**6. Biology of the hair loss and hair regrowth**

Human hair is different from hair grown by mammals due to unsynchronized growth cycles and a sensitive response to androgen.

Human hair exhibits a certain seasonal coordination, but the follicles work independently [15–17]. Latest research results sustain the idea that hair follicles act like neurons, being able to interconnect and generate hair loss and hair regrowth in a small region of the scalp. Human hair has a mosaic pattern as it consists of hair in different stages: the majority of the hair follicles (90%) being in growing phase (also known as anagen), 1–2% in regression (catagen phase), and 8–9% of the hair follicles are resting (in telogen phase) [18, 19]. The cyclic changes from anagen to telogen via catagen involve rapid remodeling of both the epithelial and dermal components of hair follicles [20, 21].

In both humans and animals, hair cycle is influenced by stimulatory and inhibitory factors, such as hormones, growth factors, cytokines, neuropeptides, and pharmaceutical products [18, 22, 23]. The dermal papilla supports an increased cell division and growth rate and induces the shift between anagen, catagen, and telogen [18, 19]. In telogen phase, the old hair is lost, but the follicle will be regenerated in early anagen, when new hair grows up [24, 25].

Current concepts of hair loss pathogenesis include genetic, genomic, hormonal, and immune contributions. Furthermore, the patient's behavior influences the hair density and its strength. In recent years, evidence has suggested that hair loss is a multifactorial disease, and the contributing factors include the resistance to insulin, local pathologies (inflammation, hypoxia, and vascular insufficiency), predisposing physiological factors (menopause and aging), association with other diseases (polycystic ovary syndrome, hirsutism, acne, hormonal imbalances, thyroid pathologies, and other autoimmune diseases). Hair loss remains a consequence of the genotype (hereditary information of the organism)-phenotype (morphology, behavior, and development) interaction [25, 26].

So far, only some of the genes involved in hair loss have been discovered: genes AR androgen receptor and EDA2R ectodysplasin A2 receptor from chromosome X, region located at 20p1 on chromosome 20, and additional loci associated with early onset baldness in Europeans, such as *HDAC9* in 7p21.1, *TARDBP* (chr1), *HDAC4* (chr2), *AUTS2* (chr7), *SETBP1* (chr18), q35

Evaluation of Animal Models Suitable for Hair Research and Regeneration

http://dx.doi.org/10.5772/intechopen.69698

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Alopecia can be a part of the normal aging process. Still, hair loss represents a great concern for patients. Several studies have shown that it generates anxiety and distress especially in

Hair loss is defined as a stressful experience for both sexes, patients being unable to cope with the progression of the disease [40, 41]. Stress functions not only as a cause, a risk factor, but also as a consequence of hair loss. Alopecia determines a poor quality of life by the physical and psychological sequelae: low self-esteem, depression, distorted social perception, and psy-

Up to the present, although many treatments have been tested, hair loss continues to be a

Two FDA-approved hair loss treatment drugs: Finasteride (acting on the hormonal cause of alopecia—the excess of androgens) and Minoxidil (acting on the physical cause—the hypoxia due to vasoconstriction), are commonly used in clinical practice in order to treat androgenetic alopecia, which represents 95% of all hair loss causes [38, 47–49]. Minoxidil (1 mg per day) is a topical formulation available in 2 and 5% concentration. It stops hair loss and promotes hair growth as it is a vasodilator and potassium channel opener, allowing more oxygen, blood, and nutrients to reach the follicle [50–53]. It has no therapeutic action on the hormonal and genetic causes of hair loss; therefore, it must be used as a continuous support for the hair follicles, otherwise the hair regrowth will cease and hair loss will begin again in 1–2 months [54–57]. Finasteride is a dihydrotestosterone-suppressing 5-alpha-reductase inhibitor, recommended for male use only, decreasing the serum levels of dihydrotestosterone, stopping hair fall (in 48% of the cases), and stimulating hair regrowth (in 51% of the cases). Studies have shown that 1 mg of finasteride oral treatment has an efficacy similar to daily topical application of minoxidil [58–60]. Given the temporary efficacy of finasteride and minoxidil and the limited number of treatments available in alopecia, new therapies are needed to prevent hair

Pharmaceutical hair loss management also includes different substances (arginine, aminexil, caffeine, and taurine), different peptides, B spectrum vitamins, zinc, or different procedures

(*WNT10A*), chr3q25 (*SUCNR1*), chr5q33.3 (*EBF1*), and chr12p12.1 (*SSPN*) [36].

**8. Consequences of hair loss**

chosocial functioning [42–45].

**9. Hair regrowth treatment**

frequent dermatological condition [46].

loss and enhance hair regrowth [61, 62].

females, affecting couple and social relationships [37–39].

The most common form of hair loss is known as "androgenetic alopecia" (AGA), which represents almost 95%. In this case, hair loss is generated by hair cycle abnormalities, such as the shortening of the anagen, within an abnormal hair cycle, and the anagen-telogen rate shifting from 6:1 to 2:1. Also, hair loss can be due to a small-sized dermal papilla. Both situations lead to shortening of hairs, decreasing hair diameter, shaft loss, and an increased number of hairs in telogen phase. In most situations, the changes of hair diameter (hair thinning) are followed by the loss of pigment: final hair (thick and pigmented) can turn back into vellus (thin and white). Studies point out that another cause of hair loss is the fact that the scalp suffers from vasoconstriction and hypoxia [27, 28].

Hair cycle disturbances are mainly caused by an excess of androgens, which alters the production of regulatory factors (soluble paracrine factors and extracellular matrix components) by the dermal papilla cells [13]. Some specific sites of the body (beard, axillary, and pubic hair) react differently than hair from the scalp, as they are androgen-sensitive [4]. Hair miniaturization and thinning, followed by hair fall is most common in the vertex and the crownfrontal area of the scalp [29, 30].

The occipital part of the scalp is an androgen insensitive area that is why in alopecia, hair is still present in this region, and hair follicles are suitable to be used in hair transplants [31, 32]. The androgen effect on hair can be summarized by the metabolization of the testosterone into 5-alpha-dihydrotestosterone by 5-alpha reductase. A good metabolization limits the hair length (in case of the beard, for example) and deficiencies of the 5-alpha reductase generate enlarged hair diameter (thicker hair in the axillary and pubic area) [19, 33–35].

Another form of alopecia is Alopecia areata (AA), a cell-mediated disease directed against active growing hair follicles. It is a nonscarring alopecia, with limited alopecic patches on the scalp or the body, sometimes affecting also the nails. The pathogenesis of AA includes an autoimmune etiology, linked to human leukocyte antigen (HLA) class II alleles and to the T lymphocytic co-stimulatory cascade [30].
