Scar: causes, symptoms, diagnosis, treatment

Cicatrix is a newly formed connective tissue in place of damaged skin and deeper tissues.

Scars are formed due to injuries, surgical incisions, as well as ulceration of a number of skin eruptions (papules, tubercles, knots, etc.). Scars are referred to a group of secondary vysypnyh elements. There are normotrophic, hypertrophic, atrophic and keloid scars.

Normotrophic scar is a scar that is located at the level of the skin.

Hypertrophic scar is a scar that protrudes above the skin level. Indicates active synthesis of fibrous structures in the newly formed connective tissue. Hypertrophic scars can occur with severe acne, especially when they are located on the skin of the chin, the lower jaw. After the resolution of inducible, phlegmonous and conglobate acne, "perverse" scars (papillary, uneven with scarring bridges) are formed, with "comedones" sealed in them. Hypertrophic scars should be differentiated from inducible acne, athere. The key point of differential diagnosis is the smoothness of the skin pattern, typical for the scar.

Atrophic scar is a scar that is below the skin level. Indicates a small number of fibrous structures in the newly formed connective tissue. Rounded atrophic scars with distinct contours are formed after chicken pox. Various atrophic scars are characteristic for acne. In some cases, when the surface perifollicular part of the dermis is damaged as a result of an inflammatory reaction, small point atrophic scars (ice-pick scars) may appear. These manifestations should be differentiated from large-porous skin, which may be a consequence of its dehydration. At the same time, the skin in the region of the cheeks, rarely the forehead, the grayish chin, is thickened, has a "porous" appearance (resembles an orange peel). Atrophic scars are often depigmented. They should be differentiated from de-pigmented secondary spots, perifollicular elastosis, vitiligo.

Keloid scar is a pathological scar that protrudes above the skin level and is characterized by active peripheral growth, especially after its excision, and subjective sensations (itching, paresthesia, soreness). Keloid scars are uncontrolled benign proliferation of connective tissue at the site of skin damage.

Exogenous predisposing factors are cuts of the skin perpendicular to the tension lines, the permanent presence of foreign bodies (earrings, ritual objects, etc.) in the skin. Endogenous factors include genetic predisposition, age and hormonal features. Clinically, the keloid is a dense tumor-like connective tissue formation of pink, red or cyanotic color, of various forms, with a shiny, smooth surface, sometimes lobular. The skin in the keloid zone is tense, and there may be telangiectasia on its surface. During the periods of active growth, the marginal zone of the keloids is the brightest, the connective tissue outgrowths ("claws of the cancer") that capture previously healthy areas of the skin are clearly visible. It is this feature that distinguishes keloids from hypertrophic scars. Areas of increased risk for localization of keloids (earlobes, neck, chest, back) and areas where they are not described (skin of the eyelids, genitals, palms, soles). There are also indications of malignization of long-lived keloids, especially in areas of permanent trauma. Keloid scars differentiate from hypertrophic scars, dermatofibromas, fibrosarcomas, scleroderm-like forms of basal cell and other dermatoses.

Fresh scars have a pinkish or reddish color due to their active vascularization. Any scar can be pigmented and depigmented. If the connective tissue is formed at the site of the pathological process without a previous disruption of the integrity of the skin, then this process is called cicatricial atrophy. It develops in tuberculous lupus, discoid and disseminated lupus erythematosus, scleroderma and some other dermatoses. A special case of cicatricial atrophy is striae, which occur at the site of chronic stretching of tissues. Striae can be formed with an increase in body weight, they are characteristic for pregnancy, as well as various endocrine disorders (eg, disease and Itenko-Cushing syndrome, including when taking systemic glucocorticosteroids). It is also possible to form striae in adolescents on the back perpendicular to the vertebral column with their rapid growth.

When the destructive pathological focus is located on the skin of the scalp in the area of cicatricial atrophy, there is no hair, so this process is called cicatricial alopecia.

The nature of the scar depends largely on the depth of action of the damaging factor, the inflammatory process, as well as on individual, genetically determined features of the formation of connective tissue on the site of a particular injury.

Let us consider some morphological features of the formation of cicatricial changes in the example of post-natal. The following phases are distinguished: traumatic edema, inflammation, proliferation, synthesis, scarring and hyalinization.

