Ophthalmic Pterygium

Pterygia are common ocular surface lesions thought to originate from limbal stem cells altered by chronic UV exposure. Traditionally regarded as a degenerative condition, pterygia also display tumor-like features, such as a propensity to invade normal tissue and high recurrence rates following resection, and may coexist with secondary premalignant lesions. This study was initiated to determine the rate of concurrent ocular surface diseases in patients with pterygia recruited from the practice of a single surgeon operating in a Sydney metropolitan hospital. One hundred pterygium specimens were histopathologically reviewed and selected cases were immunohistochemically assessed to confirm diagnosis. Along with previously documented typical features including epithelial proliferation, goblet cell hyperplasia, angiogenesis, inflammation, elastosis, stromal plaques, and Bowman’s membrane dissolution, we identified five cases of ocular surface squamous neoplasia, six cases of primary acquired melanosis, two compound nevi (one suspect invasive melanoma), and one dermoid-like lesion. In 18 specimens, clusters of basal epithelial cells that coexpressed cytokeratin15/-19 and p63were identified at the head of the pterygium, coinciding with clinical observation of Fuchs’ flecks. Our data show that significant preneoplastic lesions may be associated with pterygium and that all excised pterygia should undergo histological examination. The presence of p63-positive epithelial cell clusters supports the hypothesis that pterygia develop from limbal epithelial progenitors. (Am J Pathol 2011, 178:817–827; DOI: 10.1016/j.ajpath.2010.10.037) Pterygium is a wing-shaped ocular surface lesion traditionally described as an encroachment of bulbar conjunctiva onto the cornea. Historically, pterygia were considered degenerative lesions, exemplified by degradation of Bowman’s layer and elastosis. Currently, however, pterygia are described as a proliferative disorder resembling an aberrant wound healing response. Histopathologically, pterygia are characterized by a hyperplastic, centripetally directed growth of altered limbal epithelial cells accompanied by Bowman’s layer dissolution, epithelialmesenchymal transition, and an activated fibroblastic stroma with inflammation, neovascularization, and matrix remodeling, mediated through the concerted actions of cytokines, growth factors, and matrix metalloproteinases. Despite advances in understanding of its pathogenesis, pterygium remains an ophthalmic enigma. Intriguingly, pterygia have a predilection for the nasal limbus and affect only humans, possibly reflecting the unique ocular morphology of humans, compared with nonhuman primates and other animals. Although there is no consensus regarding the pathogenesis of pterygia, epidemiological evidence, its association with sun-related disorders such as pinguecula and cataracts, climatic droplet keratopathy, and squamous cell and basal cell carcinomas, together with our in vitro studies, support the concept that UV radiation plays a major role in development of pterygium. Furthermore, the limbal predilection may be explained by the phenomenon of peripheral light focusing, in which incidental light passes through the anterior chamber and is focused at the distal (nasal) limbus where limbal stem cells (LSCs) reside. A healthy corneal surface is maintained by self-renewing, lineage-specific stem cells (SCs) that reside in the limbus, a narrow annular transition zone that circumscribes the cornea. This regenerative capacity is regulated by exquisite programs that govern stem cell quiescence, proliferation,