We aim to find a link between keratokonus (KC) and bullous keratopathy (BK), and extra cellular matrix re-modellation molecules. The activities of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), pro-matrix metalloproteinase-13 (proMMP-13) and tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) were measured using immunoassay in three human corneal tissue layers (epithelium, stroma and endothelium) supernatants of the patients with KC and BK which underwent the perforative keratoplasty. MPP-2, MMP-9, proMMP-13 and TIMP-1 activity was detected in all samples. The epithelial layer showed significantly higher levels of MMP-9 and proMMP-13 in BK than in KC. Increased levels of MMP-2 (p=0.07) levels were found in bullous keratopathy compared to keratoconus patients. Epithelial TIMP-1 showed no significant difference in activity between KC and BK. All these findings suggest an active degradation of the extra-cellular matrix in epithelial corneal layer in Bullous Keratopathy. No difference in the concentration of MMP-2, MMP-9, proMMP-13 and TIMP-1 between KC and BK in corneal stroma and endothelium suggest that neither of these molecules play important role in KC or BK pathogenesis, at least not in stroma and endothelium.