1. The phase of traumatic edema. Immediately after the injury in the area of tissue damage, hemorrhage and edema leading to tissue hypoxia occur. Traumatic edema develops against the background of sharp disorders of blood and lymph circulation and increases over a period of 1 day. Edema can be quite pronounced, which leads to compression of surrounding tissues. Around the focus of damage, vasospasm arises, and in the future, multiple thrombi form in vessels of different calibers. Edema and thrombosis lead to local tissue necrosis in the lesion focus. Usually by the end of 3 days, traumatic edema decreases.
2. The phase of inflammation. On the 2nd-3rd day, demarcation inflammation develops. It should be emphasized that inflammation is a protective-adaptive reaction that develops on the border with necrotic tissues. Neutrophil granulocytes begin to migrate to the focus, the main function of which is the delineation of necrotic masses, resorption and phagocytosis of microorganisms. Somewhat later, macrophages appear in the lesion focus, which play a major role in the final purification of the wound. These cellular elements phagocytize tissue detritus and disintegrated neutrophilic leukocytes (the so-called neutrophil detritus). Fibroblasts also migrate to the wound.
3. The phase of proliferation. It begins on the 3rd-5th day after the injury and is characterized by active proliferation of migrated fibroblasts. As a result, the number of fibroblasts increases dramatically, and they become the predominant cells in the wound. In the future, their biological role will consist in the formation of a new connective tissue.
4. Phase synthesis. By the 5th day since the injury, fibroblasts are actively synthesizing an intercellular substance, including glycosaminoglycans and collagen protein. First, nonsulfated glycosoaminoglycans accumulate in the tissue, and then the content of sulfated (for example, chondroitin sulfates C) increases. From the collagen in the intercellular substance of the connective tissue of the dermis, collagen fibers are assembled. Simultaneously, angiogenesis occurs in the region of the former defect, the growth of numerous new blood vessels (hemocapillaries). Thus, the granulation tissue is formed. 
5. The phase of scarring. Starting from the 14th day from the moment of damage, a gradual decrease in the number of cellular elements occurs, the vessels in the granulations empty. In parallel, a mass of newly formed collagen fibers grows, which form bundles of different thickness and orientation. Fibroblasts differentiate into functionally inactive fibroblasts. So begins to form a dense unformed fibrous connective tissue of the rumen. In this case, the excessive deposition of collagen and the main substance of the connective tissue is prevented by partial death of fibroblasts, a decrease in the synthetic activity of collagen-forming cells, and an increase in the collagenolytic activities of fibroblasts and macrophages due to the enzyme collagenase (matrix metalloproteinase).
6. The phase of hyalinization. This phase is usually started from the 21st day after the damage. Characterized by impregnation with the hyaline of the already formed scar.

Simultaneously with the ripening of the rumen and hyalinization, epithelialization takes place - marginal and islet. By marginal epithelialization is meant the filling of a defect in the epidermis due to the active proliferation of basal keratinocytes from the intact skin. Ostrovaya epithelization is due to the intensive proliferation of cambial epithelial cells of the skin appendages enclosed in the tubercles of the hair follicles, as well as the terminal sections and excretory ducts of the sweat glands.

As for keloid scars, in the pathogenesis of this pathology a special place of the autoimmune theory is assigned. It is believed that when the skin is traumatized, tissue antigens are released that trigger the processes of auto-aggression and autoimmune inflammation of the connective tissue (it is assumed that antibodies to the fibroblast nuclei are present). It is shown that keloid scars develop as a result of the delay in the maturation of granulation tissue caused by high activity of fibroblasts and the preservation of a large amount of mucopolysaccharides in the interstitial material. Over time, the activity of fibroblasts may somewhat decrease, but does not completely stop (unlike other scars), the keloid continues to grow, capturing healthy skin. In the thickness of this scar are formed inferior collagen fibers, formed mainly collagen type VII, there is a large number of functionally active fibroblasts, mast cells and other cellular elements. In the course of further evolution, a distinct hyalization of keloid tissue is noted, followed by loosening and resorption of hyaline (swelling, compaction, softening phases).

It should be emphasized that knowledge of the features of the stages of scar formation can be useful for practicing specialists in choosing tactics for timely impact on the emerging and already formed scar tissue.

Principles of scar therapy

Scar treatment depends on the nature of this element and the timing of its occurrence. They use external therapy, various physiotherapy techniques, chemical and physical peelings, injections of various drugs, laser "grinding", dermabrasion, surgical excision. The most promising is an integrated approach using (sequentially or simultaneously) several techniques.

In normotrophichecic scars, external preparations are used that improve the metabolism of connective tissue (Kuriozin, Regecin, Mederma, Madecassol, Kontraktubeks), injections (intradermal injections - mesotherapy) and physiotherapy techniques. To smooth the surface of the skin, active moisturizing and superficial peels can be used. In cases of irregular form of normotrophic rumen, surgical treatment with subsequent application of "cosmetic" sutures may be indicated.

With atrophic scars, external preparations can be used that improve the metabolism of connective tissue, physiotherapy techniques. From the injection methods on some large elements apply peelings. The use of surface and medial peelings is effective for multiple atrophic scars (for example, after acne). At deep atrophic scars use a dermabrasion. In recent years, cellular technologies have become widespread.

In the case of stretch marks, a check is recommended to identify and possible endocrine predisposing factors. Recommend active hydration. External appoint as a means of affecting the metabolism of connective tissue, and special drugs (for example, Fitolastil, "Lierac", etc.). Intradermal injections of various drugs and microdermabrasion may also be indicated. It should be emphasized that the best aesthetic effect is achieved when exposed to fresh, actively blood-filled foci of pink color.

