Up to 95% of cases of baldness in the stronger sex are associated with androgenetic alopecia. In Africa and Asia, this condition is less common, and among men of the white race, more than half in the course of life encounters androgenic alopecia.
Distinctive features of such alopecia:
- hereditary predisposition;
- connection with the level of dihydrotestosterone;
- characteristic staging;
- hair loss on the parietal and frontal area.
Androgenic alopecia disrupts the normal activity cycles of the hair follicles. Hair loss is caused not so much by excessive levels of male sex hormones as by inherited hypersensitivity to them.
Physiology of hair growth
Hair follicles function in accordance with their own growth cycle. The periods of activity are not synchronous for all hair, therefore, the processes of loss and renewal proceed unnoticed.
There are 3 consecutive phases of follicle functioning:
- anagen phase (period of active hair growth);
- catagen phase (short regression period);
- telogen phase (rest period).
In long hair, the anagen stage lasts from 2 to 4 years. During this time, the length of the rod increases by about 10 mm per month. Then comes the short intermediate phase of the catagen. Its duration is no more than 3 weeks. During this transition period, the core already ceases to grow, but the processes in the hair bulb are still active. Then there is a complete cessation of elongation of the rod. This condition is called the resting phase (telogen). It lasts from 3 to 4 months. The cycle ends with hair loss. The old core is lost due to the appearance of a new one. In total for a person’s life, the same follicle undergoes up to 25 complete hair growth cycles.
Normally, the vast majority of the hair on the head is in the anagen phase, up to 10-15% – in the telogen phase, and only 1-2% – in the catagen phase. Androgenic alopecia violates the normal duration of each phase and significantly increases the percentage of follicles at rest.
Mechanisms for the development of alopecia in men
Androgenic alopecia develops due to an increase in the level of the active form of the male hormone in the skin – dihydrotestosterone acts on the hair follicles. In this case, the level of androgens in the blood can be within normal limits. Excess dihydrotestosterone most often occurs under the influence of a skin enzyme – 5-alpha-reductase. This substance helps inactive hormones inside the follicle to turn into active dihydrotestosterone.
When androgenetic alopecia is inherited:
- hypersensitivity of hair to dihydrotestosterone;
- excessive activity of 5-alpha reductase;
- a combination of these properties.
In addition, baldness can occur with an absolute increase in the level of androgens due to tumors of the testicles, adrenal glands or other diseases.
The effect of dihydrotestosterone on hair follicles varies depending on the area of the body. Male steroids regulate the type and distribution of hair growth. From their effects, the gun follicles on the skin of the face and body can begin to produce terminal (dark, stiff and long) hair. In these areas, androgens prolong the anagen stage. Dihydrotestosterone acts differently on the scalp. Because of this hormone, the phase of active growth of hair on the head is reduced, and the duration of the telogen increases. Androgen provokes degeneration of hair roots and rods. In men, the follicles most sensitive to the inhibitory effect of dihydrotestosterone are located in the forehead, temples and crown. In these areas, hair due to dihydrotestosterone prematurely enters the resting phase and begins to fall out. At the same time, update processes are slowed down.
Normal daily hair loss is up to 50-80 pieces. With androgenic alopecia, prolapse intensifies. The hair in the alopecia zone first becomes thin and colorless. The length of the rod is limited to 10-20 mm. After a few years, even such cannon hair disappears.
Stages of Androgenic Alopecia
The severity (stage) of androgenic alopecia in men is determined by the Norwood scale. According to this model, 7 stages are distinguished:
- A slight shift in hair growth from the edge. Thinning and thinning of hair in androgen-dependent zones.
- Partial hair loss in the forehead, temples, crown. The edge of facial hair growth takes the form of a triangle.
- Obvious thinning of hair at the temples or complete baldness in this area. Bald patches with a depth of 2 cm. Loss of hair in the crown of the head.
- Lack of hair on the crown of the head. Deep bald patches in the temples and forehead. Between the two zones of baldness is a strip of moderately thick hair.
- Expansion of the zones of parietal and anterior temporal alopecia. The hair on the top begins to lose its density.
- Zones of baldness on the crown of the head and forehead are separated only by individual hairs on the crown of the head.
- Zones of baldness are combined. The hair on the head continues to thin. Losses are observed on the back of the head, neck, above the ears.
With age, the prevalence of androgenic alopecia and its pronounced stages increases. According to the observations of Norwood himself, in men at the age of 25, the 3-7 stage of alopecia is detected only in 15% of cases. By the age of 35, the prevalence of baldness is already 40%. In the future, the percentage of men with alopecia progressively grows up to the age of andropause.
Diagnosis of baldness is based on data from a physical examination, medical history, and laboratory tests. Differentiate the process with other types of baldness (symptomatic, cicatricial, etc.). The diagnosis is made after dermatoscopy.
Signs of an androgen-dependent process during such an examination are:
- different diameters of hair shafts (thinning);
- empty follicles;
- pigmentation of the scalp;
- inflammation and redness of the scalp;
- peripilar rings (pigmentation around the mouths of the hair follicles).
Androgenic alopecia is confirmed by:
- thinning and hair loss in the parietal and frontal areas;
- follicular atrophy in these areas (with microscopy);
- lack of atrophy in the nape of the neck (bottom);
- an increase in the proportion of hair in the telogen phase, a decrease in the anagen phase.
Recently, the most progressive is considered a genetic study for a predisposition to androgenetic alopecia. There are different theories regarding the involvement of different loci in the inheritance of baldness.
For example, alopecia is associated with:
- with the male sex hormone receptor gene on chromosome X;
- with the IRF-1 locus on chromosome 12;
- with the cytochrome 450c17-alpha gene on chromosome 10;
- with the gene of the enzyme 5-alpha reductase on the 5 or 2 chromosome;
- with the gene locus on chromosome 20p11.22.
Treatment of androgenic alopecia
Medical care for androgenetic alopecia consists of:
- drug treatment;
- surgery (hair transplantation).
Of the drugs have proven effective:
- minoxidil (a drug for external treatment, prolongs the anagen phase);
- finasteride (for oral administration, inhibits the enzyme 5-alpha reductase).
Research is also underway on new medicines. One of the most promising is the drug with the Wnt protein. Scientists hope that this medicine will contribute to the appearance of new hair follicles on the skin.
Of the physiotherapeutic effects, the most effective low-intensity laser radiation.
The radical method is a transplant operation. The surgeon transplanted hair into the baldness area. For transplantation, own follicles from the back of the head and lateral areas of the head are used. This hair is not sensitive to dehydrotestosterone. With a successful transplant, follicular activity persists for life.
A promising development in the surgical treatment of baldness is hair cloning. Doctors plan to clone androgen-independent follicles and implant them in bald areas.