Material from the Forensic encyclopedia

Abrasion is superficial mechanical damage skin, no deeper than the papillary layer. It occurs as a result of the tangential impact of blunt or sharp (scratched) objects.

Abrasions - this is damage to certain layers of the epidermis or epithelium of the mucous membranes, in some cases, the papillary layer of the dermis is also damaged. (source?)

Depending on the depth, abrasions are divided into:

• superficial - damage only to the epidermis;
• deep - damage to all layers of the epidermis and the upper layers of the dermis.

The duration of the formation of abrasions

The average healing time is 10 to 14 days. However, the timing of the healing of abrasions can vary greatly depending on the depth of the injury and its size, on the localization (intensity of blood supply to areas of the body), age, condition immune systemcollateral damage.

V. N. Kryukov et al. (2001)

"... During external examination in the first hours after the formation of the abrasion, its bottom is sunken, the surface is pink-red, moist due to the constant release of lymph. In cases where the papillary layer is damaged, droplets of blood are added to the lymph.

After 6 hours, the bottom of the abrasion, as a rule, dries up, and a zone of hyperemia up to 1.0 cm wide is formed around it. At the same time, swelling (edema) increases and pain is noted. This process continues until the end of the first day. A crust is formed at the bottom, which has a yellowish-brown color. With deep abrasions with damage to the papillae, the crust is reddish-brown. The forming crust plays a protective biological role, protecting the damaged surface from contamination and infection.

The developing edema and cellular infiltration raise the crust, which by the end of the day is located at the level of the surrounding skin. At the end of the first day and at the beginning of the second, the crust becomes higher than the level of intact skin due to the development of a proliferative process - restoration of the damaged epidermis.

By this time the crust itself acquires a permanent dark brown color.

Since the processes of regeneration of the epidermis are more pronounced in the peripheral areas, where it is damaged, as a rule, less deeply, on the 3-5th day, peripheral exfoliation of the crust is observed ... which ends by the 7-10th day.

A pink surface remains in place of the crust that has fallen off, disappearing by the end of the second week ... "

Belikov V.K., Mazurenko M.D. (1990)

Akopov V.I. (1978)

"... the formation of a crust, on average, occurs 4-6 hours after the onset of an abrasion. The newly formed crust is tender, pale pink, located below the level of the surrounding skin. By the end of the 1st day, a clearly formed dense red crust is formed, which falls off in 7-12 days. However, a trace remaining after its fall away, we found a month or more after receiving an abrasion ... "

A.F. Kulik (1975)

"... the crust on the neck disappears in 5-6 days, on upper limbs - after 8-9, on the lower ones - after 9-11, on the stomach - after 10-13 days. "

A.F. Kulik (1985)

Stages of healing of abrasions of various ages and localization

Mukhanov A.I. (1974)

The surface of the fresh abrasion is pink-red, moist, soft, painful ...

After 6-12 hours, the bottom of the abrasion dries up; around the sediment, redness and swelling appear in the form of a ring up to 0.5 cm wide. By 24-36 hours, the surface of the abrasion becomes denser, the swelling and soreness disappear.

As noted by M.I.Raysky, in most abrasions (up to 70%) by 24 hours the bottom is covered with a brownish dense crust located above the skin level. The surface of the rest of the abrasions is sometimes moist and soft, more often dried, dense, brownish, located at the level of the skin (up to 8%) or below it (up to 21%). According to the observations of V.I. Akopov (1967), by the end of the first day, all abrasions have a crust, On the second day, the surface of the abrasions rises above the intact skin due to thickening of the crust ...

On the 3-4th day (according to V.I.Kononenko, more often on the 5th day), the crust along the edge begins to flake off and the abrasion is halved. Then there is peeling of the skin around the abrasion, its crust peels off over a large area and disappears after 1-2 weeks.

The surface at the site of the fallen off crust is at first pink, but within a week this color disappears, and the site of the abrasion ceases to differ from the surrounding skin. The healing of abrasions ends by 2-3 weeks ...

Abrasions heal faster healthy people, slower - in patients, in victims with severe injuries.

