Eyeworld

72 | EYEWORLD | SEPTEMBER 2019 C ORNEA by Stefanie Petrou Binder, MD EyeWorld Contributing Writer Contact information Tassignon: marie-jose.tassignon@uza.be PRESENTATION SPOTLIGHT bullae. Cysts are a focal collection of fluid that appear commonly in the corneal epithelium but rarely in the other layers. "We know that we need a certain number of endothelial cells in order to have a proper metabolism of the cornea. If you have fewer than 500 cells, you will have edema and loss of transparency of the cornea," Dr. Tassignon explained. The cornea is susceptible to all four types of immune responses: IgE-mediated atopic or anaphylactic reactions such as in vernal kera- toconjunctivitis; antibody-mediated cytotoxic reactions like with Mooren's ulcer; immune complex deposits as with herpes simplex stro- mal keratitis, fungi, or other infectious keratitis; and foreign body-related delayed cell-mediated responses, such as those seen with corneal grafts. More than 50 known drugs may leave deposits in the cornea, such as epinephrine and amiodarone in the epithelium. Ocular or sys- temic diseases can leave deposits of non-metab- olizable material, like copper in Wilson's disease, melanin in Descemet's, and pigment in the endothelium in pigment dispersion syndrome. Proliferation and limbal cell deficiency Proliferation is associated with abnormalities of growth. Epithelial cell proliferation is seen in LASIK cases and in patients with recurrent surgeries, causing post-surgical complications. Ectopic migration refers to epithelial ingrowth under a LASIK flap or into the anterior cham- ber and endothelial migration across the surface of the iris. The transitional zone between the cornea and the sclera is the richly vascularized limbus, which contains a reservoir of pluripotential stem cells. Limbal stem cell deficiency can be genetic in etiology, as with aniridia, or acquired, caused by chemical or thermal burns, UV and ionizing radiation, chronic inflammatory diseas- es, contact lens wear, multiple surgeries, anti- metabolites, or extensive microbial infections. P resenting a review on how the cornea reacts to insult in a session at the 23rd European Society of Cataract and Refractive Surgeons Winter Meeting, Marie-Jose Tassignon, MD, detailed the mechanisms of corneal pathologic change. Corneal basics The cornea is a highly refractive surface that covers two-thirds of the eye. It is a metabolical- ly active, avascular tissue, covered by a tear film layer, which contains diverse cytokines that are continuously secreted by the conjunctiva and the cornea. "The cornea is composed of approximately five layers, but for the purposes of the patho- logical response, I will reduce it to four: the epithelium, subepithelial zone (basement mem- brane, Bowman's layer, and anterior stroma), stroma, and the endothelium and Descemet's membrane," Dr. Tassignon said. The structures of the cornea can be affected by infection, inflammation, hypoxia, ischemia, trauma, chemical burns, drug tox- icity, primary dystrophies, systemic metabolic diseases, secondary degenerations, genetic diseases, growth disorders such as hyperplasia and neoplasia, immunopathology, desiccation, and aging. Like most tissues, however, it man- ifests only a limited number of responses to a wide variety of diseases and insults, including responses like defects, fibrosis and vasculariza- tion, edema and cysts, deposits, inflammatory and immune responses, and proliferation. Defects and deposits Corneal defects can be limited to the epitheli- um and tend to recover within 24–48 hours, or affect the stroma, typically after infections, and tend to scar with or without vascularization. Defects also occur at all layers of the cornea and are associated with a partial or complete loss of corneal tissue and may be acute, recur- rent, chronic, or persistent. Keratoconus is an example of a corneal defect affecting all layers. When endothelial cells are damaged, the cornea develops edema that can evolve into Reviewing corneal pathologic responses About the doctor Marie-Jose Tassignon, MD Antwerp University Hospital Antwerp, Belgium Relevant financial interests Tassignon: None continued on page 74

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