Acne has multiple pathogenic factors, and its pathogenesis is not well understood. Endocrine factors, the action of sebum, and microorganisms in the hair follicle are the main factors in the development of acne.
Acne is closely related to sexual endocrine secretion. It rarely develops before puberty; people who have lost or reduced sexual function, such as eunuchs who were castrated at the ancient court, do not develop acne. Acne symptoms are reduced during pregnancy, etc.
Both men and women have androgens and estrogens. The organs that secrete sex hormones are the testes and adrenal glands in men and the ovaries, placenta and adrenal glands in women. Androgens and estrogens have different ratios in men and women, and changes in these ratios may cause acne to appear. The development of sebaceous glands and sebum secretion are also associated with increased androgens, with testosterone having the strongest effect in increasing sebaceous gland activity. Progesterone and dehydroepiandrosterone (DHA) in the adrenal cortex are also involved, and the latter may play an important role in early acne. Testosterone is converted to the more active 5-alpha dihydrotestosterone by the action of 5-alpha reductase in the skin, which stimulates sebaceous gland cell turnover and lipid synthesis, resulting in increased sebum secretion and the production of thick and abundant sebum, which cannot be excreted completely and gradually accumulates in the mouth of the hair follicle. Later on, the tip exposed outside the follicular opening gradually dries out and becomes discolored by the oxidation of air, melanin deposition, and dust pollution to form blackheads.
The presence of Acinetobacter, Staphylococcus albicans and Bacillus ovalis in the hair follicle, especially Acinetobacter, contains esterases that make sebum decompose. The sebum in the hair follicle is decomposed by lipase and produces more free fatty acids, and these free fatty acids can cause a non-specific inflammatory reaction to occur in and around the hair follicle. When the pimples squeeze the nearby cells, their antibacterial power decreases and they become susceptible to bacterial infection causing inflammation, whereupon patients develop papules, pustules, sclerotia, nodules and abscesses.
In recent years, it has been suggested that the disease is immune-related and that serum IgG levels are elevated in the humoral immunity of its patients and increase as the disease worsens. Acinetobacter rotundus produces antibodies in patients, and circulating antibodies arrive locally to participate in the pathogenic process of early inflammation.
Regarding the relationship between micronutrients and acne. Recently, it has been demonstrated that low zinc in acne patients may affect the utilization of vitamin A and contribute to the keratinization of the sebaceous glands of hair follicles, and low copper weakens the body’s resistance to bacterial infection, etc. In conclusion, acne patients with low zinc, copper and iron trace elements and elevated manganese can cause a certain impact on fat metabolism and sex hormone secretion in the body, which, together with low skin resistance, may have a relationship with the development of acne.
In addition, genetics is also an important factor in the occurrence of this disease. In addition to the above factors, eating more animal fats and sugary foods, gastrointestinal disorders such as indigestion or constipation, mental stress, and hot and humid climates can have a detrimental effect on acne patients. Exposure to mineral oils or the internal use of iodides, bromides, and certain other medications can also aggravate acne.
What are the manifestations of acne and how is it diagnosed?
Blackheads composed of sebaceous keratinized and underkeratinized cells are crowded into enlarged hair follicles with inflammatory changes around the follicles. In septic damage, the affected tissue is abscessed and surrounded by many lymphocytes and multinucleated leukocytes, and sometimes staphylococci can be found. If the damage has been prolonged, plasma cells, foreign body giant cells, and proliferating fibroblasts may also be seen. In larger lesions, the sebaceous glands are partially or completely destroyed, sometimes becoming very large cysts.
Clinical manifestations
The lesions occur mainly on the face, but also on the upper chest and dorsum and shoulders, and occasionally on other sites; the periorbital skin is never involved. Patients almost always start with blackheads and oily seborrhea, and often with papules, nodules, pustules, abscesses, sinus tracts, or scarring. The various types of damage vary in size and depth, often with one or two of them predominating. The course of the disease is long, and most have no conscious symptoms. If inflammation is evident, it can cause pain and tenderness, and the symptoms are sometimes mild and severe. Most patients heal spontaneously or have reduced symptoms after puberty. Clinically, according to the main manifestations of the lesions, they can be divided into the following types.
1. Pitting acne
Blackhead acne is the main damage of acne. It is a cheese-like semi-solid stuffed at the mouth of the sebaceous glands of the hair follicles, and the outer end of the follicles is black.
2.Papular acne
The skin lesions are mainly inflammatory papules, small hard papules from millet to pea size, light red to dark red. There may be a blackheaded pimple in the center of the papule or a sebaceous plug with an unblackened tip.
3.Pustular acne
Pustular manifestations are predominant, with pustules the size of grains to green beans, follicular pustules and pustules formed at the top of the papule, with pus more viscous after breaking, leaving shallow scarring after healing.
4.Nodular acne
When the inflammation site is deeper, pustular acne can develop into thick-walled nodules of different sizes and a light red or purplish-red color. Some are located deeper and have significant elevation while in a hemispherical or conical shape. They can persist for a long time or be gradually absorbed, and some pus ulcerate to form significant scarring.
5.Atrophic acne
Papular or pustular damage destroys the glands and causes pit-like atrophic scarring. Fibrotic changes and atrophy can be caused by ulcerated pustules or naturally absorbed papules and pustules.
6.Cystic acne
The formation of sebaceous cysts of different sizes, often secondary to purulent infection, often bleeding jelly-like pus after rupture, while inflammation is often not heavy, and later the formation of sinus tracts and scarring front.
7.Coalescent acne
It is the most serious type of damage, with polymorphic lesions, many pimples, papules, pustules, abscesses, cysts and sinus tracts, scarring and keloidal clusters occurring.