Kononenko V.I. (1959)

"... 24 abrasions were observed in people aged 11 to 56 years (mostly 11, 25, 30 and 56 years old). On the first day, the observation was carried out 4 times, on the second and third - 2 times, on the rest - 1 time every day. Localization of abrasions was different: lower leg, thigh, forearms, hands, neck and chest ... "

Taikov A.F. (1952)

(quoted from A.I. Mukhanov)

Terms of healing of abrasions in days (source unknown)

Employees of the Department of Forensic Medicine of the Kiev Institute for Advanced Training of Doctors summarized the data of various authors on the timing of healing of abrasions, depending on their location and offered the following table:

The source is unknown. If you know - write on the forum

No sources specified

A.P. Gromov distinguishes between superficial and deep abrasions. In a superficial abrasion, there are no upper and partially middle layers of the epidermis or completely upper, middle and partially germ (basal) layers; the latter usually remains in the depression between the papillae of the skin itself. Lymph accumulation is observed on the surface of a superficial abrasion. The latter mixes with particles of the destroyed epidermis and foreign inclusions and dries quickly, forming a thin pink crust.

In a deep abrasion, either the entire epidermis with the tops of the papillae is absent, or the upper layers of the dermis. In such cases, there is a massive accumulation of cut and lymph on the surface of the abrasion. Mixing with the remnants of the destroyed epidermis and foreign particles, the blood coagulates, forming at first a wet, and then a drying red crust.

According to V.I. Akopov all abrasions by the end of the first day after their occurrence are covered with crusts, on the second day - the surface of the abrasions rises above the intact skin.

A.F. Taikov distinguishes four stages in the healing of an abrasion:

• 1st - minus fabric; lasts for several hours;
• 2nd - crust formation; starts after a few minutes and lasts up to 4 hours (sometimes 2-4 days);
• 3rd - epithelialization and crust falling off; lasts from 5 to 7-9 days;
• 4th - traces remaining after the crust has fallen off; are found within 9-12 days, sometimes they persist up to 25 days.

According to V.G. Naumenko and V.V. Grekhov. the crust disappears in 7-12 days, traces of abrasion disappear in 10-12 days. Rubin V.M. and Krat A.I. observed crust fall off superficial abrasions on days 7-12, deep abrasions - on days 12-21, traces of abrasions can be distinguished even after 1.2-1.5 months.

Phases of wound healing and scar formation

Scars occur as a result of surgical treatment, any trauma, as well as after thermal, chemical and radiation damage to the skin, sometimes after infections. They pose a serious problem for surgeons and patients, as they remain for life and create significant cosmetic defects and sometimes cause functional impairment in the form of restriction of joint mobility.

The wound process is a wound healing process that begins immediately after tissue damage and includes three main phases: inflammatory, the phase of formation of granulation tissue, the phase of epithelialization and the organization of the scar.

1. Inflammatory (or exudative) phase.
It starts from the moment of injury and lasts about 5-7 days.
The body's primary response to injury is to stop bleeding. During the first hours after injury, they are biologically released from damaged tissues active substanceswhich cause vasoconstriction and activation of blood clotting factors. A fresh blood clot stops bleeding and creates conditions for further wound healing. After the bleeding stops, an inflammatory reaction develops. At this stage, a cascade of complex cellular reactions occurs, aimed at implementing the mechanism of inflammation. In this case, platelets secrete cytokines (factors of intercellular interactions), which attract leukocytes and fibroblasts to the wound, and also stimulate cell division and collagen synthesis. Leukocytes accumulated in the wound phagocytose foreign bodies and bacteria. After 24 hours, macrophages appear in the wound. They not only carry out phagocytosis, but also release chemotactic factors and growth factors. Growth factors stimulate the development of skin epithelium and vascular endothelium, collagen synthesis. During this phase, the wound defect is filled with new tissue, which plays an important role in wound healing. The so-called granulation tissue develops, in the construction of which fibroblasts play a decisive role. Most often at the end of this phase, the sutures are removed. postoperative wound (for 5-7 days). If there is tension in the area of \u200b\u200bthe suture, then it can disperse, since the edges of the wound are connected by granulation tissue, and not by a scar. To avoid this, the tension should be minimal or excluded.

Type of wound on the first day after surgery.

