Alopecia Areata - Article 2
Description and Mechanism of Cause.
(see also Article 1)
Definition: Alopecia Areata (symptom-bald patches) is a worrying condition affecting either sex in which bald patches appear either singularly or in multiples. Patches may increase in numbers rapidly which may coalesce to involve much of the scalp. Other symptoms may include characteristic stubble, and the skin may appear pink and spongy. The hair may eventually re-grow. Recurrence is always a possibility. Specialist advice is available.
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This form of hair loss (sometimes abbreviated as AA) creates an absence of hair from skin areas where it is normally present. It is a microscopically-inflammatory often spontaneously reversible patchy loss of hair most often occurring in sharply-defined patches involving the scalp and/or beard, but can affect any hair-bearing area of skin. It is widely regarded as an organ-specific autoimmune response, an activity of the immune system. There may be, though not necessarily will be, an association to families where there is history of thyroid problem or of atopy (a susceptibility to eczema, asthma, hayfever). The condition has been noted in persons who through near relatives may be genetically predisposed to such type of hairloss, but equally where no familial history exists. This common but very capricious disease is believed to affect nearly 2% of the population overall. It can have a profound impact on one's life and status both at school and later at work, with its sudden onset, recurrent episodes and unpredictable course. Evidence suggests that alopecia areata can occur when excessive or sudden then prolonged stress whether mental or physical causes a breakdown within the sympathetic (and parasympathetic) nervous system, in turn adversely affecting hair-growth mechanisms. An imbalance of body-chemistry within any structure detected by this our autonomic nervous system would represent a weak link which could lead to such a breakdown. Such an imbalance might occur as result of an initiating imbalance in say the brain, and such chemical imbalance would itself initiate further imbalances along the line signaling action to be taken by the body's immune system if that system were programmed or sensitive enough to react to that imbalance. Our example of this form of hairloss is the result of just such an attack initiated by our autoimmune system. It has long been accepted that direct physical trauma, notably head injuries, may precipitate an attack at or near the injury site. From many cases observed it is also believed (though not proven) that emotional stress alone may precipitate an attack. Human emotion involves the autonomic nervous system comprising both the sympathetic and parasympathetic systems, a complex body system which to a large extent is out of our conscious control. For our purpose this system can best be described by its actions in times of stress at any age, such as undue excitement anxiety fear, post-surgical recovery or as when a direct physical or deeply mental injury has occurred. The same event, be it a family death, chronic financial crisis or physical knock will bring about different reactions in different people. That stress in our scenario may be deeply psychological and will not necessarily be accompanied by outward signs or even a consciousness of the situation. Underlying resentment of some life event is a possible example. Or the stress may simply be more physical and perhaps un-noticed. Eye-strain or infected teeth have been cited as possible examples presumably by interference with the sympathetic nerves. Certain individuals clearly possess greater innate sensitivity to such varying subconscious 'stresses' than the majority. Alopecia areata progresses as a wave of hair-follicles in a given area are prematurely caused to enter their resting-phase, severe structural changes taking place. The initial hair loss may be a result of either a localised toxic chemical-effect produced by the immune system having regarded that physical or mental stress as 'danger', sending lymphocytes already circulating in the bloodstream to attack - possibly combined with a drastic reduction in circulation of oxygenated blood to the hair papillae due to the then barrier effect of this infiltrate of lymphocytes. Within the skin at the germinal matrices of the hair-papillae some active hair-cells (melanocytes) which have a threadlike structure (ie: are dendritic) - become involved. When attacked by lymphocytes (those certain white blood cells known as T-cells) these dendritic melanocyte hair-cells do not die but leak their chemical contents into surrounding cell tissues and their contents (auto antigens) seem to be cytotoxic or poisonous giving rise to a microscopic-inflammation at the germinal matrix of each affected follicle - thus disrupting the hair's development. This might well explain why existing white or non-pigmented hairs are usually spared in the development of an alopecia areata patch - because by definition they have inactive melanocytes at their germinal matrices at the time of onset of the condition. Histologically, alopecia areata is characterised by this large number of T-cells congregating at the dermal papilla of each hair (the germinal matrix or growing area at the bottom of each hair-follicle). The consequences of penetration by these invading lymphocytes into the follicular structure, and with them the local delivery of cytotoxic (cell-poisonous) substances are: i) sudden shrinkage of the dermal papillaii) arrest of the normal differentiation program of keratinisation and pigmentation (the lack of proper manufacture, hardening, and colouring of hair-cells)iii) cell break-up in the surrounding root-sheath, with narrowing of hairshaft as it forms within the follicle. The quantity of invading lymphocytes increases with time and they continue to organise toxic conditions for the hair follicle. An accelerated telogen (the resting-phase of the hair cycle) is initiated. As the hair moves up the follicle the fragilised de-structured part (a consequence of this sudden arrest of the normal cell-differentiation process) reaches the scalp surface from where it falls away entirely from its follicle or results in hair breakage. Such broken hairs look like ' exclamation marks ' usually seen around the perimeter of a patch, and this is diagnostic of an active and possibly expanding patch of alopecia areata. Most existing affected hairs may just fall out (fall away from the follicle), their locking-mechanisms malformed and disabled. Many other hairshafts will break off at near-scalp-level as they emerge malformed from the follicle and become subject to and unable to withstand normal 'wear'. It is noteworthy that the lymphocyte attack does not and cannot destroy the hair-growing structure - since that structure is 'self'. The serious disruption of existing hair-development in that area, with a resultant bald patch, is the only consequence. When conditions within the autonomic nervous system change for the better and the causal lymphocyte activity recedes, the germinal matrix at the papilla of each hair is therefore potentially able to resume normal hair-cell production resulting in regrowth. Consequently the patch of alopecia areata is free to resolve and often does so spontaneously. This happier event may commence a few months after the initiating circumstance or may not happen for a year or two, sometimes later. The sufferer should never give up hope of recovery. Alopecia areata in very young people however is less likely to resolve than in post-pubertal adults. Once triggered, if the body response to 'danger' persists or if the mental or physical stress continues or a genetic pre- disposition takes hold, the affected area will have difficulty in resolving to regrowth. Other alopecia patches of hairloss may then develop even though an older patch might have started regrowing. In severe and more rare cases where several active patches have already merged, a whole head of scalp hair or beard may be lost (alopecia totalis). Beyond that stage - other hair-bearing areas such as eyebrows eyelashes body and limb hair may sometimes become involved - with loss from all hair-bearing skin (alopecia universalis). When at last through whatever (mysterious) reason the inflammatory attack decreases, a new hair cycle starts and a newly-synthesized hairshaft emerges at the scalp surface. This will be a vellus (baby-fine) hair usually with no pigmentation. These vellus 'recovering hairs' may be noticed developing well within the periphery and often at the centre of the earlier active patch. The vellus hair eventually grows into terminal-type hair (normal adult hair) and after a few short vellus hairgrowth-cycles the hair follicle is again enabled to construct a terminal-type hairshaft, together with its pre-accustomed pigmentation.
© D Dane 2004
