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A pterygium is characterized by abnormal fibrovascular corneoconjunctival tissue. A number of investigations have attempted to elucidate this incompletely understood pathology. Since vascular endothelial growth factor (VEGF) and p53 are known to participate in tumor vascularization, our purpose was to study VEGF and p53 expression in active primary and recurrent pterygium from Tunisian patients. To this end, 15 cases of active primary pterygium and five cases of recurrent pterygium from Tunisia were studied by immunohistochemistry. Antibodies raised against VEGF and p53 were used to analyze the distribution and expression of these markers in pterygium and normal human conjunctiva were used as negative control. VEGF and p53 proteins were found in all cases of primary pterygium in epithelial, fibroblast and vascular endothelial cells. Active primary and recurrent pterygium have different patterns of expression. In primary pterygium, an important variability of p53 and VEGF expression was observed. However, in recurrent pterygium, p53 immunoreactivity was weak to moderate, whereas VEGF immunoreactivity was strong. In normal human conjunctiva, VEGF and p53 expression was weak to negative. The overexpression of VEGF in active primary and recurrent pterygium suggests that angiogenesis may play a role in pterygium pathogenesis and the expression of p53 in active primary pterygium, which might be associated with its mutated form, supports the hypothesis that actinic radiation may be involved in the genesis of pterygium. Thus, VEGF and p53 may be useful biomarkers for understanding the physiopathology of pterygium., (Copyright © 2009 Elsevier Masson SAS. All rights reserved.)

Since mutated p53 is one of the most frequent gene abnormalities in human cancer, we hypothesized that mutation of p53 may play an important role in growth and recurrence of pterygia, a dysplasia of the conjunctiva. Therefore, we compared pterygia of Japanese and Tunisian patients using antibodies against p53, p21 and proliferating cell nuclear antigen (PCNA). In Nagasaki, 21 pterygia of Japanese individuals were removed and in Gabes, 19 primary pterygia of Tunisian individuals. Positive staining of wild type p53 was not found in the Japanese pterygia, whereas 38.1% were positive for mutant p53, none were positive for p21 and 76.2% were positive for PCNA. The incidence of mutant p53-positive staining was 50.0% in males and 22.2% in females, which was statistically significant. In the 19 Tunisian patients, positive staining of wild type p53 was not found, whereas 36.8% were positive for mutant p53, 0% for p21 and 63.1% for PCNA. Differences between Japanese patients and Tunisian patients were not significant. There were 2 types of pterygium. One type did not show mutant p53 and the other showed mutant p53 caused by ultraviolet light. However, damage caused by p53-dependent programmed cell death of pterygium cells may lead to mutations in other genes which may allow the progressive multistep development of limbal tumors. It is possible that mutant p53-positive pterygia can develop into limbal tumors.