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. 1983 Jan;90(1):96-109.
doi: 10.1016/s0161-6420(83)34594-2.

Elastodysplasia and elastodystrophy as the pathologic bases of ocular pterygia and pinguecula

Elastodysplasia and elastodystrophy as the pathologic bases of ocular pterygia and pinguecula

P Austin et al. Ophthalmology. 1983 Jan.

Abstract

Specimens of normal conjunctiva from three adult patients were examined by electron microscopy, which revealed normal elastogenesis in the substantia propria, but more prominently, in the episcleral tissues. Ultrastructural examination of eight pterygia and three pinguecula also disclosed evidence of elastogenesis, but in these lesions the morphogenetic sequence of fiber formation was distorted, and the elastic fibers were abnormal. The zone of hyalinization of the substantia propria immediately beneath the epithelium was the only site that manifested clear-cut evidence of collagen degeneration, which assumed the forms of effacement of the longitudinal periodicity of the collagen fibers, and of microfibrillar unfurling of the ends of the collagen fibers. Fibroblastic activity and elastic fiber formation were inconspicuous in this region. Beneath the hyalinized zone were collections of eosinophilic granular material. This material was shown ultrastructurally to be composed of excessive numbers of hollow-centered microfibrils (an elastic fiber precursor), with a tendency to clump centrally in the larger aggregated sheets and to acquire electron-dense inclusions. Numerous fibroblasts were found within this material. Finally, the elastotic fibers of light microscopy represented an abnormal maturational phase of elastic fiber production. These abnormal elastic fibers had microfibrils at their peripheries, but numerous electron-dense inclusions were associated with focal zones of amorphous elastin deposition. Occasionally histiocytes appeared to be engulfing these abnormal fibers. We have concluded that a large component of pinguecula and pterygia is the result of newly synthesized elastic fiber precursors and abnormal maturational forms of elastic fibers (elastodysplasia) that undergo secondary degeneration (elastodystrophy). These structures are presumed to be elaborated by actinically damaged fibroblasts of the substantia propria.

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