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What
chances have I got of spontaneous hair regrowth?
This question is very difficult to answer in relation to any one
individual case. We have no way of predicting the future course
of alopecia areata in any one person. As was written in a recently
published book "alopecia areata is only predictable in its unpredictability"
(Thompson 1996). I will have to resort to statistics to give any
form of reply. About 65% of people who have alopecia areata have
just one or two patches of hair loss which usually enter remission
after 6 months to 2 years from first diagnosis with or without treatment.
However, that leaves 35% or more who have more persistent hair loss.
This may cycle through expression or remission or become more extensive
and persistent. Only 7% of people with alopecia areata progress
to total scalp hair loss, or alopecia universalis. It has been suggested
that people who first develop alopecia areata in childhood, and/or
those with a history of allergies, are more likely to have persistent
hair loss - at least in the USA and Europe. A recent report from
India (Sharma 1996) revealed no correlation between presence of
atopy and persistence of alopecia areata which suggests regional,
or racial variations in alopecia areata presentation.
Why
does my bald skin have a bluish color?
 This may be what is unofficially
described as "melanin incontinence". This phenomenon can usually
only develop in people who have dark hair. Very occasionally the
hair follicle melanocytes, that produce pigment for incorporation
into the hair fiber, do not immediately shut down when under attack
in alopecia areata. The melanocytes continue to produce pigment,
but because there is no fiber to take it up the pigment gets dumped
at the base of the hair follicle.
Melanin is difficult to break down in large concentrations so
it builds up and this can give the skin a bluish hue. Eventually
the melanocytes do become inactive and the melanin is slowly removed
so the blue spots can slowly come and go . Melanin incontinence
is rare in humans and you won't find it described in the text books
but it has been mentioned at dermatological conferences. People
with blond or red hair are unlikely to see any discoloring of the
skin but excess production of melanin is still possible. Microscopically
pigment deposits may still be apparent but because of the pigment
color the deposits are much less likely to be seen by casual observation
of bald skin patches.
Why
is alopecia areata often expressed in well defined areas but
adjacent
hair follicles can remain unaffected?
Alopecia areata can present in a wide range of forms from small
distinct patches through larger lesions to total body hair loss
or a diffuse thinning of the hair. The reasons for this variation
in expression have only been sporadically investigated - and with
little success. Several factors have been suggested to contribute
to variable types of lesions but there is little supporting evidence.
For many years it has been questioned whether all the different
forms of hair loss are one and the same disease (Mcdonagh 1994).
Although the different types of lesions have damaged hair follicles
that look the same our definition of what does and does not look
like AA is very basic. There may be subtle differences in the disease
initiation and development that have not yet been identified which
lead to the different patterns of hair loss. As we learn more about
AA we may end up subdividing the general diagnosis of AA into groups
that have different contributing initiating factors, different methods
of development and so present as different forms of hair loss.
There has been one previous concerted attempt at classification
by Ikeda (1965) who suggested four types of AA based on observations
made in Japan. Type one was the most common affecting 83% with patchy
AA of short duration occurring in people aged 20-40 and with no
family history of AA. Type two affecting 10% of those examined occurred
in people with allergies and frequently led to more extensive alopecia
totalis. Type three occurred almost entirely in people with parents
suffering hypertension (high blood pressure). Only 4% of people
with AA were affected - initially with the reticular form of lesion
and persistent, chronic disease activity. Type four, the "combined"
type found in 3%, showed first lesion expression in people age 40+,
of persistent duration but only deteriorated to alopecia totalis
in 10% of those with the combined type. Despite this attempt to
divide AA into different subgroups further use of classification
systems has been very limited due to the lack of obvious diagnostic
features and strong evidence to permit easy and consistent subdivision.
We know that hair follicles in different positions on our bodies
can be very different in size and shape. Some respond to androgen
hormones with increased hair growth - particularly the beard region.
Other hair follicles seem to be adversely affected by the same hormones
and eventually result in male pattern baldness. In a similar way
some regions of hair follicles may be more susceptible to alopecia
areata than others - for example we know that the most common region
of hair to be affected is on the scalp.
A hypothesis of "skin mosaicism" has been put forward to at least
partially explain these differences in hair follicles. The cells
that make up our skin are descendant from a very few embryonic cells
and the skin can be divided into different regions depending on
which embryonic cells multiplied to produce it. We know that the
skin and hair of the scalp occipital region (that's the area that
runs in a band from one ear around the back of the head to the other
ear within the hair line) is derived from a different group of embryonic
cells than the hair and skin on top of the head (Ziller 1995). Particularly
intriguing is that the alopecia areata type described as "ophiasis"
is limited to hair loss in this occipital region but adjacent hair
follicles are not affected. Of course it is very tempting to speculate
that this hair loss pattern is due in part to a subtle difference
in the cells which gave rise to the occipital region - although
there is no evidence for this.
It has been suggested that pigmented hair follicles are more susceptible
to AA compared to white hair. When a lesion develops in someone
with grey hair, the pigmented follicles are usually the first to
be affected leaving just white hair surviving in a patch of AA -
although with time even white hair can be lost (Dawber 1994). As
a result of this phenomena, some dermatologists believe that immunological
action on hair follicles is specifically directed towards pigment
producing melanocyte cells (Tobin 1994).
A rare form of AA called "alopecia areata nevi" gives rise to
hair loss in the immediate area of moles or similar anomalous skin
growths. Here we might suggest that the differences within these
distinctive patches of skin somehow make hair follicles in the immediate
area more sensitive to AA. If pigmentation does make hair follicles
more susceptible then hair follicles in moles (as hyperpigmented
areas of skin) may well be more susceptible to AA.
In summary, although hair follicles cover almost all of our body
we cannot regard them as being uniform structures. Subtly different
groups of hair follicles make up a patchwork, or mosaic, over our
skin. Minor differences between each follicle type may mean some
areas of hair are more susceptible, or resistant, to development
of AA lesions. In addition the may be more than one form of alopecia
areata. Some people may develop more aggressive AA resulting in
much more extensive lesions or lesions more resistant to treatment.
These different subtypes may be indirectly influenced by the presence
of certain allergies or genes affecting our blood immune system.
The different hair loss patterns (patchy, reticular, ophiasis etc.)
could reflect different methods of disease development for different
people
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