Progressive miniaturization of terminal hair is the hallmark of pattern hair loss. Miniaturization is a process in which large, pigmented terminal hair is replaced by fine colorless vellus hair, because of the shortening of the anagen phase in consecutive hair cycles. Pattern hair loss affects both males and females as progressive thinning of hair is a pattern that is different between males and females. Male pattern hair loss (MPHL) increases in frequency and incidence as age advances after puberty. MPHL is characterized by thinning of hair in the frontal, frontotemporal, and vertex areas of the scalp with variable loss of marginal, parietal, and occipital hair. Diagnosis is made clinically based on the history of hair thinning, hair loss, local examination, and a few simple tests. Anisotrichosis is finding on dermoscopy. The two main causative factors responsible are genetic predisposition and a derivative of testosterone, dihydrotestosterone (DHT). This is autosomal dominant and polygenic. The gene is X chromosome-linked indicating maternal component. Testosterone is converted by an enzyme 5-alpha reductase, into a more potent metabolite, Dihydrotestosterone, which is responsible for MPHL There are two types of 5- alpha-reductase, type one and type two. Finasteride is a competitive inhibitor of 5 α Reductase type II, while Dutasteride inhibits both alpha type I and type II. Finasteride and minoxidil are US-FDA approved as medical treatment of MPHL. The medical treatment is effective if started in the early phase of hair loss. . There are few side effects of finasteride, but the incidence is very low, and they are reversible once the finasteride is stopped. Medical treatment is not to treat the developed baldness. The treatment of baldness is the transplantation of hair follicles.

2. OVERVIEW OF PHL
• Introduction
• Characteristics of pattern hair loss
• Epidemiology
• Pathogenesis
• Clinical manifestations
• Investigations
• Classification
• Uncommon patterns of alopecia in men
• Treatment
• Revision of key points

3. PATTERN HAIR LOSS
• 90% of male over age of 40yrs affect hair loss.
• . Clinically there is progressive thinning of hair in a pattern which is
expressed differently in males and females.

4. INTRODUCTION
• Male pattern hair loss (MPHL) or androgenetic alopecia (AGA) is
Genetically determined progressive process in which there is conversion of
terminal hair to vellus hair.
• As age advances after puberty the process increases in incidence and
severity.
• It starts from thinning of hair usually in the frontal region. As it progresses
• there is receding of the anterior hairline and deepening of the
frontotemporal area.
• There can be associated thinning or hair loss in the vertex area or there
can be thinning.
• This reduces self-esteem, loss of confidence and anxiety in the affected
man.

5. Characteristic features of Pattern Hair Loss (PHL)
are-
• 1. There is diversity of thickness of hair called an-isotrichosis means variable thickness of
hair.
• 2. Reduction of number of hairs per follicular unit.
• 3. The pattern of thinning and or loss differs in males and females, though sometimes there
may be overlap.
• 4. The anagen phase of the hair cycle shortens, making hair shorter and finer.
• 5. Telogen phase may be same or longer leading to more hair shedding and increase in the
number of empty follicles on scalp.
• 6. Hair follicles closer to the arrector pili muscles are resistant to miniaturization, compared
to the hairs further away.
• 7. PHL in males usually starts anteriorly, first involving the frontotemporal region followed by
receding of anterior hairline.
• In females PHL appears as a diffuse pattern in the frontal, mid scalp, and crown with or
without loss of frontal fringe.

6. MALE PATTERN HAIR LOSS-MPHL

7. PROCESS OF MINIATURIZATION

8. PATHOGENESIS
• The exact pathogenesis is still incompletely understood
• as there is variation in pattern
• as well as differences in response to current modalities of treatment,
• but it is clear that there is a genetic predisposition and role
of androgen in pattern hair loss.

9. MPHL
• GENETIC----Proved
• ANDROGEN----Proved
• ENVIORNMENT—Stress, Nutrition, Toxins—environmental, pesticides,
smoking and tobacco(lifestyle) ?—weak evidence (HAYAKAWA
STUDY1992)

10. EPIDEMIOLOGY
• Hamilton estimated that 30% to 50% of men developed male pattern
alopecia by the age of 502.
• Many Western studies have shown that there are racial as well as age-
related differences in the incidence and pattern of hair loss in male
pattern alopecia3

