Injury to the skin initiates a cascade of events that is collectively known as wound healing. Wound healing attempts to restore the barrier function as well the tensile strength to the injured skin. When healing deviates from its orderly pattern, abnormal or hypertrophic scarring can result. Although pigment and vascular alterations are often transient in nature,
textural changes caused by collagen disruption can be permanent, particularly in the case of keloid scarring.
The wound-healing process is divided into 3 sequential yet overlapping stages known as inflammation, granulation, and remodeling.
The initial stage is characterized by a response to cutaneous injury involving inflammatory cells.
Neutrophils are the first cells present in an injury, and they serve to debride bacteria and necrotic tissue as well as recruit other mediators.
Subsequently, macrophages arrive and elaborate a variety of cytokines, including vascular endothelial growth factor (VEGF), thereby creating an environment that promotes granulation tissue formation.
During the proliferative phase, fibroblasts arrive, proliferate, and deposit collagen, which initially consists of type III and later, type I.
Simultaneously, angiogenic factors released into the wound environment stimulate the formation of new capillaries. Keratinocytes also migrate across the wound, leading to reepithelialization.
During remodeling, there is simultaneous collagen formation and degradation, while the presence of myofibroblasts contribute to increasing the tensile strength within the wound.
Granulation tissue deposition wanes as the cells responsible during this stage undergo apoptosis; failure for this to occur may result in a hypertrophic scar.
In the case of a hypertrophic scar, an overzealous healing response occurs, in which fibroblasts, small vessels, and collagen fibers are arranged in a nodular pattern.
Alternatively, collagen can be inadequately replaced and, as a result, can form a pitted appearance resembling the surface of a golf ball.
Although scars rarely pose a significant health risk, patients with exaggerated scarring can present with physical and psychosocial distress.
The physician should aim to minimize scar formation or at least anticipate its severity, considering the patient’s history of hypertrophic/keloid scarring, as well as body site (as certain regions sustain greater tension, leading to an increased risk of scarring).
The purpose of this article is to review the strengths and limitations of current laser technology used to improve the appearance and symptomatology of hypertrophic scars, keloids, striae, atrophic scars, and acne scars.