Scars: causes, symptoms, diagnosis, treatment

A scar (cicatrix) is newly formed connective tissue at the site of damaged skin and deeper tissues.

Scars are formed as a result of trauma, surgical incisions, and ulceration of a number of skin eruptions (papules, tubercles, nodes, etc.). Scars are classified as a group of secondary eruptive elements. Normotrophic, hypertrophic, atrophic, and keloid scars are distinguished.

A normotrophic scar is a scar that is located at the level of the skin.

A hypertrophic scar is a scar that protrudes above the skin level. It indicates active synthesis of fibrous structures in newly formed connective tissue. Hypertrophic scars can occur with severe acne, especially when localized on the skin of the chin and lower jaw. After resolution of indurative, phlegmonous and conglobate acne, "vicious" scars (papillary, uneven with scar bridges) are formed, with comedones "sealed" in them. Hypertrophic scars should be differentiated from indurative acne, atheromas. The key point in differential diagnosis is the smoothness of the skin pattern, typical of a scar.

An atrophic scar is a scar that is located below the skin level. It indicates a small amount of fibrous structures in the newly formed connective tissue. Round atrophic scars with clear contours are formed after chickenpox. Atrophic scars of various sizes are characteristic of acne. In some cases, when the superficial perifollicular part of the dermis is damaged as a result of an inflammatory reaction, small point atrophic scars (ice-pick scars) may appear. Such manifestations should be differentiated from large-pored skin, which may be a consequence of its dehydration. In this case, the skin in the cheek area, less often the forehead, chin is grayish, thickened, has a "porous" appearance (resembles an orange peel). Atrophic scars are often depigmented. They should be differentiated from depigmented secondary spots, perifollicular elastosis, vitiligo.

A 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, pain). Keloid scars are uncontrolled benign proliferation of connective tissue at the site of skin damage.

Exogenous predisposing factors are skin incisions perpendicular to tension lines, constant presence of foreign bodies in the skin (earrings, ritual objects, etc.). Endogenous factors include genetic predisposition, age and hormonal features. Clinically, a keloid is a dense tumor-like connective tissue formation of pink, red or bluish color, of various shapes, with a shiny, smooth surface, sometimes lobular. The skin in the keloid zone is tense, there may be telangiectasias on its surface. During periods of active growth, the marginal zone of keloids is the brightest, connective tissue outgrowths ("cancer pincers") are clearly visible, capturing previously healthy areas of the skin. This is the feature that distinguishes keloids from hypertrophic scars. There are high-risk zones for keloid localization (ear lobes, neck, chest, back) and zones where they are not described (skin of the eyelids, genitals, palms, soles). There are also indications of malignancy of long-existing keloids, especially in areas of constant trauma. Keloid scars are differentiated from hypertrophic scars, dermatofibroma, fibrosarcoma, scleroderma-like basalioma and other dermatoses.

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

When the destructive pathological focus is localized on the scalp, there is no hair in the area of cicatricial atrophy, which is why this process is called cicatricial alopecia.

The nature of the scar largely depends 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 at the site of a particular injury.

