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Clinical Research in Dermatology: Open Access

Open AccessAndrogenetic Alopecia: a Review and Emerging
Treatments*Rubina Alves
Specialist in Dermatology, Department of Dermatology, Hospital Central do Funchal, Madeira, Portugal
Received: April 22, 2017; Accepted: June 09, 2017; Published: July 04, 2017
*Corresponding author: Rubina Alves, MD, PhD, Specialist of Dermatology, Universitat Internacional de Catalunya, Estrada Monumental, 364
3F, 9000-100 Funchal, Email: rubinaalves@gmail.com

Abstract
Androgenetic Alopecia (AGA) is the most common noncicatricial
alopecia that leads to the progressive miniaturization of the hairfollicle. Scalp terminal hairs are converted into vellus hairs, primarily
due to two factors: genetic predisposition and hormonal stimulation.
The incidence and prevalence of AGA increases with age. The
onset of AGA is gradual, and when this pathology progresses, theanagen phase shortens and the telogen phase remains constant.
The shedding area varies from patient to patient and is usually mostmarked at the vertex in men, while women with AGA generally lose
hair diffusely over the crown.
Topical minoxidil and oral finasteride (5-alpha-reductase type II
inhibitor) are the gold-standard therapies for AGA and are currently
the only Food and Drug Administration (FDA)-approved drugs for thetreatment of AGA.

The currently available treatments for AGA are sometimes
perceived as having limited effectiveness; therefore, the identificationof new therapies for this pathology is of utmost importance.
This article aims to review the pathogenesis, diagnosis of AGA andall the new emerging treatments for this entity in order to prevent its
progression and improve the results of this pathology.
Keywords: Androgenetic alopecia; Hair loss; Treatment;
Minoxidil; Finasteride; Dutasteride; Low-level-laser therapy;

Introduction

Androgenetic Alopecia is a nonscarring alopecia that affects
both men and women. It is characterized by a progressive
miniaturization of hair follicles with a characteristic pattern
distribution in genetically predisposed men and women [1]. Is
the most frequent type of hair loss in both sexes [2-4].

The onset of AGA is usually gradual and the condition slowly
develops over the years. The frequency and severity of this typeof hair loss increases with age [5]. It usually appears in the thirdand fourth decades and affects 30% to 50% of men by the age of
50 and around 80% of caucasian men aged over 70 years [1,2,69].

As in men, the frequency and severity of Female Pattern Hair
Loss (FPHL) increases with age [9]. According to Norwood [10],Symbiosis Groupafter examined a total of 1006 caucasian women, he found aprevalence of almost 30% in women over 30 years of age. Gan
DC, et al. [8] reported that prevalence of mid-frontal hair loss also
increases with age and affects 57% of women aged 80 and over.

The prevalence of AGA is different between populations;among asian, native american, and many men of african heritageis lower than that among caucasians with a decreased frequencyof frontal hair loss and less extensive hair loss [1,2,11].

Although AGA is more frequent in adults, it can also appear
in adolescents , though its prevalence among this younger
population is not well established [12,13]. On an average,adolescent AGA onset starts after puberty between 13.5 and15 years of age [14]. Although it is not expected to see AGA in
prepubertal patients without androgen levels [15, 16]. Tosti, et al.
[15] reported 20 prepubertal children with AGA with a very early
onset age between 6 and 10 years. According to the authors, allpatients had a strong genetic predisposition to the disease witha strong family history and the Dihydrotestosterone-Sulfatase(DHEA-S) levels were consistent with postadrenarche, but noneof them was affected by premature puberty, as demonstrated
by physical and laboratory assessments. In adolescents with agenetic predisposition, the first signs of AGA usually appear withrising androgens at puberty [17].
Beautiful and well-groomed hair represents youth, vitality
and energy and is important in determining one’s self-image andself-esteem [18]. In today’s society, body image is influenced bymany factors, such as the media and the fashion industry; andhair plays an important role. People who have thinning hair or
any type of hair disease may feel unattractive and have a negative
body image [19].

Embryology and Normal Hair Development

Hair follicles are derived from an interaction between theembryological ectoderm and mesoderm, which begins between 9
and 12 weeks of gestation. Human hair follicles primary develop
in the regions of the eyebrows, upper lip and chin [20].

Then, hair follicles develop over the scalp in a frontal to
occipital direction and progress over the body in a cephalocaudal*Corresponding author email: rubinaalves@gmail.com
bjamal@kau.edu.sa

The
Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

direction [21]. On the trunk and limbs, the hair germ development
is delayed and appears around the sixteenth week [22].

By 18–20 weeks of gestation, the entire initial populationof follicles has formed, including those on the scalp, althoughfollicular development is in different stages of evolution [23].
Human Follicles (HFs) develop through complex
morphogenetic processes resulting from reciprocal molecularinteractions between epithelium and underlying mesenchyme
during embryonic development [24].

At birth, within anatomical regions and most of the scalp
hair, all hairs are initially synchronous in anagen phase [25,26].
However, in the occipital scalp, telogen phase is delayed until
after birth and this can give rise to a path of hair loss in this regionof the scalp [27].
Initially, this Transient Neonatal Hair Loss (TNHL) also known
as ‘neonatal occipital alopecia’ was thought to be secondary tofriction due to babies sleeping in the supine position [20]. A
prospective study was performed, and as stated by the authors,
TNHL is related to the physiology of hair shaft shedding, itappears in healthy babies from birth until approximately thesecond month of life without accompanying symptoms and withspontaneous resolution [23].

