The retina is the light-sensitive tissue lining the back of the eye, responsible for transmitting visual signals to the brain. When this delicate tissue is damaged by disease or injury, the body attempts repair. This process often results in the formation of abnormal tissue known as retinal scar tissue, medically referred to as fibrosis or gliosis. The resulting abnormal tissue contracts, causing distortion and wrinkling of the retina, which severely compromises vision.
The Body’s Response: How Scar Tissue Forms in the Retina
The mechanism of retinal scarring involves a unique healing response distinct from scar formation elsewhere in the body. Since the retina is part of the central nervous system, its primary response to injury is reactive gliosis. This involves the activation of specialized support cells, specifically Müller cells and astrocytes, which multiply and change shape to wall off the damaged area.
These activated glial cells increase the production of structural proteins like glial fibrillary acidic protein (GFAP), making the tissue more rigid. This contributes to the formation of a glial scar, which acts as a barrier but also physically distorts the retinal architecture. Another source of scar tissue involves the retinal pigment epithelial (RPE) cells, which normally lie beneath the retina. When the retina is breached, RPE cells can migrate and transform through fibrous metaplasia, taking on the characteristics of fibroblast-like cells.
These transformed cells multiply and secrete components of the extracellular matrix, forming a dense, contractile sheet. The most common manifestation is an Epiretinal Membrane (ERM), a transparent layer of scar tissue that forms directly on the retina’s surface. As this membrane matures, its contraction pulls and puckers the underlying tissue, leading to visual distortions.
Scarring Caused by Physical Injury and Separation
Acute physical trauma or the mechanical separation of retinal layers severely triggers the body’s scarring response. The most dramatic example is retinal detachment, where the retina pulls away from its underlying support layers. This separation exposes the cells to inflammatory signals and growth factors that initiate aggressive scar tissue formation.
The most severe form of scarring linked to detachment is Proliferative Vitreoretinopathy (PVR), the leading cause of failed retinal reattachment surgery. PVR involves the widespread proliferation of RPE cells, glial cells, and inflammatory cells that migrate into the vitreous cavity and onto the retinal surface. These cells form thick, contractile membranes that exert tractional forces, pulling the retina into fixed folds or causing recurrent detachment.
Direct ocular trauma, such as a penetrating injury or blunt force, also initiates a rapid scarring cascade. The breach of the retina and the blood-retinal barrier allows cells and proteins to enter the vitreous, immediately triggering the PVR mechanism. The resulting mechanical stress and inflammatory environment drive the formation of these scar sheets, which can lead to permanent loss of vision.
Scarring Caused by Chronic Vascular Damage
Long-term, systemic diseases that compromise the retinal blood supply are a major source of scar tissue. This mechanism is primarily driven by chronic oxygen deprivation, or ischemia, which causes the retina to release growth factors. The two most common conditions resulting in this type of scarring are advanced diabetic retinopathy and wet Age-Related Macular Degeneration (AMD).
In Proliferative Diabetic Retinopathy (PDR), uncontrolled high blood sugar damages small vessels, leading to areas of non-perfusion and hypoxia. In response, the retina increases the production of Vascular Endothelial Growth Factor (VEGF). This factor stimulates the growth of new, abnormal, and fragile blood vessels—a process called neovascularization—on the retinal surface and into the vitreous gel.
These new vessels are structurally weak and are often accompanied by a fibrovascular scaffold of scar tissue, formed by the proliferation of glial cells and fibroblasts. As this fibrovascular tissue contracts, it pulls on the retina, causing a Tractional Retinal Detachment (TRD), a characteristic complication of PDR. Similarly, Wet AMD involves the abnormal growth of vessels, known as choroidal neovascularization (CNV), which originate from the choroid beneath the retina.
These fragile CNV vessels leak fluid and blood beneath the macula, causing direct injury to the overlying light-sensing cells. To contain the damage, the body forms a dense collection of scar tissue and blood vessels known as a disciform scar. This final, irreversible fibrovascular scar physically replaces the macula’s neurosensory tissue, resulting in a permanent blind spot in the center of vision.