Regression after laser:
why it is rare, its causes
and how to manage it.

Regression — the partial return of the refractive defect after laser — is the most common fear among patients considering refractive surgery. It is a legitimate concern. But the clinical reality is very different from common perception: significant regression is rare, its causes are well understood, and when it occurs, it is manageable.

In our case series of over 25,000 procedures with the AMARIS laser, the vast majority of results are stable long-term. When regression occurs, it is typically mild, early and predictable.

What is not a regression

First of all, it is important to distinguish true regression from defect progression. If a 22-year-old patient is treated for -4.00 D of myopia and presents -0.75 D three years later, the most likely cause is not corneal regression: the myopia continued to progress because it was not stabilised at the time of surgery. This is why we insist on documented refractive stability before operating.

Likewise, the refractive change related to ageing — presbyopia, a slight hypermetropic shift after 50 — is not a laser regression. It is physiology.

The biological causes of true regression

1. Epithelial hyperplasia

This is the main mechanism of regression after surface refractive surgery (PRK, TransPRK). The corneal epithelium — the most superficial layer, approximately 50-55 µm thick — has a natural ability to remodel its thickness to compensate for changes in the underlying stromal profile.

After a myopic treatment, the laser thins the central stroma. The epithelium tends to thicken centrally to partially fill the depression created by the ablation — a process called compensatory epithelial hyperplasia. This thickening partially reduces the effect of the ablation and produces refractive regression.

The extent of hyperplasia is proportional to the depth of ablation: the more dioptres corrected, the more the epithelium tends to compensate. For low myopia (< -3.00 D), hyperplasia is minimal and clinically insignificant. For high myopia (> -6.00 D), it can rarely produce a regression of 0.50-1.00 D in the first 3 to 6 months.

2. Stromal remodelling

The corneal stroma — the tissue the laser removes — also has a remodelling capacity, although slower and less pronounced than that of the epithelium. After ablation, the stromal collagen fibres undergo a wound healing process that can slightly alter the curvature achieved. This process is more relevant after hypermetropic treatments (where ablation is peripheral and the biomechanical response less predictable) than after myopic treatments.

Stromal remodelling is typically complete within 3-6 months. Refraction stabilises and remains stable. In our 30-year case series (since 1996), we do not observe significant late stromal regressions.

3. Lens changes

The lens changes with age: it becomes stiffer (presbyopia), opacifies (cataract), and changes its own refractive index. These variations can produce a refractive shift — typically myopic (nuclear cataract) or hypermetropic (cortical cataract) — which is perceived by the patient as a "regression" of the laser. In reality, the cornea is stable: it is the lens that has changed.

Risk factors for regression

Not all patients have the same risk. Factors that increase the likelihood of clinically significant regression include: high corrections (myopia beyond -6.00 D, hypermetropia beyond +3.00 D), thin corneas with deep ablations, young age at the time of surgery (greater tissue plasticity), prolonged prior contact lens wear (which alters epithelial biology), and individual predisposition to wound healing — a genetically determined factor that is not always predictable.

Regression and surgical technique

The surgical technique influences the type of regression, not its complete absence.

TransPRK / PRK — surface treatment. The epithelium is removed and regenerates completely in 3 to 5 days. Epithelial hyperplasia is the predominant regression mechanism. The advantage: the epithelium can be monitored via the MS-39 epithelial map, and enhancement is straightforward — the laser works on the surface again without having to re-lift a flap.

LASIK — the flap protects the interface from direct epithelial regeneration, reducing hyperplasia. However, the flap-stroma interface can develop epithelial ingrowth (epithelial growth beneath the flap) and stromal remodelling under the flap is less predictable. Enhancement requires re-lifting the flap — a procedure that is not always straightforward when performed years later.

SMILE — similar to LASIK in terms of epithelial protection. However, enhancement after SMILE is more complex: there is no flap to re-lift, and a second treatment requires either a conversion to surface PRK or the creation of a new cap — technically more demanding procedures.