Each follicle is capable of producing three different types ofhair as follows: lanugo, vellus and terminal hairs. The initial hairproduced is the lanugo hair. The type of hair originated by anindividual follicle can change with age or under the influence ofhormones [28].

Lanugo hair is nonmedullated, fine (typically less than 30 µm
in diameter), soft, and usually non pigmented hair which cover
the whole body of the newborns [20]. Is typically shed between
the thirty-second and thirty-six weeks of gestation, although
it can remains by 3–4 months after birth in an unsynchronizedwave pattern. Then he is replaced by vellus hair [12].
Vellus hair is short, light-colored, barely noticeable, andcovers almost the whole body. Around puberty, there is anincrease of the circulating adrenal androgens, which leads to asite-specific response from the hair follicles. With the presence of
androgens, the hairs of the scalp miniaturize, while the hair of the
body enlarges. At this time, the hairs of axillary, pubic, chest, andbeard (boys) change from vellus to terminal hair, contributing to
the development of the secondary sex characteristics [21,28].

Terminal hair is larger (approximately 1 to 100 cm of length)
and thicker usually with more than 60 µm in diameter. This typeof hair is strongly pigmented and is found on the scalp, eyebrows,
axillary and pubic areas, chest and face [21]. In patients with AGA,
terminal hairs follicles in the scalp convert to miniaturised hairfollicles (< 30 µm in diameter).

Anatomy and Hair cycle

The hair follicle is anatomically divided into three parts:

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Jamal,
et al.
©2017
Alves
R

upper (infundibulum), middle (isthmus) and lower part
(inferior segment). The infundibulum and isthmus comprise thepermanent portions of the hair follicle and is a relatively constant
structure, while the inferior segment is transient and undergoes
cyclical regeneration [29]. A fourth segment of the pilosebaceous
follicular unit would comprise the sebaceous gland [26].

In the permanent part, the infundibulum extends fromthe skin surface to the insertion of the sebaceous duct at thejunction with the isthmus whereas the isthmus begins below the
sebaceous duct and extends to the bulge or area of attachment for
the arrector pili muscle [22].

The lower segment of the follicle is the site of the majorityof activity in the hair follicle. Is comprised of three layers fromoutermost to innermost: Outer Root Sheath (ORS), Inner Root
Sheath (IRS) and Hair Shaft (HS).
The inner part of hair bulb is invaginated at its base by the
Dermal Papilla (DP). The IRS and HS are derived from epithelial
cells surrounding the DP, a region known as the hair bulb matrix
or germinative epithelium.

Dermal papilla size is dynamically regulated during the haircycle [30]. Cells emigrate from the DP during catagen and thenrepopulate it in anagen [31,32]. The DP is a condensation ofmesenchymal cells at the proximal end of the hair follicle, which
determines hair shaft size and regulates matrix cell proliferationand differentiation. In large follicles the DP often contains a loopof capillary blood vessels. DP cells have the ability to regenerate
new hair follicles. These cells tend to aggregate both in vitro andin vivo. This tendency is associated with the ability of papilla cells
to induce hair growth [33]. The follicle miniaturization seen in
AGA is thought to be driven by dysfunctional DP cell.
The human skin supports approximately 5 million hairfollicles, of which approximately 100,000 are on the scalp [23].

Human hair grows in a continuous cyclic pattern presentswith different phases: the anagen or growth phase, which lasts
between 2 and 7 years, the catagen or regression phase, which
has a duration of 2-3 weeks, the telogen phase, which lasts 3
months, and the shedding exogen phase [20].
The duration of hair cycle phases can be modulated bydifferent physiological conditions in the same individual, in
accordance with stages of postnatal, sexual development or
seasonal environment [34]. The normal hair cycle results in thereplacement of every hair on the scalp every 3–5 years [28].

The anagen phase receives signals from the cells of the germto regenerate. The interface between the hair follicle epithelium
and the mesenchyme increases progressively and the cells of thehair bulb matrix reproduce with a high mitotic rate and stem cells
in the bulge give rise to hair germs to create a new HF [27,35].
When the period of active growth ends, the follicle growth
stops and enters in a transitional physiological involution stage,
the catagen phase. In catagen, bulbar portion of the follicle is

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164(2) 1-13.
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1):Page 2 of 13

The
Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

degraded but HF stem cells are maintained in the bulge [24, 36].
At this time, the follicle decreases in size as the DP cells move
together [37]. After catagen, follicles undergo apoptosis and enterin the telogen phase. The hair filament remains in the telogen
phase which later is detached during exogen [38].

The telogen or resting phase is followed by exogen in which
the hair filament is detached.
The regenerative hair cycle is regulated by different molecularsignals between follicular epithelium and mesenchymal DP
cells [24]. The growth and development of HFs is influenced
by a number of signals, different Growth Factors (GFs) andtheir receptors and cytokines. These signals also comprisetranscription factors, nuclear receptors, neurotrophins andintracellular signaling pathways [27].
There is a balance of negative and positive influences
regarding the activation or down-regulation of hair cycle and thatis distinct for each phase of the hair cycle [39].
It has been described that anagen phase is activated by
Wnt (wingless) /β-catenin (Beta-catenin) / LEFT (T-cell factor
lymphoid enhancer), Sonic hedgehog (Shh) and the proteyoglican
versican [40,41,33]. This molecules have been used as anindicator of hair inductiveness, many of which are also associatedwith aggregative behaviour.

Other GFs are involved in promoting the hair regrowth
including Fibroblast Growth-Factor (FGF), Insulin-like Growth
Factor 1 (IGF-1), Hepatocyte Growth Factor (HGF), Keratinocyte
Growth Factor (KGF) and Vascular Endothelial Growth Factor(VEGF) [42-44,39]. This activation signalling leads to thestimulation of the hair germ in anagen phase.

