Retinal Scarring: Causes, Symptoms, and Treatment Options

Retinal scarring, sometimes called subretinal fibrosis, is permanent structural damage to the light-sensitive tissue at the back of the eye that almost always results in some degree of irreversible vision loss. It develops as an end-stage wound-healing response to a range of insults, from age-related macular degeneration to retinal detachment to infections contracted before birth. Once a scar has fully formed, the delicate photoreceptor cells beneath it are typically destroyed, and no current treatment can restore them. That makes the story of retinal scarring as much about prevention and early intervention as it is about treatment after the fact.

Why the Retina Scars in the First Place

The retina lines the inside of the eye like wallpaper, and just behind it sits a single layer of support cells called the retinal pigment epithelium (RPE). Under normal conditions, RPE cells stay put and perform housekeeping duties: recycling visual pigments, feeding photoreceptors, and clearing waste. When the retina is injured, though, these cells can undergo a dramatic identity shift. They lose their specialized traits and start behaving more like wound-repair cells, gaining the ability to migrate and multiply. This transformation is driven largely by a signaling molecule called TGF-β, which kicks off a cascade that ultimately produces collagen and other scar-forming proteins.

Preclinical studies have confirmed that RPE cells retain a surprising capacity to swing between their normal, anchored state and this wound-repair mode, a process researchers call epithelial-mesenchymal transition.

¹ TGF-β is a central driver of this process in RPE cells, triggering signaling chains that stimulate both the cell transformation and the deposition of fibrous tissue.² Another protein, connective tissue growth factor (CTGF), has been found to correlate strongly with the severity of fibrosis across a range of vitreoretinal conditions, suggesting it plays a major downstream role in the scarring process.³

The practical takeaway is that the retina scars through the same basic wound-healing program the body uses everywhere else. The problem is that unlike skin or muscle, the retina cannot afford scar tissue. Photoreceptors are exquisitely organized, and a clump of collagen in their place means permanent blindness in that spot.

Common Causes of Retinal Scarring

Several conditions can set off the scarring cascade. They share the common thread of retinal injury or chronic inflammation, but the specific path to fibrosis differs for each.

Neovascular Age-Related Macular Degeneration

Wet (neovascular) AMD is one of the most common causes of retinal scarring in older adults. Abnormal blood vessels grow beneath or through the retina, leaking fluid and blood. The body’s attempt to seal off this damage produces subretinal fibrosis. The natural course of untreated nAMD leads to scarring and vision loss, and even with modern anti-VEGF injections, fibrosis can develop in roughly half of treated eyes within two years.⁴ Eyes with “classic” lesion types, where the abnormal vessels have broken through the RPE layer into the subretinal space, appear more prone to scarring than those with “occult” lesions that remain beneath the RPE.

Proliferative Vitreoretinopathy

When the retina detaches, the resulting breach of the blood-retinal barrier floods the vitreous cavity with growth factors and inflammatory signals. RPE cells and glial cells migrate onto the retinal surface, where they form contractile membranes that pull and distort the retina. This process, called proliferative vitreoretinopathy (PVR), represents the end stage of wound healing after retinal detachment and is a leading cause of surgical failure in retinal reattachment procedures.⁵ The detachment itself triggers glial cells to release inflammatory signals that promote cell proliferation and tissue remodeling, creating a vitreous environment that favors de-differentiation and scar formation.⁶

Diabetic Retinopathy

Advanced proliferative diabetic retinopathy (PDR) can produce fibrovascular membranes that adhere to and pull on the retina, sometimes causing tractional retinal detachments.⁷ CTGF plays a particularly important role in diabetic scarring. As the disease progresses, the balance between VEGF (which drives new blood vessel growth) and CTGF (which drives fibrosis) shifts, leading to what researchers describe as an “angio-fibrotic switch” in which the disease transitions from a vascular problem to a fibrotic one.⁸

Infections and Inflammatory Conditions

Certain infections can leave retinal scars, sometimes with devastating results. Congenital toxoplasmosis, an infection passed from mother to child during pregnancy, can produce large macular scars visible on examination, sometimes spanning several times the diameter of the optic disc.⁹ Ocular histoplasmosis syndrome, caused by the fungus Histoplasma capsulatum, is a major cause of central vision loss in young adults living in endemic regions. Choroidal neovascularization triggered by the infection can produce scarring similar to that seen in AMD, though the affected population is much younger.

