Embryological Basis in the Pathogenesis of Vitiligo

Authors

  • Nayan Kumar S Ph.D Scholar, Department of Kaumarabhritya, Sri Dharmasthala Manjunatheshwara College of Ayurveda and Hospital, Tanniruhalla, Hassan, Karnataka, India
  • Shailaja U Professor of Kaumarabhritya & Principal, Sri Dharmasthala Manjunatheshwara College of Ayurveda and Hospital, Tanniruhalla, Hassan, Karnataka, India
  • Inchara P PG Scholar, Department of Kaumarabhritya, Sri Dharmasthala Manjunatheshwara College of Ayurveda and Hospital, Tanniruhalla, Hassan, Karnataka, India

Keywords:

Vitiligo, Embryological basis, Switra

Abstract

Vitiligo (Switra) is a chronic skin condition characterized by the loss of pigmentation due to melanocyte destruction. Despite its prevalence, the exact etiopathogenesis remains complex and poorly understood. This article explores the embryological basis of vitiligo, with a particular focus on neural crest cell migration and its disruption, which may contribute to melanocyte loss. Embryological factors such as abnormal neural crest cell migration, defective melanocyte colonization, and genetic predisposition are highlighted as potential causes. Furthermore, Ayurvedic perspectives are integrated, emphasizing the role of maternal and nutritional factors in the development of the skin, which may predispose individuals to conditions like vitiligo. Ayurvedic concepts such as the influence of Matruja Bhava (maternal factors), Satmyaja Bhava (adaptation factors), and genetic inheritance provide additional insights into the skin’s development and its susceptibility to diseases. The article suggests that a deeper understanding of both embryological and Ayurvedic perspectives could pave the way for more effective prevention and management strategies for vitiligo.

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Published

2025-02-17

How to Cite

S, N. K., U , S., & P, I. (2025). Embryological Basis in the Pathogenesis of Vitiligo. World of Medicine : Journal of Biomedical Sciences, 2(2), 63–65. Retrieved from https://wom.semanticjournals.org/index.php/biomed/article/view/298

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