PRK Scars: Key Insights on Healing and Recovery

Photorefractive keratectomy (PRK) is a widely used laser eye surgery for vision correction, but the healing process can sometimes lead to corneal scarring. While most patients experience smooth recovery, some develop scars that affect visual clarity. Understanding how and why these scars form is essential for managing expectations and optimizing outcomes.

The way the cornea heals after PRK determines whether scarring will occur and how it might impact vision. Several biological processes influence this healing, leading to variations in scar appearance and severity.

Early Corneal Healing Mechanisms

The initial phase of corneal healing after PRK begins immediately after the epithelial layer is removed. Epithelial cell migration is the first step in restoring the corneal surface. Within hours, basal epithelial cells at the wound margins flatten and extend filopodia, allowing them to move across the exposed stroma. This process is facilitated by integrins and fibronectin, which provide adhesion points for advancing cells. Studies show that epithelial closure typically occurs within three to five days, depending on patient age and preoperative corneal health (Wilson, 2020, Experimental Eye Research).

As the epithelial layer regenerates, stromal keratocytes undergo changes in response to laser-induced injury. Normally responsible for maintaining corneal transparency by producing organized collagen, these cells transition into an activated state, increasing proliferation and extracellular matrix remodeling. Growth factors such as transforming growth factor-beta (TGF-β) and platelet-derived growth factor (PDGF) regulate this process. Excessive activation of these pathways can lead to disorganized collagen deposition, increasing the likelihood of post-PRK haze (Jester et al., 2019, Investigative Ophthalmology & Visual Science).

During this phase, the cornea experiences temporary hydration increases due to the loss of epithelial barrier function, which can affect corneal thickness and refractive outcomes. Matrix metalloproteinases (MMPs) play a critical role in degrading damaged extracellular components and facilitating tissue remodeling. However, an imbalance in MMP activity has been linked to delayed healing and irregular stromal remodeling, contributing to persistent visual disturbances (Torricelli et al., 2021, Progress in Retinal and Eye Research).

Transition to Fibrotic Changes

As healing progresses, the reparative process shifts toward long-term tissue stabilization. Fibroblastic and myofibroblastic pathways become central in determining whether scarring will occur. Myofibroblasts, derived from activated keratocytes, secrete dense extracellular matrix components and contractile proteins that can impair corneal clarity. Their persistence is strongly associated with subepithelial haze, a form of fibrosis that can reduce visual acuity (Zieske, 2021, Experimental Eye Research).

TGF-β plays a key role in fibrotic transformation by promoting myofibroblast differentiation and suppressing collagen degradation. Elevated TGF-β levels correlate with increased haze formation, particularly in patients with higher refractive corrections requiring deeper stromal ablation (Reinstein et al., 2020, Journal of Cataract & Refractive Surgery). The duration and intensity of TGF-β activity influence whether corneal opacity is temporary or leads to long-term fibrosis.

The structural integrity of the stromal collagen network is also affected by laser ablation. Disruptions in collagen arrangement can increase light scatter and reduce optical quality. Research using second-harmonic generation imaging has shown that persistent PRK haze is associated with misaligned collagen bundles, while properly healed corneas maintain an organized fibrillar structure (Morishige et al., 2019, Investigative Ophthalmology & Visual Science).

Variations in Scar Appearance

Corneal scars after PRK vary based on stromal remodeling, collagen deposition patterns, and tissue alteration depth. Some individuals develop transient haze that resolves within months, while others experience persistent opacity affecting vision. Deeper ablations are generally linked to denser scarring due to increased collagen irregularities.

Scar morphology ranges from faint haze to well-defined fibrotic plaques. Mild cases typically cause slight contrast sensitivity reduction without significant vision impairment. Severe fibrosis can create localized, elevated lesions leading to irregular astigmatism, glare, and halos, particularly in low-light conditions. Optical coherence tomography (OCT) imaging has shown that denser scars coincide with areas of increased backscatter, indicating disorganized collagen fibrils that disrupt corneal smoothness.

The location of scarring also affects visual impact. Central corneal scars, especially those near the visual axis, cause more noticeable disturbances than peripheral haze, which may be less symptomatic. Confocal microscopy studies have found that central scars often exhibit higher cellular density and extracellular matrix deposition, contributing to greater light diffraction. This explains why patients with similar levels of post-PRK haze may experience different degrees of visual impairment.

Methods for Evaluating Scarring

Assessing corneal scarring after PRK requires imaging techniques and clinical evaluations to determine structural and optical changes. Slit-lamp biomicroscopy is widely used to grade the density and distribution of scarring based on standardized scales such as the Fantes grading system. While effective for qualitative assessment, it lacks precision in quantifying scar depth and microstructural characteristics.

Anterior segment optical coherence tomography (AS-OCT) provides high-resolution cross-sectional scans, revealing scar thickness and reflectivity. Increased backscatter in AS-OCT images correlates with areas of disorganized collagen, offering insight into post-PRK fibrosis severity. Unlike slit-lamp exams, AS-OCT allows longitudinal tracking of scar evolution.

Confocal microscopy provides real-time visualization of cellular changes within corneal layers. This technique helps differentiate transient haze, primarily consisting of activated keratocytes, from persistent fibrosis, characterized by dense extracellular matrix deposition. The ability to assess cellular density and morphology makes confocal microscopy valuable for identifying prolonged myofibroblast activity contributing to visual disturbances.

Biological Factors Influencing Recovery

Corneal healing after PRK varies due to biological factors influencing tissue repair. Differences in cellular response, genetic predisposition, and systemic health conditions determine whether a patient experiences minimal haze or persistent scarring. Fibroblast and myofibroblast activity regulation is a key factor, as prolonged myofibroblast persistence can interfere with corneal transparency restoration.

Age plays a role in recovery. Younger patients often heal faster but face a higher risk of haze due to increased fibroblast activity, while older individuals may experience slower epithelial regeneration, prolonging inflammation and increasing irregular stromal remodeling risk. Systemic conditions like diabetes can impair healing by disrupting cellular signaling pathways. Studies indicate that diabetic patients have delayed epithelial closure, leading to prolonged stromal exposure and increased collagen deposition risk. These biological differences explain why some individuals recover with minimal scarring while others develop persistent fibrosis affecting vision.

Associations With Other Ocular Conditions

Pre-existing ocular conditions significantly influence PRK healing outcomes. Patients with dry eye disease often experience delayed epithelial regeneration due to insufficient tear film support, prolonging inflammation and increasing stromal irregularity risk. A compromised tear film slows epithelial migration and affects the distribution of growth factors essential for balanced collagen synthesis, leading to uneven healing and increased post-surgical haze.

Individuals with keratoconus or forme fruste keratoconus face a heightened risk of unpredictable stromal remodeling. These conditions weaken corneal structure and disrupt collagen organization, increasing the likelihood of excessive thinning and irregular fibrosis post-surgery. While PRK is often preferred over LASIK in patients with subtle corneal ectasia to avoid flap creation, altered biomechanical properties can still result in suboptimal healing.

Patients with a history of herpetic eye disease are also at risk, as PRK can trigger viral reactivation, leading to an inflammatory cascade that worsens scarring. Understanding these associations helps clinicians tailor treatment plans and manage patient expectations regarding healing and visual outcomes.