Autoimmune thyroiditis is a frequent cause of goiter in children and studies point to the increasing prevalence of juvenile autoimmune thyroiditis (JAT) in children and adolescents. Clinically, JAT can manifest, depending on the presence or absence of goiter, as either a goitrous form or atrophic form. Both are characterized by the presence of thyroid antibodies in serum, with the goitrous form being more common in children. Recent evidence suggests that thyroid autoimmunity originates from an interaction of genetic, endogenous and environmental factors which end up activating thyroid-specific autoreactive T-cells in susceptible children. In addition to underlying genetic/HLA predisposition, factors including sex hormones, glucocorticoids, low birth weight, radiation and drugs may play a role in thyroid autoimmunity. Patients with JAT can present due to thyroid enlargement or symptoms arising due to hypothyroidism. Asymptomatic enlargement of the thyroid gland is a common presenting complaint, especially in older children and adolescents. Thyroid function can vary from euthyroidism to subclinical or overt forms of hypothyroidism and less commonly hyperthyroidism. Accordingly, patients can be symptomatic. There is considerable debate regarding the management of patients with euthyroidism or subclinical hypothyroidism. Available evidence indicates the presence of residual goiter in endemic form and a high prevalence of JAT in children. It is suggested that children should be screened for goiter as part of school health examinations, and goitrous children should be monitored for thyroid function.