Acne (a synonym for acne vulgaris, acne) belongs to a special group of skin diseases – psychosomatic dermatoses. Acne (Greek άκμή – inflammation of the sebaceous glands) is a polymorphic multifactorial disease of the apparatus of the sebaceous glands. The term “acne” is used to emphasize the chronic, often recurring course of dermatosis, the complexity of its etiopathogenesis and the need for an integrated approach to the treatment of the disease.
Despite the emergence of modern methods of treatment, acne is still one of the most common dermatoses in young people. The incidence of acne not only does not have a clear downward trend, but also increases significantly. Acne belongs to one of the most common skin diseases and in the puberty (transitional) period, it is noted in varying degrees of severity in almost 100% of boys and 90% of girls. The peak incidence, as a rule, falls on 14-17 years, which leads to special attention to the treatment of this disease in adolescents. At the same time, a high incidence of the disease was also found in young people aged 18–25 years (up to 80–85%), as well as at the age of 25–34 and 35–44 years, respectively, 8 and 3%. In young men, the disease is more common and severe.
Acne at the age of 12-24 is called acne vulgaris or common acne. In most cases, by the age of 18–20 years begin to notice signs of spontaneous regression of the disease. In some patients, the disease acquires a chronic relapsing character, in some cases with the formation of “late acne” ( acne tarda ) by the age of 30–40 years . It has been proven that in recent years, the number of women with late forms of acne has been increasing. According to Ch. Colleir et al. (2008), in adolescent patients, the incidence of acne is almost the same in both sexes, while late acne is much more common in women.
Thus, according to various studies, the proportion of patients with acne rash aged 25–40 years is 40–54%. In studies conducted by G. Dummont – Wallon et al. (2008), J. Rosso, C. Williams et al. (2007), the average age of women with acne was 26.5–31.8 years. In a multicenter study conducted in the United States between 1990 and 1999, it was found that the average age of acne patients increased from 26.5 to 40.5 years.
The detectability of severe forms, according to various authors, is 5-14% of the total incidence of acne. Many patients have a relapsing course, often complicated by taking many medications that are used independently and, in most cases, are ineffective.
Why does acne occur? The background for the development of this disease is seborrhea – a special condition associated with overproduction of sebum and a change in its composition. Normally, sebum is used to lubricate the surface of the epidermis. The sebaceous glands that produce sebum are located throughout the skin, with the exception of the palms and soles, and are usually in close contact with the hair follicles, forming a common greasy hair follicle (SVF). According to the degree of fat content, the skin is divided into normolipic (normal fat content), hypolipic (dry), seborrheic (oily) and hyperseborrheic (with acne). Seborrheic skin (oily) (lat. Sebum – “fat”, rheo – “leak”) is characterized by increased release of fat by the sebaceous glands. At first glance, its structure seems rough, similar to the peel of an orange, oily and even oily in appearance. The pores are wide, funnel-shaped, gaping. However, they are empty, there are no greasy plugs or comedones (two interpretations are possible – lat. Comedo, comedonis – glutton and a synonym for blackhead ; from novolat. Acne comedonica – cyst). With age, the amount of fat released decreases and can normalize.
Hyperseborrhoeic skin (with acne) is characterized by quantitative and qualitative disorders of the function of fat secretion and the accumulation of cells of the stratum corneum in the mouths of the sebaceous glands, as a result of which the formation of the water-lipid mantle becomes uneven and comedones appear in the seborrheic zones. Seborrheic zones are called areas of the skin on which the content of large, multi-lobed sebaceous glands is increased and there are from 400 to 900 of these glands per 1 cm 2 .
Seborrheic zones include the scalp, the region of the eyebrows, the nose and nasolabial triangle, the chin, the axillary region, the chest and the back, and the perineum.
