Radiation-induced thyroiditis is rare with an incidence of approximately 0.1–0.7%. The thyroid gland is extremely susceptible to radiation, whether external or internal, and can be compromised in a wide radiation dose range, especially in higher doses. Radiation treatment of neck cancer such as tonsillar carcinoma and lymphoma can cause thyroiditis, followed by destruction of thyroid cells and consequently hypothyroidism. Irradiation to the thyroid during therapy for breast cancer can also induce hypothyroidism. Patients who receive radioactive iodine (RAI) for ablation of Graves’ disease or toxic multinodular goiter (MNG) occasionally develop severe thyroid pain 7–10 days after therapy due to the development of acute thyroiditis. Historically, hypothyroidism after external beam radiotherapy (EBRT) of the thyroid gland in adulthood was considered not to develop below a dose threshold of 10–20 Gy. More recent data from patients receiving EBRT suggest a dose threshold for an increased risk of hypothyroidism of 10 Gy. Data from patients with Graves’ disease after radioactive iodine (RAI-131I) therapy (internal radiotherapy) indicate that hypothyroidism rarely occurs below thyroid doses of 50 Gy. Irradiation from atom bombs or nuclear reactor accidents can also cause acute thyroiditis among survivors. Generally, therapy should be directed toward the primary disease rather than the thyroid, but administration of thyroid hormone may be necessary if destruction of thyroid tissue is sufficient to produce hypothyroidism. The conventional treatment of radiation-induced thyroiditis commonly involves medications and is based on the phase of thyroiditis and its symptoms. In any case, follow-up of thyroid function after EBRT or RAI is mandatory so that patients with hypothyroidism needing thyroid hormone replacement will not be overlooked.