**Acknowledgements**

(melanocytopenic), which is related to the melanin pigment, and (b) non-melanopenic, which is not related to the melanin pigment. Melanopenic hypopigmentation mainly occurs due to the disruption in the complex process of skin pigmentation. Non-melanopenic hypopigmen‐

Vitiligo is a hypopigmentary disorder of the skin in which cutaneous and ocular melanocytes are selectively destroyed that result in loss of pigmentation. It affects 1–2% of the population including both sexes and all races equally [102]. Multiple theories have been proposed, including genetic, neural, biochemical, viral, and autoimmune mechanisms. However, an autoimmune mechanism has been proposed as the most accepted cause of vitiligo. In previous studies, it has been demonstrated that most important feature in vitiligo is alternation of the melanocyte ratio at the dermal-epidermal junction [103,104]. The long dendritic, melanin granules filled, dopa positive melanocytes were found to be prominent in the outer peripheries

Study conducted by Mohamed and El-Saman [106] on vitiligo patients using light and electron microscopy, showed complete loss of melanin pigment granules in the epidermis, mononu‐ clear cellular infiltration in the dermis, and marked positive ICAM-1 expression over kerati‐ nocytes in the epidermis and around endothelial and inflammatory cells in the dermis of the vitiligo sections. The above authors have reported that the biopsies of vitiligous skin samples exhibited significant ultrastructural changes of degenerative nature in the keratinocytes. This was conspicuous by the presence of electron dense cytoplasm with vacuolization and frag‐ mentation of keratin tonofilaments. Large, irregular indented nuclei were also observed in the biopsies. Besides, the cytoplasm of keratinocytes becomes completely deficient of melano‐ somes in contrast with the control group. Dilated intercellular spaces (edema) and loss of intercellular junctions with or without remnants were also observed. Complete absence of melanocytes and obvious presence of lymphocytes in the basal layer and dermis were evident. These findings give strong fine structural evidence that the vitiligo leads to the degenerative

We have recently shown that active ingredients of plants like *psoralea corylifolia,* (psoralen), *nigella sativa* (thymoquinone), *piper nigrum* (piperine), and *withania somnifera* (withaferin), *berberis vulgaris* (berberine) all have powerful melanogenic (skin darkening) properties and are excellent activators of melanosomal receptors, which when properly stimulated can cause skin darkening in some of the animal models studied in our laboratory [107–112]. Whether these have a similar role in mammalian melanocytes and specific cell lines is yet to be determined at the cellular level. Therefore, it could be an interesting possibility to further explore the herbal ingredient-activated melanosomal receptor signaling cross talk within the melanogenetic pathways, where different receptors participate in skin pigmentation and its dysfunctions.

The morphoanatomical activities of the melanocytes have evolved to enable them to perform specific functions with great efficiency: the regulated production and distribution of melanin

tary disorders may be associated with anemia, edema, and Raynauld's phenomenon.

**a. Vitiligo**

276 Muscle Cell and Tissue

of vitiligo lesions [105].

changes in the structure of melanocytes.

**6. Conclusion**

The authors extend heartfelt appreciation to the Secretary and Principal of Saifia College of Science, Bhopal, India, for encouragement.
