Ways of skin regeneration

In response to damage to the skin, neuro-humoral mechanisms come into play that aim to restore the body's homeostasis through the closure of a wound defect. And the faster is the restoration of the integrity of the skin (there is epithelization of the wound), the greater the likelihood of obtaining either an abruptly healing or healing with the formation of aesthetically acceptable scars. The speed of reparative processes in the skin depends on the area and depth of damage, the state of reactivity of the macroorganism, the presence of concomitant pathology, the state of the microcirculatory bed, the microelement composition of the tissues, the degree of infection of the wound, the rationality of treating the wound defect and. Etc.

The result of a skin injury can be:

• complete restoration of the skin, without visible differences from healthy skin;
• hyperpigmented skin;
• depigmented skin:
• atrophic skin;
• one of the variants of physiological scars;
• pathological scars.
• cicatricial contractures.

The speed of epithelialization of the wound is one of the key moments in the optimal restoration of the skin defect. The epithelial potential of the wound, in turn, directly depends on the remaining fragments of the basal membrane with the basal keratinocytes of the epidermis: epithelial cells of the hair follicles, sebaceous and sweat glands and wound area, and also from the area of the injury.

1. Surface trauma of the rut, with damage to the epidermis to the basal membrane and the tips of the papillae, always heals without scarring due to increased proliferation of basal keratinocytes.

The dermis in this case remains practically intact, therefore the healing speed depends on the proliferative capacity of keratinocytes. Such a trauma can be with medial peelings, sandblast dermabrasion, abrasions, scratches, polishing of the skin with an erbium laser, surface burns of the second degree.

2. Trauma of the skin, located deeper than the tips of the papillae, causes damage to the basal membrane and capillaries of the superficial vasculature. Bleeding and pain are the first symptoms of such trauma.

Such damage to the skin occurs with operative dermabrasion by Schuman's cutter, carbon dioxide laser, deep peelings or a burn of II-IIIa degrees and heals, as a rule, without scars at the expense of preserved fragments of the basal membrane with basal keratinocytes, epithelial cells of the hair follicle and epithelium of gland ducts .

Keratinocytes survived near the skin defect, after receiving the information on the damage, begin to actively divide and rush to the bottom of the wound, crawl from the edges, creating first a monolayer of cells, and then a multilayered layer, under which the process of repairing the skin defect and restoring the skin .

When the skin is damaged at a given depth, hyperpigmentation may occur under the influence of solar radiation. Especially it concerns the skin of III and IV phototypes according to Fitzpatrick. An inflammatory reaction that occurs when the capillaries loops, leads to the stimulation of mast cells, the release of a large number of biologically active molecules, mediators of inflammation, histamine, stimulating the synthetic activity of melanocytes. They produce more melanin, which is transferred to keratinocytes and causes focal post-traumatic hyperpigmentation.

In aggravating circumstances (attachment of a secondary infection, a decrease in immunity, endocriomyopathy, thin skin treatment with a solution of potassium permanganate and other cases), the skin defect deepens below the basal membrane where the melanocytes are located. In these cases, after repair of the skin defect, a depigmented spot or atrophic skin may remain in its place, and in the absence of basal keratinocytes on the basal membrane and scar.

In addition, the probability of skin depigmentation is possible:

• at I and II skin phototypes;
• with chemical traumas that led to toxic damage to melanocytes;
• if there is a history of vitiligo;
• with deficiency of copper, iron, zinc, selenium, amino acid tyrosine, tyrosinase, etc.

3. Skin trauma below the scallops of the epidermis at the border of the papillary and reticular layer of the dermis almost always ends in scarring.

In the event that there are many skin appendages with preserved epithelial cells on the wound site, the reactivity of the organism is high, good blood supply, for example in children, the trauma can also end without the formation of pronounced scars, but the skin is most likely to be thin, atrophied with depigmented and sites. This, in fact, a happy occasion. Unfortunately, almost always after such an injury there are scars. In depth, such wounds are comparable to third-degree burns. The type of scars in this case can be different - from normo-atrophic to hypotrophic and keloid.

In the case of secondary infection, the presence of concomitant aggravating factors that reduce the reactivity of the organism, a protracted inflammation is possible, leading to a transition to an inadequate inflammatory reaction, an expansion and deepening of the area of destruction, and the appearance of hypertrophic or keloid scars.

The hypertrophic scar is equal to or even slightly smaller than the area of the wound defect, due to the contraction of the collagen fibers, but its relief extends beyond the level of the surrounding skin, creating the effect of (+) tissue.

Keloid scars also have (+) tissue, but they extend beyond the area of the previous wound.

4. Deep injuries with the destruction of underlying tissues, namely the pronounced layer of subcutaneous fat always heal with the formation of deforming scars. With the development of an adequate pathophysiological inflammatory reaction, scars of a hypotrophic type appear.

With the development of protracted inflammation, prerequisites arise for the formation of hypertrophic scars. Inflammatory reaction, converted into inadequate inflammation, in the presence of predisposing factors, leads to the accumulation of information and other biologically active molecules in the scar tissue that lead to the appearance of atypical fibroblasts with increased metabolism and corresponding secretory activity, which can become a morphological substrate for the appearance of a keloid scar.

When uninfected deep chipped or cut wounds of a small area below the scallops of the epidermis, the process of restoring the integrity of the tissue passes very quickly due to the adhesion of the edges of the wound and the marginal creeping of the keratinocytes. In this case, as a rule, normotrophic scars are formed.