Sir,

We read this case report with great interest. The authors described a case of a persistent corneal epithelial defect, stromal changes, and wound leak following a penetrating keratoplasty in an eye which had undergone a pterygium excision and conjunctival autograft.1 The authors allude the epithelial defect noticed on the first postoperative day to be due to limbal stem cell deficiency. It may be plausible to provide an alternative explanation for the reported finding. The epithelial defect and corneal stromal changes were noticed to a site adjacent to the previous pterygia. Recent studies have shown evidence to suggest that the development of pterygia is linked to matrix metalloproteinases (MMPs) overexpressed by altered limbal epithelial basal cells.2 MMPs are a family of more than 21 genetically distinct proteases, which are produced in small amounts under normal physiological conditions by fibroblasts and epithelial cells.3 These MMP's being proteases dissolve and remodel extracellular matrix that includes fibronectins, collagen, and basement membrane.3 During the development of pterygia, there is overexpression of MMPs that go on to dissolve Bowman's layer, which in turn triggers the fibrovascular pannus formation.2

The epithelial and stromal changes observed might have resulted from abnormal activity of MMPs from the previous site of the pterygium. Further, the figure shows the epithelial defect to be involving the donor corneal button as well on day 1. This was a very rapid change and manifestations of limbal stem cell deficiency are generally slow in onset.4 The epithelial defect in this patient may be due to altered MMP expression resulting in dissolution of Bowman's layer leading to a corneal epithelial defect. The rapid healing of the epithelial defect following limbal stem cell graft may be contributed to the removal of source of the MMPs.

We would be most grateful for the view of the authors