Psoriasis is a chronic autoimmune skin disorder characterized by red, well-demarcated plaques with silvery scales, commonly affecting the extensor surfaces and scalp. While fibrosis is not a primary feature of psoriasis, chronic inflammation associated with the condition can occasionally result in fibrotic alterations in the skin or joints. Psoriasis affects approximately 4.4% of the global population, with variations based on geographic location and ethnicity. Triggers like drugs, infections, lifestyle factors, or genetic predisposition (HLA-Cw6) initiate an inflammatory cascade in the dermis. A regulatory T-cell defect permits overactivation of immune cells, which migrate to the epidermis and release pro-inflammatory cytokines. This stimulates keratinocyte proliferation, resulting in epidermal thickening and rapid turnover of the stratum corneum. The excess keratinocytes form characteristic silvery scales and plaques, often with dilated capillaries and perivascular inflammation in the dermis. Neutrophil accumulation can also form pustules. Current psoriasis treatments may cause adverse effects, leading to poor patient adherence. There remains an unmet need for safer and more durable therapeutic options.