2. Proliferation (phase of formation of granulation tissue)
With a favorable course wound process this phase begins on the 7th day and lasts up to 4 weeks on average. In this phase, the wound defect continues to fill with granulation tissue, in the construction of which fibroblasts play a decisive role. They are responsible for both collagen production and the main substance of the extracellular space. Subsequently, the maturation of granulation tissue occurs, which consists of connective tissue, new germinating capillaries and inflammatory cells. For the growth of blood vessels and the maturation of collagen, the presence of cytokines in the wound, a sufficient content of oxygen, zinc, iron, vitamin C. When the granulation lining is ready, epithelial cells settle on it and close the wound. At the end of this stage, the edges of the wound are already connected by a young, immature scar, which still remains relatively easily extensible and well visible due to the large number of vessels it contains.
The scar at this time has a bright red color.

3. Formation and organization of the scar.
This phase starts around the 4th week and lasts for about 1 year. Starting from the 4th week, the number of cellular elements and vessels in the scar tissue decreases significantly. There is a transformation of a brighter and more visible scar into a scar less bright and therefore less noticeable. The wound is finally filled with connective tissue and epithelium. Collagen continues to grow: the delicate primary collagen is replaced by a coarser and stronger one. As a result, a scar is formed, the strength of which is 70–80% of the strength of the skin.
At the end of this phase, due to the contraction of smooth muscle cells, the edges of the wound converge.

During the wound process, there are three main periods.

First periodcharacterized by the melting of necrotic tissues, their sequestration into the external environment and cleansing of wound detritus. The duration of this period is determined by the amount of damage, the degree of infection of the wound, the characteristics of the organism and averages 3-4 days.

The initial reaction of the body to injury is vasospasm in the area of \u200b\u200bthe wound defect, followed by their paralytic expansion, increased permeability of the vascular wall and rapidly growing edema, which is called traumatic. The acidosis developed as a result of metabolic disorders and a change in the state of colloids contribute to the progression of traumatic edema.

The vasodilatation is accompanied by a violation of their permeability and is associated with the release of mainly histamine and partly serotonin. In response to damage and exposure to microbes, white blood cells migrate in large numbers from the blood vessels into the wound. This applies mainly to neutrophils capable of phagocytosis. Along with other enzymes, they secrete leukoprotease, which is used to destroy cell debris and phagocytosed microorganisms. In addition, a large number of histiocytes, macrophages, lymphocytes and plasma cells accumulate in the tissues. Along with this, in normal plasma there are oxins that facilitate phagocytosis, agglutinins that help to adhere and destroy bacteria, a factor that stimulates an increase in the release of leukocytes from the blood.

Concerning the mechanism of lysis of non-viable tissues and wound cleansing, the role of the microbial factor in this process should also be emphasized.

The inflammatory reaction can grow rapidly and already during the first day a so-called leukocyte shaft is formed, which develops on the border of viable and dead tissues, being a demarcation zone. All these processes lead to the preparation of damaged tissues for the healing process. In particular, fibrin deposited in the wound undergoes local fibrinolysis of plasmin, which appears due to the activation of plasmin by kinase. This leads to unblocking of lymph gaps and blood vessels, and inflammatory edema disappears. Starting from the third day, along with the predominant catabolic processes, anabolic processes come into play, the synthesis of the basic substance and collagen fibers by fibroblasts increases and capillaries are formed.

An increase in blood supply to the area of \u200b\u200binjury causes a decrease in local acidosis.

Second period -the period of regeneration, fibroplasia, begins from 3 to 4 days after injury. It is shorter, the less cells and tissues were injured when injured. A distinctive feature of this period is the development of granulation tissue, gradually completing the wound defect. In this case, the number of leukocytes sharply decreases. Macrophages continue to play an important role, but capillary endothelium and fibroblasts acquire great importance during the regeneration period.

Granulation tissue begins to form in the form of separate foci at the bottom of the wound. These foci are characterized by intensive neoplasm of capillaries as a result of the secretion of biologically active substances by mast cells. Granulation tissue, due to its richness in blood vessels and cells, looks juicy, bleeds easily and has a pinkish-red color. appearance granulations can be judged on the state of wound healing. Usually healthy granulations have a grainy appearance, bright red color, and their surface is moist and shiny. Pathological granulations are characterized by a smoother surface, they look pale, flaccid, vitreous-edematous, covered with a layer of fibrin. Their cyanotic shade indicates a deterioration in venous outflow, which causes such a color. In sepsis, the granulations are dark red and appear dry.

