When the skin is damaged, following an injury or due toacne for instance, it responds by initiating several defence mechanisms to combat inflammation. Immune cells, such as macrophages, are first recruited to the injury site. They eliminate cellular debris and bacteria present in the wound, thus promoting an environment conducive to tissue regeneration. As inflammation subsides, the phase of cellular proliferation begins. Fibroblasts, specialised cells, multiply and migrate towards the wound. They are responsible for the production of collagen, a protein essential for the formation of scar tissue, as well as other components of the extracellular matrix.
Simultaneously, the process ofangiogenesis is initiated, meaning that new blood vessels are formed from the existing vessels damaged by the injury. The endothelial cells within the blood vessels respond to the damage by dividing and migrating towards the injured area. They then form new blood vessels, which allows for the delivery of nutrients, oxygen, and growth factors necessary for healing.
Finally, the healing process continues with the re-epithelialisation, or the regeneration of the epidermis. This occurs via the activation of keratinocytes, the constitutive cells of the epidermis. The keratinocytes located at the periphery of the wound multiply and migrate towards the injury zone, interacting with the components of the extracellular matrix. During their migration, they differentiate, meaning they undergo morphological and molecular changes to transform into mature epithelial cells. These differentiated cells form a new layer of epidermis, similar to the one that existed before the injury.