When hypertrophic scars are used as external means, improving the metabolism of connective tissue, and topical glucocorticoids. The external preparation Dermatix, possessing both an occlusive effect, and influence on a metabolism of a connecting tissue is popular also. From injecting techniques, the cicatrixation of the cicatrix with glucocorticosteroids is used. Assign also laser resurfacing. Individual hypertrophic scars are removed surgically or with the help of a laser. In the future, chemical and physical peels are used. In recent years, cell technologies have become widespread.

With keloid cicatrices, the question of a single therapeutic approach to their treatment has not yet been resolved, and the problem of radical treatment of keloids remains unsolved. In the literature, many methods of systemic therapy of keloids have been described (cytotoxic drugs, glucocorticosteroids, synthetic retinoids, preparations of alpha, beta interferon), which have not justified themselves for therapeutic effectiveness. At the same time, their side effects are heavier than keloids. Some authors persistently suggest destructive methods of influence on keloid scars (surgical excision, laser destruction, electrodiathermocoagulation, cryodestruction, etc.).

Long-term experience of conducting such patients testifies to a categorical contra-indication of destructive methods of influence without further inhibition of fibroblast activity. Any keloid injury leads to even more severe relapses of keloids, accelerating their peripheral growth.

At various stages of the formation of keloids, general and local therapeutic effects are used, often combining them. Thus, with relatively "fresh" and small-sized keloids existing no more than 6 months, the method of intra-arterial administration of preparations of prolonged steroids in the form of suspensions (Diprospan, Kenalog, etc.)

Given the resorptive effect of drugs, one should remember the general contraindications to the administration of systemic glucocorticosteroid hormones (peptic ulcer of the stomach and duodenum, diabetes mellitus, chronic foci of infection, the age of patients, etc.). The single dose and the frequency of administration depend on the area of keloids, the tolerability of the drug, and the presence of contraindications. This therapeutic effect allows to achieve the suppression of the fibroblast activity in the keloid and to start the processes of atrophy. Clinical effect is estimated not earlier than 2-3 weeks: blanching, flattening and wrinkling of the scar, reduction of itching, soreness. The need to reintroduce the steroid into the scar is evaluated individually based on the clinical results achieved, but not earlier than 3 weeks after the first administration (taking into account the general resorptive effect of the drug). It is necessary to take into account possible side effects that arise in connection with the intra-administration of prolonged steroids:

• painfulness at the time of administration (it is advisable to mix the suspension of the steroid drug with local anesthetics);
• a few days after the administration, the appearance of local hemorrhages in the scar tissue with the development of necrosis;
• the formation of milium-like inclusions at the site of drug administration (aggregation of the drug base);
• with the introduction of prolonged steroids into keloids located near the face (earlobes, neck), some patients experience regional steroid acne;
• with long courses of administration and large quantities of the drug, complications that are identical to systemic steroid therapy are possible.

The method of choice can be a combination of surgical excision and intraocular steroids. Surgical excision of old and extensive keloids is carried out under the conditions of a surgical clinic (preferably in a plastic surgery clinic) followed by the imposition of an atraumatic suture. After 10-14 days (after removal of stitches) in a fresh linear scar It is advisable to introduce prolonged steroid preparations by diffuse infiltration. This tactic prevents the re-formation of the keloid and gives a good cosmetic effect.

In cases of multiple and large areas of keloids, the impossibility of glucocorticosteroid therapy, it is possible to administer long-term courses of D-penicillamine at a daily dose of 0.3-0.5 g for 6 months under the control of platelet levels in peripheral blood and individual tolerability. The exact mechanism of action of this drug on the state of connective tissue is not clear. It is known that it destroys circulating immune complexes, reduces the autoantigenicity of immunoglobulin G, inhibits the production of rheumatoid factor and the formation of insoluble collagen. This method is less effective and can be accompanied by many-numbered side effects, which makes it difficult to use in a cosmetology salon.

The method of choice is intramuscular injection every other day 5 ml. Solution of unithiol in a course dose of 25-30 injections, combining this therapy with occlusive dressings of topical steroids. It is permissible to carry out cryomassage of keloids (but not cryodestruction!). These techniques give a positive effect in the form of pitting and flattening of keloid scars, as well as cessation of their peripheral growth, a significant reduction in subjective unpleasant sensations.

Very popular, but not always effective pressure bandage, clip, etc. Outside, in addition to the above means, affecting the metabolism of connective tissue, use the drug Dermatics.

Nevertheless, it should be noted that none of their known methods of therapy do not lead to the complete disappearance of keloids, but only to a certain decrease in their activity. Any destructive methods without subsequent intra-intramuscular administration of glucocorticosteroids only make the situation worse, leading to even more severe relapses.

[1], [2], [3], [4]