The causes of poor granulation formation can be both general and local. After their elimination, the appearance of granulations quickly changes and the process of filling the wound with scar tissue is restored.

Due to the large number of fibroblasts that form collagen fibers and interstitial substance, the wound cavity fills and at the same time the epithelium begins to creep from the edges due to the migration of cells to the newly formed granulations. The second fibroplastic period lasts from 2 to 4 weeks, depending on the location and size of the wound.

Third period- the period of scar reorganization and epithelialization, begins without any transition on the 12-30th day from the moment of injury and is characterized by a progressive decrease in the number of vessels, they become desolate. the number of macrophages, fibroblast mast cells decreases. In parallel with the maturation of granulation tissue, wound epithelialization occurs. The overly formed scar tissue rich in collagen fibers undergoes restructuring. These processes are typical for all tissues, they differ only in time. For example, skin heals much faster than fascia and tendons, which take 3-6 months to heal. At the same time, restoration of the skin begins after 24-48 hours and is determined by migration, division and differentiation of epithelial cells. With the primary wound healing, its epithelialization occurs on the 4th-6th day.

Phases of wound healing (according to M.I.Kuzin, 1977)The first phase is inflammation. The initial period of this phase in the wound is characterized by vasodilation, exudation, hydration and migration of leukocytes. Then phagocytosis and autolysis intensify, which helps to cleanse the wound from necrotic tissues. The duration of this phase is 1-5 days. In this phase, there is pain, fever, infiltration, and swelling in the wound.

The second phase is regeneration. During this period, recovery processes prevail in the wound. Tissue exudation is reduced. The synthesis of collagen and elastic fibers increases, which fill the tissue defect. The wound is cleansed, granulation tissue appears in it. Signs of local inflammation decrease - pain, temperature, infiltration. The duration of this phase is about a week (from 6 to 14 days from the beginning of the injury).

The third phase is the formation and reorganization of the scar. There is no clear boundary between the second and third phases. During this period, the scar thickens and contracts. The duration of this phase is up to 6 months.

Each anatomical region has its own characteristics of wounds. This determines the tactics of performing surgical operations, pain relief, etc.

The wound process is a set of successive changes occurring in the wound, and the reactions of the whole organism associated with them.

Conditionally, the wound process can be divided into general reactions of the body and wound healing itself.

General reactions

The complex of biological reactions of the body in response to damage during the wound process can be considered as two successive stages.

First phase

Within 1-4 days from the moment of injury, excitation of the sympathetic nervous system, the release of hormones of the adrenal medulla, insulin, ACTH and glucocorticoids into the blood. As a result, vital processes are enhanced: body temperature and basal metabolism increase, body weight decreases, the breakdown of proteins, fats and glycogen increases, the permeability of cell membranes decreases, protein synthesis is suppressed, etc. The significance of these reactions is to prepare the whole organism for life in conditions of alteration.

In the first period, a moderate increase in body temperature, weakness, and decreased performance are observed.

Blood tests show an increase in the number of leukocytes, sometimes a slight shift leukocyte formula to the left, protein may appear in urine tests. With profuse blood loss, there is a decrease in the number of erythrocytes, hemoglobin, hematocrit.

Second phase

Starting from 4-5 days, the character general reactions due to the predominant influence of the parasympathetic nervous system.

Growth hormone, aldosterone, acetylcholine are of primary importance. In this phase, body weight increases, protein metabolism normalizes, and the reparative capabilities of the body are mobilized. With an uncomplicated course, by the 4th-5th day, the phenomena of inflammation and intoxication are stopped, the pain subsides, the fever stops, the laboratory parameters of blood and urine are normalized.

Healing wounds

Wound healing is the process of repairing damaged tissues with the restoration of their integrity and functions.

To close a defect formed during injury, three main processes occur in the wound:

Collagen formation by fibroblasts. During wound healing, fibroblasts are activated by macrophages. They proliferate and migrate to the site of injury by binding to fibrillar structures via fibronectin. At the same time, fibroblasts intensively synthesize substances of the extracellular matrix, including collagens. Collagens ensure the elimination of tissue defect and the strength of the formed scar.

