There is great anecdotal evidence that an autoimmune disorder causes the destruction of melanocytes, and this theory is now generally accepted as the common cause of vitiligo. It is known vitiligo appears in conjunction with several other autoimmune disorders, such as juvenile diabetes mellitus, Addison's disease, and pernicious anemia, and additionally organ-specific antibodies can often be seen in patients with vitiligo. If the immune system raises antibodies or cytotoxic T cells to damage melanocytes, the mode of action the cells take against the melanocytes could be apoptosis induction directly against melanocytes or Ig induced complement-both are demonstrated in figure 3. Proving this theory, there is histological evidence in vitiligo patients that apoptosis is occurring in the unpigmented skin lesions]
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Figure 3. Autoimmue theory of vitiligo showing both cell-mediated and humoral autoimmune responses. Figure from Expert Reviews on Molecular Medicine online; permission pending.
[b]Neural Theory]
There is also evidence that peripheral nerve endings may secrete a substance that is cytotoxic to melanocytes and causes their destruction. This is supported by the segmental variety of vitiligo, which occurs in specific dermatomes, indicating the skin is possibly only being affected by the nerves of that specific dermatome. Additionally, vitiligo appears with certain neurological disorders such as encephalitis, and trauma that causes peripheral nerve damage. Nerve endings in depigmented areas were seen to produce abnormal neuropeptides and nerve growth factors, and displayed axonal degeneration-these abnormal chemicals may be toxic to melanocytes. Additionally, depigmented areas showed some abnormal autonomic function, such as increased adrenergic tone, increased norepinephrine, and an increased concentration of catecholamines. These data then suggest that neurotransmitter release could, directly or indirectly, have an affect on melanocyte destruction and depigmentation.
[b]
Self-Destruct Theory]
It is known that some of the intracellular pre-melanogenesis metabolites are toxic to melanocytes, such as dopa and dopachrome. Normally melanocytes possess cellular measures to counteract these toxic substances, but it is believed that cells may lose the ability to counteract these toxic metabolites and are destroyed by leakage of metabolites into the cytoplasm and eventually cell lysis. There is evidence that points to this in that certain hydroquinone derivatives that are similar to these intra-cellular metabolites cause leukoderma experimentally.
[b]Growth Factor Defect Hypothesis]
A study in the 1980's found that melanocytes in lesions from vitiligo patients contained melanocytes, but that these cells exhibited "defective growth and passage capacities." The researchers then noted that the growth defects of the melanocytes were partially corrected by adding a growth factor to their culture, additionally suggesting that growth defects may be part of the pathology of vitiligo. In depigmented areas, cellular analysis showed that there were melanocytes but that they grew poorly. These data suggest that, whether a primary or secondary cause, growth defects appear to play a role in leukoderma and vitiligo (Njoo & Westerhof 2001).
Genetic Influences]
There does appear to be a strong genetic influence in vitiligo]
A team of researchers used the family histories kept by the American Vitiligo Foundation to examine the Mendelian inheritance of vitiligo, and found that most instances of the disease were clustered in families. They found that for patients of vitiligo, offspring have the highest chance of developing the disease, followed by siblings, parents and grandparents (Majumder et al. 1988). Before this work Majumder's team published a report in 1988 suggesting a multiple recessive homozygous model for the disease. In 1994 a seperate team of researchers validated Majumder's proposition of multiple homozygous recessive alleles, causing non-Mendelian inheritance of the disease; this team found that 3 "epistatically interacting autosomal diallelic loci" are involved in the pathogenesis of the disease and affected individuals exhibit homozygous recessive genotypes for all 3 loci (Nath et al. 1994).
[b]Convergence Theory]
Following genetic studies, researchers have begun to lean towards a multi-faceted etiology for vitiligo, that combines components of the aforementioned theories and genetics. This theory states that genetic influences have a role in causing vitiligo in addition to other elements, such as stress, accumulation of toxic compounds, infection, autoimmunity, mutations, and impaired melanocyte proliferation (Njoo & Westerhof 2001).
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