Wound healing has variable mechanisms and consequences in different ocular tissues. The processes summarized in the following sections are also discussed in other volumes of the BCSC. Also see the appropriate chapters in this volume for the topography of a specific ocular tissue.
A corneal abrasion, or corneal epithelial defect, refers to a wound that is limited to the surface corneal epithelium, although Bowman layer and superficial stroma may also be involved. Within an hour of injury, the parabasilar epithelial cells begin to migrate across the denuded area until they touch other migrating cells; then contact inhibition stops further migration. Simultaneously, the surrounding basal cells undergo mitosis to supply additional cells to cover the defect. Reepithelialization occurs at a rate of 2 mm per day, on average. Although a large corneal abrasion is usually covered by migrating epithelial cells within 24–48 hours, complete healing, which includes restoration of the full thickness of epithelium (5–8 layers) and re-formation of the anchoring fibrils, takes 4–6 weeks. If a thin layer of anterior corneal stroma is lost with the abrasion, epithelial cells will fill the shallow crater, forming a facet. The Bowman layer is not replaced when it is incised or destroyed.
Corneal stromal healing is avascular and occurs via the process of fibrosis rather than by the fibrovascular proliferation seen in other tissues (Fig 4-2). Following a central corneal wound, neutrophils arrive at the site via the tears (Fig 4-3), and the edges of the wound swell. The corneal matrix glycosaminoglycans, keratan sulfate and chondroitin sulfate, disintegrate at the edge of the wound. The stromal keratocytes (fibroblast-like cells) are activated and eventually migrate across the wound, laying down collagen and fibronectin. The spacing of the keratocytes is not regular, and collagen fibers are not parallel to the stromal lamellae. Hence, cells are directed anteriorly and posteriorly across a wound that will always be visible microscopically as an irregularity in the stroma and clinically as an opacity. If the wound edges are not well-apposed, the gap will not be completely filled by the proliferating keratocytes, resulting in focal stromal thinning.
Both the epithelium and the endothelium are critical to good central wound healing. If the epithelium does not cover the wound within a few days of injury, healing of the subjacent stroma will be limited and the wound will be weak. In addition, growth factors from the epithelium stimulate and sustain healing. The surface of a healed ulceration is covered by epithelium, but little of its lost stroma is replaced by fibrous tissue. The endothelial cells adjacent to the wound slide across the posterior cornea; a few cells are replaced through mitosis. The endothelial cells lay down a new thin layer of Descemet membrane. If the internal aspect of the wound is not covered by Descemet membrane, stromal keratocytes may continue to proliferate onto the posterior surface of the membrane as fibrous ingrowth, or the posterior wound may remain open permanently. In the late months of healing, the initial fibrillar collagen is replaced by stronger, thicker collagen fibers.
Excerpted from BCSC 2020-2021 series: Section 4 - Ophthalmic Pathology and Intraocular Tumors. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.