Epithelialization of the wound occurs as epithelial cells migrate from the edges of the wound to its surface. Completed epithelialization of the wound defect creates a barrier for microorganisms.

The tissue constriction effect, to a certain extent due to the contraction of myofibroblasts, ensures the reduction of wound surfaces and wound closure.

These processes occur in a certain sequence, which is determined by the phases of wound healing (phases of the wound process).

Phases of wound healing according to M.I. Kuzinu (1977):

Phase I - inflammation phase (1-5 days);

Phase II - regeneration phase (6-14 days);

Phase III - the phase of scar formation and reorganization (from the 15th day from the moment of injury).

Inflammation phase

I phase of wound healing - the phase of inflammation, proceeds in the first 5 days and combines two consecutive periods: vascular changes and wound cleansing from necrotic tissues. Vascular reactions and extravascular changes occurring in the wound are closely related.

The period of vascular changes. In response to trauma, a number of disorders develop that affect the microvasculature. In addition to the direct destruction of blood and lymphatic vessels, which contributes to a violation of the outflow of blood and lymph, a short-term spasm occurs, and then a persistent paretic expansion of microvessels. Participation in the inflammatory reaction of biogenic amines (bradykinin, histamine, serotonin), as well as the complement system, leads to persistent vasodilation and an increase in the permeability of the vascular wall.

Decreased perfusion leads to deterioration of tissue oxygenation in the wound area. Acidosis develops, carbohydrate and protein metabolism is disturbed. During the decay of cellular proteins (proteolysis), K + and H + ions are released from the destroyed cells, increasing the osmotic pressure in the tissues, water retention occurs, tissue edema (hydration) develops, which is the main external manifestation of inflammation.

Prostaglandins, metabolites of arachidonic acid released from destroyed cell membranes, take an active part in this phase.

The period of cleansing the wound from necrotic tissue. In cleaning the wound, the most significant role is played by blood corpuscles and enzymes. Already from the first day, neutrophils appear in the tissues and exudate surrounding the wound, and lymphocytes and macrophages appear on days 2-3.

Regeneration phase

Phase II of wound healing - the phase of regeneration, takes place from 6 to 14 days from the moment of injury.

Two main processes take place in the wound: collagenization and intensive growth of blood and lymphatic vessels. The number of neutrophils decreases and fibroblasts - connective tissue cells with the ability to synthesize and secrete extracellular matrix macromolecules - migrate to the wound area. An important role of fibroblasts in wound healing is the synthesis of connective tissue components and the construction of collagen and elastic fibers. The bulk of collagen is formed precisely in the regeneration phase.

At the same time, recanalization and growth of blood and lymphatic vessels begin in the wound area, which helps to improve tissue perfusion and feed fibroblasts that need oxygen. Mast cells concentrate around the capillaries, which contribute to the proliferation of the capillaries.

For biochemical processes in this phase, a decrease in acidity, an increase in the concentration of Ca2 + ions and a decrease in the concentration of K + ions, and a decrease in metabolism are characteristic.

The III phase of wound healing - the formation and reorganization of the scar, begins approximately from the 15th day and can last up to 6 months.

In this phase, the synthetic activity of fibroblasts and other cells decreases and the main processes are reduced to strengthening the formed scar. The amount of collagen practically does not increase. Its restructuring and the formation of cross-links between the collagen fibers occur, due to which the strength of the scar increases.

There is no clear border between the regeneration phase and scarring. Maturation of connective tissue begins in parallel with the epithelialization of the wound.

Factors affecting wound healing:

The patient's age;

Nutritional status and body weight;

The presence of a secondary wound infection;

The immune status of the body;

The state of blood circulation in the affected area and the body as a whole;

Chronic concomitant diseases (diseases of the cardiovascular and respiratory systems, diabetes mellitus, malignant tumors etc.).

Classic types of healing

With a possible variety of options for the course of the wound process, depending on the nature of the injury, the degree of development of microflora, the characteristics of the violation of the immune response, they can always be reduced to three classical types of healing:

Healing by primary intention;

Healing by secondary intention;

Healing under a scab.

