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Histopathological
features of alopecia areata
Under normal circumstances hair growth in each hair follicle
occurs in a cycle. There are three main phases of the hair growth
cycle; anagen, catagen, and telogen (Dry 1926). Anagen is the
active growth phase when hair fiber is produced. This is followed
by catagen,
a period of controlled regression of the hair follicle. Ultimately
the hair follicle enters telogen where it is in a so-called resting
state. Anagen is the longest phase with up to 90% of follicles
on
a normal human scalp in this active hair growth state at any given
time. The average rate of hair fiber growth is around 0.35mm a
day
but this rate varies depending on the site of the hair follicle
and the age of the individual (Pelfini 1969). The length of the
anagen growth phase for scalp hair is around 4-10 years while
telogen lasts just 30-90 days (Van Scott 1957). The total number
of hair
follicles for an adult human is estimated at 5 million with 1
million on the head of which 100,000 alone cover the scalp (Szabo
1958).
See the Hair Biology section of
this web site for more details.
 Alopecia areata is widely regarded as an autoimmune disease where
the anagen hair follicles apparently become the target for an immune
cell attack (Ranki 1984, Perret 1984). It is generally thought that
in the clinical condition the affected follicles involuntarily leave
anagen under the immune cells' influence, enter catagen and then
shed the hair fiber on entering telogen. This increase in telogen
shedding of hair is usually focal and later expands outwards in
a wave-like pattern (Eckert 1968). The follicles may then proceed
back into the next anagen growth phase but, as a result of the continued
activity of the immune cell infiltrate, the hair follicles produce
poor aberrant hair fiber - the follicle is described as being in
a dystrophic anagen state. The affected hair follicles may continue
to oscillate through several rapid cycles of dystrophic anagen and
telogen (Messenger 1986). What happens beyond this is a matter of
some argument (McDonagh 1994). Some researchers believe the hair
follicles continue indefinitely in this dystrophic anagen/rapidly
cycling state (Van Scott 1958, Messenger 1986). Others believe many
of the follicles are eventually arrested in telogen (Swanson 1981).
There is no actual loss of hair follicles even in hairless lesions.
Rather, the follicles are not producing visible hair fiber. Associated
with this disruption of hair fiber production is a perifollicular
(around the hair follicle) and intrafollicular (within the hair
follicle) inflammatory infiltrate. This infiltrate is often described
as like a "swarm of bees" around the hair follicle bulbs.
The immune cells have been identified as primarily T lymphocytes,
with the CD4+ cell subtype twice as common as the CD8+ cell subtype
(Perret 1984, Ranki 1984, Gollinck 1990, Rook 1991). The inflammatory
infiltrate also contains a handful of macrophages, Langerhan’s
cells and granulocytes.
We find that in long term chronic alopecia areata the intensity
of inflammation very slowly decreases and fewer lymphocytes,
macrophages,
Langerhan's cells are found around affected hair follicles. The
cells are still there in numbers greater than we would normally
expect for people without alopecia areata but it is as if the
immune
system has decided that once it has gained territory in the initial
battle it leaves a skeleton crew to maintain control. It may
be
that the hair follicles gradually become less active over the long
term and so become less stimulating to the immune system. Hair
follicles
are extremely robust and capable of taking a lot of punishment.
Despite the disruption by immune cells the hair follicles are
capable
of regeneration given the right conditions, even after many years
of immune cell insult.
Histopathological
features of alopecia areata references
- Kim IH,
Jo HY, Cho CG, Choi HC, Oh CH. Quantitative image analysis of
hair follicles in alopecia areata. Acta Derm Venereol. 1999 May;79(3):214-6.
- Freyschmidt-Paul
P, Hamm H, Happle R, Hoffmann R. Pronounced perifollicular lymphocytic
infiltrates in alopecia areata are associated with poor treatment
response to diphencyprone. Eur J Dermatol. 1999 Mar;9(2):111-4.
- Kossard
S. Diffuse alopecia with stem cell folliculitis: chronic diffuse
alopecia areata or a distinct entity? Am J Dermatopathol. 1999
Feb;21(1):46-50.
- McElwee
KJ, Boggess D, Olivry T, Oliver RF, Whiting D, Tobin DJ, Bystryn
JC, King LE Jr, Sundberg JP. Comparison of alopecia areata in
human and nonhuman mammalian species. Pathobiology. 1998;66(2):90-107.
- Tobin SJ.
Morphological analysis of hair follicles in alopecia areata. Microsc
Res Tech. 1997 Aug 15;38(4):443-51.
- Elston
DM, McCollough ML, Bergfeld WF, Liranzo MO, Heibel M. Eosinophils
in fibrous tracts and near hair bulbs: a helpful diagnostic feature
of alopecia areata. J Am Acad Dermatol. 1997 Jul;37(1):101-6.
- Nutbrown
M, MacDonald Hull SP, Baker TG, Cunliffe WJ, Randall VA. Ultrastructural
abnormalities in the dermal papillae of both lesional and clinically
normal follicles from alopecia areata scalps. Br J Dermatol. 1996
Aug;135(2):204-10.
- Ghersetich
I, Campanile G, Lotti T. Alopecia areata: immunohistochemistry
and ultrastructure of infiltrate and identification of adhesion
molecule receptors. Int J Dermatol. 1996 Jan;35(1):28-33.
- Elieff
D, Sundby S, Kennedy W, Hordinsky M. Decreased sweat-gland number
and function in patients with alopecia areata. Br J Dermatol.
1991 Aug;125(2):130-5.
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