The process of wound healing and eventually scar formation includes 3 overlapping phases that restore the skin. In order, the stages are inflammatory, proliferative, and remodeling.⁸,⁹ The first phase, inflammatory, takes 1 to 3 days and is characterized by hemostasis. Hemostasis is the process by which the body stops bleeding by the formation of clot composed of platelets and clotting factors. At the same time, neutrophils, macrophages, and other immune cells arrive to fight foreign particles at the wound site. The next phase is the proliferative phase and lasts from 4 to day 21. In this stage of wound healing, certain cells perform specific tasks. To restore the integrity of the skin, the cells work together; keratinocytes multiply and cover the epidermis, the outermost skin layer, in a process called re-epithelialization; endothelial cells generate blood vessels; and fibroblast cells form new collagen. The final stage of the wound healing
process, the remodeling phase, lasts from day 21 to year 1. Throughout this phase, new collagen replaces the old tissue and the wound begins to contract, prompted by myofibroblast cells. This action establishes scar formation and enhances wound strength and takes more than a year.⁸ Ideally, by the end of the wound healing process, the scar will form with a faint, fine skin-colored scar line without any other symptoms. Especially during the last remodeling phase, if anything goes wrong during the wound healing process, the wound may heal abnormally with pathological scarring.⁹

Certain risk factors contribute to particular people developing abnormal scars. The size and depth of the scar as well as the direction are intuitive factors. Anatomical location of the wound is also a risk factor. The shoulders, anterior chest, lower abdomen, and skin over bony prominences, as well as other locations with little blood supply, scar poorly.¹⁰ Personal and family history of scars, age, and skin tone are other factors that contribute to the scar formation.¹⁰ Medication being taken can also interfere with the wound healing process. The doctor should be informed of any of the above-mentioned known risk factors before surgery or procedure so that prophylactic treatment can be assigned before the scar itself needs to be treated.

In surgical hypertrophic scars, the cause of the scar is the surgery itself. Specifically, traumas to the lower deep dermis layers in areas where the skin is tighter or there is additional muscle tissue are most susceptible to the development of hypertrophic scars. Adverse healing factors such as infection, excess tension, and repeat traumas are associated with hypertrophic scars.¹¹ Hypertrophic scars form in the presence of elevated levels of TGF-β. Their characteristic elevated, uneven appearance is due to the body producing new collagen fibers at a rate that exceeds the destruction of old collagen.¹¹ In this case, the proportion of type III to type I collagen in the scar is higher than in normal skin. The accumulation of excess collagen results in the raised hypertrophic scar.¹¹

Keloids form by the random organization of type III collagen fibers in a dense connective tissue matrix. This ratio of type III to normal collagen is higher in keloid scars than in other scars.¹¹ This is contrary to normal scars that feature collagen bundles arranged parallel to the skin surface. Keloids are ischemic as compared with adjacent normal tissue. It is thought that the greater expression of hypoxia-induced factor-1α and a marked decrease in vascular density contribute to this nature. Research suggests that fibroblasts and myofibroblasts are responsible for the increased deposition of collagen.¹¹ This is indicated by the increased levels of fibronectin produced by fibroblasts. Other theories show keloid formation as stimulated by an allergic, hormone-stimulated, or hypoxia-induced response. Recent studies report keloids as a product of insulin-like growth factors. Scientists generally believe genetic factors impact keloid formation, as certain populations and families form keloids more often (see also chapter 8.2).