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Experimental eye research
12, 2020;201 108295.

The cornea in keratoconjunctivitis sicca.

Stephen C Pflugfelder, Michael E Stern
Author Information
  1. Stephen C Pflugfelder: Department of Ophthalmology, Baylor College of Medicine, Houston, TX, United States. Electronic address: stevenp@bcm.edu.
  2. Michael E Stern: Department of Ophthalmology, Baylor College of Medicine, Houston, TX, United States; ImmunEyez, Mission Viejo, CA, United States. Electronic address: michaelestern4@gmail.com.
PMID: 33038387 DOI: 10.1016/j.exer.2020.108295

Abstract

The lacrimal functional unit (LFU) regulates tear production, composition, distribution and clearance to maintain a stable protective tear layer that is essential for maintaining corneal epithelial health. Dysfunction of the LFU, commonly referred to as dry eye, leads to increased tear osmolarity and levels of inflammatory mediators in tears that cause ocular surface epithelial disease, termed keratoconjunctivitis sicca (KCS). Corneal changes in KCS include glycocalyx loss, barrier disruption, surface irregularity inflammatory cytokine/chemokine production, cornification and apoptosis. These can reduce visual function and the increased shear force on the corneal epithelium can stimulate nociceptors sensitized by inflammation causing irritation and pain that may precede frank clinical signs. Therapy of keratoconjunctivitis sicca should be tailored to improve tear stability, normalize tear composition, improve barrier function and minimize shear forces and damaging inflammation to improve corneal epithelial health.

Keywords

Barrier function Cornea epithelium Dry eye Dry eye disease Hyperosmolarity Nociceptor Pain Tear stability

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Grants

  1. P30 CA125123/NCI NIH HHS
  2. P30 EY002520/NEI NIH HHS
  3. P30 EY020799/NEI NIH HHS
  4. R01 EY011915/NEI NIH HHS

MeSH Term

Cornea
Humans
Keratoconjunctivitis Sicca
Osmolar Concentration
Tears
Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

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