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Source :Rooks text book of dermatology 9th edition
Bolognia text book of dermatology
IADVL text book of dermatology 4th edition
Fitzpatrick text book of dermatology 8th edition
levers histopathology of skin 11th edition
Hair Cycle
 follicle passes through 3 phases
Anagen hair
Catagen
hair,
Telogen hair
New
Anagen hair
• histologic appearance of hair follicles changes in hair
cycle,
IN ADULT HAIR CYCLE
Anagen -- phase of active
growth—lasts 3 yrs;
Catagen--phase of
regression—lasts 3 wks
Telogen-- resting period—
lasts 3 months
Hair Follicle stem cells
 Hair follicle stem cells govern the cyclical
regeneration
 Initially thought- “secondary germ” is located at the
base of the telogen hair follicle.
 Secondary germ is a transient structure that forms at
the end of catagen from cells in the lower bulge
 SC Permanently located in the bulge
 bulge cells give rise to all epithelial layers of the hair
follicle, confirmed by using lineage analysis
 Lgr5- exclusive marker of secondary germ cells(marks
bulge cells)
 Lgr6, a gene related to lgr5, is expressed in an area
above the bulge in the upper isthmus.
Anagen
 Anagen can be divided into 7
different stages:
 Stage I—growth of the dermal
papilla and onset of mitotic
activity in the germ-like
overlying epithelium
 Stage II—bulb matrix cells
envelop the dermal papilla and
begin differentiation, evolving
bulb begins descent along the
fibrous streamer
 Stage III—bulb matrix cells
show differentiation into all
follicular components
 stage IV—matrix melanocytes
reactivate
 stage V—hair shaft emerges
and dislodges telogen hair
 stage VI—new hair shaft
emerges from skin Surface
 stage VII—stable growth
 During proliferation and migration of keratinocytes
into the dermis to reform the new lower follicle,
proteases and collagenases appear at the leading
edge of the downgrowth
 Growth factors and their receptors are upregulated
similar to an epithelial wound
•Expression of keratin 6
•Dermal papilla moves
downward
•Neurocutaneous and vascular
networks are remodelled
•Melanocytes proliferate and
repopulate
Catagen
 2-3 weeks
 1% of follicles in this stage
 Cessation of the mitotic activity of the matrix cells
 Apoptosis in the cyclic portion of the hair follicle
 Pigment production by melanocytes ceases
leading to a nonpigmented proximal end in the
telogen club hair
 Melanin engulfed by macrophages
 Perifollicular sheath
collapses,vitreous or glassy
membrane thickens.
 Lower follicle retracts upward
with the dermal papilla.
 Perifollicular sheath forms a
fibrous layer comprised of
fibroblasts, small blood vessels,
and collagen.
 Dermal papilla becomes situated
immediately below the bulge at
the lower portion of the isthmus
 Dermal papilla, protected from the
surrounding apoptosis and
destruction (perhaps because it
expresses bcl- 2, an antiapoptotic
factor12) condenses and begins to
move upward to come to rest below
the bulge during telogen.
 FGF-5 and EGF, neurotrophins and
TGF-β1 induce premature catagen -
shortening of hair length by 15 %
Telogen
• Period of complete inactivity
lasting about 100 days
(3 months) in the scalp.
• 5-10% of follicles
Shedding is an active
process.
•Scalp loses 100-150
telogen hairs a day
•Club Hair either falls
out during telogen or
is pushed out by new
hair growth during the
next anagen phase.
Exogen
 Milner et al proposed distinguishing hair shedding as a
separate phase called exogen.
 Exogen is a highly controlled
and timed event ,shed on a
seasonal basis.
Exogen is an active stage is supported by
Headington’s description of one type of telogen
effluvium he termed immediate telogen release.
• Hair shedding might involve release by
desmoglein 3 which is believed to anchor the club
hair during telogen.
Kenogen
 Usually whenever a telogen hair is shed, an anagen
hair is already present in the follicle to replace it.
 At times the follicle stays empty after telogen
sheds, this is known as kenogen.
 May last from weeks to months, seen in patients
of androgenetic alopecia, prepubertal children.
Control of Hair growth cycle
 Androgens- Act through receptors in the dermal
papilla.
 Increases length of anagen, diameter, and growth
rate in susceptible follicles.
 Paradoxically cause shorter anagen time,
miniaturization, and slower growth in areas such as
the scalp
 Axillary & Pubic hair respond to testosterone, rest of
body hair only responds to DHT made by 5-alpha
reductase type2
 Estrogens
 Prolongs anagen but decreases the growth rate.
 Responsible for the post-partum telogen effluvium.
 Thyroxine
 Advances onset of anagen
 increases growth rate.
 Excesses can be stressful and lead to telogen
effluvium.
 Deficiency results in slowing growth rate.
.
