garments applied post- (once tolerable, typically after 2 weeks) provide sustained compression to prevent and , worn 23 hours daily for 6-12 months or longer as needed. Optimal timing for these interventions is crucial, with most guidelines recommending surgical action within 24-48 hours post-injury after initial to balance risk and scar prevention benefits. Delaying beyond this window increases the likelihood of entrenched and denser deposition, whereas prompt execution—once hemodynamic stability is achieved—yields the best functional and aesthetic results in preventing contractures.

Treatment

Topical and Dressing Therapies

Topical and dressing therapies represent a cornerstone of non-invasive scar management, primarily targeting the modulation of scar maturation through surface application to alleviate symptoms such as itching, , and . These treatments work by influencing the epidermal barrier and underlying dermal processes, often by promoting hydration or applying mechanical force to limit excessive deposition during the remodeling phase of . As of 2025/2026, there is no single "best" scar treatment cream, as effectiveness varies by scar type, age, skin type, and individual response. Dermatologists generally recommend silicone-based gels or sheets as the most evidence-based option for reducing scar appearance, often over onion extract creams like Mederma. Popular and frequently recommended products include silicone gels such as ScarAway, Kelo-cote, or Dermatix; Mederma Advanced Scar Gel or PM Intensive Overnight Cream (onion extract-based); and Bio-Oil (for moisturizing and older scars). Consultation with a dermatologist is advised for personalized advice, as early treatment and consistent use are key. Silicone-based products and pressure garments are among the most established options, with onion extract gels offering additional benefits, though evidence varies in strength across modalities. Silicone gels and sheets, such as ScarAway, Kelo-cote, or Dermatix, hydrate the via an occlusive barrier, which maintains optimal moisture levels and reduces excessive production by fibroblasts, thereby flattening and softening scars. This mechanism helps normalize the and decreases , leading to improved scar pliability and reduced . Application typically involves 12 to 24 hours of daily use for 2 to 3 months, starting once the has epithelialized, with meta-analyses demonstrating significant reductions in scar height, pigmentation, and pliability compared to no treatment or placebos. For instance, postoperative scars treated with gel showed marked improvements in these parameters, supporting its role in both preventive and therapeutic contexts. Onion extract, derived from Allium cepa, is incorporated into topical gels such as Mederma Advanced Scar Gel for its anti-inflammatory properties, primarily through like and , which inhibit release, leukotriene synthesis, and proinflammatory cytokines, ultimately softening scars and improving organization. These gels are applied once or twice daily to mature scars, often in combination with other agents like or to enhance bacteriostatic effects and reduce scar elevation. Systematic reviews indicate limited but positive evidence for scar softening and cosmetic improvement after 4 to 8 weeks of use, though onion extract performs comparably to alone without superior efficacy in meta-analyses of randomized trials. Pressure garments apply sustained mechanical compression, typically at 20 to 30 mmHg, to hypertrophic scars, which mechanically limits blood flow and proliferation, promoting parallel alignment and scar maturation akin to normal . Custom-fitted garments are worn for 23 hours per day over 6 to 12 months, with prophylactic initiation as early as 2 weeks post-injury yielding optimal results in burn-related scarring. from systematic reviews shows improvements in scar height and redness, with some studies reporting up to 60-80% reduction in hypertrophic features when combined with other topicals, though overall certainty remains moderate due to heterogeneous trial designs.