Laser Injury and Photocoagulation

Accidental laser exposure can cause deep retinal scarring and retinal traction, particularly in cases severe enough to produce vitreous hemorrhage.¹⁰ Intentional laser photocoagulation, used to treat diabetic retinopathy and other conditions, also produces scars by design. Traditional parameters produce a stable scar roughly the size of the laser beam, though newer approaches using shorter pulses and lighter burns may allow the damaged photoreceptor layer to recover, reducing side effects like blind spots.¹¹

What Retinal Scarring Feels Like

The symptoms depend heavily on where the scar sits. A scar in the peripheral retina may cause no noticeable symptoms at all and be found only during a routine eye exam. A scar at or near the macula, the small central area responsible for sharp, detailed vision, is a different story entirely.

The most characteristic symptom of macular scarring is metamorphopsia: straight lines appear wavy, bent, or distorted. This distortion arises when the scar disrupts the orderly alignment of retinal layers in the macula. Imaging studies have shown that metamorphopsia correlates with measurable misalignment of both inner and outer retinal layers at affected sites.¹² You might also experience a central scotoma, a blank or dark patch in the center of your vision. Research on macular holes, a related condition, found that the majority of patients reported perceiving visual distortions such as bending, thinning, or a break in a straight line when looking through the affected eye.¹³

People with macular scars often notice difficulty reading, recognizing faces, or performing tasks that require fine central vision, even though their peripheral vision remains intact. This can be profoundly disorienting because you can see the world around you, just not the thing you are trying to look directly at.

How Retinal Scars Are Detected

Optical coherence tomography (OCT) is the workhorse of retinal scar diagnosis. This noninvasive imaging technique produces cross-sectional views of the retina at micrometer resolution, allowing clinicians to see fibrotic tissue, fluid pockets, and structural disruption in remarkable detail. In the context of nAMD, OCT can identify precursors to scarring before a scar is fully established. A study analyzing data from a large treatment trial found that the presence of abnormal new vessels, subretinal hyperreflective material, and certain fluid collections at baseline strongly predicted which spots would eventually develop fibrotic scars.¹⁴ More than three-quarters of the pixels that became fibrotic scars by years two and five were preceded by abnormal vessels at baseline, meaning early imaging can flag high-risk areas years before vision loss occurs.

OCT has also sharpened the ability to distinguish scars from other structures. Outer retinal tubulation, for example, is a tubular formation in the outer retinal layers that can look similar to fluid-filled cysts on routine scans but is actually a distinct finding associated with chronic damage. Higher-resolution OCT modes can differentiate it from active fluid, preventing unnecessary treatment.¹⁵ Fundus autofluorescence, another imaging modality, helps map the extent of healed choroidal lesions, particularly in inflammatory conditions like tubercular serpiginous-like choroiditis, where it tends to pick up more healed lesions than OCT-based angiography.¹⁶

Current Treatment Options

The honest reality is that once a retinal scar has fully formed, no approved therapy can reverse it. Treatment focuses on two goals: preventing scars from forming in the first place, and surgically removing scar tissue in specific situations where the tissue itself is causing ongoing mechanical damage.

Anti-VEGF Injections

For nAMD, anti-VEGF drugs like bevacizumab and ranibizumab are the standard of care. By blocking the growth factor that drives abnormal blood vessel formation, these injections reduce leaking and bleeding, slowing the progression toward scarring. A major comparison trial found that the two drugs produced similar rates of scar development, and that monthly versus as-needed dosing schedules did not meaningfully differ in scar risk.¹⁷ Anti-VEGF therapy is not a cure for scarring; it is a strategy to keep the disease controlled long enough to prevent scars from forming. And it does not always succeed: that same trial documented continued scar formation in many treated eyes, and eyes that developed fibrotic scars by year one lost an additional average of about 13 letters of vision between years one and five.¹⁸

Surgery for Epiretinal Membranes and PVR

When scar tissue forms on the retinal surface as a membrane, vitrectomy surgery with membrane peeling can physically remove it. One study of this procedure found that about 83% of patients gained two or more lines of vision, and 93% of those interviewed reported improved functional vision, especially a reduction in distortion.¹⁹ Surgeons sometimes also peel a deeper layer called the internal limiting membrane (ILM) to reduce the chance of the membrane growing back. A meta-analysis found that while skipping ILM peeling produced slightly better short-term vision (within 12 months), peeling the ILM led to better vision after 18 months and a markedly lower recurrence rate of the membrane.²⁰

For PVR, surgery is more complex and outcomes are less predictable. The contractile membranes that form in PVR can be extremely adherent to the retina, making clean removal difficult. Even after successful surgery, re-proliferation of scar tissue is a common complication.

Therapies Under Investigation

Because existing treatments cannot reverse established scars, researchers are pursuing strategies aimed at the molecular machinery of fibrosis itself. Several targets are showing promise in preclinical work.

