Ocular inflammation is regulated by complicated mechanism that are responsible for the rupture of the blood-ocular barrier and the attraction of leukocytes towards the eye. This cellular trafficking is regulated by the liberation of inflammatory mediators and cytokines.
The main effects of prostaglandins that are described in the literature were reviewed.
Despite the fact that the inhibitory action of aspirin and NSAIDs on prostaglandins secretion is known since 1971, it is quite recently that two isoenzymes of cyclooxygenase were discovered. The Cyclooxygenase-1 (COX-1) is constitutive and is responsible for the production of PGE2. This prostaglandin is related to the housekeeping functions such as gastric protection, platelet aggregation and maintenance of renal function. The expression of the cyclooxygenase 2 (COX-2) is induced by inflammation. The presence of COX-2 could be demonstrated in many ocular tissues (corneal epithelium and endothelium, pigmentary epithelium etc. ...). The use of NSAIDs in clinical practice allows a good control of ocular inflammation, of pain, of the maintenance of a good mydriasis during surgery and are impending the onset of postoperative cystoid macular edema.
Prostaglandins are potent anti-inflammatory agents but their use is limited in the presence of severe dry eye syndrome or allergy towards NSAIDs.