Injectable and Pharmacological Interventions

Injectable and pharmacological interventions for scar management primarily target pathological scarring such as keloids and hypertrophic scars through direct delivery of agents that modulate , activity, and production. These treatments are often administered intralesionally to achieve localized effects, minimizing systemic exposure, and are typically used as monotherapy or in combination to enhance efficacy and reduce recurrence rates. Common agents include corticosteroids, antimetabolites, sclerosing agents, and , with administration frequencies ranging from every 4-6 weeks depending on the drug and scar response. Dermal fillers, such as hyaluronic acid-based products or autologous fat transplantation, are utilized for volume restoration in atrophic scars, elevating depressed areas to improve skin contour. Hyaluronic acid fillers provide temporary improvement, while autologous fat grafting offers potentially longer-lasting volume restoration and regenerative benefits through tissue integration and stimulation of collagen production. These interventions are often combined with subcision to release underlying fibrotic adhesions, laser resurfacing, skin boosters, or other therapies to enhance overall scar improvement outcomes. Corticosteroids, particularly (TAC), are among the most established injectable therapies for reducing scar volume and symptoms in keloids and hypertrophic scars. Administered via intralesional injections every 4-6 weeks at concentrations of 10-40 mg/mL, TAC works by suppressing , inhibiting fibroblast proliferation, and decreasing synthesis, leading to scar flattening in up to 50-80% of cases with short-term use. However, its efficacy may be limited for long-term control, with recurrence rates around 50% after cessation, and common side effects include skin atrophy, , and . A confirmed TAC's benefits for short-term management but noted superior outcomes with alternatives like 5-fluorouracil or verapamil in some comparisons. Combinations with other agents, such as 5-FU, have shown improved results, with balanced efficacy and tolerability in treating keloid scars. 5-Fluorouracil (5-FU), an agent, inhibits in fibroblasts, thereby reducing proliferation and excessive deposition in pathological scars. It is typically injected intralesionally at 50 mg/mL every 1-4 weeks, often combined with corticosteroids like TAC to mitigate pain and enhance flattening, achieving >50% improvement in scar appearance across diverse anatomical sites in over 250 treated . This approach is considered a safe and practical alternative to steroids alone, with lower risks of , though potential side effects include ulceration, , and flu-like symptoms. A of monotherapy demonstrated consistent keloid improvement without severe adverse events, supporting its role in recurrent or steroid-resistant cases. Bleomycin, a sclerosing derived from verticillus, induces and inhibits , making it effective for treatment through monthly intralesional injections at doses of 0.1-1.0 units/mL. Clinical studies report high , with up to 70-90% scar flattening or resolution, outperforming TAC and 5-FU in meta-analyses for reduction and symptom . Side effects are generally mild, including local pain and , with rare systemic risks like at low doses used for scars. Its antimitotic action targets proliferating fibroblasts, contributing to durable responses in refractory . Verapamil, a , reduces transforming growth factor-beta (TGF-β) expression and production by fibroblasts, promoting scar remodeling when injected intralesionally at 2.5 mg/mL every 2-4 weeks or applied as a topical . It achieves comparable or superior flattening to TAC in hypertrophic scars and keloids, with 50-70% improvement rates and fewer adverse events such as . A randomized study highlighted verapamil's safety profile as a viable alternative, particularly for patients intolerant to steroids, and combinations with TAC yield long-term stable results. These interventions collectively address cellular targets like fibroblasts to inhibit scar progression, though optimal outcomes often require multimodal approaches tailored to scar characteristics.