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

1. Traumatic edema phase. Immediately after the injury, hemorrhage and edema occur in the area of tissue damage, leading to tissue hypoxia. Traumatic edema develops against the background of sharp disorders of blood and lymph circulation and increases over the course of 24 hours. The edema can be quite pronounced, which leads to compression of the surrounding tissues. Vasospasm occurs around the site of injury, and subsequently multiple thrombi form in vessels of different calibers. Edema and thrombosis lead to local tissue necrosis in the site of injury. Usually, by the end of 3 days, traumatic edema decreases.
2. Inflammation phase. On the 2nd-3rd day, demarcation inflammation develops. It should be emphasized that inflammation is a protective and adaptive reaction that develops at the border with necrotic tissues. Neutrophilic granulocytes begin to migrate to the site, the main function of which is to delimit necrotic masses, resorption and phagocytosis of microorganisms. Somewhat later, macrophages appear in the site of injury, which play a major role in the process of final wound cleansing. These cellular elements phagocytize tissue detritus and disintegrated neutrophilic leukocytes (the so-called neutrophilic detritus). Fibroblasts also migrate to the wound.
3. Proliferation phase. Begins on the 3rd-5th day from the moment of injury and is characterized by active proliferation of migrated fibroblasts. As a result, the number of fibroblasts increases sharply, and they become the predominant cells in the wound. In the future, their biological role will be to form new connective tissue.
4. Synthesis phase. By the 5th day from the moment of damage, fibroblasts begin to actively synthesize the intercellular substance, including glycosaminoglycans and collagen protein. First, non-sulfated glycosaminoglycans accumulate in the tissue, and then the content of sulfated ones increases (for example, chondroitin sulfates C). Collagen fibers are assembled from collagen in the intercellular substance of the connective tissue of the dermis. At the same time, angiogenesis occurs in the area of the former defect - the growth of numerous new blood vessels (hemocapillaries). In this way, granulation tissue is formed.
5. Scarring phase. Starting from the 14th day after the injury, the number of cellular elements gradually decreases, and the vessels in the granulations become empty. In parallel, the mass of newly formed collagen fibers increases, forming bundles of varying thickness and orientation. Fibroblasts differentiate into functionally inactive fibrocytes. Thus, dense, unformed fibrous connective tissue of the scar begins to form. At the same time, 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 activity of fibroclasts and macrophages due to the enzyme collagenase (matrix metalloproteinase).
6. Hyalinization phase. This phase usually starts on the 21st day from the moment of injury. It is characterized by the saturation of the already formed scar with hyaline.

Simultaneously with the maturation of the scar and hyalinization, epithelialization occurs - marginal and insular. Marginal epithelialization is understood as filling the epidermal defect due to the active proliferation of basal keratinocytes from the side of the intact skin. Insular epithelialization occurs 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, the autoimmune theory plays a special role in the pathogenesis of this pathology. It is believed that when the skin is injured, tissue antigens are released, which triggers the processes of auto-aggression and autoimmune inflammation of the connective tissue (the presence of antibodies to fibroblast nuclei is assumed). It has been shown that keloid scars develop as a result of delayed maturation of granulation tissue due to high activity of fibroblasts and the preservation of a large number of mucopolysaccharides in the interstitial substance. Over time, the activity of fibroblasts may decrease somewhat, but does not stop completely (unlike other scars), the keloid continues to grow, capturing healthy skin. In the thickness of such a scar, defective collagen fibers are formed, formed mainly by collagen type VII, there is a large number of functionally active fibroblasts, mast cells and other cellular elements. With further evolution, distinct hyalinization of the keloid tissue is noted, followed by loosening and resorption of hyaline (phases of swelling, compaction, softening).

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

Principles of Scar Therapy

Scar therapy depends on the nature of the element and the time of its occurrence. External therapy, various physiotherapeutic methods, chemical and physical peels, injections of various drugs, laser "polishing", dermabrasion, surgical excision are used. The most promising is a comprehensive approach using (sequentially or simultaneously) several methods.

For normotrophic scars, external preparations are used to improve connective tissue metabolism (Curiosin, Regecin, Mederma, Madecassol, Contractubex), injection (intradermal injections - mesotherapy) and physiotherapeutic methods. Active moisturizing and superficial peelings can be used to smooth out the skin surface. In cases of irregularly shaped normotrophic scars, surgical treatment with subsequent application of "cosmetic" sutures may be indicated.

In case of atrophic scars, external preparations that improve connective tissue metabolism and physiotherapeutic methods can be used. Of the injection methods, peelings are used on individual large elements. The use of superficial and median peelings is effective for multiple atrophic scars (for example, after acne). In case of deep atrophic scars, dermabrasion is used. In recent years, cellular technologies have become widely developed.

