Although the biology of corneal wound healing is only partly understood, healing after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK) differs in many respects, and the mechanisms appear to be differently controlled. There is less of an inflammatory and healing response after LASIK, but a longer period of sensory denervation. The cellular, molecular, and neural regulatory phenomena associated with postoperative inflammation and wound healing are likely to be involved in the adverse effects after LASIK, such as flap melt, epithelial ingrowth, and regression. Interface opacities in the early postoperative period include diffuse lamellar keratitis (DLK), microbial keratitis, epithelial cells, and interface opacities. Diffuse lamellar keratitis (sands of the Sahara syndrome) describes an apparently noninfectious diffuse interface inflammation after lamellar corneal surgery probably caused by an allergic or a toxic inflammatory reaction. Noninfectious keratitis must be distinguished from microbial keratitis to avoid aggressive management and treatment with antimicrobial drugs. Microbial keratitis is a serious complication after LASIK, but a good visual outcome can be achieved following prompt and appropriate treatment.