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The pigmentary unit is a pear-shaped black structure at the tip of dermal papilla in pigmented hair. In gray hair, the pigmentary unit becomes fuzzy, the melanocytes become few and rounded, and lightly pigmented oligodendritic melanocytes become visible in the proximal hair bulb. During anagen, there is a marked reduction in the number of melanocytes in the hair follicles through autophagolysosomal degeneration leading to pigment loss. This is thought to be central in the pathogenesis of graying. Defective melanosomal transfer to cortical keratinocytes or melanin incontinence due to melanocyte degeneration contributes to graying. Degenerative changes within the hair follicle are associated with an increase in dendritic cells in the hair follicle. Eventually, there are no melanogenic melanocytes in the hair bulb.
Genetic and environmental elements influence the hair follicle stem cells and melanocytes. Telomere shortening, decrease in cell numbers, and certain transcription factors have all been implicated in this process of aging. In turn, these molecular alterations lead to structural modifications of the hair fiber, decrease melanin production, and lengthen of the telogen phase of the hair cycle.
Perhaps the role of reactive oxygen species (ROS) on graying of hair is most studied. During active growth phase, i.e., anagen phase there is active melanogenesis in the hair follicle. This involves hydroxylation of tyrosine and oxidation of dihydroxyphenylalanine to melanin causing enormous accumulative oxidative stress. The failure of antioxidant effect could damage melanocytes leading to decreased pigmentation.[12,22] Wood et al. demonstrated that the accumulation of hydrogen peroxide in hair follicles and absent expression of antioxidants such as catalase and methionine sulfoxide reductase in gray hair follicles. Their experiment supported the theory of prooxidant role in graying of hair. Oxidative stress can also be a result of ultraviolet (UV) rays, pollution, emotional factors, or inflammatory causes. Experiments have shown melanocyte apoptosis and oxidative damage in graying hair follicles. Furthermore, exogenous oxidative stress showed increased graying in the hair follicles. An experiment on mice demonstrated that UV radiation could cause oxidative damage on hair follicles causing hair graying. They also demonstrated that the protective effect of an antioxidant superoxide dismutase. Numerous studies have demonstrated increased oxidative load due to psychological stress implying that even emotional factors play a role in premature graying.[25,26] A recent study on young adults in Turkey revealed that PGH is closely related to factors causing oxidative stress such as emotional stress, alcohol consumption, and chronic diseases in genetically predisposed men and women. Daulatabad et al. made an attempt to measure oxidative stress load in PGH. They demonstrated an increase in prooxidants such as serum malonaldehyde, whole blood reduced glutathione, and serum ferric reducing antioxidant potential and decrease in antioxidants. Shi et al. demonstrated compromised antioxidant activity in gray hair follicles. Their experiments revealed that catalase protein expression and hydroxyl radical-scavenging activities are strongly repressed in unpigmented hair follicles.
Progeroid syndromes are associated with defective