11. PATHOGENESIS
• James Hamilton,11 was the first who found the role of testosterone in MPHL. Eunuchs
and men who have undergone castration before puberty do not develop male pattern
baldness.
• MPHL is because of a sensitivity to androgens in a genetically susceptible individual.10
• Testosterone is converted into a more potent metabolite, Dihydrotestosterone by an
enzyme named 5-alpha reductase.
• The 5-alpha reductase has been found in many parts of the body but is more
concentrated in scalp.
• There are two types of reductase, type one and type two.
• Type one alpha reductase is present in pilosebaceous and sebaceous glands.
• type two alpha reductase is found in prostate, dermal papilla and outer root sheath of
hair follicle.12
• DHT has five times more affinity for androgen receptors.
•

12. Evidence in favor of androgens causing MPHL
• People with genetic deficiency of type II reductase do not show
MPHL;
• similarly alpha reductase inhibitors also have proved to be beneficial
to treat MPHL.

13. Genetic evidence
• As per Osborn’s study,13 MPHL is autosomal dominant.
• MPHL is also polygenic; more than one gene is responsible, but
among all, the androgen receptor AR gene is most important.
• The evidence supports that AR gene location is on X-chromosome,
explaining the maternal component or inheritance.
• Other evidence proves there is higher expression of the AR gene in
balding scalp compared to non-balding scalp.
• It is found that men with Kennedy disease, do not show MPHL
because there is a genetic defect in AR gene.14

14. Other factors affecting hair growth
• Hair growth is also affected by the level of insulin growth factor I
(IGF1), basic fibroblast growth factor(FGF) , and vascular endothelial
growth factor (VEGF). These are anagen maintaining factors and
promote hair growth.
• Hair growth is adversely affected by premature apoptosis of dermal
papilla cells which may take place through the production and release
of cytokines such as transforming growth factor ß1, Interleukin1alpha
and tumour necrosis factor.

15. CLINICAL MANIFESTATIONS
• complaints of either increasing hair shedding or loss of volume.
• The patient often shows increased hair shedding, especially while combing.
• There is a decrease in anagen phase duration and increase in telogen phase.
• Reduction in anagen phase reduces the length of hair shaft, and over time, the
length of the hair fibre is reduced to the extent that the hair is not long enough
to reach the scalp surface and the follicle looks empty.
• Kenogen phase becomes much longer or there is a delay in replacement of
telogen hair, so the area finally becomes bald.
• Commonly there is receding of the anterior hairline and deepening of
frontotemporal angle
• Patients may also present with diffuse hair loss and or thinning and loss of hair
only in the vertex region .
• The presentation may vary, but the presence miniaturization of hair is a
characteristic feature of MPHL/AGA resulting in a heterogeneous population of
hair shaft thickness.
• Norwood, Hamilton and a few others have developed classifications of male
pattern hair loss.
• Most commonly used is the Norwood classification.

17. INVESTIGATIONS

18. Scalp Dermoscopy
• It shows a heterogeneous population of hair shaft thickness -
anisotrichosis, miniaturized vellus like hair and perifollicular brown
halos may be seen.17 (FIG 19.3)
thick
Intermediate
thin
anisotrichosis

20. Hair Pull Test
• In the early phase of PHL there is a positive hair pull test except in the
occipital area. Later, when hair loss stabilize, and the hair pull test
may not be positive

21. Histopathology
• The findings are-
• 1. Decrease in terminal and anagen hair,
• 2. Increased vellus and telogen hair.
• 3. Increase in follicular stelae (presence of fibrous track at place of terminal
• hair) ending in superficially located miniaturized follicles.
• 4. Mild peri-follicular lymphocytic infiltrates primarily around upper follicle.
• 5. Concentric perifollicular fibrosis may be present.
• 6. Sebaceous gland remains intact.
•

22. HISTORY OF HAIR LOSS
EXAMINATION OF HAIR & SCALP
GROSS & DERMOSCOPY
BLOOD INVESTIGATIONS-CBC, Vit
B12,vit D, S.Ferritin etc
COORELATE ALL FINDINGS OF 1,2,3
DIAGNOSIS NOT CLEAR
SPECIFIC TEST-hair pull
test, biopsy
MAKE DIAGNOSIS
PLAN THE TREATMENT
SURGICAL
MEDICAL
ADJUVANT-
PRP, LTTT etc

23. CLASSIFICATION OF MPHL
• There are many classifications, more common is Norwood Stage and
its variation.
• Others includes Hamilton’s classification

