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. 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 (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. Collagen synthesis 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; 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 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. 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 (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, which is a specialized contractile fibroblast. These cells express α-smooth muscle actin (α-SMA). The myofibroblasts are absent in the first trimester in the embryonic stage where damage heals scar free; in 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 stay around 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.
symptom of Acne
symptom of Croup
symptom of Mouth breathing
symptom of Pharyngitis
symptom of Dermatitis
symptom of Rosacea
symptom of Epiglottitis
symptom of Sinusitis