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
