Patterned hair loss is
thought to be caused by both inherited and physiological backgrounds. Patterned
hair loss gradually proceeds following a specific pattern in front and on top
of the scalp. Among males, hair shedding often begins after puberty due to the
effect of the male hormone, androgen, and is named male pattern baldness, also
known as androgenetic alopecia (AGA). The major cause of AGA in human is
thought to be as follows; the human hair follicle follows a cycle of a
relatively long-lasting anagen phase and relatively short catagen and telogen
phases. Each hair follicle is replaced with a revitalized newly generated hair,
but when AGA occurs, the anagen phase becomes shorter and the hair follicle
does not fully grow and enter the next hair cycle, which results in increasing
amounts of short and thin hairs (miniaturized hairs), and eventually the temporal
or forehead scalp surface skin becomes visible (Sakamoto et al., 2017).
Androgen are known to
cause cell regression and balding of the scalp in AGA individuals. Testesterone
and dihydrotesterone (DHT), which is formed by action of 5?-reductase (5?R), are two major
androgens and DHT are considered more potent to trigger hair loss. Androgens
also affect the dermal papilla (DP) of hair follicle, which produces paracrine
signals that stimulate or inhibit the growth of follicular epithelium. These
include insulin-like growth factor-1 (IGF-1) and vascular endothelial growth
factor (VEGF). Other growth factors are also found to be involved in the hair
growth regulation such as keratinocyte growth factor (KGF) and hepatocyte
growth factor (HGF) have a stimulatory effect on hair follicle growth, while
epidermal growth factor (EGF) and transforming growth factor-b (TGF- b) have an
inhibitory effect on hair follicle growth (Roh et al., 2002).
drugs for hair loss treatment
present there are few drugs are used to treat androgenic alopecia (AGA). The
first drug approved for enhancing scalp hair growth was minoxidil (RogaineR).
It causes vasodilation (widening of blood vessels), thus increasing circulation.
In about a third of the people who try it, minoxidil improves hair growth, causing
scalp follicles to enlarge and lengthening the growth cycle. For many, however,
the hair growth is meager. Minoxidil does not help people who already are bald (Tortora & Derrickson, 2009).
Minoxidil was first used as a
vasodilator to treat cardiovascular disorders, but the unexpected side effect
of hirsutism led to its topical use as a hair-growth stimulator. The mechanisms
involved in AGA treatment are still unclear. It seems to open potassium
channels and increase the proliferation and differentiation of epithelial cells
in the hair shaft. However, local irritation, itching, dryness and erythema may
occur when minoxidil is topically used, as well as systemic side effects such
as dizziness and tachycardia. Serious side effects, such as an increase in left
ventricular end-diastolic volume, cardiac output, and left ventricular mass,
have been reported with the use of 2% minoxidil solution. Unfortunately,
another potential drawback of minoxidil therapy is the loss of newly grown hair
within one to three months after discontinuation of the medicine (Kumar, Rungseevijitprapa, Narkkhong, Suttajit, &
A low strength of finasteride is
also licensed in treatment of AGA. It is specific 5?-reductase inhibitors which
metabolizes testosterone into more potent androgen, dihydrotestosterones (DHT).
The active metabolite of dihydrotestosterone (DHT) will binds to androgenic
receptors in the hair follicle and then activates the genes responsible for
hair follicle regression (Herman & Herman, 2016) . But these
drugs may possess certain side effects include impotence, decreased libido,
ejaculation disorders and breast tenderness and enlargement (Committee, 2013).