24. NORWOOD STAGE I
NS I –Minimal recession along the anterior border of the hair line

25. NORWOOD STAGE II
• NS II –Mild recession in frontotemporal area, with thinning along the
anterior margin of the forelock. The recession in frontotemporal area
is no further posteriorly than approximately 2 cm anterior to a
coronal line joining two external auditory meatus.
>2CM

26. NORWOOD STAGE III
• NS- III –The hair loss leads to deep frontotemporal recession. The
recession extends further posteriorly than a line 2 cm anterior to a
coronal line drawn between two external auditory meatus.
<2CM

27. NORWOOD STAGE IV
• NS I-V –Frontal and frontotemporal recession are more severe that in
type III, (baldness extending more than a coronal line joining two
external auditory meatus.)
• There is also hair loss or sparse hair in the vertex. But there is a hair
bearing area present between the frontal area of baldness and vertex
bald area

28. NORWOOD STAGE V
• NS V –Hair loss or baldness in both the vertex and frontotemporal
area. hair bearing area between both frontal and vertex bald areas is
very narrow or sparse hair is present.

29. NORWOOD STAGE VI
• NS VI –hair from the hair bearing area between frontal and vertex
which was present in grade V has now disappeared. There is no
hair on the top of the head. Also, there is further hair loss laterally ,
posteriorly.

30. NORWOOD STAGE VII
• NS VII –The hair loss is much severe than stage VI leading to a narrow
horseshoe shaped band of hair in the occipital zone . this hair band
begins laterally just anterior to the ear and extends posteriorly on the
side & quite low on the occipital area.
•

31. VARIATION GRADE II A, IIIA, IVA, VA
• The variants of the Norwood scale described as
GRADE IIA, IIIA, IVA, VA, have
• two major characteristics present: minor
characteristics may or may not present.
• The major feature—First, the recession involves
the entire frontal border with no sparing of the
mid frontal region (hair loss in both
frontotemporal and mid frontal areas).
• Second, there is no associated hair loss in the
vertex area.
• The minor variation is that there can be few
hairs in the area of recession, with a
• horseshoe shaped fringe of hair remaining on
the sides and back of the scalp is that
• is wider than non-type A cases.

33. DIFFUSE UN PATTERN HAIR LOSS
Diffuse thinning across
the entire scalp
including
Occipital region

34. DIFFUSE PATTERN HAIR LOSS
• Diffuse patterned alopecia
(DPA) - there is diffuse
thinning and hair loss
without complete balding
as in male pattern baldness
but without involvement of
the occipital area.

35. MPB with Persistent MFF
• MPB with persistent mid
frontal forelock. Any grade
of baldness but hair remains
present in forelock area

36. • Senile alopecia.- usually
seen in old age, decrease in
density over entire scalp. In
some cases, thinning is seen
from nape of neck towards
safe donor area this is
known as reverse pattern
androgenetic alopecia

37. • Persistent anterior
fringe. Baldness of any
extent but anterior
hairline is preserved.

38. TREATMENT
• There are effective medical treatments for male AGA. If started in
early phase the treatment can effectively control ongoing hair loss
and can prevent progressive baldness. US FDA approved treatment
for male AGA is use of topical minoxidil and oral finasteride.
• LLLT is US FDA cleared—safe for AGA
• PRP-off label treatment of AGA
• Food suppliants, vitamins and others off label

39. Minoxidil
• The drug minoxidil was first used in the 1970s as an oral
medication for refractory hypertension.
• The topical solution of minoxidil 2 to 5% is US FDA approved
treatment of androgenetic alopecia for both men and women.

40. EFFECT OF MINOXIDIL ON HAIR
1. Premature entry into anagen from resting phase. Abel24reported an increase in anagen telogen
ratio after 12 months of its use.
2.It elongates anagen and shorten telogen.25
3.There is an overall increase in follicle size and increase in mean hair diameter.
4.There is histological and clinical evidence of reversal of miniaturisation.26
5. Minoxidil is more useful in maintaining & thickening pre-existing hair, rather than re growing new
hair.
6. Use of topical minoxidil in peri operative period prevent the usual shedding that occurs one to
two weeks after transplantation and reduces the time for regrowth by one to two months. Minoxidil
should be stopped 2 – 3 days before surgery to minimize skin irritation which reduce theoretical risk
of intraoperative bleeding.
7. The half-life of minoxidil is 22 hrs and its peak effect comes in 40 weeks of its continuous
application.
8. Twice a day 5% minoxidil on dry scalp for man is recommended

41. MINOXIDIL Side effects
1. Hypertrichosis means unwanted hair growth over face and other
part of body, which is more commonly seen in females even at lower
dose. Spillage of minoxidil solution over forehead and face my induce
hair growth. The systemic is discontinued.
2. Irritant reaction leads to scalp irritation and pruritus.
3.Worsening of seborrheic dermatitis.
4.Contact dermatitis. Allergic reaction is mainly because of propylene
glycol, less commonly because of minoxidil salt it self.27 allergic reaction
is less with minoxidil foam.

