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S. R. Massei, C. Nabavi, J. Tao, J. R. Paugh, C. Nien-Shy, J. V. Jester; Effects of Age and Dysfunction on Human Meibomian Gland Growth, Differentiation, and Leukocyte Infiltration. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4259.
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Recently, we have identified specific age-related changes in the mouse meibomian gland (MG), including: cytoplasmic to nuclear redistribution of the lipogenesis differentiation factor, PPARγ; decreased basal acinar cell Ki67 nuclear staining indicating cell cycle exit; and increased acinar/ductal infiltration by CD45+ leukocytes. The purpose of this study was to determine if human MG undergoes similar age-related changes.
Patients undergoing horizontal lid tightening procedures were enrolled in this study. Dermatologic history, age, and presence of meibomian gland dysfunction (MGD) were recorded. Collected tissue was then frozen and sections stained with antibodies specific for; (1) peroxisome proliferator activator receptor (PPARγ) to assess MG differentiation, (2) Ki-67 nuclear antigen to assess cell cycle entry, and (3) common leukocyte antigen (CD45) to assess leukocyte infiltration.
A total of 42 patients have thus far been enrolled in this study. Patient ranged in age from 59 to 93 years old, and averaged 75 years old. PPARγ staining was predominantly nuclear within differentiating meibocytes and cytoplasmic within basal acinar cells. There was, however, an increase in cytoplasmic staining of meibocytes seen in the younger individuals 59-70 years old. Ki67 staining revealed a low number of cells entering the cell cycle with less than 5 positive cells/250 µm length along the basal cell layer, similar to what is detected in older mice. CD45 staining showed a highly variable pattern of infiltrating leukocytes that ranged from highly infiltrated acini, ducts and interstitial tissue to complete absence. The CD45 staining appeared to be correlated to MGD grade with MGD 3 and 4 (marked gland dropout and highly viscous excreta) showing the greatest leukocyte infiltration. No associations were noted between patient history/MGD diagnosis and PPARγ/Ki67 staining patterns.
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