Pterygium Pathogenesis, Actinic Damage, and Recurrence

Pterygium, perhaps the most obvious of the ophthalmohelioses (sun-related eye diseases) 1 , 2 has proven to be an ophthalmic enigma. 3 It is potentially the Cinderella ocular disease—considered a diminutive condition and previously described as a degenerative condition. Increased understanding of its pathogenesis holds the key to further improvement in treatment modalities and outcomes. There is now strong evidence that ultraviolet (UV) light plays a major role in its development 4–6 and this is consistent with early evidence of an association with skin malignancy. 7 The likely involvement of both corneal epithelial stem cells and nerves provides an interesting model for their interaction with UV radiation in a transparent tissue. The active processes unleashed include inflammation, tissue invasion and degradation, angiogenesis, fibrosis, proliferation and apoptosis with involvement of matrix metalloproteinases (MMPs), cytokines, and growth factors (GFs). The presence of an inflammatory mass on the ocular surface may predispose the patient to a “pseudo-dry eye syndrome.” 8 A better understanding of the molecular biology of this disease may result in the development of better medical treatments and may provide some insight as to why surgery sometimes fails.