The hair cycle is regulated through other pathways with adown-regulation affected, which are also essential for the proper
hair formation. Others GFs exert their action through an inhibitory
effect and down-regulation on hair growth and that may be
involved in the beginning of the catagen phase [39]. Some of these
GFs include: growth factor bone morphogenetic protein-4 (BMP4), transforming growth factor-β (TGF-β), interleukin-1α (IL-1α)
and tumour necrosis factor-α (TNF-α) [45,46].
The knowledge of these molecular targets could help us to
identify the potential therapeutic target of platelet-rich plasma,as described below.

Pathophysiology of Androgenetic Alopecia

The pathogenesis of AGA is influenced by two main factors:
heredity and androgen action. AGA is considered a disease with agenetic predisposition, but the mode of inheritance has not been
well characterized [47].
Inheritance is almost certainly polygenic, with genetic
input from both parents. Studies performed on monozygotic
twins showed strong concordance rates between 80 and 90%,
reinforcing the implication of a genetic basis [12,48].

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R
2017
Jamal,
et al.

Family history predisposes to early development and rapid
progression of the alopecia [3]. Its etiology is multifactorial andpolygenetic [1,49].

For the development of AGA, the presence of androgens,in combination with genetically susceptible hair follicles, isnecessary [50].

The modulation of hair growth androgens is very important.
Androgens such as testosterone are responsible for the conversionof vellus hair into terminal hairs of facial, trunk, extremities,
pubic and axillary areas. The growths of these areas are similar
in both sexes and begin around puberty. The growth of scalp hair
is not dependent of the androgens, although it is well known they
are necessary for the development of balding [51].
So, androgens will have a different effect regarding the locationof the hair follicle. They are able to stimulate both the growthof hair (pubic, axilar, beard, chest) and also promote the loss ofcertain hair in the scalp, in genetical susceptible individuals.
The androgen hormones testosterone and Dihydrotestosterone(DHT) each have selective roles at puberty. Testosterone isconverted to DHT by the enzyme 5-alpha-reductase that has two
isoenzymes: 5-alpha-reductase type I (present in the liver andsebaceous glands) and 5-alpha-reductase type II (present in thescalp, beard, chest, liver and prostate gland).

Testosterone is associated with increased muscle mass,
growth of the scrotum, voice change, and the presence of terminal
pubic and axillary hair fibers. An increased activity of 5-alphareductase type II plays an important role in the development of
AGA; Levels of this isoenzyme are higher in men than in womenand in the areas affected by AGA [1,3].
DHT is associated with temporal scalp hair recession, acne,
growth of the prostate gland, and the development of terminal
hairs in the beard region, external ears, and limbs.

The hormone DHT activates the genes responsible for the
shortening of hair growth cycle as well as the transformation oflarge hair follicles into smaller follicles that progressively become
miniaturized [16].

AGA is characterized by the miniaturization of the hair that
only occurs in certain areas: the frontotemporal and vertex area
in men and the crown region in women. These scalp regions
are susceptible to the effects of androgens. During the gradualtransformation of the miniaturized follicles (from terminal tovellus-like follicles), the anagen phase shortens, and for thisreason more hairs are in telogen phase [50]. There is no loss ofhair follicles in AGA, just miniaturized [12]. DHT has been shownto inhibit hair growth in mouse models through blocking theactions of growth factors such as insulin-like growth factor 1(IGF-1) [37,52].

Diagnosis of Androgenetic Alopecia

Most patients with AGA will be easily diagnosed by a clinical

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164(2) 1-13.
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1):Page 3 of 13

The Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

history and clinical examination, according to the condition of thecharacteristic distribution pattern [53]. Male pattern baldness ischaracterized by a receding hairline at the temples and baldingof the vertex, which gradually enlarges to link together. In thefemale pattern, there is a diffuse decrease in density over thecrown of the head and the frontal hairline is preserved.

Some noninvasive techniques such as trichoscopy and hairpull test help to perform the correct diagnosis. In some cases,
it might be necessary to do a more extensive examination
using other diagnostic tools, such as scalp biopsy. A laboratory
examination might be extremely useful in some patients,
especially in women, to evaluate any associated diseases. Global
photographies performed at baseline are helpful to compare theefficacy of the treatment, both for patient and physician.
In the presence of a patient with hair loss the first to perform
is a detailed clinical history. The history should include all
demographic data of the personal history of the patient including
age, sex, age at the first manifestation and grade of evolution of
the hair loss, through time.

The family history of AGA is important because of the role ofgenetics in this pathology. Although a positive family history isfrequent, a negative family history of AGA does not exclude thediagnosis [1,54].

An exhaustive history of associated diseases, systemic
alterations and drug history are of utmost importance, as there
are different factors such as nutritional or endocrine diseases
and drug intake that could precipitate or aggravate the severityof the hair loss. Several environmental factors such as exposure
to ultraviolet radiation and smoking have been associated withthe development of AGA, so these aggravating factors should also
be considered when performing the clinical history of the patient[55-58].
In the physical examination, besides the scalp skin and hairit should also be evaluated the facial and body hair and the nails.
The skin of the scalp should be examined to exclude signs oferythema, scaling, inflammation and atrophy. Usually, in patientswith AGA, the scalp skin has no alterations although somepatients can present with a discrete erythema and scaling relatedwith seborrheic dermatitis that can be an aggravating factor. Jang
WS, et al. [47] in a retrospective review found that seborrheic
dermatitis was the most common associated disease in male andfemale patients with AGA.
In patients with advanced AGA, the skin of the scalp becomessmooth and shiny but in some cases a discrete atrophy can bepresent [1]. Nevertheless, the presence of atrophy should alert toanother type of alopecia such as scarring alopecia.

