![]() One study suggested that 83% of patients (n=12) with Mooren's ulcer were HLA-DR17 positive, and 83% were HLA-DQ2 positive, as compared to control populations where frequencies varied between 5% and 40%. It has been found that certain HLA alleles may be associated with Mooren's ulcer. However, Mooren's ulcer has not been proven to be more prevalent in endemic areas of ascariasis. Receptors for this antigen have also been found on the surface of certain helminths, which has led to speculation regarding an association with helminthic infections. This molecule has also been found in circulating polymorphonuclear leukocytes. Gottsch and colleagues have suggested that this disorder can result from a host response to calgranulin C, a normally hidden antigen expressed by keratinocytes in the corneal stroma. EtiologyĪlthough the etiology of Mooren’s ulcer is unknown, there is evidence suggesting an autoimmune basis, and possibly genetic and environmental factors contribute to the pathogenesis. Neovascularization can occur up to the advancing edge of the ulcer but not beyond it. The central edges of the ulcer can develop an overhanging edge with or without opacification, and neovascularization of the cornea can occur, extending from the limbus into the ulcer bed. Destruction of the cornea generally affects stromal tissue only, leaving behind an intact endothelium and epithelium. Inflammation is not seen in the sclera adjacent to the peripheral ulcers, nor does it affect the underlying Descemet’s membrane. Alternatively, they can completely consume the corneal stroma, replacing it with a thin fibrovascular membrane. These ulcers are often described as crescent-shaped and can leave behind an opaque and edematous central cornea. The bed of the furrow becomes vascularized, with vessels advancing into the base of the undermined edges of the ulcers (figure 1). ![]() Corneal changes begin within 2-3 mm from the limbus, first appearing as grey swellings that rapidly furrow, affecting the superficial one-third of the cornea and then proceeding circumferentially and centrally over 4-12 months. The disease generally begins with intense limbal inflammation and swelling in the episclera and conjunctiva. Mooren’s ulcer is characterized by painful peripheral corneal ulceration of unknown etiology. ![]()
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