Glucocorticoids (GC) can regulate aqueous humor outflow and have often been associated with primary open angle glaucoma (POAG). The ocular or systemic administration of glucocorticoids can cause the elevation of intraocular pressure by increasing aqueous humor outflow resistance via morphological and biochemical changes in the trabecular meshwork (TM). The ability of glucocorticoids to induce ocular hypertension is dependent on individual responsiveness, the potency of the glucocorticoid, the route of administration, and the duration of treatment. Glucocorticoid-induced ocular hypertension occurs not only in humans, but also in rabbits, cats, dogs, and nonhuman primates. Glucocorticoids have a multitude of effects on trabecular meshwork cells causing changes in TM protein expression, cytoskeletal organization, extracellular matrix deposition, cell shape, and cell function. Many of these changes in the TM may be responsible for the generation of glucocorticoid-induced ocular hypertension. There have been several reports of increased cortisol levels, altered cortisol metabolism, and differential glucocorticoid responsiveness in patients with ocular hypertension and POAG. However, there is as yet no clear evidence for a causal role between glucocorticoids and primary open angle glaucoma. Finally, there is evidence that a variety of steroids of differing pharmacological steroid classes can lower the elevated intraocular pressure (IOP) in glucocorticoid-induced ocular hypertension and/ or in glaucoma patients. Continued research in the coming years should (a) identify the molecular mechanisms responsible for glucocorticoid-induced ocular hypertension and glaucoma, (b) determine whether glucocorticoids play a role in the pathogenesis of primary open angle glaucoma, and (c) determine the therapeutic utility of anti-glaucoma steroids.