June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Morphological Meibomian Gland Changes in Experimental Dry Eye
Author Affiliations & Notes
  • Carolina Kunnen
    The Ocular Surface Institute / College of Optometry, University of Houston, Houston, Texas, United States
  • Rose Y Reins
    The Ocular Surface Institute / College of Optometry, University of Houston, Houston, Texas, United States
  • Carolina Lema
    The Ocular Surface Institute / College of Optometry, University of Houston, Houston, Texas, United States
  • Rachel L Redfern
    The Ocular Surface Institute / College of Optometry, University of Houston, Houston, Texas, United States
  • Footnotes
    Commercial Relationships   Carolina Kunnen, None; Rose Reins, None; Carolina Lema, None; Rachel Redfern, None
  • Footnotes
    Support  NIH-NEI Grant EY023638
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 2239. doi:
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    • Get Citation

      Carolina Kunnen, Rose Y Reins, Carolina Lema, Rachel L Redfern; Morphological Meibomian Gland Changes in Experimental Dry Eye. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2239.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Meibomian gland dysfunction (MGD) is the leading cause of dry eye disease. Exposure to environmental stress is thought to alter the meibomian gland function and impact tear quality. These functional changes can in turn result in morphological changes to the meibomian glands. This study evaluates the morphological meibomian gland changes in an experimental dry eye (EDE) mouse model using meibography.

Methods : EDE was induced in 12 week old C57BL/6 mice by subcutaneous scopolamine injection (TID) and desiccating stress for 5 days. Following treatment, EDE (n=4) and untreated (UT) (n=5) age-matched mice were euthanized and the eyelids were removed for imaging of the meibomian glands using the Keratograph 5M infrared camera (OCULUS). A region of interest from the center of the eyelid containing the superior (185x400 pixels), inferior (160x400 pixels), and combined meibomian glands (250x400 pixels), was selected from 14 images and processed using a custom designed software developed in MATLAB. The relative proportion of meibomian gland coverage and average gland length were compared between EDE and UT mice.

Results : Overall, a significant larger relative proportion of meibomian glands were observed in the EDE (n=7) eyelids compared to the UT (n=7) eyelids (35.2 ± 1.6% vs. 32.8 ± 1.5%, p = 0.01). Morphological changes in EDE were mainly observed in the inferior glands compared to the UT (28.8 ± 2.7% vs. 26.1 ± 1.3%, p = 0.04). No significant difference was observed for the superior glands between EDE and UT (39.3 ± 1.3 vs. 38.2 ± 1.4%, p = 0.12). No significant difference in gland length was observed for either superior or inferior meibomian glands between the EDE and UT mice (Superior: 1.29 ± 0.06mm vs. 1.25 ± 0.06mm, p = 0.25; Inferior: 0.77 ± 0.06mm vs. 0.79 ± 0.07mm, p = 0.63).

Conclusions : After 5 days of EDE, there was an increase in relative proportion of the meibomian glands compared to UT mice. This was attributed to the enlargement of the inferior glands suggesting their involvement in the early pathogenesis of MGD. This enlargement appears to be caused by widening of the glands, as no significant differences in the length of the glands was observed. Widening of the meibomian glands is believed to be the first sign of meibomian gland dysfunction that ultimately leads to meibomian gland atrophy.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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