The pathogenesis of corneal epithelial defects

Determination of plasminogen activator activities in normal and pathological human tears. The significance of tear plasminogen activators in the inflammatory and traumatic lesions of the cornea and the conjunctiva

“…This explanation is seemingly contradictory to the observations of Salonen et al (1988), who 'in order to clarify whether the plasmin activity was due to elevated levels of plasminogen activator', performed an assay for this enzyme (PA) in the tears of 4 patients with negative results. Our findings in pathological human tears are more in agreement with the view of Berman and others, who, based on histological studies and tissue culture experiments, emphasized the importance of plasminogen activators deriving from different cells of the ulcerating (Berman et al 1980(Berman et al , 1983 and wounded (Chan 1986;Berman 1989; corneas.…”

Rate of epithelialisation and re-operations in corneal ulcers treated with amniotic membrane transplantation combined with botulinum toxin-induced ptosis

“…Comparably, neurotrophic keratopathy and rheumatoid arthritis were demonstrated to be the main causes of failure in previous studies [17,29]. To prevent existing inflammation from causing more damage to the surface, systemic immunosuppression maybe helpful in preparing such eyes for reconstruction [2,14].…”

“…Physiological wound healing is often hindered by accompanying inflammation and therefore becomes ineffective. If PED remains unattended, corneal ulceration and melting, the formation of descemetoceles, and corneal perforation might occur, leading subsequently to the loss of sight [2]. A healthy basement membrane as well as a reduced inflammation are thus crucial for promoting epithelialisation and lasting therapeutic success.…”

Upregulation of Matrix Metalloproteinase in Tear Fluid of Patients with Recurrent Corneal Erosion

“…14,15 Laminin is present mainly in the lamina lucida and plays a critical role in attachment of epithelial basal cells to type IV collagen and proteoglycan. 16 Furthermore, laminin and type IV/VII collagen are co-occur in anchoring plaques. 17 Therefore, as those structural components are also substrates of gelatinase, the excessive degradation of the ECM may be a causative factor of RCE.…”