42. MINOXIDIL-Contra indication
• 1. The use of minoxidil during pregnancy and breast feeding is
taken as category C drug.28, so during pregnancy and breast feeding,
minoxidil shall not be used and or be prescribed.
•
• DOSE—In male AGA 5% minoxidil solution twice a day. The
solution is to be applied on the dry scalp. If foam is used then once a
day can be applied.29,30

43. Finasteride
• Finasteride is a competitive inhibitor of type II 5-alpha reductase,
taken orally it reduces DHT levels in serum and in scalp by up to
70%31,32. .
• There are 2 main isoenzymes of 5 alpha reductase.
• Type I is found mainly in the liver and sebaceous glands in the skin.
• Type II - Prostate and Hair follicle. Finasteride molecules inhibit the 5
alpha reductase type II and thus helps in reducing the serum and
scalp levels of DHT

44. Effects of Finasteride in Males
• Increase ratio of anagen to telogen hair.
• Increase in hair weight.
• Hair weight increases more than the hair count.
• Better at increasing the growth rate (length) & thickness of hair.

45. FINASTERIDE
•
• 1. The blockage of 5α Reductase type I cause 30% reduction of
serum DHT level.
• 2. The blockage of 5α reductase type II causes 70% reduction of
serum DHT.
• The Finasteride act on type II, decreasing DHT levels by 70% in
skin, scalp, tissue and serum.

46. Effects of Finasteride on Men
• Sperm
• No significant effect on sperm count, total sperm per ejaculate, sperm motility or
sperm morphology on 1 mg finasteride every day. May occur at higher dose of
5mg/day but reversible once the drug is stopped.37,38,39
• Prostate
• Finasteride is neither promoter nor preventer of prostate cancer41,42.
Finasteride causes decrease in prostatic volume.
•
• Sexual adverse effects
• Decreased libido, erectile dysfunction, ejaculatory disorder may find in patients.
The incidence is less than 2% in the finasteride group and less than 1% in the
placebo group. These symptoms are reversible after stopping of drug.40
•

47. Effect on other body parts 43,44
1. Gynaecomastia and pain in male breast (Mastalgia) incidence 0.4%
2. Exfoliative dermatitis
3. Perioral numbness
4. Swollen salivary glands
5. Depression
• Side effects are reversible after stopping the drug.

48. Post finasteride syndrome (5 alpha reductase
inhibitor syndrome)
• Persistent sexual, physical and neurological adverse reactions in patients
who have taken finasteride.
• the symptoms are depression, loss of libido, erectile dysfunction, suicidal
ideation, anxiety, panic attacks, gynecomastia, muscle atrophy, penile
shrinkage, cognitive impairment, insomnia, severely dry skin and tinnitus.
• Symptoms start showing after a few weeks of stopping finasteride.
• This is a controversial issue and yet no detailed scientific data is available. A
causal relationship has not been established.
• Pre-existing mental health issues, such mood or anxiety disorders, bipolar
or obsessive compulsive disorders seem to be risk factors for development
of the uncommon syndrome45.
• Due caution should be taken with prescribing of finasteride to these
patients.

49. Dutasteride
• Dutasteride inhibits both type I and type II 5 alpha reductase
isoenzyme. It is 100 times more potent at inhibiting the type I enzyme
and three times more potent in inhibiting type II enzyme as compared
to Finasteride.46
• Dose of Dutasteride is 0.5mg/ day
• Decrease scalp DHT by 51% to 79% in comparison to finasteride,
(Finasteride decreases DHT by 34 – 41 %.).
• The serum DHT level is reduced by more than 90 % as compared to
70% by finasteride