These signs would easily help differentiate AGA from othertypes of hair loss or infections.
Hair examination includes the hair of the scalp, facial and thewhole body.

Copyright:
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Jamal,
et al.
©2017
Alves
R

The scalp hair of patients with AGA is a miniaturized hairwith variation of hair calibre, length and re growth. It follows acharacteristic pattern of distribution, which is different between
sexes. Male pattern is characterized by recession of hairline,
frontotemporal and vertex areas while in the female pattern,
there’s usually a diffuse distribution of hair loss, more pronounced
in frontal and mid scalp areas. Unlike in male pattern, the frontal
hairline in women is typically preserved.
Although, these are the most frequent patterns in bothgenders, there are other types of pattern distribution whichhave specific classifications, such as Hamilton-Norwood scale
for men and Ludwig for women, the most frequently used. The
Classifications of AGA are described below.

The examination of the facial and body hair will give further
information, regarding differential diagnosis or associatedpathologies. The absence or reduced of eyebrows/ eyelashes
may suggest a frontal fibrosing alopecia or Alopecia Areata (AA)[1]. Regarding body hair examination, an excessive hair growth
could lead the physician to think in hypertrichosis or signs ofhyperandrogenism such as hirsutism.
To analyse with more detail the hair scalp, some noninvasive
diagnostic tools may be helpful.

A hair pull test, also known as “traction test” or “Sabouraud’ssign” helps distinguishes between active and non-active hairloss from follicles. To perform this test, around 50–100 hairs
are grasped between the index finger and thumb and then lifted
proximally to distally, with gentle traction [20]. This procedure
is repeated in different areas of the scalp: frontal, occipital andtemporal regions. The hair pull test is considered positive if morethan 10% of telogen hairs are released, this means that if thepull test has more than 5 or 6 hair indicates ongoing hair activity[54,59].

False positives can occur if the test is performed on a day inwhich hair has been washed. A positive hair pull test will indicate
an active hair shedding. Hair pull test in positive in Telogen
Effluvium (TE). In patients with AGA, the hair pull test is usuallynegative, with the exception of active periods when a moderate
telogen hair shedding is present in a pattern distribution [1].

Trichoscopy is a noninvasive technique performed using ahandheld dermoscopy or a digital video dermatoscopy system.
The handle dermoscopy usually has a 10-fold magnification of
the skin surface while the video dermoscope, which is equippedwith a software, will have the benefit of larger magnification(ranging from 10-70 fold) and the conversion of measurement
results into a database Trichoscopy adds important informationfor establishing the correct diagnosis and it is also a useful tool
for assessing disease activity and monitoring treatment efficacy[18,60,61].
In AGA, trichoscopy will easily identify the abnormalities
present in this type of alopecia. Male and female AGA sharesimilar trichoscopic features.

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164(2) 1-13.
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1):Page 4 of 13

The Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

The most important trichoscopic feature is hair shaft
thickness heterogeneity, which means the presence of hairs withdifferent thickness such as thin, intermediate and thick hairs [61].
Other features include vellus hairs (decreased terminal to vellus
hair ratio), predominance of HF units with single hairs, yellow
dots (hair follicles filled with hyperkeratotic plugs), perifollicular
discolouration, wavy hair and honeycomb pigmentation [60,62].

The videodermoscope with an automatic digitalised system
will add more information of the analysed images regarding
hair parameters such as number of hairs (number of hairs/0.65cm2), hair density (n per cm2), terminal hair density (n percm2), anagen and telogen hairs (%) and anagen/telogen ratio.
In patients with AGA, frontal hair density is decreased whencompared with occipital areas and anagen/telogen ration isnormal or decreased [1].
The trichogram is a quantitative technique that provides
information on the ability of hair growth and its alterations.
Although an useful technique, it requires prior training andis time consuming [63]. Usually is not a frequent diagnostic
technique used for the diagnosis of AGA.
Usually, scalp biopsy is the standard technique for diagnosing
different types of scarring alopecia [54]. In addition, scalp biopsy
could give relevant information in difficult cases of non scarring
alopecia, where the diagnosis of the type of alopecia is uncertain.
In few cases, the diagnosis of AGA is not clear, such as alterationsof the scalp suggestive of scarring alopecia or diffuse AA, and ascalp biopsy may be needed to obtain the final diagnosis [1].

The scalp biopsy should be performed with a cylindrical punchof 4 to 6 mm in diameter, in an area representative of the hair loss
[26]. Biopsies taken with a smaller punch than 4 mm in diameterare not recommended as it would give less number of follicle
units, and as the follicles are not always affected simultaneously
by a such disease it would diminishes the probability of a correct
diagnosis [26]. The biopsy specimen should include the entire
follicular unit and reach into the subcutaneous tissue where
normally are the bulbs of anagen hair follicles [54,64].
According to Blume-Peytavi, et al. [1], it should be obtained
two 4-mm punch biopsies in which 1 biopsy is for verticalsectioning and the other biopsy for horizontal sectioning.

A horizontal sectioning of the scalp biopsy specimen would
give more quantitative and morphometric data and allowed avisualization of a larger number of follicles, diameter and grouping
whereas the vertical section would provide more information
about the length of the hair follicle and full dermal thickness andthis was a diagnostic advantage, especially in scarring alopecia[54, 65, 66]. It remains uncertain if biopsies should be oriented
horizontally or vertically [26].
Recently, DU X, et al. [66] published a systematic review metaanalysis to evaluate the value of horizontal sections comparedto vertical sections in the diagnosis of alopecia and found “nosignificant difference exists between horizontal and vertical

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Alves
R
2017
Jamal,
et al.

sectioning techniques in the diagnosis of alopecia”, althoughmore studies are needed.

