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Purpose The pathogenesis of pterygium is not well known, and controversy exists about the cell origins and the nature of initial trigger required for its development. We investigated whether endothelial progenitor cells (EPCs) are involved in pathogenesis of pterygium and the mechanism underlying the selective recruitment of EPCs during this process. Methods We studied 13 normal controls and 28 pterygium patients (primary (n ¼ 15), recurrent (n ¼ 13)). Substance-P, vascular endothelial growth factor (VEGF), and stem cell factor (SCF) were measured in plasma and tears using ELISA, and circulating CD34 þ and c-kit þ mononuclear cells (MNCs) by flow cytometry. Anterior segment fluorescein angiography (FAG) was performed to evaluate hypoxic conditions in the early stage of pterygium. Surgically removed pterygial tissues were analyzed immunohistochemically using the progenitor cell markers, CD34, c-kit, VEGFR-1, and VEGFR-2. Results Anterior segment FAG findings showed an increase in non-perfusion areas and attenuated vessels in the nasal limbus during early-stage pterygium. Circulating CD34 þ MNCs and c-kit þ MNCs were increased in pterygium groups compared with normal controls. Systemic and local cytokines including SP, VEGF, and SCF in pterygium groups were also elevated and showed positive correlations with CD34 þ and c-kit þ MNC numbers. Immunohistochemical analysis of pterygium showed strong progenitor cell marker immunoreactivities. Conclusions EPCs might be involved in pterygium development, and ocular hypoxia triggers this neovascularization by recruiting EPCs derived from the bone marrow via the production of systemic and local cytokines.

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Pterygia are considered to be induced by predisposing factors such as the external toxic environment. Glutathione transferases (GSTs) have a role in the detoxication of toxic chemicals. Transglutaminases (TGases) are involved in apoptosis, cellular adhesion and the wound healing process. As their expressions may be changed in abnormal conditions, we evaluated the clinicopathological status of pterygia by immunohistochemical study with GST-pi and TGase C. Twenty one pterygia, two pseudopterygia and five normal conjunctival specimens were used. The formalin-fixed samples were embedded in paraffin blocks, which were subjected to be stained with anti-GST-pi and anti-TG polyclonal antibodies immunohistochemically. They were graded from negative to strong. Staining patterns of GST-pi ranged from negative to weak in normal conjunctival epithelium, while in pterygia and pseudopterygia, one was weak, seven mild, ten moderate and five strong. As for TGase C expression, normal tissues were weak to mild, but ten were mild, nine moderate and four strong in pterygia and pseudopterygia. The general staining patterns of GST-pi and TGase C were prominent, ranged from moderate to strong in pterygia and pseudopterygia with basophilic degeneration and keratinization. On the corneal side of pterygia, TGase C was strongly positive in the basal epithelium on destroyed Bowman's layer and in conjunctival fibrous tissue. We suggest that GST-pi and TGase C are responsible for the process of pathogenesis of pterygia and pseudopterygia.

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