50. DUTASTERIDE-Side effects
• Side effects
• Effects of Dutasteride are long lasting because of its long half-life
which is 5 weeks as compared to finasteride. (Finasteride half-life is
6 to 8 hrs.)
• The 0.5 mg daily dose of Dutasteride decreases sperm count by 28%
in 26 weeks, decreases semen volume, decreases Sperm motility but
no significant change found in sperm morphology.46,47,48,49
• Not approved by the FDA for the treatment of AGA.
• Dutasteride is a potent teratogen and its use is contraindicated in
women of child bearing age. (refer to chapter 22 for details)

51. 1.Mechanism of action
2.USFDA Approval for MPHL
3.Dose
4.Half life
5.Scalp DHT
6.Serum DHT
7.Scalp testosterone
8. Serum Testosterone
9. Sexual Side effects
10 .Effect on sperm
Finasteride
inhibits Type II 5 alpha reductase
approved
1mg / day
6-8 hours
Decrease by 34 to 41%
Decrease by 70 %
increases
increases depending on dose
approximately in 2% male in the
form of decreased libido, erectile
dysfunction, ejaculatory disorders.
these s/e are reversible as half life
is only 6-8 hrs.
no significant effect on Sperm
count, morphology and motility
Dutasteride
Both type I and type II 5Alpha
reductase inhibited.
not approved.
https://www.youtube.com/watch?
v=ky7kzIOwI0s&t=21s
0.5 to 2.5 mg /day
5 weeks
Decrease by 51 to 79%
decrease by more than 90%
increases
increases
S/E is long lasting and more difficult
to reverse as half life is 5 weeks.
Significant decreases in sperm
count and motility but no
significant change in sperm
morphology.

52. Topical Ketoconazole
• Ketoconazole is known for its antifungal property commonly used to
treat dandruff (Pitriasis Capatis).
• It has anti-inflammatory properties and anti DHT action also.
• One study50shows 2%ketoconazole with 2% minoxidil shows better
growth as compared to without ketoconazole.
• Another study51,52 says ketoconazole used with finasteride may lead
to complete reduction of DHT.
• AGA with seborrheic dermatitis are benefited by ketoconazole.

56. OTHER OTC Products for hair growth over the
counter
• Saw palmetto (Serenoa repens )
• Biotin (vit H or B7)
• Nioxin scalp therapy.
• Procerin tablet & topical serum.
• Tricomin shampoo.
• Camouflage
• Wigs & hair pieces
• VITAMINS
• FOOD SUPPLEMENTS
• PRP
•

57. SURGICAL MANAGEMENT
• FUSS (FUT)
• FUE
• BHT

62. TP
FTP
MFP
Relocate FTP and MDP

63. Before After

64. Before After

65. KEY POINT
• Progressive miniaturization of terminal hair is the hallmark of pattern hair loss.
• Miniaturization is a process in which large, pigmented terminal hair is replaced by fine colourless vellus hair, because of shortening of the anagen
phase in consecutive hair cycles.
• Pattern hair loss affects both males and females as progressive thinning of hair is a pattern which is different between males and females.
• Male pattern Hair loss (MPHL) increases in frequency and incidence as age advances after puberty.
• MPHL is characterized by thinning of hair in the frontal, frontotemporal and vertex area of scalp with variable loss of marginal, parietal and occipital
hair.
• Diagnosis is made clinically based on the history of hair thinning, hair loss, local examination and a few simple tests. Anisotrichosis is finding on
dermoscopy.
• The two main causative factors responsible are genetic predisposition and a derivative of testosterone, dihydrotestosterone (DHT).
• This is autosomal dominant and polygenic. The gene is X chromosome linked indicating maternal component.
• Testosterone is converted by an enzyme 5-alpha reductase, into a more potent metabolite, Dihydrotestosterone, which is responsible for MPHL
• There are two types of 5- alpha reductase, type one and type two.
• Finasteride is a competitive inhibitor of 5 α Reductase type II, while Dutasteride inhibits both alpha type I and type II.
• Finasteride and minoxidil are US-FDA approved as medical treatment of MPHL.
• The medical treatment is effective if started in the early phase of hair loss.
• . There are few side effects of finasteride, but the incidence is very low, and they are reversible once the finasteride is stopped.
• Medical treatment is not to treat the developed baldness. The treatment of baldness is transplantation of hair follicles.
•

66. Advise
• After listening this is is advisable to read the chapter 19 from the
book ‘practical guide to hair transplantation----’
• These tutorial are designed based on chapter
• Fore details on examination and treatment read other chapters in the
book and listen tutorial of related chapter.
• For any quarry email to me—anilgarg61@yahoo.com. I will be happy
to answer.
• Best whishes
• Thanks