Article
Pathogenesis of "Floppy Eyelid Syndrome" (FES): involvement of Matrix metalloproteinases in elastic fiber degradation
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Authors
Published: | September 22, 2004 |
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Outline
Text
Objective
To analyze eyelid biopsy specimens in patients with FES with special regard to elastic fiber content and ultrastructure as well as expression of elastin-degrading enzymes.
Methods
Horizontal pentagonal lid resections of 16 upper eyelids were performed in 11 patients with FES. Full thickness lid specimens and controls from 9 age-matched patients with basal cell carcinoma were studied by light and transmission electron microscopy, semiquantitative morphometry and immunohistochemistry using antibodies against matrix metalloproteinases 2, 7, 9 12 and neutrophil elastase.
Results
Histopathologic studies revealed a significant decrease of elastic fibers within the posterior (tarsus) and anterior eyelid lamella (skin) as compared to controls. Residual elastic fibers showed an abnormal ultrastructure with a diminished elastin core. Immunohistochemically, there was an increased immunoreactivity for elastolytic proteases (esp. metalloproteinases 7 and 9) in areas of elastin depletion.
Conclusions
Upregulation of elastolytic enzymes, most probably induced by mechanical stress, contributes to elastic fiber degradation with subsequent tarsal laxity and eyelash ptosis in patients with FES. Nocturnal eversion and poor contact of the lax eyelids with the globe my further enhance secondary keratoconjunctivitis.