In case of stretch marks, an examination is recommended to identify possible endocrine predisposing factors. Active moisturizing is recommended. Externally, both agents that affect the metabolism of connective tissue and special preparations (for example, Fitolastil, Lierac, etc.) are prescribed. Intradermal injections of various preparations and microdermabrasion may also be indicated. It should be emphasized that the best aesthetic effect is achieved when acting on fresh, actively blood-supplied pink foci.

For hypertrophic scars, both external agents that improve connective tissue metabolism and topical glucocorticoids are used. The external drug Dermatix is also popular, having both an occlusive effect and an effect on connective tissue metabolism. Of the injection methods, glucocorticosteroid injections are used. Laser resurfacing is also prescribed. Individual hypertrophic scars are removed surgically or with a laser. Chemical and physical peels are then used. In recent years, cellular technologies have begun to develop widely.

In the case of keloid scars, the issue of a single therapeutic approach to their treatment has not yet been resolved, and the problem of radical treatment of keloids remains unresolved. The literature describes many methods of systemic therapy of keloids (cytostatic drugs, glucocorticosteroids, synthetic retinoids, alpha-, beta-interferon drugs), which have not proven themselves in terms of therapeutic effectiveness. At the same time, their side effects exceed the severity of keloids. Some authors persistently propose destructive methods of influencing keloid scars (surgical excision, laser destruction, electrodiathermocoagulation, cryodestruction, etc.).

Many years of experience in treating such patients indicate a categorical contraindication to destructive methods of treatment without further suppression of fibroblast activity. Any injury to a keloid leads to even more severe relapses of keloids, accelerates their peripheral growth.

At various stages of keloid formation, general and local therapeutic effects are used, often in combination. Thus, with relatively "fresh" and small keloids that have existed for no more than 6 months, the method of intra-focal administration of prolonged steroids in the form of suspensions (Diprospan, Kenalog, etc.) is very effective.

Given the resorptive effect of the 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, age of patients, etc.). A single dose and frequency of administration depend on the area of keloids, drug tolerance, and the presence of contraindications. Such therapeutic effects allow one to achieve suppression of fibroblast activity in the keloid and initiate atrophy processes. The clinical effect is assessed no earlier than after 2-3 weeks: blanching, flattening and wrinkling of the scar, decreased itching and soreness. The need for repeated administration of the steroid into the scar is assessed individually based on the achieved clinical results, but not earlier than 3 weeks after the first administration (given the general resorptive effect of the drug). One should take into account possible side effects arising in connection with the intra-scar administration of prolonged steroids:

• pain at the time of administration (it is advisable to mix the suspension of the steroid drug with local anesthetics);
• a few days after the injection, local hemorrhages may appear in the scar tissue with the development of necrosis;
• formation of milium-like inclusions at the injection sites (aggregation of the drug base);
• when introducing 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 identical to systemic steroid therapy are possible.

The method of choice may be a combination of surgical excision and intralesional steroid administration. Surgical excision of old and extensive keloids is performed in a surgical clinic (preferably in a plastic surgery clinic) with subsequent application of an atraumatic suture. After 10-14 days (after removing the sutures), prolonged steroid drugs are administered into the fresh linear scar using the diffuse infiltration method. Such tactics prevent recurrent keloid formation and provide a good cosmetic effect.

In cases of multiple and large keloids, impossibility of glucocorticosteroid therapy, it is possible to prescribe long courses of D-penicillamine in a daily dose of 0.3-0.5 g for 6 months under the control of the platelet level in the peripheral blood and individual tolerance. The exact mechanism of action of this drug on the condition of connective tissue has not been clarified. 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 numerous side effects, which complicates its use in a beauty salon.

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

Pressure bandages, clips, etc. are very popular, but not always effective. Externally, in addition to the above-mentioned means that affect the metabolism of connective tissue, the drug Dermatix is used.

However, it should be noted that none of the currently known methods of therapy leads to the complete disappearance of keloids, but only to a certain decrease in their activity. Any destructive methods without subsequent intra-scar injection of glucocorticosteroids only aggravate the situation, leading to even more severe relapses.

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