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Abstract Androgenetic alopecia (AGA) is a common hair disorder that presents as patterned, progressive hair loss across the frontotemporal and vertex scalp regions of men and women. Androgenetic alopecia advances with age and diminishes body image satisfaction among sufferers. Androgenetic alopecia affects at least 50% of men by the age of 50 years, and up to 70% of all males in later life. Its etiology is purported to be polygenic and androgenic, but the underlying molecular mechanisms governing its onset and progression are not fully understood. Androgenic alopecia’s pathobiological suspects include androgens (i.e., 5α-dihydrotestosterone), hair-cycle-regulating signaling proteins (i.e., interleukin 6, transforming growth factor β 1& 2), inflammatory fatty acid derivatives (i.e., prostaglandin D2), signaling pathways and pathway inhibitors (i.e., Wnt/β-catenin, dickkopf-1), and concomitant morphology. (i.e., vascularity, perifollicular fibrosis). Trichoscopy (Scalp dermoscopy) is a fast and noninvasive method for evaluating hair density. This method is simple, quick, easy to perform, well-accepted by patients, and useful for monitoring treatment, determining severity of the disease and follow-up. Oral finasteride and topical minoxidil are the only FDA-approved treatment for AGA management. Finasteride is a 5α-reductase inhibitor, which prevents the conversion of testosterone to dihydrotestosterone (DHT). Oral minoxidil is an antihypertensive and a vasodilator. Topical minoxidil has a complex mechanism of action. It results in the synthesis of prostaglandins and vascular endothelial growth factors in dermal papilla Summary 92 and the opening of potassium channels, resulting in increasing anagen to telogen ratio. Botox (botulinum toxin type A) is a ne |