1. Molecular Pathophysiology of Melanocyte Loss
Vitiligo is an acquired autoimmune depigmentation disorder affecting approximately 0.5–2% of the world population. Auto-reactive CD8+ cytotoxic T lymphocytes infiltrate the dermo-epidermal junction, producing interferon-gamma (IFN-γ) and activating CXCL10/CXCR3 signaling, which leads directly to targeted melanocyte apoptosis.
2. Classification & Clinical Staging
Divided into Non-Segmental Vitiligo (generalized, symmetric macules on acrofacial and periorificial surfaces) and Segmental Vitiligo (unilateral dermatomal distribution, rapid stabilization, lower association with systemic autoimmunity).
3. Therapeutic Interventions & JAK Inhibitors
Front-line therapy combines Narrowband UVB (NB-UVB 311nm) phototherapy with topical calcineurin inhibitors (Tacrolimus 0.1%) and newly approved topical Janus kinase (JAK) inhibitors (Ruxolitinib 1.5% cream) to halt immune destruction and recruit follicular melanocyte stem cells.