February 1971
Volume 10, Issue 2
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Articles  |   February 1971
Electron Microscopic Studies on the Pupillary Membrane: The Fine Structure of the White Strands of the Disappearing Stage of this Membrane
Author Affiliations
  • NOBUHIKO MATSUO
    Department of Opthalmology, Columbia University, New York, N. Y.
  • GEORGE K. SMELSER
    Department of Opthalmology, Columbia University, New York, N. Y.
Investigative Ophthalmology & Visual Science February 1971, Vol.10, 108-119. doi:
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      NOBUHIKO MATSUO, GEORGE K. SMELSER; Electron Microscopic Studies on the Pupillary Membrane: The Fine Structure of the White Strands of the Disappearing Stage of this Membrane. Invest. Ophthalmol. Vis. Sci. 1971;10(2):108-119.

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

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Abstract

When the pupillary membrane atrophies late in gestation, it appears as white strands of tissue in the slit lamp. The purpose of this paper is to report the morphology of these disappearing strands. These ran completely across the pupillary area from the lesser circle of the iris. The younger, still functional pupillary membrane was partially covered by fibroblasts, and the vessels within it were enveloped by a thin basement membrane and a few collagen fibrils. The structure of the white strand varied from the center of the pupil to the iris. It consisted of one or two layers of fibroblasts arranged concentrically amid collagen fibrils and an amorphous ground substance. The fibroblasts were active, as shown by their cytologic structure. Remnants of a few vessels were seen enveloped by a thick basement membrane and many collagen fibrils. Macrophages appeared on the surface of the white strand and within the lumen of the vessels. In some areas the fibroblasts were very few in number, and collagen fibrils were degenerating into a homogeneous granular substance. Several cellular functions are involved in the disappearance of the pupillary membrane, including synthetic activity of some fibroblasts, degeneration of other fibroblasts and collagen fibrils, macrophage activity causing destruction of the tight junctions of the endothelial cells, and, finally, phagocytic activity of the macrophages. Dysfunction of any of these processes, could play a role in the persistence of pupillary membranes seen clinically.

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