Contamination of contact lenses is another cause as fungi, bacteria and parasites, microscopic parasite acanthamoeba, in particular, could inhabit the surface of the carrying case of the contact lens. When placing the contact lens to ones eyes, invisible microorganisms may contaminate the cornea resulting in PUK. An extended period of wearing contact lenses could also cause damage on the cornea surface, allowing the entry of microorganisms to the cornea. Other than contamination of contact lenses, contamination occurring in water could also cause PUK. Especially in places like the ocean, rivers, lakes and hot tubs, massive amounts of bacteria, fungi, and parasites exist. When there is an injury on the cornea surface, contact with contaminated water could transfer unwanted microorganisms into the cornea resulting in PUK. Virus and bacteria are sources of infection to the cornea. Herpes virus and bacteria that cause gonorrhea are some examples. Anatomy and pathogenesis
The corneal epithelium consists of five to six layers of cells with a total thickness of around 0.52mm. The cornea thickens to 0.65mm towards the periphery of the cornea. Stroma, which accounts for 90% of the corneal thickness, refers to the middle layer between epithelium and endothelium. It is present in the peripheral cornea to act as a transitional zone between the sclera and cornea. Limbal vasculature, deriving from capillaries that surround the peripheral cornea, supplies the stroma. Various molecules normally diffuse from these capillaries at the periphery to the central cornea.
With limited diffusion, there is a higher concentration of IgM, factor C1 of the complement cascade, and Langerhans cells. Any kind of inflammatory stimulus present in the peripheral cornea results in recruitment of neutrophil and activation of both classical and alternative pathways of immune response, namely the humoral and cell-mediated autoimmune responses. These responses will lead to the formation of antigen-specific antibodies to combat foreign antigens. However, antigen-antibody complexes formed may deposit in the vascular endothelium and activate complements leading to severe local inflammation. Under this circumstance, inflammatory cells, such as macrophages and neutrophils, enter the peripheral cornea. These inflammatory cells release enzymes protease and collagenases, causing potential disruption of the corneal stroma. The additional release of cytokines, for example, interleukin-1, from these cells further accelerates the process of stromal destruction. Moorens ulcer and relevant classification
Moorens ulcer is a common form of PUK. One classification of Moorens ulcer, based on the clinical presentation, includes bilateral indolent moorens ulcer, bilateral aggressive moorens ulcer and unilateral moorens ulcer. Unilateral moorens ulcer, meaning ulcer of one eye, mainly affects elderly above 60 years old. Rapid onset with redness and severe pain of the affected eye and either slow or extremely quick progression are some typical characteristics of unilateral moorens ulcer. Bilateral aggressive moorens ulcer is prevalent in Indian between age 14 to 40. The common presentation includes the appearance of lesions in one eye, followed by the development of lesions in another eye. Finally, bilateral indolent moorens ulcer is common in patients of at least 50-year-old.