Could apoptosis change the way we do PRK?

Just when we thought photorefractive keratectomy (PRK) had achieved a level of safety and predictability in correcting refractive errors in our patients, new wounding healing information regarding apoptosis (programmed cell death) surfaces to show us that the way we remove the corneal epithelium matters a great deal in how the corneal stroma responds to our treatment.1 Excimer laser manufacturers have previously adjusted the algorithms for PRK to include anti-central island software, multizone treatments, and astigmatism conversion factors. LASIK surgeons have created their own algorithms for correcting refractive errors under a flap because of perceived benefits of LASIK over PRK, including the absence of central epithelial and stromal wound healing. Now PRK may be in store for yet another change in algorithms to compensate for the regional variation in epithelial thickness when performing transepithelial ablation. Kim and coauthors (pg. 526-533), describe the relative absence of keratocyte apoptosis following transepithelial excimer laser ablation compared to transepithelial ablation followed by mechanical scraping prior to excimer laser photorefractive keratectomy. This relative paucity of apoptosis with transepithelial ablation means that fewer keratocytes die and fewer need to be replaced by activated keratocytes that produce collagen and proteoglycans that are involved in wound healing, and that lead to regression and haze. These results suggest that minimizing apoptosis would improve the outcome and stability of excimer laser PRK by reducing the variable of wound healing which is experienced differently among patients. This leads to the question: Could apoptosis change the way we do PRK?