Li Z Y, Wallace R N, Streeten B W, Kuntz B L, Dark A J
Department of Ophthalmology, State University of New York Health Science Center, Syracuse 13210.
Invest Ophthalmol Vis Sci. 1991 Apr;32(5):1573-85.
The nature of the abnormal elastotic materials seen in pingueculae and their insensitivity to elastase are poorly understood. The authors investigated their composition by immunoelectron microscopy using antibodies to elastic fiber components, serum and tissue components known to be associated with elastosis in other sites. The abnormal elastic fibers showed labeling for elastin, microfibrillar protein, and amyloid P where these components never co-localize normally, indicating the fibers are not simply immature but aberrant in organization. There was mild positivity for the serum protease inhibitor alpha-1 antitrypsin at the edges of the abnormal elastic tissue and marked positivity for lysozyme. The more superficial region of pingueculae had similar elastic constituents but no fiber formation and a paucity of elastic microfibrils. The subepithelial dense concretions showed strong staining for lysozyme, the first component to be identified in these aggregates. Amyloid P and lysozyme are characteristic components of dermal elastosis, postulated to have an inhibitory effect on elastolytic processes, indirectly affecting the control of elastogenesis. The greater prominence of nonfiber-forming aggregates in pingueculae may be related to their marked deficiency of elastic microfibrils compared with dermal elastoses. This difference speaks for more severe actinic cellular damage in the poorly protected conjunctival tissue.