In areas affected by AGA is possible to identify an increased
number of miniaturized follicles, and a ratio telogen-vellus of <3:1 when compared to a ratio telogen-vellus of < 7:1, in patients
without AGA [1,67].
The main histologic features in AGA are slight perifollicularlymphohistiocytic infiltration with a perivascular degeneration of
the lower one third of the connective tissue [68].

The examination of the nails can add important informationand is important for the differential diagnosis of other types ofalopecia. Nail abnormalities such as pitting can be present in AA
and liquen planus. Patients with AGA typically don’t have any
alteration in nails.

In women, although the majority has a normal hormonal
function, a careful evaluation regarding gynaecological history
should be done to exclude hormonal dysregulations [1].
Regarding laboratory examination and according to Camacho
and colleagues in their protocol, the most important laboratory
tests to be considered are levels of free testosterone, 5-α-DHT,
DHEA-S, 17-beta-hydroxyprogesterone, prolactin, delta-4androstenedione, sex-hormone-binding globulin (SHBG),
3-α-androstanediol glucuronidel and prostatic-specific antigen(PSA) in both, premenopausal (normal levels ≦ 0.02 ng/mL) andpostmenopausal women (nL ≦ 0.04 ng/mL) [63].

The global photography of the scalp is a non-invasive anduseful method for determining clinical changes in the patient
over time in a standardized manner.

Classifications of Androgenetic Alopecia

There are several classifications that help to determine thedegree of androgenetic alopecia for male and female patients.
This allows staging the degree of alopecia at the time of diagnosis
and control the evolution and response to the treatment.
For male pattern hair loss, the classification widely used is:

Hamilton-Norwood Classification: the most widelyclassification used for MPHL [10]. There are seven stages of
evolution, involving the frontotemporal area and evolution of hairloss to the vertex. There are absence of frontal hairline, however,in some cases, men develop diffuse thinning of the crown withretention of frontal hairline that resembles a female patternobserved in Ludwig Classification.
For female pattern hair loss, the most common classifications
are:Ludwig’s Classification: divided into three progressive
stages based on hair density: I - minimal alopecia; II - Moderated
alopecia and III - severe alopecia [69].
Ebling’s Classification: includes a five stage classification
system for FAGA. The first two stages are the same as the Ludwig

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

Page 5 of 13

The Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

Copyright:
Copyrights:©
2017
Jamal,
et al.
©2017
Alves
R

system. Type III includes the diffuse hair loss and the initial lossof hair from the frontotemporal hair line; Type IV besides the
diffuse loss there’s evidence of frontotemporal recession; type V,
appears like the male pattern of baldness (MPHL) with a there iscomplete loss of hair on the top of the scalp [70].

Lachgar, et al. [73] performed a study to evaluate if minoxidil
could affect the expression of VEGF. According to the authors,minoxidil caused an elevation of VEGF and should be consider anindirect inducer of angiogenesis through an up regulation of theexpression of VEGF in DP cells, during the anagen phase.

Savin Scale: a recent classification scale of 8 levels
similar to Hamilton–Norwood’s classification with frontal andlateral views of the hair loss patterns, that uses a computer
analysis based in “the density of hair by unit of area” [63].

The literature has demonstrated that topical minoxidil is as aneffective treatment for AGA by promoting hair growth Minoxidil
is available in 2% and 5% solutions and it is used twice a day indoses of 1 mL [76].

Olsen’s Classification: classification proposed by
Olsen with 3 degrees of severity. The main characteristic of thisclassification is the “christmas tree” distribution, with a frontal
accentuation in a triangular [71].

Treatment of Androgenetic Alopecia

The treatment of androgenetic alopecia should be initiate
as early as possible as untreated androgen-dependent alopecia
progressively deteriorates [72].
There are several treatment options available for the treatmentof hair loss, although currently, only topical minoxidil and oral
finasteride have the approval of Food and Drug Administration(FDA) for the treatment of AGA.

Minoxidil

Initially, oral minoxidil was used to treat high blood pressure.
As a side effect of the treatment was an increased hair growth.
Since then, topical minoxidil has been used to treat hair loss [6].
The 2% topical minoxidil received the approval by US-FDA for
the treatment of AGA in male and female patients in 1998 and2001, respectively.

The 5% topical minoxidil was approved for the treatment of
AGA in men, in 2007 and the 5 % foam minoxidil in 2006 also forthe treatment of AGA in men [49]. The 5% solution and 5% foam
are not licensed by the FDA for use in women, but it is commonlyused off-label for this purpose [12].
Minoxidil is a pyrimidine derivate that needs to be converted
to its active metabolite, minoxidil sulphate, to exert its action.
Minoxidil is thought to promote hair regrowth through its ability
to open ATP-potassium channels. Although the exact mechanismof action of minoxidil is not fully understood, minoxidil has
vasodilatory, proliferative and anti-inflammatory effects [53].
There are different possible mechanisms in which minoxidil
could act to induce hair regrowth.

VEGF is known to increase angiogenesis and also promoteperifollicular vascularization, hair growth rates, and increased
follicle and hair size [44]. An VEGF mRNA is strongly expressedin DP cells during anagen phase with a substantial decrease of
expression during catagen and telogen phases Topical minoxidil
on the hair follicle can increased the expression of VEGF mRNA,
presented in the DP cells [49,73,74].

