Skin atrophy is a heterogeneous group of chronic diseases, the main symptom of which is the thinning of the components of the skin: the epidermis, dermis and subcutaneous fat. The process is based on the complete or partial destruction of collagen and elastic fibers – one of the main components of the connective tissue of the dermis. The elasticity of the skin suffers, hence the second name of skin atrophy – elastosis. The etiology and pathogenesis are individual for each type of atrophy, most of them have not been fully studied. The clinical diversity of the manifestations of the disease, methods of treatment, diagnosis, prevention, prognosis are proportional to the number of pathologies included in the group.
General information
Skin atrophy is a pathological process as a result of age–related, metabolic, inflammatory, trophic changes in all layers of the dermis and epidermis, leading to degeneration of connective tissue in the form of a decrease in the volume of collagen and elastic fibers with an outcome in thinning of the skin. Such a structural restructuring of the skin is also called elastosis (colloidal dystrophy as a result of aging of the dermis).
Various forms of skin atrophy were first described by independent scientists as a symptom of somatic pathology. For example, when studying progeria, a hereditary disease of adults, skin atrophy was described by the German doctor O. Werner in 1904, and in children, the phenomenon of premature aging accompanied by skin atrophy was first described by J. Getchinson back in 1886. The causes of the occurrence and development of many forms of skin atrophy are not clear today. The clinical diagnosis is made on the basis of the pathomorphological picture of the disease. The urgency of the problem is connected not only with aesthetic aspects, but also with the ability of some forms of skin atrophy to degenerate into cancer.
Causes
It is customary to distinguish two ways of occurrence and development of skin atrophy: physiological and pathological. The physiological includes aging and pregnancy, all other cases are the result of pathology. Skin aging begins with damage to cell membranes by free radicals – molecules with an unoccupied electron actively involved in various chemical reactions. Free radicals are the result of natural biochemical processes inside the human body, but they can also be formed under the influence of toxic substances (exhaust gases, cigarette smoke, contaminated products).
The “behavior” of these active elements is regulated by the antioxidant system of the body – a combination of enzyme and non-enzyme mechanisms of inhibition of autooxidation of cells. Normally, free radicals help a person cope with infections, improve blood clotting, and saturate cells with oxygen. However, with age, the number of free radicals increases critically, they cease to play a positive role and begin to destroy cells. This leads to an intradermal cellular imbalance, degenerative processes in the skin with the development of areas of atrophy. Dermatologists believe that this process is aggravated by an age-related violation of the lipid barrier of the skin (due to a decrease in estrogen levels, menopause), leading to the destruction of the stratum corneum of the epidermis, the destruction of structures capable of retaining moisture, which contributes to the development of atrophy.
Another mechanism of formation of atrophic scars – striae – during pregnancy. One of the most significant reasons for their occurrence is considered to be a decrease in the ability of skin cells (fibroblasts) to synthesize collagen and elastin while maintaining the synthesis of enzymes that destroy this collagen and elastin. The skin loses its strength, the collagen and elastic fibers of the dermis are torn, unable to withstand the constant overgrowth of the skin by the growing fetus, while the epidermis retains its integrity. A defect is formed – a site where active fibroblasts flock to fill it with collagen and elastin. The stage of active scarring begins. Later, the activity of collagen and elastin production decreases, the connective tissue at the site of the “failure” is compacted, squeezing the lumen of blood and lymphatic vessels inside the emerging scar. Nutrition and metabolism of this part of the dermis are disrupted, inflammation is replaced by dystrophy. This is how an irreversible skin defect is formed – a stretch mark, or an atrophic scar.
Skin atrophy as a result of pathological processes depends on the characteristics of the disease of which it is a symptom. However, all types of skin atrophy resulting from pathology have common features. The essence in this case is to reduce the volume of tissues that make up the skin. Part of the cells of the skin for one reason or another is destroyed and ceases to perform their usual functions: protection (water-fat “mantle” of the skin), thermoregulation and respiration (pores), participation in metabolic processes (synthesis of vitamin D in the epidermis), neuroregulation (receptors).