Peripheral haze: the phenomenon that causes unnecessary alarm

There is a post-operative phenomenon that is not a regression, not a complication, and has no clinical significance — but that can alarm the patient if they are not informed about it: peripheral corneal haze.

After every excimer laser treatment — TransPRK, PRK, and also PresbyMAX — a natural process of stromal scarring occurs in the transition zone between the treated and untreated cornea. Stromal keratocytes activate, produce new collagen, and for several weeks or months the cornea may show a slight opaque halo at the periphery, visible at the slit lamp. This is haze.

Mild peripheral haze is physiological. It is not located in the central optical zone — where the light passes to form the retinal image — and does not affect vision. With modern lasers such as the AMARIS 1050RS and Smart Pulse technology (which produces a smoother stromal surface after ablation), the incidence of clinically significant haze is extremely low: less than 3% at 6 months in moderate-to-high myopic treatments, and in these cases it is almost always mild haze (grade 1) that resolves spontaneously.

Scarring response by technique

TransPRK / PRK — scarring occurs on the stromal surface, directly beneath the epithelium. Haze is subepithelial: superficial, monitorable, and treatable. Preventive treatment with post-operative steroid eye drops is routinely prescribed in our protocol, and clinically significant central haze has become extremely rare with modern lasers and Smart Pulse technology. In my personal experience: 20 cases out of 30,000 eyes treated — 0.067%. In all cases, haze resolved with prolonged steroid eye drops or spontaneously. No case of permanent haze.

LASIK — there is no surface haze (the flap protects). But there is a far more concerning phenomenon: Diffuse Lamellar Keratitis (DLK), also called "Sands of Sahara". It is an inflammation of the flap-stroma interface affecting 2-4% of LASIK patients. Haze is deep — in the interface, not on the surface — and in severe cases (stage 3-4) can cause permanent interface opacity, loss of corrected visual acuity down to 20/200, and in extreme cases stromal melting (stromal melt). DLK requires aggressive treatment with high-dose steroids, and in resistant cases lifting the flap and irrigating the interface. Unlike the subepithelial haze of TransPRK, deep DLK rarely regresses completely when it reaches the advanced stages, and can reappear even years after surgery — cases of late DLK up to 15-18 years after LASIK are documented.

SMILE — scarring occurs within the stroma, in the interface of the extracted lenticule. A deep intrastromal opacity is documented in the literature and visible on OCT even when it is not at the slit lamp. As with LASIK, this is deep haze that is difficult to resolve. Cases of DLK after SMILE and after enhancement PRK post-SMILE are also documented.

In all cases, mild peripheral haze that resolves spontaneously does not require treatment. Haze that persists beyond 6 months and affects vision should be assessed by the surgeon.

When we intervene

Not every regression requires an enhancement. A return of -0.25 / -0.50 D of sphere is often functionally insignificant. Residual astigmatism is corrected with contact lenses from 0.75 D — below this threshold, laser touch-up is rarely justified — the patient does not wear glasses and does not notice the difference. We intervene when regression is stable (no longer progressing — typically after 6 to 12 months), functionally significant (the patient notices a visual decline that limits their activities), and the residual corneal thickness allows it.

The decision is based on three data points: current refraction, the MS-39 epithelial map (to quantify hyperplasia), and residual stromal pachymetry. The ForeSight system simulates the enhancement outcome before proceeding.

How common is it in our case series

In our experience with TransPRK SmartSurfACE and the AMARIS 1050RS laser, the percentage of patients requiring an enhancement for regression is very low. The vast majority of results are stable long-term — confirmed by our 30-year case series (since 1996). When an enhancement is necessary, it is performed under optimal conditions: same laser, same diagnostic equipment, same surgeon, same guarantee.

The 5-year guarantee

All our procedures include a 5-year guarantee. If a clinically significant regression occurs within 5 years of the procedure and corneal conditions permit, the touch-up is included — subject to an annual paid check-up. This is not a commercial gesture: it is the logical consequence of a protocol we believe in.