Healing by primary intention is the most economical and functionally beneficial, it occurs in a shorter time with the formation of a thin, relatively strong scar.

By primary intention, surgical wounds heal when the edges of the wound are in contact with each other (connected by sutures). The amount of necrotic tissue in the wound is small, the inflammation is insignificant.

Only wounds without an infectious process heal by primary intention: aseptic operating or accidental wounds with minor infection, if microorganisms die within the first hours after injury.

Thus, in order for the wound to heal by primary intention, the following conditions must be met:

No infection in the wound;

Tight contact of the edges of the wound;

Absence of hematomas in the wound, foreign bodies and necrotic tissues;

Satisfactory general state patient (lack of general adverse factors).

Healing by primary intention occurs in the shortest possible time, practically does not lead to the development of complications and causes small functional changes. it best type healing wounds, to which one should always strive, to create the necessary conditions for it.

Healing by secondary intention - healing through suppuration, through the development of granulation tissue. In this case, healing occurs after a pronounced inflammatory process, as a result of which the wound is cleared of necrosis.

Healing conditions by secondary intention:

Significant microbial contamination of the wound;

A significant defect in the skin;

The presence of foreign bodies, hematomas and necrotic tissues in the wound;

Unfavorable state of the patient's body.

There are also three phases in secondary intention healing, but they have some differences.

Features of the phase of inflammation

In the first phase, the phenomena of inflammation are much more pronounced and the cleansing of the wound takes much longer. At the border of the penetration of microorganisms, a pronounced leukocyte shaft is formed. It helps to differentiate infected tissues from healthy ones, demarcation, lysis, sequestration and rejection of non-viable tissues occur. The wound is gradually clearing. As the areas of necrosis melt and the products of decomposition are absorbed, intoxication of the body increases. At the end of the first phase, after lysis and rejection of necrotic tissues, a wound cavity is formed and the second phase begins - the phase of regeneration, the peculiarity of which is the emergence and development of granulation tissue.

Granulation tissue is a special type of connective tissue formed during wound healing by secondary intention, contributing to the rapid closure of the wound defect. Normally, without damage, there is no granulation tissue in the body.

Healing under a scab - Healing of a wound under a scab occurs with small superficial injuries such as abrasions, damage to the epidermis, abrasions, burns, etc.

The healing process begins with the clotting on the surface of the lesion of the outflowing blood, lymph and tissue fluid, which dry out with the formation of a scab.

The scab has a protective function and is a kind of "biological dressing". Rapid regeneration of the epidermis occurs under the scab, and the scab is rejected. The whole process usually takes 3-7 days. In the healing under the scab, the biological characteristics of the epithelium are mainly manifested - its ability to line living tissue, delimiting it from the external environment.

Wound healing is a dynamic process with three overlapping stages: inflammation, granulation tissue formation, skin maturation or remodeling. The contribution of each of these stages to the healing process depends on the depth of the injury.

Shallow wounds. Shallow wounds involve the epidermis and the upper layers of the dermis. Skin appendages (hair follicles, sweat and sebaceous glands) are preserved. Thrombus formation, inflammation and the formation of granulation tissue are insignificant. At the heart of the healing of shallow wounds is epithelialization due to the preserved appendages of the skin and the marginal epidermis, which ultimately leads to a complete and rapid restoration of the skin with invisible scars or even without them. Hyper- or hypopigmentation may remain at the wound site.

Deep wounds. A necessary stage in the healing of deep wounds is the formation of a blood clot to stop bleeding from relatively large vessels of the deep layers of the dermis. Inflammation and the formation of granulation tissue are important healing steps along with skin tension, which brings the wound edges closer together to promote epithelialization. Since the appendages of the skin are damaged, epithelization of deep wounds occurs only due to the marginal epidermis and the lost tissues are replaced by scar tissue.

To understand the pathogenesis of scarring, it is necessary to know how wound healing occurs normally.

Inflammation stage

The first thing that happens during wound healing is the formation of a hematoma. This ensures the cessation of bleeding from damaged vessels and the creation of a barrier that prevents microorganisms from entering the wound. A thrombus is a temporary matrix into which inflammatory cells migrate. When platelets are destroyed, many growth factors are released, incl. transforming growth factor (TGF-β1), epidermal growth factor, insulin-like growth factor type 1 (IGF-1) and platelet growth factor, which attract inflammatory cells, promote extracellular matrix synthesis and vascular germination.

