Abstract
Purpose :
The aim of this retrospective analysis was to ascertain if differences existed in staining patterns, lid hyperkeratinization, and/or blink patterns in two disease populations: dry eye disease (DED) and meibomian gland dysfunction (MGD).
Methods :
Objective signs of DED and MGD were assessed in DED subjects (n=16), MGD subjects (n=33), and normals (n=10). MGD subjects had to have a documented history of MGD, Schirmer’s >5 mm, TFBUT <5 sec, corneal fluorescein staining >0.5. DED subjects had to have documented history of dry eye, and a symptom score >1 (Ora Calibra® Ocular discomfort and 4-symptom questionnaire). Normal subjects had to have <2 on the same scale, corneal fluorescein staining <2. Corneal and conjunctival staining in five regions was assessed with standardized and reproducible scales, and blink rates measured. Lid hyperkeratinization, a component of the clinically validated Ora CalibraTM Lid Margin and Ocular Surface Staining Scales, was also assessed on a 4-point scale. P values were calculated by unpaired, equal variance t-test (p<0.05).
Results :
Blink rate (blinks/min) was significantly higher in the MGD group (24.76±15.8) compared to normals (12.79±11.4, p=0.03), and higher but not significantly than the DED group (19.29±14.1, p=0.24). Lissamine staining in 2 regions was higher in the MGD group: inferior cornea (2.14±0.83 vs. 1.56±0.64, p=0.02) and central cornea (0.72±0.77 vs. 0.15±0.44, p<0.01). Conversely, fluorescein staining was higher in 3 regions in the DED group: superior cornea (2.16±0.57 vs. 1.68±0.80, p=0.04), temporal conjunctiva (2.13±0.50 vs. 1.60±0.76, p=0.01), and nasal conjunctiva (2.21±0.68 vs. 1.62±0.78, p=0.01). Sum scores of all 5 regions also reflected these differences. Lid hyperkeratinization was significantly worse in MGD (2.84±0.31) than DED (1.97±0.67, p<0.01) and normals (1.80±0.42, p<0.01).
Conclusions :
In the MGD population, significant hyperkeratinization, as assessed by the Lid Margin ScaleTM, as well as the observed increased blink rate, may contribute to mechanical disruption of glycoprotein secretions of ocular surface mucins, resulting in increased lissamine staining. These results support development of clinical methods to distinguish MGD-derived DED with precise anatomical and functional assessments of the lids and ocular surface.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.