Thyroid eye disease is an autoimmune condition characterised by an active inflammatory phase in many cases, with soft tissue inflammation and oedema in the eyelids and orbital tissues. Glucocorticoids (GCs) offer broad non-specific suppression of the immune system and reduction of inflammation and have long been a first-line treatment for active TED. They have a role in the treatment of active disease, acute treatment of dysthyroid optic neuropathy, and prevention of TED activation in high-risk patients receiving radioiodine treatment for Graves’. Their low cost, familiarity and widespread availability mean that they remain the initial treatment of choice in most parts of the world despite their side-effect profile and the arrival of newer biologic drugs for TED. They are increasingly used alongside steroid-sparing second-line agents such as mycophenolate. Organisations such as the European Group on Graves Orbitopathy have drawn up guidelines for the use of steroids in TED based on available evidence and championed a shift from oral towards pulsed intravenous administration. Local administration of steroid injections has also been described for TED. Further research is needed into potential combination treatment with other modalities such as the newer biologic drugs. This chapter examines the evidence for the role of corticosteroids in TED and how they can be used safely and effectively.