Vitiligo is an acquired pigmentry disorder of the skin and mucous membranes which manifests as white macules and patches due to selective loss of melanocytes (Bishnoi and Parsad, 2018).
Vitiligo affects 0.5% to 2% of the world's population, without clear preference for race or sex, although women may be more likely to present for treatment and respond to surveys. Almost 50% of patients present before 20 years of age, and many of these present before 10 years of age (Rodrigues et al., 2017).
Vitiligo is a “complex disorder, termed polygenic and multifactorial, reflecting simultaneous contributions of multiple genetic risk factors and environmental triggers (Spritz and Andersen, 2017).
Patients with vitiligo and their first-degree relatives have an increased prevalence of autoimmune thyroid disease, type 1 diabetes mellitus, pernicious anemia, rheumatoid arthritis, Addison disease, lupus, and Guillain–Barré syndrome (Gill et al., 2016).
There is no cure for vitiligo but several treatment options are available. A successful strategy to treat vitiligo should incorporate three distinct approaches: reducing melanocytes stress, regulating the autoimmune response, and stimulating melanocyte regeneration (Rashighi and Harris, 2017).
Replenishing the skin with new melanocytes is needed during the repigmentation process and is dependent on existence of stem cells. Narrow band ultra violet radiation induces repigmentation in distinctive patterns such as follicular, marginal, and diffuse (Awad, 2014).
Known sources of melanocytes for repigmentation include the hair follicle unit, the depigmented epidermis and the edge of vitiligo lesions (Goldstein et al., 2015). Dogra and Vinay (2014), reported that inactive melanocytes in the outer root sheath (ORS) mature as they reach the nearby epidermis. Also, immature dendritic, tyrosinase negative, and c‐kit‐positive pigment cells mainly concentrated around the follicular ostium, rete pegs, and outer root sheath were also a source of epidermal repigmentation.
Further research into stem cells has shown that the primary melanocyte germ cell is present in the hair follicle bulge region while a possible secondary melanocyte source composed of c‐kit+ melanocytes is found in the infundibulum and interfollicular epidermis, as is evident in UV‐treated vitiligo lesions (Goldstein et al., 2015).
Jang et al. (2014), showed that the depigmented epidermis may still contain melanocytes and these can recover their functionality both in vivo and in vitro. Moreover, non‐melanogenic melanocytes exist in several adnexal exocrine compartments of the skin, including sebaceous glands.
Zhou et al. (2019), suggested that specific cytokeratins are markers for stem cells activation. Abbas and Bhawan (2011), suggested cytokeratin (CK) 15 was as a specific stem cell marker and demonstrated its restricted expression in the bulge region of murine and human hair follicles. However, El-Khoury et al. (2016), revealed that, in addition to the bulge region, CK15 expression also involves part or all the outermost layer of the outer root sheath of the human hair follicle, the basal layer of the epidermis, and even eccrine glands.
Cyokeratin19, is an acidic cytokeratin with a molecular weight of 44kDa, was initially thought to be restricted to the human hair follicle bulge, but after that, has demonstrated in the outermost layer of ORS in the bulge region as well as the outer root sheath proximal and distal to the bulge (Dai et al., 2018). Hulst et al. (2015), have shown that CK19 was important in the commitment of stem cells to an epidermal cell fate and differentiation.
Abbas et al. (2010), proved that CK15 and CK19 are valuable tools to monitor tissue homeostasis and the potential to self-renew.
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