THANKS

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Dermatology Textbooks Guide Hair Cycle Phases

  • 1. Source :Rooks text book of dermatology 9th edition Bolognia text book of dermatology IADVL text book of dermatology 4th edition Fitzpatrick text book of dermatology 8th edition levers histopathology of skin 11th edition
  • 2. Hair Cycle  follicle passes through 3 phases Anagen hair Catagen hair, Telogen hair New Anagen hair • histologic appearance of hair follicles changes in hair cycle,
  • 3. IN ADULT HAIR CYCLE Anagen -- phase of active growth—lasts 3 yrs; Catagen--phase of regression—lasts 3 wks Telogen-- resting period— lasts 3 months
  • 4. Hair Follicle stem cells  Hair follicle stem cells govern the cyclical regeneration  Initially thought- “secondary germ” is located at the base of the telogen hair follicle.  Secondary germ is a transient structure that forms at the end of catagen from cells in the lower bulge  SC Permanently located in the bulge
  • 5.  bulge cells give rise to all epithelial layers of the hair follicle, confirmed by using lineage analysis  Lgr5- exclusive marker of secondary germ cells(marks bulge cells)  Lgr6, a gene related to lgr5, is expressed in an area above the bulge in the upper isthmus.
  • 6.
  • 7. Anagen  Anagen can be divided into 7 different stages:  Stage I—growth of the dermal papilla and onset of mitotic activity in the germ-like overlying epithelium  Stage II—bulb matrix cells envelop the dermal papilla and begin differentiation, evolving bulb begins descent along the fibrous streamer
  • 8.  Stage III—bulb matrix cells show differentiation into all follicular components  stage IV—matrix melanocytes reactivate  stage V—hair shaft emerges and dislodges telogen hair  stage VI—new hair shaft emerges from skin Surface  stage VII—stable growth
  • 9.  During proliferation and migration of keratinocytes into the dermis to reform the new lower follicle, proteases and collagenases appear at the leading edge of the downgrowth  Growth factors and their receptors are upregulated similar to an epithelial wound
  • 10. •Expression of keratin 6 •Dermal papilla moves downward •Neurocutaneous and vascular networks are remodelled •Melanocytes proliferate and repopulate
  • 11. Catagen  2-3 weeks  1% of follicles in this stage  Cessation of the mitotic activity of the matrix cells  Apoptosis in the cyclic portion of the hair follicle  Pigment production by melanocytes ceases leading to a nonpigmented proximal end in the telogen club hair  Melanin engulfed by macrophages
  • 12.  Perifollicular sheath collapses,vitreous or glassy membrane thickens.  Lower follicle retracts upward with the dermal papilla.  Perifollicular sheath forms a fibrous layer comprised of fibroblasts, small blood vessels, and collagen.  Dermal papilla becomes situated immediately below the bulge at the lower portion of the isthmus
  • 13.  Dermal papilla, protected from the surrounding apoptosis and destruction (perhaps because it expresses bcl- 2, an antiapoptotic factor12) condenses and begins to move upward to come to rest below the bulge during telogen.  FGF-5 and EGF, neurotrophins and TGF-β1 induce premature catagen - shortening of hair length by 15 %
  • 14. Telogen • Period of complete inactivity lasting about 100 days (3 months) in the scalp. • 5-10% of follicles Shedding is an active process.
  • 15. •Scalp loses 100-150 telogen hairs a day •Club Hair either falls out during telogen or is pushed out by new hair growth during the next anagen phase.
  • 16. Exogen  Milner et al proposed distinguishing hair shedding as a separate phase called exogen.  Exogen is a highly controlled and timed event ,shed on a seasonal basis.
  • 17. Exogen is an active stage is supported by Headington’s description of one type of telogen effluvium he termed immediate telogen release. • Hair shedding might involve release by desmoglein 3 which is believed to anchor the club hair during telogen.
  • 18. Kenogen  Usually whenever a telogen hair is shed, an anagen hair is already present in the follicle to replace it.  At times the follicle stays empty after telogen sheds, this is known as kenogen.  May last from weeks to months, seen in patients of androgenetic alopecia, prepubertal children.
  • 19. Control of Hair growth cycle  Androgens- Act through receptors in the dermal papilla.  Increases length of anagen, diameter, and growth rate in susceptible follicles.  Paradoxically cause shorter anagen time, miniaturization, and slower growth in areas such as the scalp  Axillary & Pubic hair respond to testosterone, rest of body hair only responds to DHT made by 5-alpha reductase type2
  • 20.  Estrogens  Prolongs anagen but decreases the growth rate.  Responsible for the post-partum telogen effluvium.  Thyroxine  Advances onset of anagen  increases growth rate.  Excesses can be stressful and lead to telogen effluvium.  Deficiency results in slowing growth rate.
  • 21. .