Type: Research
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Before we consider alopecia and associated conditions it is important to understand normal hair growth. Hair is a skin appendage that is of great importance skin properties. Each strand of hair goes through a unique life cycle and has its own stage of development at any taken moment. Usually, three phases are recognized to compose the hair lifespan: anagen, catagen and telogen. The growth itself is the anagen phase, the one during which hair elongates rapidly and gets pigmented. Followed by catagen, a phase of organ involution (apoptosis) to allow the follicle to renew itself. Telogen is the period of rest before the next anagen starts.

Hair growth cycle. Anagen phase may last years and during this stage cells in the papilla divide to produce new fibers. Catagen usually lasts weeks to detach the hair follicle from the nourishing dermal papilla, at this phase the hair does not grow. During rest (telogen) which takes months normal hair loss takes place.

This cycle depends on stem cells, called keratinocytes. Together with pigmented cells called melanocytes they are the target for the inflammatory attack in alopecia.

I B1 Definition of alopecia

Alopecia manifests as loss of hair. Thus, it may be regarded as baldness. Most papers I acquainted claim alopecia a putative autoimmune hair loss disease. Petukhova et al (2010) emphasize:

‘The phenomenon of ‘sudden whitening of the hair’ is ascribed to the acute onset of alopecia at times of profound grief, stress or fear, in which the pigmented hair  is selectively shed while the white hair persists’

Generally, alopecia may be defined as an inflammatory hair loss. A disease that may affect men and women of all ages, but does not lead to scar formation.

I B 2 Clinical presentation and diagnosis of alopecia

Alopecia is seen as patches of hair loss. Alopecia usually manifests as hair loss most commonly on the scalp. The disorder looks like circumscribed patches of normal skin on the scalp or in the beard. The rapid onset may progress the disease to the point of total hair loss all over the body within just weeks. However, variants have been described: ophiasis (occipital scalp), diffuse and sudden graying. Although regarded as a merely cosmetic defect, alopecia may influence self-esteem considerably. The disorder may affect children and teenagers. The diagnosis of alopecia is clear from  its clinical course. Should controversy occur, skin biopsy to reveal follicle infiltration may be performed.

II A Immune privilege theory

When reading articles about alopecia it occurred to me that human immune system is an extremely wise and a careful structure. For example, there are numerous immune cells (T – and B- lymphocyte, different leukocytes, monocytes and so on), but all of them somehow know accurately what is alien, bad (i.e. a virus of flue) and what good, mine (i.e. cell of an organ). Moreover, when an organ becomes disease, the immune network will detect it and react adequately. This is amazing to me.

Normal hair follicle also represents an immune privilege locus. Today, it is accepted that when immune tolerance fails to proceed, the hair follicle is under attack of immune cells. Petukhova et al (2010) note that stem cells, which are capable to regenerate are usually left intact, while only those at the base of the follicle are disrupted. I suppose this is the clue to understanding why alopecia is potentially treatable. Nevertheless, Martinez-Mir et al (2007) mind there has been no antigen of alopecia identified yet.

II B Alopecia is one of the most prevalent autoimmune diseases

The lifetime risk of alopecia is around 1.7%, making it one of the most common autoimmune conditions. In the United States, 14.5 million people of both genders at all ages and in all ethnic groups are affected with alopecia.

II C Challenging factors of alopecia

As seen in the previous section, autoimmune theory seems to be rather logical and evidence-grounded. However, there are still some observations that are not so easy to explain from the point of immunology. For example, why is it so that spontaneous re-growth is possible. I mean, if the immune barrier is disrupted, the auto-aggression is practically unstoppable. What makes it regress? I did not find the answer and the authors from my bibliography do not seem to ask that question to themselves.

Another challenging problem is mild type of the disease. As Gilhar et al (2012) write alopecia presents as “typical round areas of complete hair loss in normal-appearing skinâ€. Auto-immune attacks are known not to have mercy on a piece of organ here and to destroy it there. Let us say, autoimmune thyroiditis is associated with alopecia. This means that the whole thyroid gland is affected. Now, how can happen so that some hair follicles remain untouched while the other (like occipital) specifically affected?

