傷口癒合概論
語言：中文
Wound healing requires a complex interaction and coordination of different cells and molecules. Any alteration in these highly coordinated events can lead to either delayed or excessive healing. Wound healing without complications is critical to the survival, as it restores the integrity of the skin and protects the individual from infection and dehydration. Adult wound healing involves a well orchestrated series of events leading to the repair of injured tissues, resulting in scar formation. The goal of any surgical or aesthetic procedure is to leave no scarring. For this, it is essential that wound healing should be optimized so that the skin heals without scars and as quickly as possible. A lot of research has been done on wound healing, but how much of this translates into actual clinical results remains to be seen.
Healing of acute wounds, triggered by tissue injury, consists of overlapping and highly coordinated phases of hemostasis, inflammation, proliferation and remodeling. When a breach of the skin’s integrity occurs, hemostasis is initiated by platelets through fibrin clot formation. Platelets also release various mediators of wound healing to attract macrophages and fibroblasts to the site of tissue injury. The inflammatory phase begins with the arrival of neutrophils followed later by macrophages and lymphocytes at the wound site. The proliferative phase is characterized by new blood vessel formation (angiogenesis), synthesis of extracellular matrix (ECM) components and re epithelialization. Following the proliferative phase, collagen remodeling begins, along with vascular maturity and regression; this process typically lasts 6 24 months from the time of injury.
The wound healing cascade may be arrested in any of these phases, leading to the formation of a chronic nonhealing wound. Many mediators including inflammatory cells, growth factors, proteases such as matrix metalloproteinases (MMPs) and cellular and extracellular elements play important roles in the process of wound healing. Alterations in one or more of these components may lead to the impaired healing.
Wound healing can also be negatively influenced by many exogenous factors, including concurrent diseases, such as diabetes, renal failure, malnutrition, smoking, radiation exposure, infection and an immunocompromised state. In the presence of these factors, wounds can fail to heal adequately, resulting in chronic wound formation. The wound healing process can occasionally go into overdrive, resulting in excessive healing and the formation of fibroproliferative scar like keloids and hypertrophic scars. This review provides a general overview of the physiology of wound healing, focusing specifically on how recent advances could translate into improved clinical outcomes.
