Histopathological Features of Vitiligo and Melanocyte
Degeneration
The affected skin in vitiligo demonstrates melanin loss and absence of
or reduced numbers of melanocytes in the epidermis [16]. This
decrease varies according to the disease stage [13]. Melanocytes as
revealed by using an appropriate monoclonal antibody technique or the
Fontana Masson (FM) stain, remain present, however, they disappear from
affected skin of vitiligo as the disease progress [17].
Immunohistochemical studies of vitiligo lesions show the absence of
melanocytes from the basal layer, but they may exist in decreased
numbers and can demonstrate degenerative changes [18].
Even though it is clear that depigmentation in vitiligo results from
melanocyte loss from the skin, it remains unclear whether this occurs
through a degenerative or autoimmune process. Defective in vitrogrowth of melanocytes derived from individuals with vitiligo [19,
20] and increased susceptibility of vitiligo melanocytes to exogenous
stimuli suggests that degeneration may elucidate melanocyte loss
[21].
Melanocytes from vitiligo subjects were shown to poorly proliferate
compared to healthy normal melanocytes [19] and also they show
inadequate antioxidant activity with high levels of superoxide dismutase
and low levels of catalase [22]. Under normal circumstances,
superoxide dismutase catalyses the first step of dismutation by
converting the superoxide anion into oxygen and hydrogen peroxide and
then catalase enzyme transforms hydrogen peroxide into water and oxygen,
protecting cells from reactive oxygen species (ROS). In fact,
melanocytes synthesise high ROS levels as by-product of melanogenesis.
Therefore, compensatory media supplements such as growth factors or
catalase are required to culture melanocytes derived from vitiligo
patients [20, 23]. Also, increased expression of hydrogen peroxide
and elevated oxidative by-products within vitiligo patient skin has been
reported [22, 24, 25]. In addition, melanocytes from vitiligo
patients were more sensitive to in vitro oxidative therapies such
as cumene hydroperoxide and UVB light [26, 27]. However, exogenous
treatment of catalase (pseudocatalase), which was proposed to cure
vitiligo by regulating ROS, was ineffective in treating vitiligo lesions
[28]. Thus, dysregulated redox balance in vitiligo might be a
consequence, but not a cause, of vitiligo. Melanocytes from vitiligo
patients show morphological and physiological abnormalities. Those in
peri-lesional borders are seen to be enlarged with longer dendritic ends
than normal melanocytes [29]. However, rapid regimentation of the
skin following engrafting of human vitiligo lesional skin on nude mouse
was achieved, indicating that intrinsic melanocyte defect was not the
only cause of melanocyte destruction in vitiligo [30]. Histochemical
and immunohistochemical examination shows infiltration of a large number
of T lymphocytes at the edge of vitiligo lesions with a complete
microscopic loss of melanin in lesional skin [31]. Therefore, it is
certain that vitiligo melanocytes are abnormal compared to healthy
melanocytes, but this abnormality does not seem to be sufficient for the
disorder.