Ways to restore the skin

In response to skin damage, neurohumoral mechanisms come into effect, aimed at restoring the body's homeostasis by closing the wound defect. And the faster the restoration of the integrity of the skin occurs (the wound epithelialization occurs), the greater the likelihood of either scarless 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 tissues, the degree of wound infection, the rationality of the treatment of the wound defect, etc.

Skin trauma can result in:

• 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 rate of wound epithelialization is one of the key moments in the optimal restoration of a skin defect. The epithelialization potential of a wound, in turn, directly depends on the preserved fragments of the basement membrane with basal keratinocytes of the epidermis: epithelial cells of hair follicles, sebaceous and sweat glands and the area of the wound, as well as on the area of the injury.

1. Superficial trauma to the rut, with damage to the epidermis down to the basement membrane and the tips of the papillae, always heals without scars due to increased proliferation of basal keratinocytes.

In this case, the dermis remains practically intact, so the healing rate depends on the proliferative capacity of keratinocytes. Such trauma can occur with median peelings, sandblasting dermabrasion, abrasions, scratches, skin polishing with an erbium laser, and superficial second-degree burns.

2. Skin trauma located deeper than the papillary tips results in damage to the basement membrane and capillaries of the superficial vascular network. Bleeding and pain are the first symptoms of such trauma.

Such skin damage occurs during surgical dermabrasion with a Schumann cutter, carbon dioxide laser, deep peelings or a burn of II - IIIa degrees and it heals, as a rule, without scars due to the preserved fragments of the basement membrane with basal keratinocytes, from the epithelial cells of the hair follicle and from the epithelium of the gland ducts.

The keratinocytes remaining near the skin defect, having received information about the damage through neurohumoral mechanisms, begin to actively divide and rush to the bottom of the wound, crawling from the edges, creating first a monolayer of cells, and then a multilayer layer, under which the process of reparation of the skin defect and restoration of the skin is completed.

When the skin is damaged at this depth, hyperpigmentation may occur under the influence of solar radiation. This is especially true for skin of Fitzpatrick phototypes III and IV. The inflammatory reaction that occurs when the capillary loops are damaged leads to stimulation of mast cells, the release of a large number of biologically active molecules, inflammation mediators, histamine, stimulating the synthetic activity of melanocytes. They produce a larger amount of melanin, which is transferred to keratinocytes and causes focal post-traumatic hyperpigmentation.

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

In addition, the possibility of skin depigmentation is possible:

• for skin phototypes I and II;
• in case of chemical injuries that lead to toxic damage to melanocytes;
• if there is a history of vitiligo;
• in case of deficiency of copper, iron, zinc, selenium, amino acid tyrosine, tyrosinase, etc.

3. Skin injuries below the ridges of the epidermis at the border of the papillary and reticular layers of the dermis almost always end in scarring.

In the event that there are many skin appendages with preserved epithelial cells at the site of the wound, the body's reactivity is high, there is good blood supply, for example in children, the injury may also end without the formation of pronounced scars, but the skin will most likely be thin, atrophied with depigmented areas. This is, in fact, a lucky chance. Unfortunately, scars almost always appear after such an injury. In terms of depth, such wounds are comparable to third-degree burns. The type of scars may vary - from normo-atrophic to hypotrophic and keloid.

In the case of a secondary infection, the presence of concomitant aggravating factors that reduce the body's reactivity, prolonged inflammation is possible, leading to a transition to an inadequate inflammatory reaction, 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 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 destruction of underlying tissues, namely a 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 prolonged inflammation, prerequisites for the formation of hypertrophic scars arise. The inflammatory reaction that has turned into inadequate inflammation, in the presence of predisposing factors, leads to the accumulation of information and other biologically active molecules in the resulting scar tissue, leading 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.

In uninfected deep punctured or cut wounds of small area below the ridges of the epidermis, the process of tissue integrity restoration occurs very quickly due to the adhesion of the wound edges and the marginal creep of keratinocytes. In this case, normotrophic scars are usually formed.