Scar
A scar is an area of fibrous tissue that replaces normal skin following 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 results in some degree of scarring. An exception is animals with complete regeneration, which regrow tissue without scar formation.
Scar tissue is composed of the same protein 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 randomised alignment. For example, scars in the skin are less resistant to ultraviolet radiation, and sweat glands and hair follicles do not grow back within scar tissues. A myocardial infarction, commonly known as a heart attack, causes scar formation in the heart muscle, which leads to loss of muscular power and possibly heart failure. However, there are some tissues that can heal without any structural or functional deterioration.
Types
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. 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, both of which experience excessive stiff collagen bundled growth overextending the tissue, blocking off regeneration of tissues. Another form is atrophic 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 are regarded as scars by some.High melanin levels and either African or Asian ancestry may make adverse scarring more noticeable.
Hypertrophic
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.Keloid
Keloid scars are a more serious form of excessive scarring, because they can grow indefinitely into large, tumorous 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, 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. Surgical removal of keloid is risky and may exacerbate the condition and worsening of the keloid.
Atrophic
An atrophic scar takes the form of a sunken recess in the skin, which has a pitted appearance. These are caused when underlying structures supporting the skin, such as fat or muscle, are lost. This type of scarring is often associated with acne, chickenpox, other diseases, surgery, certain insect and spider bites, or accidents. It can also be caused by a genetic connective tissue disorder, such as Ehlers–Danlos syndrome.Stretch marks
Stretch marks are also a form of scarring. These are caused when the skin is stretched rapidly, or when skin is put under tension during the healing process. This type of scar usually improves in appearance after a few years.Elevated corticosteroid levels are implicated in striae development.
Umbilical
Humans and other placental mammals have an umbilical scar 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.Pathophysiology
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. When the extracellular matrix senses elevated mechanical stress loading, tissue will scar, and scars can be limited by stress shielding wounds. Small full thickness wounds under 2mm reepithelize 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 the regulation of body temperature. Elastic fibers are generally not detected in scar tissue younger than 3 months old. In scars, rete pegs are lost; through a 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 on a monthly basis. All other adult tissues, upon rapid shedding or injury, can scar.
Prolonged inflammation, as well as the fibroblast proliferation, can occur. Redness that often follows an injury to the skin is not a scar and is generally not permanent. The time it takes for this redness to dissipate may, however, range from a few days to, in some serious and rare cases, a few years.
Scars form differently based on the location of the injury on the body and the age of the person who was injured.
The more severe the initial damage is, the more significant the scar will generally be.
Skin scars occur when the dermis 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 more significantly than wounds from primary closure.
Collagen synthesis
An injury does not become a scar until the wound has completely healed; this can take many months, or years in the worst pathological cases, such as keloids. To begin to patch the damage, a 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 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
The scarring is created by fibroblast proliferation, a process that begins with a reaction to the clot. To mend the damage, fibroblasts slowly form the collagen scar. The fibroblast proliferation is circular and cyclically, the fibroblast proliferation lays down thick, whitish collagen inside the provisional and collagen matrix, resulting in the abundant production of packed collagen on the fibers giving scars their uneven texture. Over time, the fibroblasts continue to crawl around the matrix, adjusting more fibers and, in the process, the scarring settles and becomes stiff. This fibroblast proliferation also contracts the tissue. In unwounded tissue, these fibers are not overexpressed with thick collagen and do not contract.EPF and ENF fibroblasts have been genetically traced with the Engrailed-1 genetic marker. EPFs are the primary contributors to all fibrotic outcomes after wounding. ENFs do not contribute to fibrotic outcomes.
Myofibroblast
Mammalian wounds that involve the dermis of the skin heal by repair, not regeneration. 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. 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, which is a specialized contractile fibroblast. These cells express α-smooth muscle actin.
The myofibroblasts are absent in the first trimester in the embryonic stage where damage heals scar-free; in small incisional or excision wounds less than 2 mm that also heal without scarring; and in adult unwounded tissues where the fibroblast in itself is arrested; however, the myofibroblast is found in massive numbers in adult wound healing which heals with a scar.
The myofibroblasts make up a high proportion of the fibroblasts proliferating in the postembryonic wound at the onset of healing. In the rat model, for instance, myofibroblasts can constitute up to 70% of the fibroblasts, and is responsible for fibrosis on tissue. Generally, the myofibroblasts disappear from the wound within 30 days, but can remain in pathological cases in hypertrophy, such as keloids. Myofibroblasts have plasticity and in mice can be transformed into fat cells, instead of scar tissue, via the regeneration of hair follicles.