Laser and Light-Based Treatments

Laser and light-based treatments utilize targeted energy devices to address scar , redness, and texture irregularities, offering minimally invasive options for improving scar appearance without surgical intervention. These therapies work by selectively heating specific chromophores in the skin, such as in blood vessels or in tissue, to promote vascular reduction and dermal remodeling. Clinical applications focus on hypertrophic, atrophic, and pigmented scars, with treatments typically administered in outpatient settings and spaced several weeks apart to allow for healing. Treatment selection should account for skin type and scar severity to optimize efficacy and reduce risks like post-inflammatory hyperpigmentation. The pulsed dye laser (PDL), operating at wavelengths of 585-595 nm, specifically targets in dilated blood vessels within scars, leading to and subsequent reduction in and vascularity. This makes PDL particularly effective for early hypertrophic and scars, where redness is prominent, with meta-analyses demonstrating significant decreases in Vancouver Scar Scale (VSS) scores after treatment. Patients generally require 3-6 sessions, spaced 4-8 weeks apart, to achieve optimal vascular improvement, with the showing a favorable safety profile and minimal side effects like transient . Fractional CO2 laser treatment employs ablative resurfacing to create microthermal zones in the skin, vaporizing damaged tissue while sparing surrounding areas, which is ideal for atrophic scars such as boxcar scars from or . By delivering intense thermal energy, it profoundly stimulates neocollagenesis, tissue remodeling, and epidermal regeneration, yielding improved scar depth and texture, particularly in moderate to severe atrophic cases. Fractional picosecond lasers offer similar collagen regeneration benefits with potentially fewer adverse effects, making them a promising option for facial atrophic scars. For acne scars, a prevalent form of atrophic scarring, no single treatment completely erases the lesions, but combination professional therapies such as fractional lasers, picosecond lasers, microneedling, subcision, and others can achieve 50–80% improvement in appearance; results vary by scar subtype, patient age, skin tone, and treatment adherence. Effective strategies prioritize controlling active acne first, anticipate gradual progress over months, and involve dermatologist consultation. Treatment protocols often involve 3-4 sessions at 6-week intervals, with studies reporting enhanced and reduced atrophic features. Intense pulsed (IPL) delivers a broad-spectrum (typically 500-1200 nm) that non-selectively addresses multiple chromophores, including and oxyhemoglobin, to correct pigmentation irregularities and refine scar texture. IPL is versatile for superficial pigmented scars and vascular components, promoting even tone and flexibility through photothermolysis of abnormal vessels and melanocytes. Similar to other modalities, 3-6 sessions spaced 4 weeks apart are commonly recommended, yielding gradual enhancements in scar color and surface smoothness. Clinical trials across these therapies indicate 50-75% overall improvement in hypertrophic scar characteristics, including reduced height, pliability, and pigmentation, as assessed by standardized scales like the VSS or Patient and Observer Scar Assessment Scale. These outcomes highlight the role of and light-based approaches in remodeling, where thermal stimulation accelerates activity and extracellular matrix reorganization for long-term scar maturation.

Surgical Corrections

Surgical corrections for scars involve invasive procedures aimed at improving the appearance, function, or symptoms of problematic , particularly when non-surgical methods are insufficient. These techniques are typically performed by surgeons or dermatologic surgeons and are reserved for mature scars (at least 6-12 months post-injury) to minimize further distortion. The choice of procedure depends on scar type, location, size, and patient factors such as type and propensity. Excision and closure is a foundational surgical approach for removing hypertrophic or scars, where the is precisely cut out and the is closed primarily with sutures to create a finer linear scar, or closed with grafts or flaps if tension is high. For severe ice-pick type scars or narrow deep boxcar scars, punch excision is commonly employed to remove the scar tissue, followed by suturing or grafting to achieve a less noticeable result. For , which extend beyond the original boundaries and have high recurrence rates, complete excision is often combined with undermining of surrounding to reduce tension, though simple excision alone results in recurrence in up to 45-100% of cases without adjunct therapies. may be used for larger keloids on areas like the trunk, providing coverage while allowing the donor site to heal with a less conspicuous scar. Scar revision techniques focus on reorienting or redesigning the scar to align with natural tension lines or blend with surrounding features, thereby camouflaging it. Geometric rearrangements, such as the or pinwheel methods, involve excising the scar in a specific pattern—e.g., the technique removes elliptical and repositions adjacent skin flaps to break up the linear appearance—reducing visibility and improving . These methods are particularly effective for wide or irregular scars on the face or limbs, with studies showing improved patient satisfaction scores post-revision compared to untreated scars. The pinwheel excision, useful for circular or stellate scars, rotates triangular flaps to irregularize the scar edge, minimizing shadowing and . Tissue expansion is employed for extensive scars causing significant deformity or coverage deficits, where a silicone balloon is surgically placed beneath intact skin adjacent to the scar and gradually inflated over weeks to months to generate additional . This expanded is then advanced or rotated to replace the scarred area, providing like-with-like tissue with matching color and texture. The technique is ideal for large defects on the , , or extremities, with success rates exceeding 90% in generating sufficient tissue for reconstruction when managed properly. To prevent recurrence, especially in keloids and hypertrophic scars, adjunctive therapies are integrated postoperatively. Intralesional corticosteroid injections, such as , are administered starting immediately after and continued at intervals to suppress activity, reducing recurrence to 10-20% in some series. External beam , delivered in low doses (e.g., 15-20 Gy over fractions) within 24-48 hours post-excision, inhibits keloid reformation by targeting proliferating cells, with recurrence rates of 10-45% reported, compared to 45-55% without intervention. These adjuncts are selected based on scar location and patient risk, with avoided in areas like the due to potential long-term risks. For functional scars leading to joint restriction, release may be briefly incorporated to restore mobility alongside cosmetic revision. Treatment outcomes vary depending on scar type, severity, individual differences, and often require multiple sessions or combined approaches for optimal results. It is essential to consult a professional dermatologist or plastic surgeon for thorough evaluation and personalized treatment, as improper management or self-treatment can worsen the scar or cause additional complications.

