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A
definition of alopecia areata
Alopecia areata (AA) is a non-scarring, inflammatory, hair loss
disease that can affect men, women and children. The factors that
activate the onset of alopecia areata and the mechanisms of its
development are not fully understood. Circumstantial evidence suggests
alopecia areata is an autoimmune disease where cells of an individual's
own immune system prevent hair follicles from producing hair fiber.
Although alopecia areata is not life threatening, the pressures
of an image orientated society can make hair loss psychologically
devastating for those affected, their families, and friends.
A
brief history of alopecia areata
Although Hippocrates first used the term alopecia (literally translated
as "fox's disease"), the characteristics of the hair loss
disease we now know to be alopecia areata (AA) were first described
by Cornelius Celsus in 30 A.D. Celsus described two forms of alopecia.
The first he described as complete baldness occurring in people
of all ages. The second he called "ophiasis", which literally
translates as "snake", due to the winding way the bald
region spread across the skin. He suggested ophiasis was only seen
in children. Alopecia areata is sometimes known as "area celsi"
in tribute to Cornelius Celsus. Alopecia areata has been given many
different names throughout history. However, the actual term "alopecia
areata" was first used by Sauvages in his "Nosologica
Medica", published in 1760 in Lyons, France.
 From
the 1800's onwards there was considerable debate about the cause
of alopecia areata. Two main hypotheses were put forward, one based
on parasitic infection (Gruby 1843, Radcliffe-Crocker 1903), the
other based on a nervous disorder (Von Barensrung 1858). The parasitic
hypothesis drew support from the way the hair loss lesion developed
- slowly expanding in size just as a local infection would. Even
more significant were the apparent epidemics of alopecia areata
reported to occur in institutions such as orphanages and schools
(Bowen 1899, Colcott Fox 1913, Davis 1914). However, many attempts
to isolate an infective organism and to transfer alopecia areata
by inoculation have failed (Sabouraud 1896, Ormsby 1948, Ikeda 1967).
The initiation of alopecia areata by a nervous disorder, variously
known as the trophoneurotic, neurotrophic, or neuropathic hypothesis,
eventually gained the support of most dermatologists of the day.
This vague hypothesis could be supported by the apparently frequent
clinical observations of emotional or physical stress and trauma
that were associated with the onset of alopecia areata and often
reported in the medical journals at that time (Sequeira 1913, Kingsbury
1909). Emotional stress and physical damage were believed to adversely
affect hair follicles via the nervous system and Joseph (1886) showed
that patchy hair loss could apparently be induced by cutting nerves
in the necks of cats (it was later suggested that the hair loss
was actually due to the cats scratching themselves). This highly
circumstantial, but compelling evidence drew popular support for
the trophoneurotic hypothesis. The idea circulated among dermatologists
for many years because it was (and still is) very difficult to fundamentally
prove or disprove that alopecia areata was a nervous disorder. The
hypothesis is still supported by some dermatologists today.
 One
of the more unusual variations on the neuropathic origin of alopecia
areata was put forward by Jacquet (1902) who suggested alopecia
areata was initiated by sources of nerve irritation such as defective
and diseased teeth. Jacquet's hypothesis was apparently confirmed
by others (Decelle 1909). Although Baily (1910) showed dental disease
to be equally frequent in people without alopecia areata. Eye strain
was another suggested cause of alopecia areata (Kinnear 1939).
With the start of the twentieth century alopecia areata was known
to be associated with disorders of the endocrine glands (Sabouraud
1913), particularly the thyroid. As such, some believed the underlying
cause of alopecia areata was due to a hormone dysfunction. By the
1920's most dermatologists had abandoned the parasitic theory of
alopecia areata and favored variations on the trophoneurotic and
endocrine theories - often combining the two.
Sufferers of alopecia areata were certainly under extensive mental
stress, not least from fear that they would be suspected of having
ringworm or syphilis. Until the advent of antibiotics, syphilis
was a widespread, contagious disease. It often manifests itself
by sudden, rapid loss of hair in well defined patches, just like
alopecia areata (Ormsby 1948, Roxburgh 1950), before progressing
to development of lesions and sores. Syphilis in the secondary stage
can also affect finger nails (Roxburgh 1950). To further complicate
the matter, some dermatologists suggested that alopecia areata could
be found in increased association with syphilis - as distinct from
the direct action of syphilis on hair follicles. Syphilis was believed
to induce alopecia areata by the mental distress it created and
its possible upset of the endocrine system (Savill 1939). These
clearly visible symptoms of syphilis were often confused with alopecia
areata by the general population and resulted in social ostracism
for the sufferer (Ormsby 1948).
The early 20th century saw the development of another hypothesis
of alopecia areata induction based on toxic agents. An unknown poison
was believed to be introduced to the hair follicle via the blood
system inducing hair loss (Adamson 1912). The sudden remission and
relapse of alopecia areata and its action simultaneously over the
body was believed to support the idea. Also in support, injection
of thallium acetate (rat poison) was shown to induce alopecia areata
like hair loss in some people (Adamson 1912, Dixon 1927, Ormsby
1948), with expression of exclamation mark hairs - a diagnostic
feature of alopecia areata (Roxburgh 1950). However, the toxic origin
of alopecia areata never gained widespread popularity against the
neuropathic and endocrine hypotheses and has long since fallen from
grace.
It is now widely believed that alopecia areata is an autoimmune
disease. Even though studies more than 100 years old showed that
alopecia areata affected hair follicles were invaded by inflammatory
cells (Giovannini 1891), the inflammatory autoimmune disease hypothesis
did not become popular until the 1960s. The idea was first proposed
by Rothman in a discussion of a paper by Van Scott (1958). Autoimmune
disease occurs when a patient's immune system mistakes part of his
or her own tissue for a foreign invading organism, attacks, and
attempts to destroy, that part of the tissue. Increasingly, hard
evidence is being produced in support of this hypothesis over the
previous suggestions.
A
brief history of alopecia areata references
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