A number of other signaling molecules, for example, fibrinolysis products, attract neutrophils and monocytes to the wound. These cells come from the bloodstream by diapedesis through the endothelium of the capillaries adjacent to the wound. The main function of neutrophils is phagocytosis and the destruction of microorganisms inside cells. In addition, neutrophils produce inflammatory mediators, under the influence of which keratinocytes and macrophages can be activated already at this stage of healing.

At the end of an acute inflammatory reaction (after 1-2 days), monocytes migrated from the bloodstream become macrophages and destroy the remaining microorganisms and dead cells. These macrophages also serve as a source of growth factors and inflammatory mediators, in particular platelet growth factor, which attract fibroblasts to the site of injury.

Proliferation stage

Fresh granulation tissue is very rich in blood vessels and cells. Since epithelization alone is not enough for the healing of deep wounds, the proliferation of fibroblasts of the dermis adjacent to the wound begins already in its first stages. Fibroblasts migrate into the wound, lining the extracellular matrix of fibrin, fibronectin, vitronectin, and glycosaminoglycans. In fresh granulation tissue, the ratio of type III collagen to type I collagen is high.

In response to the action of growth factors in the wound, the proliferation of keratinocytes and fibroblasts begins. With the formation of granulations and the appearance of excess collagen matrix, the number of cells decreases by apoptosis. How apoptosis is triggered is unknown. Under the influence of substances that stimulate angiogenesis, which serve as inducers of endothelial growth factor, TGF-β1, angiotropin and thrombospondin, vessels begin to grow into the extracellular matrix.

Myofibroblasts contribute to the convergence of the edges of extensive wounds, which reduces the amount of granulation tissue required to fill the wound cavity and reduces the area of \u200b\u200bepithelialization. Due to the contractile proteins actin and desmin, fibroblasts also contribute to the convergence of the edges of the wound. The mechanical stress that occurs after the edges of the wound are closed gives a signal to stop the tension.

Epithelialization begins within a few hours after the appearance of the wound. Migrating keratinocytes activate tissue plasminogen activator and urokinase and increase the number of urokinase receptors, which in turn promotes fibrinolysis, an important step for keratinocyte migration. To pass through the temporary matrix formed by the thrombus, keratinocytes form additional receptors for fibronectin and collagen. Keratinocyte migration and epithelialization are facilitated by the tension of the wound edges.

Maturation and restructuring stage (complete healing)

At the restructuring stage, excess collagen and temporary matrix are removed by tissue enzymes, and inflammatory cells leave the wound. When the scar matures, a balance arises between the processes of destruction of the temporary matrix and collagen synthesis.

On the one hand, fibroblasts synthesize collagen, contractile proteins and extracellular matrix, on the other hand, fibroblasts, mast cells, endothelial cells and macrophages secrete a number of enzymes (matrix metalloproteinases) necessary for destruction and restructuring. The balance between these proteinases and their tissue inhibitors plays an important role in the repair of damaged tissues.

Interferons, produced by T-lymphocytes (interferon-γ), leukocytes (interferon-α) and fibroblasts (interferon-β), prevent the development of fibrosis and suppress the synthesis of collagen and fibronectin by fibroblasts.

The restructuring process lasts from 6 to 12 months, but it can take years. The strength and elasticity of the scar is usually only 70 - 80% of that of intact skin, so scars are more susceptible to repeated injury.

Factors affecting wound healing and scarring

Age. Unlike adults, fetal skin wounds heal quickly and without scarring. The mechanism of scarless healing is unclear, however, it is known that inflammation is weak in this case, a large amount of hyaluronic acid is present in the wound contents, collagen fibers are stacked in a certain order.

The body of the fetus is significantly different from the adult body. The main difference is in the features of tissue oxygenation: the oxygen content in them remains relatively low throughout the entire period of intrauterine development. Inflammation in wounds in the fetus is mild due to neutropenia. As the fetal immune system develops, the inflammatory response becomes more pronounced and scars may form at the site of the wounds.