Blackheads ( acne ) are the result of occlusion and inflammation hyperplastic sebaceous glands. The mechanism of acne development is quite complicated, but the main links of pathogenesis are currently defined:
1) hyperplasia and hypersecretion of the sebaceous glands,
2) follicular hyperkeratosis,
3) colonization of the ducts of the sebaceous glands with propionic acid bacteria,
The secretion of sebum is regulated by several mechanisms, which include the suppressive effects of estrogen and stimulating the production of sebum, the influence of androgens, progesterone and glucocorticosteroids. The sebaceous glands have steroid-sensitive (androgen-sensitive) receptors that regulate their secretory activity. Given that acne vulgaris usually appears in the puberty, when the sex glands begin to function actively, the role of sex steroid hormones in the pathogenesis of acne is discussed.
The skin takes an active part in the metabolism of steroid sex hormones, in particular in the extraglandular formation of androgens from precursor steroids, being simultaneously the main target tissue for androgens. For such a type of dermatosis as acne vulgaris, possible predisposing factors are an increase in blood levels of testosterone and an increased sensitivity of hair follicles and sebaceous glands to androgens. Hyperandrogenism leads to hypertrophy and increased functioning of the sebaceous glands. Stimulation of androgen receptors increases mitotic activity and differentiation of epidermal cells, enhances desquamation of follicle epithelial cells, increases the synthesis of intercellular lipids, stimulates hair growth and sebum secretion.
There is a correlation between increased sebum formation and severity of acne. So, the production of sebum with mild acne increases by 1.3 times, with moderate – 1.7 times, and with severe – 1.9 times. An imbalance of lipids also develops : in an increased volume of sebum, the concentration of essential α-linolenic acid decreases (the main regulator of differentiation of keratinocytes of the SVF duct) and the expression of the transglutaminase enzyme increases.
This leads to the predominance of dyskeratosis and proliferation processes over desquamation of SVF epithelium, which ultimately cause follicular retention hyperkeratosis of SVF – a thickening of the stratum corneum of the epidermis due to excessive keratin content. The mechanism of its formation is to slow down the process of exfoliation of the cells of the stratum corneum, which is due to an increase in the content of glycosaminoglycans in the stratum corneum, which, in turn, makes it difficult to separate the corneous cells and their physiological rejection.
In acne, both processes – follicular hyperkeratosis and increased adhesion of corneocytes – disrupt keratinization at the mouth of the hair follicles, where the lumen of the sebaceous gland opens. This leads to clogging of the follicular duct of the sebaceous gland with horny scales and the formation of micro comedone. With hyperkeratosis of the outer (epidermal) part of the follicular canal, open comedones are formed , the black color of which is due to the oxidation products of sebum lipids, mainly squalene. With deep keratosis, the outlet of the follicular canal does not expand, but is filled with fat and detritus, closed comedones form .
Follicular hyperkeratosis, obstruction of the SVF duct, and lipid-rich sebum lead to clogging of the follicle and hindering the penetration of air into the canal and the creation of anaerobic conditions favorable for the development and reproduction of facultative anaerobes – Propionibacterium acnes and Propionibacterium granulosum microform and other representatives of microfacial and other conditional microforms ( Staphylococcus epidermidis, Staphylococcus aureus, Pityrosporum ovale ). These microorganisms produce the enzyme lipase, which breaks down diacyl and triacyl glycerides to glycerol and free fatty acids.
The addition of microorganisms involves in the pathological process neutrophils and phagocytes of peripheral blood producing pro-inflammatory cytokines, interleukins-1α, -1β and -8; tumor necrosis factor α (TNF-α). These cytokines activate the enzyme cyclooxygenase, which contributes to the formation of arachidonic acid, the main inflammatory mediator – leukotriene B4 (LTB4). LTV4 stimulates neutrophils, T-lymphocytes, monocytes and eosinophils, followed by their release of hydrolytic enzymes and nitrogen monoxide (NO). This leads to the destruction of the wall of the sebaceous gland with the release of its contents into the dermis and the development of an inflammatory reaction. At the same time, coccal microflora (strepto- and staphylococci) join, which is clinically manifested in the form of purulent-inflammatory elements of the rash – papules, pustules, nodes and cysts.
Thus, in the formation of acne, the leading role belongs to hypertrophy and increased functioning of the sebaceous glands, follicular hyperkeratosis, activation of microorganisms with subsequent inflammation.