Complications

Physical and Functional Issues

Scars can lead to , which are tightenings of the that restrict joint mobility and limit , particularly in injuries where up to 58.6% of affected joints show limitations at 3-6 weeks post-injury, declining to 20.9% at 12 months. These often affect the upper body more frequently and can impair daily activities by causing functional deficits, such as reduced ability to extend or flex limbs. In severe cases, they result from excessive deposition and activity, leading to persistent shortening of the tissue across joints. Pain and pruritus (itching) are common sensory disturbances in scars, often arising from neuropathic mechanisms such as nerve entrapment or damage during the process. may stem from injured sensory nerves regenerating aberrantly, while pruritus can be triggered by release from mast cells as part of the inflammatory response in healing wounds. In scars, these symptoms frequently co-occur due to chronic inflammation and neural hypersensitivity, affecting quality of life through persistent discomfort. Scar tissue is often fragile and less elastic than normal , increasing the risk of ulceration, especially in areas subject to or . This vulnerability arises because scars have reduced tensile strength and poor , making them prone to breakdown and chronic wounds, such as in post-burn lesions where malignant degeneration like can develop over time. Sites subject to or are particularly susceptible, leading to recurrent ulceration if not managed. In children, scars can interfere with normal growth, as the fixed scar tissue does not expand proportionally with the body's development, resulting in facial or limb distortion over time. Pathologic scars disrupt this process through ongoing contraction driven by myofibroblasts, potentially causing skeletal or muscular abnormalities as the child matures. This growth interference can lead to functional and aesthetic issues.

Psychological Impacts

Scarring can profoundly affect , leading to significant emotional distress among affected individuals. Surveys and clinical studies indicate that between 20% and 50% of patients with visible scars report symptoms of depression or anxiety, with higher rates observed in those with acne-related or burn-induced scarring. This distress often manifests as dissatisfaction with appearance, with over half of patients expressing unhappiness about their scar aesthetics, contributing to altered self-perception and emotional vulnerability. Visible scars, particularly facial keloids, are frequently associated with and , exacerbating psychological burdens. Research on keloid patients reveals that approximately 49% feel stigmatized, and 36% report limitations in social interactions due to judgmental attitudes from others. Such experiences can lead to avoidance of social interactions and heightened feelings of isolation, especially in professional or public settings where scars are perceived as disfiguring. The overall for individuals with scars is often diminished, characterized by reduced and maladaptive behaviors such as withdrawal from social activities. These impacts are particularly pronounced in adolescents, where post-acne scars have been shown to significantly impair and daily functioning, prolonging negative thought patterns initiated during active skin conditions. In burn survivors, scarring contributes to (PTSD), with up to 30-40% experiencing persistent symptoms like intrusive memories and linked to their altered appearance. Psychological interventions, such as (CBT) and counseling, are recommended to address these impacts by targeting unhelpful beliefs about appearance and promoting coping strategies, though access remains limited for many patients.

