Abstract

Hyperosmolarity is a central mechanism causing ocular surface inflammation and eye irritation in typical patients suffering from tear dysfunction. Tear composition in dry eyes, or dysfunctional tear syndrome, may destabilize the tear film and cause ocular surface epithelial disease. Increased activity of matrix metalloproteinases (MMPs), especially MMP-9, plays a critical role in wound healing and inflammation and is primarily responsible for the pathologic alterations to the ocular surface that leads to a dysfunctional tear state. Altered corneal epithelial barrier function is the cause for ocular irritation and visual morbidity in dry eye disease. The increased MMP-9 activity in dry eyes may contribute to deranged corneal epithelial barrier function, increased corneal epithelial desquamation, and corneal surface irregularity. Dry eye is one of the most common complications of photorefractive keratectomy and laser in-situ keratomileusis (LASIK). LASIK has both a neurotrophic effect on the cornea and leads to a physical change in corneal shape that results in a change in tear dynamics, leading to ocular surface desiccation. The reduction in tear function after LASIK may induce an increase in osmolarity and consequently raise the concentration of proinflammatory cytokines and MMP-9 in the tear film, which results in dry eyes and insufficient attachment between the corneal flap and the corneal bed. Appropriate diagnosis and management of dysfunctional tear syndrome may lead to less postoperative LASIK complications.

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