Other effects of minoxidil to induce hair regrowth could
be the activation of activation of cytoprotective prostaglandin
synthase-1 and increased expression of HGF, both hair growthpromoters [49,74,75].

Several studies have demonstrated that minoxidil applied
twice a day is an effective treatment for AGA, in both men andwomen [5,49,77-81].

Olsen, et al. [79] performed a Randomized Clinical Trial (RCT)comparing the use of 5% topical minoxidil versus 2% topicalminoxidil and placebo in the treatment of AGA in men. The
authors refer that the men who used 5 % topical minoxidil had
an earlier response to treatment than those who used 2% topicalminoxidil. Both 2 and 5% topical minoxidil solutions were welltolerated by the men without evidence of systemic effects.
Concerning the treatment of FPHL, either 2 or 5% (used offlabel) topical minoxidil solution appears safe to use in womenwith AGA. The only additional risk of the 5% topical minoxidil
solution over the 2% topical minoxidil solution reported was thehigher incidence of facial hypertrichosis [9].
Recently, 5% minoxidil foam has received specially attention
because of the good compliance of the patient and as hydroalcohol-based vehicle with absence of propylene glycol, presented
in minoxidil topical solutions.

Blume-Peytavi, et al. [82] performed a randomized, singleblind study of 5% minoxidil foam once daily versus 2% minoxidil
solution twice daily to compare their efficacy and safety in thetreatment of AGA in women. According to the authors, both
treatments were equally effective for improving hair loss,
although once daily 5% MTF was better tolerated (lower incidenceof pruritus and dandruff) with greater aesthetic advantages incomparison with twice-daily 2% minoxidil solution.
Another study reported that 5% minoxidil foam could be
more convenient with a better compliance of the treatment andwas not associated with greater side effects. The present article
provides update and reliable information that 5% minoxidil foam
is a very good option for women patients with hair loss [83].

Some clinicians prescribe minoxidil in combination withother active ingredients, such as tretinoin. Bazzano GS, et al. [84]studied the combination of topical tretinoin with minoxidil andfound a terminal hair regrowth in 66% of the patients, after 1
year of treatment. Another study compared the efficacy of 5%

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

Page 6 of 13

The
Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

minoxidil alone (twice-daily) versus the combination of 5%minoxidil solution and 0.01% tretinoin (once daily) for MPHL. In
this randomized, double-blind trial, the authors reported that theefficacy and safety of both treatments appear to be equivalent,with no statistical differences between the two treatment groups[85].

To assess the efficacy the patient should wait at least 6months before considering if the treatment is effective. To ensure
the compliance of the patient to the treatment, the physician haveto inform about the transitory hair shedding that occurs after 2
months of the beginning of the treatment. The main side effects
reported with the use of minoxidil are hypertrichosis and contact
dermatitis.

Alpha Reductase Inhibitors

There are two types of 5α-reductase enzymes, which have to
be considered. Type 1 5α-reductase enzyme predominates in thesebaceous gland, liver, skin and scalp while type 2 predominantly
is mainly present in the prostate and certain regions of terminal
hairs The 5α-reductase inhibitors regulate the transformation of
testosterone to DHT in DP cells of the follicular units [49].
The main 5α-reductase inhibitors are finasteride anddutasteride.

A daily oral dose of 1 mg finasteride reduces scalp DHT by
64% and serum DHT by 68%. Dutasteride can decrease serum
DHT by more than 90%, while finasteride decreases serum DHT
by 70% [6].

Oral finasteride is a competitive and specific inhibitor of type2 5α-reductase. In men with AGA, the balding scalp contains
miniaturized hair follicles and increased amounts of DHT if
compared to the hairy scalp. The administration of finasteridedecreases scalp and serum DHT concentrations in bald scalp andincreases scalp testosterone, as stated by Dallob and colleagues[86].

Finasteride has been investigated extensively and it is widely
accepted as one of the more effective therapies for AGA in men[49,87].
Mella, et al. [88], published a systematic review to assess theefficacy and safety of finasteride therapy for AGA, when comparedto placebo. The authors report that moderate-quality evidenceof the studied articles showed that daily use of oral finasteride
increases hair count and improves patient and investigatorassessment of hair appearance.
Treatment with finasteride should be life-long as its
interruption is followed by gradual hair loss, with return to thepre-treatment status within 1 year.

The optimal dose of finasteride for male AGA was identified
as 1mg/day [63].
Regarding the use and of finasteride in women, its efficacy
is not well-established and is used as an off-label treatment of

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Alves
R
2017
Jamal,
et al.

2.5-5mg/day [89-91]. Two RCT have demonstrated that theuse of 1mg/day is not effective in women. Price VH, et al. [92]published a double-blind, placebo-controlled, randomized,
multicenter study and reported that after 12 months of treatment
with finasteride 1mg/day in postmenopausal women there was adecrease in hair count from baseline and that finasteride was noteffective in improving hair loss [92,93].
Oral dutasteride is an 5α-reductase inhibitors of both type
1 and 2 enzymes and is prescribed as an off-label treatment for
AGA.

Although with few studies published until now, the use ofdutasteride appears to be safe and efficacious in the treatment ofpatients with AGA [94,95].

In a recently published clinical trial, Tsunemi, et al. [96]reported that patients who took 0.5 mg of oral dutasteride once
daily for 52 weeks improved the hair regrowth, at 26 and 52
weeks. Of notice, between weeks 26 and 52 the proportion ofpatients who improved from baseline increased, which meansthat the effects of dutasteride are still progressing and thatdutasteride needs a longer follow-up. The present study reportsthat dutasteride exhibited long-term safety, tolerability andefficacy for male AGA.
Different studies compared dutasteride versus finasteride inorder to assess its efficacy and safety.

