A characteristic of dry eye disease (DED) is the presence of inflammation, a significant driving factor of the vicious circle that is DED. TFOS second dry eye workshop (TFOS DEWS II) aptly described this process as being initiated by evaporative water loss leading to hyperosmolar tissue damage. This contributes to the inflammatory cascade, with an increased presence of inflammatory markers in the tear film, such as matrix metalloproteinase-9 (MMP-9). These changes cause damage to both epithelial and goblet cells, manifesting in the clinical signs of corneal and conjunctival staining and reduced tear break-up time. This further feeds into the initial hyperosmolarity, perpetuating the process. This cycle of events also causes damage to the corneal nerves which provide nutritional support to the corneal epithelium by releasing factors important for growth and wound healing, such as substance P. Epithelial cells reciprocate by providing support to corneal nerves by secreting growth factors that promote nerve growth. In DED, the equilibrium of these supporting growth factors and inflammatory markers is affected.
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