Reply to Contact Lens-Based Expansion and Transplantation of Autologous Epithelial Progenitors for Ocular Surface Reconstruction: Crossover Control
Parmar et al. recommend that we design a crossover control using a bandage contact lens (CL) alone for future patients managed with our novel technique (1). Bandage CLs are known to facilitate healing of persistent corneal epithelial defects and are often used in conjunction with conventional medication (2) in patients with limbal stem-cell deficiency (LSCD). Our technique for expansion and transplantation of autologous epithelial progenitors involved removal of irregular epithelium and conjunctivalisation from the corneal surface (superficial keratectomy)before placement of a stem-cell–laden CL.The use of a crossover control design would not be feasible because the keratectomy could not be performed twice. In addition, patients enrolled in our study had failed medical therapy for LSCD, including bandage CL wear. Parmar et al. highlight the work of Ozbek and Raber (3) who managed corneal epithelial breakdown in an aniridic patient with monthly bandage CL replacementover4years, butitwasunclearwhether the patient remained on this management strategy indefinitely. Indeed, the patient we reported on with aniridia (1) had previously failed bandage CL wear. Interestingly, the Acuvue CL (Johnson & Johnson Vision Care, Jacksonville, FL) used in the study of OzbekandRaber (3) was unable topromote cell expansion in our hands. Furthermore,
prolonged CL wear is itself associated with increased risk of infection (4), limbal stemcell failure (5), and the need for meticulous follow-uptoreplaceCLsandmonitorforCL loss, the later was believed to be responsible for recurrent episodes of epithelial deterioration in their patient (3). Parmar et al. used a crossover control study design to treat three patients with persistent epithelial defects by transplanting each with human amniotic epithelial cells that were seeded on a collagen shield, which in turn was supported by a bandage CL (6). Of note, there were four main differences in their study compared with our recent investigation (1); (i) the authors treated persistent epithelial defects not LSCD, (ii) the authors used nonocular allogeneic cells (amniotic epithelial cells), (iii)
the authors used fetal calf serum-infused media, and (iv) they introduced an animalderived collagen shield. Furthermore, the shield was implanted multiple times due to rapid dissolution, and the mean patient follow- up was only 6.3 months. We too have tried nurturinghumanlimbal epithelial progenitors on collagen shields (SurgiLens; Bausch & Lomb, Irvine, CA) supplemented with 10% autologous serum. However, cells were nonadherent and eventually clumped as the shield underwent rapid dissolution. It is tempting to speculate that high failure rate recorded by He et al. (7) in experimental transplantation of limbal epithelial cells was due to the instability of collagen shields.
Department of Pathology
School of Medical Sciences
University of New South Wales
Sydney, Australia
Stephanie L. Watson
Department of Ophthalmology
Prince of Wales Hospital
Sydney, Australia
Address correspondence to: Nick Di Girolamo,
Ph.D., Department of Pathology, School of Medical Sciences, University of New South
Wales, Sydney, Australia.
E-mail:
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Received 20 October 2009.
Accepted 23 October 2009.
Copyright © 2010 by Lippincott Williams &
Wilkins
ISSN 0041-1337/10/8904-484
DOI: 10.1097/01.TP.0000368789.42492.f2
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