In 2004, Olsen EA, et al. [97] performed study in which men
with AGA were randomized to receive daily dutasteride (0.05,
0.1, 0.5, or 2.5 mg), finasteride (5 mg), or placebo. After 24 weeks
of treatment, both dutasteride and finasteride were superior
to placebo and the group of 2.5mg dutasteride had a statisticalsignificant improvement when compared with 5 mg finasteride.
Tsunemi, et al. [96] reported that 0.5 mg of dutasteride
exhibited long-term safety, tolerability and efficacy for male
AGA. Another study performed by Boersma, et al. [98] reported
that 0.15 mg of oral dutasteride appears to be significantly more
effective than 1.25 mg of oral finasteride in women under 50
years of age.

Both finasteride and dutasteride are frequently prescribed
as off-label treatments for women with AGA. These drugs crossthe blood-brain barrier and might cause the feminisation of amale fetus, which means that they are contraindicated for use
in women with child-bearing potential and during pregnancy(Pregnancy Category X) [6]. Thus, special attention is neededin fertile women of childbearing age, for whom contraceptive
measures are obligatory [6].

Antiandrogens

Oral antiandrogen therapy such as cyproterone acetate,
spironolactone or flutamide are used in the treatment of FPHL,
although evidence of efficacy for any of these treatments islimited [49]. Oral antiandrogens are used in women and arecontraindicated in men due to their feminizing action.

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

Page 7 of 13

The
Effect of Smoking
on Facial
Aging Amongin Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Females
Emerging
Treatments

Cyproterone Acetate (CA) is an androgen receptor blocker
and potent progestin It has been in common usage for over 40
years in the treatment of hirsutism but the limited controlled trial
evidence has shown little evidence of efficacy in FPHL.

The mechanism of action of CA is to block androgen
receptors and decrease testosterone levels by suppressing
luteinizing hormone and follicle-stimulating hormone release[63,99]. It seems that CA may be more effective in women withhyperandrogenism.
There are no dose-ranging studies, but most practitioners
use CA 50 to100 mg/day from the fifth to the 15th day of themenstrual cycle for a 6-month period. The first 10 days of eachmenstrual cycle, then followed by 2mg/d from the first day ofthe cycle to the 21st, with a week of rest, for 18 months [63].
In premenopausal women, oral contraceptives such as ethanol
estradiol should be added as it stabilizes menstrual irregularities.
For postmenopausal women, CA may be used continuously.

The side effects of CA are dose dependent and this medication
is absolutely contraindicated in patients with liver disease. In
addition, feminization of a male fetus may occur and so patientsshould be advised to cease the medication before conception.
According to Camacho et al opinion’, CA is the best treatment for
the FPHL [63].
Spironolactone is a potassium-sparring diuretic, structurally
related to aldosterone (antagonist) that acts as an anti-androgenic
by reducing the levels of total testosterone and competitively
blocking the androgen receptor in target tissues [99]. Its primary
use is as a diuretic and antihypertensive. There are no controlled
trials in FPHL.
The dosage range from 50 mg/day to 200 mg/day for at least
6 months. The beginning is made with a starting low dose of 50
mg/day and increasing the monthly dose by 50 mg to a final doseof 200 mg/day [63,100].
Side effects are dose related and include menstrualirregularities (menorrhagia), postmenopausal bleeding, breast
tenderness, hyperkalemia and fatigue. In healthy young women,
the risk of hyperkalemia is very low, although check of the serum
potassium levels should be performed periodically [63].
This drug is category X for pregnancy, as it has as the potential
to feminize a male fetus.

Flutamide is a pure, nonsteroidal antiandrogen that acts by
inhibiting androgen uptake and by inhibiting nuclear binding of
androgen within the target tissue. It is the treatment of choice
when hair loss and hirsutism are associated with each other[101]. The most severe side effect is hepatotoxicity. Other side
effects described include lethargy, mood change, and loss oflibido. Is also contraindicated in pregnancy and lactancy as it may
cause feminization of the male fetus.

Emerging treatments

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Copyrights:
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©2017
Alves
R
2017
Jamal,
et al.

The currently available treatments for AGA are sometimes
perceived as having limited effectiveness; therefore, theidentification of new therapies for this pathology is of utmost
importance [102,103]. New possible offline treatments for AGA,
such as topical finasteride, injectable dutasteride, laser therapy
and PRP, have recently emerged and have been claimed to have
hair growth-promoting or anti-hair loss effects.

Topical finasteride

Topical finasteride is being investigated as a new treatment
for AGA with fewer side effects than oral finasteride. According
to Caserini, et al. [104], a daily application of a 0.25% solutionof finasteride (doses of 100 and 200 μL) leads to the inhibitionof scalp DHT and may minimize the untoward sexual side effects
that are linked to systemic DHT reduction [6].
A RCT compared oral finasteride and topical finasteride in
45 male patients with AGA. Patients were randomized in two
groups to receive 1) twice daily finasteride gel 1% preparationand placebo tablets 2) oral finasteride 1% and placebo gel, for
6 months [105]. According to the authors, the results showedsimilar efficacy for the two therapies, although not statisticallysignificant.

