Hair loss in children encompasses a spectrum of conditions congenital and acquired, originating from hair shaft, follicular, or infectious causes. A congenital hair abnormality may be an isolated finding in an otherwise healthy child or a feature suggestive of a multisystem syndrome. Both congenital and acquired alopecia may be irreversible, resulting from destruction of hair follicles and replacement by fibrous scar tissue. Disease processes that lead to follicular loss are known as scarring alopecia, whereas follicles are generally preserved in non-scarring alopecia .

A basic understanding of hair biology enables consideration of normal versus abnormal hair loss in pediatric patients. Hair consists of the proteinaceous shaft and the root, anchored in the follicle, an involution of the epidermis. Hair follicles contain rapidly dividing cells, but the only visible portions are the follicular ostia, through which hair fibers emerge. Humans are born with a population of approximately five million preformed follicles. Follicles can produce lanugo, vellus, or terminal hairs. Newborns are covered in soft lanugo hair, which is replaced by downy, fine vellus hair after 3–4 months. At puberty, androgens transform most vellus hair into thicker, more pigmented terminal hair. Terminal hairs undergo cyclical growth with up to 90% of follicles in active growth (anagen phase); 1–3% in a brief involutionary transition (catagen phase); and 5–10% in dormancy (telogen phase). Hair is shed after 2–3 months in telogen phase, after which anagen begins again, and the cycle repeats. Daily loss of 50–150 telogen hairs is normal, but the number of hairs shed is roughly equal to the number of follicles entering anagen