TGF-β, the master switch of retinal fibrosis, is an obvious target. In a mouse model, antibodies that neutralize TGF-β reduced subretinal fibrosis by about 65% compared to untreated controls.²¹ Nintedanib, a drug already approved for lung fibrosis, has been shown in lab studies to prevent TGF-β from triggering the epithelial-mesenchymal transition in RPE cells, suggesting it could potentially be repurposed for retinal use.²² Another line of research targets the Notch signaling pathway, which cooperates with TGF-β to amplify scar protein production in retinal glial cells. A compound called RO4929097, which blocks Notch signaling, reduced fibrosis-related protein buildup in both cell and animal experiments.²³

None of these have reached large-scale human trials for retinal fibrosis yet, and TGF-β is involved in so many body processes that blocking it systemically raises safety concerns. Still, the convergence of multiple research groups on the same signaling pathways suggests a growing understanding of where the fibrosis process can be interrupted.

Regenerative Approaches

Perhaps the most ambitious frontier is replacing the damaged RPE entirely. RPE transplantation, using cells derived from stem cells, is moving from animal experiments into early human trials. A 2025 review of the field noted that replacement of the RPE is emerging as a promising approach for degenerative retinal diseases in which RPE function cannot otherwise be restored, with early human results indicating potential efficacy.²⁴

In one recent trial, strips of RPE cells derived from induced pluripotent stem cells were transplanted into patients with macular degeneration and retinitis pigmentosa. All patients met the primary endpoint of graft survival at one year, and one patient with dry AMD showed improvement in retinal sensitivity and vision-related quality of life.²⁵ These are very early results in a handful of patients, so caution is warranted. But the fact that transplanted cells can survive in the human eye for at least a year is itself a meaningful milestone. The major unsolved problem is that transplanted RPE may not help much if the overlying photoreceptors have already been destroyed by scarring, which is why these approaches work best when applied before end-stage disease.

Living with Retinal Scars

When a macular scar has destroyed central vision and no further medical or surgical intervention can help, low-vision rehabilitation becomes the practical path forward. The brain has a remarkable ability to adapt. When the fovea (the central point of sharpest vision) is knocked out by a scar, many people unconsciously begin using a nearby, undamaged area of retina as a substitute fixation point, known as a preferred retinal locus. Rehabilitation training can strengthen and stabilize this adaptation.

Eccentric viewing training teaches patients to consciously use their preferred retinal locus for reading and other tasks. A study of patients with central scotomas found that while this training did not significantly improve best-corrected visual acuity on an eye chart, reading speed and patient satisfaction scores increased substantially.²⁶ A more targeted approach uses biofeedback, in which the patient receives audio cues that reward them for directing their gaze toward the optimal retinal location. In a pilot study, patients who underwent ten weekly sessions of biofeedback training showed improvements in visual acuity, fixation stability, retinal sensitivity, and reading speed, with reading speed increasing from an average of about 64 words per minute to 92.²⁷ The mechanism appears to involve strengthening the neural connections between the substitute retinal area and the brain’s visual processing centers.²⁸

Magnification devices, specialized reading glasses, electronic screen readers with adjustable contrast, and smartphone accessibility features round out the toolkit. Many people with macular scars retain enough peripheral vision to navigate, cook, and perform most daily activities, even if reading standard print or driving is no longer possible. The adjustment is difficult, but the degree of functional independence achievable with good rehabilitation often surprises patients who initially feared total blindness.

Why Early Treatment Matters So Much

The research on retinal scarring points to a frustrating asymmetry: the window for preventing a scar is far wider than the window for treating one. In nAMD, prompt and consistent anti-VEGF treatment limits the leaking and bleeding that trigger the wound-healing cascade. The finding that more than three-quarters of eventual scar sites in a large trial already showed abnormal vessels at baseline underscores how early the process begins.¹⁴ In diabetic retinopathy, controlling blood sugar and blood pressure reduces the risk of reaching the proliferative stage where fibrous membranes form. In retinal detachment, timely surgical repair minimizes the inflammatory exposure that drives PVR.

For infections like toxoplasmosis, prenatal screening and treatment in endemic regions can prevent the congenital form that produces massive macular scars in newborns. And for occupational or recreational laser hazards, proper eye protection is the only reliable prevention; once a laser burn penetrates the retina deeply enough to cause hemorrhage, scarring is essentially inevitable.

The gap between the ease of prevention and the difficulty of reversal is the central theme in retinal fibrosis research. New anti-fibrotic drugs and regenerative cell therapies may eventually narrow that gap, but for now, the strongest message from the evidence is that preserving retinal tissue before it scars is far more effective than trying to restore it afterward.