The cornea and precorneal tear film combine to function as a strong refractive lens. To produce such an optically powerful structure, the corneal microanatomy consists of an epithelium and thin epithelial basement membrane, a thick relatively acellular stroma, Descemet's membrane, and a monolayered endothelium. The corneal epithelium is 10 to 15 cell layers thick. The basement membrane of the epithelium is composed of type IV, VI, and VII collagen as well as laminin, hyaluronans, and fibronectin [1]. The stroma comprises most of the corneal thickness and consists of multiple contiguous layers of thin and uniformly positioned collagen microfibrils surrounded by an extracellular matrix (ECM) of collagen types I, III, V, VI, and XII; stromal glycosaminoglycans (keratan sulfates, dermatan sulfates, and chondroitin sulfates); and glycoproteins [1]. A limited number of stromal keratocyte/fibroblasts are present. Descemet's membrane is the acellular basement membrane of the endothelium. This ever-thickening basement membrane contains collagen types I, III, IV, V, VI, and VIII; laminin; fibronectin; and heparan sulfates [1]. The corneal endothelium produces Descemet's membrane and contains an energy-dependent pump to maintain corneal deturgescence. The precorneal tear film is a lipid-bilayered and aqueous mucin-dominated gel that aids lubrication, transfers oxygen to the cornea, and smoothes out small surface irregularities in the anterior corneal epithelium to maintain a uniform optical surface. The tear film also removes exfoliating corneal epithelial cells and provides a means for inflammatory cells to reach the central cornea. Inflammatory conditions of the cornea or conjunctiva tend to produce a shift toward a more acid tear film [2]. Tear film proteins serve to control infectious agents and lower the surface tension, enabling the tear film to cover the conjunctival and corneal surfaces better. Proteins in the tears are species specific and include albumin; the immune globulins IgA, IgG, IgD, and IgE; ceruloplasmin and transferrin; histamine; plasminogen activator; complement; interferon; prostaglandins; the antimicrobial proteins lysozyme, beta-lysin, and lactoferrin; and the tear film proteinases [2]. Damage to the cells of the corneal epithelium and stromal ECM results in what is referred to as an abrasion or ulcer. Most superficial uncomplicated corneal ulcers in animals heal without incident, because corneal wound healing is remarkably well regulated thanks to a natural harmonious balance between mechanisms of corneal repair and degradation. Infected corneal ulcers or ulcers with extensive stromal involvement may, however, progress to corneal perforation in as little as 24 hours. This rapidly progressive corneal deterioration is described clinically as keratomalacia, or corneal "melting," with the primary mediators of this corneal stromal degeneration being microbial-, leukocyte-, tear film-, and corneal cell-derived enzymes called proteinases [3-5].
