The pathogenesis of allergic rhinitis has been classified by nasal challenge studies from which response effects and inflammatory events have been better categorized. Allergic rhinitis follows a classic type I hypersensitivity reaction model comprised of an early phase response, which is immediate, a late phase reaction, which occurs 3-10 hours after the first challenge, and a rechallenge phase, 12-24 hours after the initial challenge. Corticosteroids reduce the number of basophils on the epithelial surfaces of the nose and the number of eosinophils in the nasal mucosa, which allows them to be effective in the inhibition of late and rechallenge phases; whereas they show lesser activity on the early phase due to their greater effect on the delayed inflammatory events, which include the late phase reaction, mediator release recurrence, cellular influx, and heightened reactivity to allergens or mediators. The newer topical intranasal steroids (beclomethasone dipropionate, flunisolide, triamcinolone, and budesonide) have been proved effective in the management of allergic rhinitis, on the basis of controlled clinical trials, with minimal side effects. Intranasal steroids are indicated in patients with rhinitis who do not do well on antihistamines and decongestants. The agents that allow once-daily dosing provide an advantage for improved compliance. At recommended dosages, patients appear to be free of major side effects; however, the lowest dose for the shortest period of time required for symptom control should be utilized.