Society and

Intentional Scarring Practices

Intentional scarring, known as , has been practiced across various cultures as a deliberate form of to signify rites of passage, social identity, and spiritual beliefs. In many African societies, particularly among the of , facial and body scarification involves making precise incisions into the skin to create raised patterns that serve as markers of tribal affiliation and maturity. These marks, often applied during or ceremonies, symbolize endurance and , with patterns varying by lineage or region to denote specific social roles. Among other sub-Saharan African groups, such as the Ga'anda and Bétamarribé, scarification employs techniques like superficial cutting, etching, or branding with heated tools to produce permanent designs linked to agricultural motifs, , or protection against evil. These practices, rooted in communal rituals, reinforce group cohesion and personal status, where the pain endured is viewed as a test of resilience essential for adulthood. Branding, in particular, creates keloid-like scars through controlled burns, while incisions are often rubbed with ash or irritants to enhance visibility and texture. Historical evidence from ancient civilizations also reveals intentional scarring for status and identity. In and , depictions in art show facial scarification among Nubians, likely used to indicate ethnic origin or social standing, with incisions creating linear patterns that distinguished individuals in hieroglyphic scenes. Similarly, in Polynesian cultures, early tattooing practices incorporated by cutting designs into the skin and rubbing in pigments or irritants to form darkened, raised scars, symbolizing ancestry, protection, and warrior status during rites of passage. tāmoko, a Polynesian variant, uses chiseling to produce grooved scars on the face, blending incision with pigmentation for deep cultural significance. In contemporary contexts, intentional scarring persists as a form of cosmetic within alternative communities, including tattoo enthusiasts and practitioners, where it is pursued for aesthetic, erotic, or expressive purposes rather than ritual obligation. Designs are created through cutting, branding, or chemical means to achieve textured, three-dimensional effects that complement or replace traditional tattoos, often customized to reflect personal narratives or subcultural affiliations. This modern adaptation emphasizes individual autonomy and artistic innovation, though it remains niche due to its permanence and intensity. Despite its cultural value, intentional carries notable health risks, primarily from the open wounds created during the process. Infections, such as bacterial or viral transmission via unsterilized tools, pose a significant threat, particularly in non-clinical settings where or can spread if equipment is shared. Additionally, individuals with darker tones or genetic predispositions are at higher risk for formation, where scars grow excessively beyond the original incision, leading to raised, itchy, or painful hypertrophic tissue that may require medical intervention. The involves dysregulated with excessive deposition in response to the intentional trauma.

Historical and Etymological Context

The word "scar" derives from the escharre, meaning "scab" or "scab-like mark," which entered around the to describe a mark left by a healed . This term traces back further to eschara and ultimately to eskharā, referring to a "scab" or "burn mark," evoking the or fireplace due to the charred appearance of such lesions. In ancient civilizations, scar management relied on natural substances to promote healing and minimize disfigurement. , as documented in the (c. 1550 BCE), applied to wounds for its antibacterial properties and used compounds, such as , as astringents to aid closure and reduce scarring. Similarly, Greek physicians like (c. 460–370 BCE) advocated mixed with for effects on open wounds, reflecting early recognition of scars as permanent gaps or notches in the skin. By the , mechanical interventions emerged alongside evolving surgical practices. Pressure therapy, involving compression to flatten raised scars, gained traction; American surgeon John Collins Warren Jr. in 1893 endorsed elastic bandages and splints for keloids, building on earlier observations that constant pressure could inhibit excessive growth. This period marked a shift in viewing scars not just as inevitable but as manageable through physical means. Cultural perceptions of scars evolved significantly from the Victorian era's emphasis on bodily perfection to contemporary integration in reconstructive medicine. In the 19th century, visible scars were often stigmatized as deformities, symbolizing moral or social failing, particularly for women, and prompting early plastic surgery efforts to conceal them. By the mid-20th century, this gave way to acceptance in fields like post-war reconstructive surgery, where scars became emblems of resilience rather than shame. Key milestones include the 1980s introduction of silicone gel sheeting for scar flattening, first observed effective by Australian burn units, and the advent of laser therapies, such as CO2 and pulsed-dye lasers, which targeted vascular and textural abnormalities to improve appearance.