The third troubling issue is scar formation. It is well known that after organ damage the connective tissue develops. No matter what was the problem – a skin burn, an autoimmune thyroiditis, or a peptic ulcer, scar must remain. However, as described, no scars evolve should alopecia affect skin.

According to novel investigations of Petukhova et al (2011), cytomegalovirus may trigger alopecia by modification on of proteins. In this case, it is not clear what makes the virus affect only the hair follicle and not other organs as usual.

II D Treatment review

To treat alopecia is not a thanksgiving job. Curative therapy does not exist. No matter how strange it may seem, but some physicians rely on natural chance to natural remission. Immunosuppressive regimen may be applied to acute onset of alopecia. This may be a immunomodulating hormone (triamcinolone) injected into follicles, or rarely, systemic glucocorticoids. Contact sensitizers that provoke hair growth may be applied in chronic cases. Laser therapy technologies, commonly used to treat hypertrichosis have been shown to provoke paradoxical hair growth. Ranwala (2012) reports that the first success to treat alopecia with an appropriate laser length dates to 2004. Laser radiation may decrease inflammation and enhance stem cells regeneration. In the future, cytokines and other derivates of biologically active molecules might find their use.

III A Clinical evidence of alopecia inheritance

Family cases of alopecia have been described. Patients with a family history of alopecia also have a personal or family history of atopy, Down’s syndrome, autoimmune disorders. First-degree relatives and twin studies support genetic determinants of alopecia. Martinez-Mir et al (2007) have clearly shown 20 family histories of alopecia and supported their clinical observations with genetic research. Relatives of the affected are at considerably increased risk for alopecia.

III B Laborotary data that support genetic impact

An inbred laboratory mice strain that develops alopecia in adulthood carries genes associated with alopecia. In a laboratory mouse with deficient gene involved in keratinocyte differentiation total baldness develops. Thus, when genes involved in hair cycle are damaged alopecia may develop.

III C Genotype survey on alopecia

In their fundamental survey, Martinez-Mir et al (2007) studied 20 families and encompassed more than 100 patients with alopecia. Although, a validation set not included, the research team managed to identify at least four chromosomes involved. Another reliable study of Petukhova et al (2011) collected a big collection of patients to compare them to healthy people. They identified both innate and acquired immune nucleotide polymorphisms associated with alopecia.

In conclusion, both studies identified susceptibility loci common to alopecia on chromosomes 6p (HLA), 6q (UL 16 binding protein [ULBP]), 10p (IL2RA), and 18p (PTPN22).

III D Chromosomes and genes linked to alopecia

IV Discussion and conclusion

The skin is the largest organ of the body and hair plays a major role in its homeostasis. Although referred to a merely cosmetic defect, alopecia is a disease that affects millions of people worldwide. Clinical observations, as well as recent studies clearly demonstrate alopecia has genetic determinants. However, neither the immune theory itself, nor the genetic surveys are capable to explain the clinical course that very often takes place. Moreover, treatment approaches a still disappointing reflecting poor understanding of the disorder.

In this paper, I collected evidence-based manuscripts concerning alopecia to describe up-to-date approaches. One must agree that a considerable progress had been done with the introduction of modern technologies into this area. However, immune theory does not answer all questions, and what is more important, immune treatments do not meet patients’ requirements now. In the future most probably, new insights into molecular pathogenesis of alopecia will stimulate search for remedies of new generation. Genetic factors for no doubt play a major role in alopecia, but how can it be that now this is almost baldness and later of no apparent reason it may be not so?

What is most challenging to me is how laser technologies may start a revolution in alopecia management pattern. These results seem to be encouraging, but to find application into practice, further studies and randomized controlled trials are needed.

None of the existing theories explain alopecia in complete, but in all they provide us important insights into the disease. I think that combination therapies of the various treatment modalities for alopecia will give a chance for the patients in the near future.

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