The fetal skin is constantly bathed in warm sterile amniotic fluid, which contains many growth factors. But this alone does not explain scarless healing. In experiments on fruit of lambs, isolation of the wound from amniotic fluid with a silicone bandage did not prevent scarless healing; on the other hand, the adult skin grafted to the fetus engrafted with the formation of a scar despite contact with amniotic fluid.

The high content of hyaluronic acid in the extracellular matrix increases the mobility of cells, enhances their proliferation, and hence the restoration of the damaged area. This allows us to consider hyaluronic acid as the main factor in scarless healing. A glycoprotein was found in fetal wounds, which is absent in adult wounds. This glycoprotein stimulates the synthesis of hyaluronic acid. In addition, it is believed that its long-term presence in fetal wounds contributes to the orderly deposition of collagen during their healing. When treated with hyaluronic acid, perforated eardrum rats not only recovered faster than in control animals, but there was less scar tissue at the site of injury, and collagen fibers were arranged in an orderly manner.

Rapid epithelialization of fetal wounds may be due to early accumulation of fibronectin and tenascin in the wound contents. Fetal and adult fibroblasts are different. Fibroblasts of the fetus at the beginning of intrauterine development produce more collagen of types III and IV, while fibroblasts of an adult produce mainly type I collagen. In addition, fetal fibroblasts are able to simultaneously proliferate and synthesize collagen, and in an adult, fibroblast proliferation precedes collagen synthesis. Thus, in adults, during wound healing, the appearance of collagen deposits is somewhat delayed, which leads to the formation of scars. Skin tension does not play a role in scarless healing, because fetal wounds are practically devoid of myofibroblasts.

Inflammation plays a key role in repairing damaged tissue and forming scars. In the fetus, in the absence of inflammation, wounds heal without scarring. It is believed that wound healing deteriorates with age. As the body ages, its inflammatory response decreases due to the weakening of the function of macrophages and T-lymphocytes, loss of reactivity and mobility of fibroblasts, a decrease in the number and other distribution of growth factors and their receptors, incl. receptor TGF-β. All of this can explain the difference in the speed and quality of wound healing at different ages.

Although wounds heal more slowly in older people, they have better scar quality, which may be due to a decrease in the level of transforming growth factor (TGF-β) in the damaged skin. It is also possible that fibroblasts of the fetal subtype appear in the wounds of the elderly, which leads to wound healing, like in the fetus. Reducing hormone levels, particularly estrogens, during menopause may also contribute to slower wound healing and reduced scarring.

Estrogens. In vitro studies have shown that sex hormones affect important stages of wound healing such as inflammation and proliferation. Estrogens regulate the production of TGF-β isoforms and the formation of their receptors, which play a significant role in the development of fibrosis and scar formation. In healthy postmenopausal women, wound healing slows down, but the quality of scars improves, which is associated with a decrease in the level of TGF-β1 in wounds.

Against the background of hormone replacement therapy, wounds begin to heal faster, which suggests a direct or indirect regulation of healing by sex hormones. Studies have shown that menopausal women have hormone therapy within 3 months. accelerates epithelialization and collagen deposition in wounds.

The presence of estrogen receptors on the surface of fibroblasts indicates the possibility of direct regulation of the function of these cells by estrogens. In addition, estrogens increase TPP-β1 levels in vitro.

These data suggest the involvement of estrogens in the regulation of the production of skin fibroblasts and TGF-β1. Finally, it has been noted that systemic administration of estrogen antagonists inhibits wound healing in humans. A preliminary study of scars in women who received wounds during administration of the estrogen antagonist tamoxifen showed that these scars were best qualitythan the scars left after the healing of the same wounds in women who did not receive tamoxifen.

Heredity. There is evidence of the existence of a hereditary factor that affects the wound healing process, activating abnormal (pathological) scarring, which leads to the appearance of hypertrophic and keloid scars. Both autosomal dominant and autosomal recessive inheritance of keloid scars have been reported. Often keloid scars are noted in the patient's relatives with similar scars. In addition, the prevalence of keloid scars is significantly higher in dark-skinned populations, reaching 4.5 to 16% in Africans and Hispanics. The frequency of keloid scars is high in carriers of HLA-β14 and HLA-BW16, in individuals with blood group A (II) and those suffering from Rubinstein-Teibi syndrome.