Background/Aim: In literature, few studies have examined the diagnostic or prognostic potential of matrix metalloproteinases (MMP) in pterygium, whose formation and progression are closely related to imbalance in the extracellular microenvironment. In this study, we investigated the contribution of MMP7 promoter (A-181G and C-153T) polymorphic genotypes to pterygium risk. Materials and Methods: A total of 134 cases and 268 controls were collected and their MMP7 genotypes at A-181G and C-153T were examined by polymerase chain reaction-restriction fragment length polymorphism methodology. Results: The AA, AG and GG genotypes at MMP7 promoter A-181G were nonsignificantly differentially distributed between the two groups at 85.8, 11.2 and 3.0%, respectively, in pterygium cases and 88.4, 9.7 and 1.9% in controls, respectively (p for trend=0.6822). There was no polymorphic genotype for MMP7 C-153T among our Taiwanese cohort. Conclusion: A-181G and C-153T genotypes at MMP7 do not have a direct role in determining Taiwanese susceptibility to pterygium. Pterygium is a disease presenting an abnormal wing-shaped outgrowth of fibrovascular conjunctival tissues invading the clear cornea. The etiology of pterygium is still largely unclear. The incidence of pterygium is epidemiologically due to several factors, such as overexposure to sunshine, UV light, heat, dust, and other particles in the atmosphere (1-3). In the past two decades, mounting evidence has supported the concept that variations in our genome play a critical role in the determination of the etiology and development of pterygium (4-11). Many theories for pterygium have been proposed, such as imbalances in immunological mechanisms, growth factors, cytokines, apoptosis, angiogenesis (12-15), and most interestingly but complicatedly, an imbalance in the extracellular microenvironment and the involvement of matrix metalloproteinases (MMPs) (16-19). MMPs are a group of zinc-binding endopeptidases responsible for regulating the components of the extracellular matrix microenvironment (20). The activation of MMPs generally takes place in the extracellular space, and interacts with various other proteases, teaming up to regulate the behaviors of cancer cells including viability, cell differentiation, programmed cell death, angiogenesis, immune surveillance, invasiveness and migration capacity (21, 22). The smallest MMP member, MMP7 (matrilysin), is responsible for the metabolism of a broad spectrum of substrates including fibronectin, vitronectin, elastin, collagen IV, aggrecan, and proteoglycans (23). In addition, MMP7 is involved in inflammatory responses via its capacity to promote cell-surface processing of cytokines such as tumor necrosis factor a (24). MMP7 activation was first proposed to be involved in the pathogenesis of pterygium as early as 2001 by Girolamo and colleagues (25). In their analysis of cultured pterygial and conjunctival tissues from eight pterygium cases at Wales hospital in Sydney, basal and activated MMP7 levels were 1.4-and 2.7-fold higher, resp...