Research

Ongoing Studies

Recent genome-wide association studies (GWAS) have advanced the understanding of susceptibility through genetic mapping, identifying more than 10 loci associated with the condition using post-2020 data. A multi-ancestry published in 2025 detected 26 independent loci across diverse populations, with 12 replicating in an independent dataset, highlighting variants in fibroproliferative pathways that contribute to excessive scarring. These findings build on earlier GWAS by increasing the number of confirmed loci and providing estimates of 6% in Europeans, 21% in East Asians, and 14% in multi-ancestry cohorts, emphasizing ancestry-specific genetic risks. Biomarker research has targeted circulating microRNAs (miRNAs) for early prediction of pathological scar formation, offering non-invasive diagnostic potential. Studies have shown that miR-365a/b-3p is significantly upregulated in both tissues and serum from mouse models, with fold-changes indicating its role in differentiation and progression. This miRNA's elevated circulating levels correlate with scar severity, positioning it as a promising for identifying at-risk patients shortly after injury, as validated through and qRT-PCR analyses in and animal samples. Animal models remain central to testing anti-fibrotic interventions, particularly using excisional assays to evaluate in mimicking scar . In these models, full-thickness excisional wounds are created on the dorsal , allowing assessment of markers like deposition and alpha-smooth muscle expression over 14-21 days. A 2025 study utilized this approach to test YAP inhibitors, demonstrating reduced mechanotransduction signaling that prevented hypertrophic scarring and promoted regenerative without . Clinical trials are investigating type A (BoNT-A) in phase II settings to reduce wound tension and mitigate scar formation, with updates from 2023-2025 protocols reporting a mean reduction of 3.1 points on the Scar Scale and improvements in scar width. These trials, such as randomized controlled evaluations of intradermal BoNT-A injections post-excision, target high-tension areas like the face and trunk, showing reduced activity and tension-mediated compared to saline controls. Meta-analyses of these efforts confirm BoNT-A's role in early intervention, with significant improvements in scar pliability and observed in 644 participants across 12 studies.

Emerging Therapies

Stem cell therapy utilizing adipose-derived stem cells (ADSCs) represents a promising avenue for modulating scar remodeling by promoting tissue regeneration and reducing . These cells secrete factors that inhibit excessive deposition and , leading to improved scar pliability and appearance in early clinical trials. For instance, a 2025 review of 43 preclinical and clinical studies found that ADSC products, including exosomes and conditioned media, significantly decreased thickness and vascularity, with some combination therapies showing up to 50% improvement in scar scores compared to controls. Ongoing phase I/II trials, such as one evaluating allogeneic ADSCs for burn scar remodeling, report preliminary reductions in scar volume by approximately 30% after 6 months, attributed to enhanced collagen reorganization without adverse events. Gene editing technologies, particularly / targeting the TGF-β pathway, are under investigation in preclinical models to disrupt fibrotic signaling and prevent pathological scar formation. TGF-β overexpression drives differentiation and accumulation in scars; -mediated or activation of related genes, such as TGIF1, has demonstrated reduced markers and in corneal and fibroblast models. A 2022 genome-wide screen identified key TGF-β mediators in hepatic stellate cells, with analogous applications in dermal showing decreased scar in mouse wound models by inhibiting downstream Smad signaling. These approaches build briefly on ongoing genetic studies of scar , offering potential for precise, localized interventions. Nanotechnology enables targeted delivery of anti-fibrotic agents through nanoparticles designed for sustained release, minimizing systemic side effects and enhancing efficacy in scar prevention. Polymeric nanoparticles loaded with drugs like or siRNA against TGF-β provide prolonged inhibition of fibrogenic pathways, with preclinical studies in excisional models reporting 40-60% reductions in scar index due to controlled release over 2-4 weeks. A 2023 review highlighted liposomal and micellar nanoparticles that promote anti-inflammatory M2 polarization, leading to flatter scars in hypertrophic models. Early translational efforts focus on and for clinical translation. Bioengineered skin substitutes incorporating 3D-printed scaffolds with anti-scarring matrices aim to recapitulate native dermal architecture while suppressing during closure. These scaffolds, often composed of hydrogels embedded with growth factors or decellularized matrices, facilitate vascularization and epithelialization without excessive deposition; a 2024 rat model using 3D-bioprinted double-layer skins reduced scar formation by promoting regenerative phases. As of 2025, phase I trials are evaluating safety and integration of such constructs for full-thickness wounds, with initial data indicating improved tensile strength and minimal hypertrophic response in human volunteers.

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