Turning to the discussion of the wound healing process itself, there are several important points to keep in mind. As we age, obeying the Heiflick rule (limited number of cell divisions), the number of niche cells decreases. As a consequence, the concentration of a person's own signaling molecules decreases, gradually reducing the skin's ability to repair. This is easily confirmed by a simple observation.
Reparation is triggered due to damage, with a continuous regeneration process, and is characterized by three phases:
Phase 1 - vascular reactions, exudation, edema, swelling, infiltration, fibrin shedding, and formation of the lesion;
Phase 2 - production of collagen, new formation of vessels, and most importantly - development of granulation tissue. At a young age, up to 12 years, this phase begins simultaneously with the first one, with a high concentration of niche cells and signaling molecules, which is why children rarely have residual scars;
Phase 3 - starts in the middle of the second phase and the older the person is, the earlier it "starts" and runs simultaneously with the second phase, lasts up to a year, leaving a scar.
Thus, the practical task is to activate the ancient evolutionary mechanism of wound healing by artificially increasing the concentration of signaling molecules in the wound. The higher the concentration of molecules, the earlier phase 2 starts, as in children, promoting faster and, importantly, scarless healing.
Traditionally, healing is characterized by two types of tension. Primary tension occurs without suppuration and formation of interstitial tissue with subsequent development of a linear scar; it proceeds in wounds with even and viable edges not more than 1 cm apart in the absence of wound infection. Secondary tension of the wound closes through suppuration with formation of visible connective tissue and subsequent development of rough scars; it occurs in case of wound infection development and presence of defects which do not allow the wound walls to close. The processes of inflammation and hypoxia contribute to excessive activation of fibroblasts, which actively produce collagen, the excess of which can disrupt the natural healing process and create a poor-quality scar.
It is important to note that healing under a scab (blood clot) occurs without formation of a scar with the preserved growth layer in the presence of fibrin and blood-forming elements. This is the next important detail for our attention - something has to fulfill the role of a scab. Usually it happens through hematoma formation, which provides stopping of bleeding from damaged vessels and creation of barrier preventing entry of microorganisms into the wound.
Simultaneously, a number of molecules of non-protein nature are released from the surface of the niche cells, which trigger the processes of active basal cell division, as it is known, forming the basis of granulation and epithelization islets.
Thus, artificially increasing the concentration of signaling molecules on the wound surface, we managed to stimulate granulation tissue growth hundreds of times faster than fibroblasts produce collagen. And the presence of a biopolymer film holding the exposure of these molecules in the wound, acting as a scab, only increased the efficiency.