The retina is made of terminally differentiated cells that typically do not regenerate when injured. Because the retina is part of the central nervous system (CNS), glial cells (eg, Müller cells, astrocytes), rather than fibroblasts, proliferate in response to retinal injury. Surgical techniques to close holes or tears in the neurosensory retina are successful when the retina and retinal pigment epithelium (RPE) are injured (eg, as a result of cryotherapy, photocoagulation), forming an adhesive, atrophic scar between the neurosensory retina and Bruch membrane (see Chapter 11, Fig 11-27).
The internal limiting membrane (ILM) and Bruch membrane provide the architectural anchors for glial scarring; adhesions between the ILM and Bruch membrane may incorporate a rare residual glial cell, and variable numbers of retinal and RPE cells may be present between the membranes. If the wound has damaged Bruch membrane, choroidal fibroblasts and vessels may participate in the formation of the final scar. The end result is a metaplastic fibrous or fibrovascular plaque in the sub–neurosensory retina and sub-RPE regions. The RPE usually undergoes hyperplasia in such scars, causing the dense pigmented clumps seen clinically on fundus examination.
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.