Pathophysiology
If a wound becomes covered with epithelial tissue within two weeks, minimal collagen will be deposited and no scar will form. Generally, if a wound takes longer than three to four weeks to become covered, a scar will form. Deep second-degree burns heal with scarring and hair loss. Sweat glands do not form in scar tissue, which impairs the regulation of body temperature.
The scar is a result of the body's repair mechanism after injury in many tissues.
Any injury does not become a scar until the wound has completely healed; this can take many months, or years in the worst pathological cases, such as keloids. To begin to patch the damage, a clot is created; the clot is the beginning process that results in a provisional matrix. In the process, the first layer is a provisional matrix and is not scar. Over time, the wounded body tissue then 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.
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.
The fibroblast involved in scarring and contraction is the myofibroblast, which is a specialized contractile fibroblast. These cells express a-smooth muscle actin (a-SMA).
The myofibroblasts are absent in the first trimester in the embryonic stage; damage then heals scar free; small incisional or excision wounds less than 2 mm also heal without scarring; and in adult unwounded tissues where the fibroblast in itself is arrested; however, the myofibroblast is found in massive numbers in adult wound healing which heals with a scar.
The myofibroblasts make up a high proportion of the fibroblasts proliferating in the postembryonic wound at the onset of healing. In the rat model, for instance, myofibroblasts can constitute up to 70% of the fibroblasts, and is responsible for fibrosis on tissue. Generally, the myofibroblasts disappear from the wound within 30 days, but can stay around in pathological cases in hypertrophy, such as keloids.
Prolonged inflammation, as well as the fibroblast proliferation can occur. Redness that often follows an injury to the skin is not a scar, and is generally not permanent (see wound healing). The time it takes for this redness to dissipate may, however, range from a few days to, in some serious and rare cases, a few years.
Scars form differently based on the location of the injury on the body and the age of the person who was injured.
The worse the initial damage is, the worse the scar will generally be.
Skin scars occur when the dermis (the deep, thick layer of skin) is damaged. Most skin scars are flat and leave a trace of the original injury that caused them.
Wounds allowed to heal secondarily tend to scar worse than wounds from primary closure.
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