A study conducted by Tanglertsampan C compared thesafety and efficacy of 3% minoxidil solution (MNX) versus the
combination of 3% minoxidil and 0.1% finasteride solution(MFX) in the treatment of men with AGA [106]. At 24 weeks, there
was an increase of hair count from baseline in both groups, but
no statistical difference. The assessment by global photography
showed significantly greater improvement in the MFX group thanthe MNX group.
Another study assessed the efficacy of 5% topical minoxidil
fortified with 0.1% finasteride in patients with AGA who had
been medicated with 5% topical minoxidil and oral finasteride in
the previous two years [107]. The aim was to assess the efficacy
of maintaining the hair growth. Eighty-four percent maintained agood hair density after 12 months of treatment with minoxidilfinasteride combination.

There are few published articles regarding topical finasterideand usually topical finasteride is used in combination with othermedication. At this moment, there is insufficient evidence tosupport the use of topical finasteride [49]. Additional studies
using the topical finasteride alone are needed to assess its efficacy.

Injectable dutasteride

Injectable dutasteride might be a promising treatment
for AGA. In 2013, Moftah, et al. [108] published a study that
evaluated the efficacy and safety of mesotherapy using adutasteride-containing preparation (0.5 mg of dutasteride, 20
mg of biotin, 200 mg of pyridoxin and 500 mg of D-panthenol)in female patients with hair loss. The authors concluded that thispreparation was effective, tolerable and yielded better response
among females with a shorter duration of disease. More studies

Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

Page 8 of 13

The
Effect of Smoking
on Facial
Aging Among
Females in Saudi
ArabiaAndrogenetic
Alopecia:a Review
and Emerging
Treatments

are needed with the use of injectable dutasteride alone, to assess
its efficacy.

Low-level laser therapy

The laser therapy is the application of Light of Low-Level
Laser (LLL) or Laser-Emitting Diodes (LED) with a spectral of
600 - 1000 nm and is used to treat several conditions such as
pain reduction, inflammation and to promote wound healing
and tissue regeneration [109,110]. Recently, it has been use
to promote hair regrowth. For its used in hair loss, most of theavailable devices use a wavelength of 655 nm.
The first LLLT device, the Hairmax Lasercomb® wasapproved by the US FDA and received clearance as a safe therapy
for the treatment of male AGA in 2007 and female AGA in 2011
[111,112].

Although the exact mechanism of LLLT is not clear, this laser
phototherapy might induce proliferation, migration, oxygenationand stimulate the transition from telogen hair follicles to anagen[110,111,113].
A systematic review was carrying out and found and the
majority of studies covered in the review found an overall
improvement in hair regrowth, thickness, and patient satisfaction
following LLLT therapy [114].

Another evidence-based review stated that LLLT devices areboth safe and effective for the treatment of FPHL and MPHL [113].
Avram MR, et al. [115] performed a study in 7 patients toinvestigate the efficacy of LLLT in hair regrowth and found a notstatistical significance decrease in the number of vellus hairs, anincrease in the number of terminal hairs, and an increase in shaft
diameter. No improvement in hair density was noted.
Although published articles found that LLLT could improve
hair regrowth, the LLLT results are limited with a low numberof patients. More studies, including RCT are needed to support
its efficacy. In addition, the optimum dose, wavelength,
coherence and dosimetric parameters remain to be determined[113,116,117,110].

As stated by Gupta AK, et al. [110], clinical studies should be
conducted and published in peer-reviewed journals and althoughmanufacturers believe in the quality and efficacy of their device,this might not be “sufficient for physicians to accept LLLT for hairloss and widely promote it, without reservation, to patients”.

Prognosis of Androgenetic Alopecia

There have been a number of studies regarding a relationshipbetween AGA and associated diseases, such as hypertension,
hyperlipidemia, diabetes mellitus, and Coronary Artery Disease(CAD).
Ahouansou, et al. [118] evaluated the association between
AGA and hypertension and found that men, aged between 19 to 50
years and who have early AGA (occurring before 35 years of age),

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Alves
R
2017
Jamal,
et al.

had an increased incidence of hyperinsulinemia and disorders
associated with insulin resistance, such as obesity, hypertension,and dyslipidemia [47,119].
Patients with AGA might be at an increased risk of CAD which
increases with increasing grade of AGA [120].

Arias-Santiago, et al. [121] performed a case control study with
154 participants, to analyze the presence of the cardiovascularrisk factors and the prevalence of carotid atheromatosis inmale and female patients with AGA in comparison with control
subjects. According to author’s results, the metabolic syndrome
was diagnosed in 60% and 48.6% of male and female patientswith AGA, respectively; Atheromatous plaques were more
frequent in patients with AGA than in controls and that was
statistical significant.
Therefore, the determination of metabolic syndrome,
ultrasound study of the carotid arteries in patients with AGA
may be useful screening methods to detect risk of developing
cardiovascular disease in patients with early-onset AGA andsignal a potential opportunity for early preventive treatment.

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Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access4(4): 1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
The EffectSmoking
on Facial
Among
Females
DOI:
http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

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on Facial
Aging Among
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ArabiaAndrogenetic
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and Emerging
Treatments

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Alves R
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B, Alsayeda B,
Filemban
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The EffectSmoking
on Facial
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Females
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http://dx.doi.org/10.15226/2378-1726/4/4/00164
in
Saudi
Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

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and Emerging
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Alves R
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Treatments.
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Dermatol
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Citation: Jamal
Alves R
(2017)
Androgenetic
Reviewand H,
Emerging
Treatments.
ClinofRes
Dermatol
OpenAging
Access.
4(4): Females
1-13
BT,
BokhariA, AljahdaliAlopecia:
B, Alsayeda B,
Filemban
et al.. (2017)
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on Facial
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http://dx.doi.org/10.15226/2378-1726/4/4/00164
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Arabia. Clin Res Dermatol Open Access 4(1): 1-13.

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