Skin color is determined by melanin, oxygenated (reduced) hemoglobin and carotenoids. Their proportions and depth in the skin and epidermal thickness and selective scattering of light affect skin color. Blue nevi and Mongolian spots are brown pigments in the dermis that appear blue-gray. Interface dermatitis such as lichen planus or lupus erythematosus appear as cyanotic. Red furunculosis of the hair appears orange-red, and xanthomatosis or cortical cysts appear yellow due to the lipid content. Common hypopigmented disorders include pemphigus foliaceus, anemic nevus, leprosy, nodular sclerosis, idiopathic hypopigmented spots, ito hypopigmented disease. Pigment deficiency disorders include vitiligo, anaplastic nevus, halo nevus, scleroderma, scleroderma, and sclerosis. The whitening of the skin in vitiligo is due to a wide variety of melanocyte destruction factors. Albinism is a genetic factor resulting in the inability to synthesize pigment-saturated melanin vesicles. Freckles in localized increased pigmentation are epidermal melanin amounts that are normal but they produce too much pigment. Pigmented nevi are the result of benign proliferation of melanocytes and can be understood as a benign tumor. Black freckle-like nevi are hyperpigmentation of the basal layer and marked melanin within the stratum corneum. Epidermal hyperpigmentation is seen in pigmented nevi, melanomas, café au lait, melasma and freckle-like nevi and can be more obvious with Wood’s lamp. Post-inflammatory hyperpigmentation is often dermal pigmentation, and golden moss is caused by iron deposition. Post-inflammatory hyperpigmentation or deposition of metallic/drug/ or denatured dermal material is not evident by wood lamp irradiation.