As a result, there is a failure in the blood supply, innervation, nutrition of the skin, there are foci of inflammation with trophic disorders, its structure changes: the number of collagen and elastic fibers in the connective tissue of the dermis, cells of the basal layer of the epidermis decreases. The skin is dehydrated. All this leads to the thinning of its layers, a decrease in their volumes, that is, to the formation of foci of atrophy. It should be noted that in some cases, skin atrophy can be common.
Classification
In dermatology, there are many approaches to the classification of skin atrophy. In our opinion, the most rational is the division of pathology into congenital and acquired:
1 Congenital atrophy of the skin – dysplasia of the ectoderm (the source of epithelial cells of the skin), affecting not only the skin itself, but also its appendages (hair, sebaceous and sweat glands, sometimes nails, teeth).
- Atrophic nevus is a birthmark in the form of a limited plaque, localized in the epidermis and dermis, without the interest of subcutaneous fat
- Atrophic aplasia is the absence of skin on limited areas of the scalp
- Hemiatrophy of the facial skin is an asymmetric thinning of the skin affecting all layers of the dermis, with the involvement of the underlying muscle tissue in the process.
2 Acquired skin atrophy is a consequence of somatic pathology, exposure to physical or other factors.
- Primary – occurs against the background of complete well-being, the etiology is unclear
- Involutive – wrinkles of various localization
- Secondary – a consequence of exposure to radiation, X-rays, sunlight on the skin; a symptom of chronic diseases.
Symptoms
The symptoms of skin atrophy of any etiology and localization are identical: in the focus of atrophy, the skin is thinned, dry, soft, painless, without hair, sebaceous and sweat glands, with vessels shining through it. It easily gathers into a fold, like tissue paper, when stroked it resembles wet suede; dyschromia is noted (from all shades of red to whitish). Parallel formation of areas of compaction is possible due to the proliferation of connective tissue, which increases the chances of degeneration of skin atrophy into cancer.
Skin atrophy has many faces. During puberty, pregnancy, and obesity, foci of striatoid atrophy are formed, mainly of hormonal genesis with metabolic disorders (Itsenko-Cushing syndrome). They are located on the abdomen, mammary glands in the form of pinkish-whitish stripes, are able to ulcerate. Localization of foci on the back is described – such atrophy is provoked by lifting weights. Spotted and white skin atrophy have vascular genesis. Idiopathic progressive skin atrophy is an illustration of borreliosis. Vermiform atrophy of the skin is observed in the puberty period. Foci of atrophy are small, symmetrical, localized on the cheeks, have inclusions in the form of follicular horn plugs, inflammation (unlike acne) is absent.
Skin atrophy is a symptom of many diseases: pigmented xeroderma, actinic keratosis (elastosis), lupus erythematosus, pyoderma, tuberculosis, syphilis, porphyrin disease, poikiloderma, lichen planus, progressive facial hematrophy, multicolored lichen and many others.
A special kind of skin atrophy is corticosteroid atrophy, which occurs as a response to the vasoconstrictive effect of hormones. They inhibit the synthesis of dermal fibers, increasing their destruction. External ointments leave superficial local foci of atrophy; corticosteroid injections cause destruction of the deep layers of the dermis and underlying tissues. The most serious negative effect is created by tablet corticosteroids. They provoke universal skin atrophy with total thinning of the skin, with multiple telangiectasias and traumatic pseudo–scar changes on the back of the hands – stellate skin atrophy.
Diagnosis and treatment
The diagnosis of skin atrophy does not cause difficulties, in difficult cases, histological examination helps. Skin atrophy is irreversible, disrupts the quality of life. Drugs that improve trophism (xanthinol nicotinate), the functioning of the nervous system (B6 + magnesium), vitamin therapy (A and D) are shown. Carbon dioxide baths, paraffin applications, natural creams are advisable. With corticosteroid atrophy, the intake of drugs is corrected, up to their complete cancellation. Borreliosis is treated with antibiotics, and aesthetic problems are solved with the participation of a cosmetologist and a plastic surgeon.
Prevention consists in the treatment of the underlying pathology. Corticosteroid therapy should be performed in the evening, when the proliferation of skin cells is minimal. The prognosis for life is favorable. Regular observation by a dermatologist is shown in order not to miss the possible transformation of skin atrophy into cancer.
