Axial length stability and shortening in clinical studies

We expect axial length to grow during childhood—whether in the context of myopia progression or even normal emmetropisation. Hence, when axial length is stable or shortens, this challenges our understanding of normal ocular growth and raises questions about the mechanisms at play. Recent studies have reported instances of axial length shortening in children receiving myopia control treatment. This article reviews the documented magnitudes of axial shortening across various treatment modalities and highlights key considerations—such as instrument repeatability—when interpreting these outcomes.

Axial length shortening has been documented in various studies using different myopia control interventions. Notably, these are as follows.

In a retrospective study investigating the effects of weekly 1% atropine in Chinese children, a mean axial shortening of −0.033 mm at 7 days, −0.072 mm at 2 months, and −0.033 mm at 6 months was reported.1

There is a small amount of data that has documented axial shortening in myopia control spectacle lens wearers. In a retrospective study looking at defocus incorporated multiple segment (DIMS) lenses in Chinese children (n=489), they found that 2.7% of DIMS wearers had axial shortening of −0.13 ± 0.07 mm over 2 years that also corresponded with a reduction of myopia of 0.09D.2 In a randomized controlled trial looking at highly aspherical lenslet (HAL) lenses in Chinese children (n=154), they found 3 of the study participants experienced axial length shortening of −0.04 mm, -0.09 mm and −0.27 mm after 2 years.3

Axial length shortening has been reported in several large-scale retrospective studies of orthokeratology. In one study of 37 Chinese children, the mean axial shortening was −0.18 mm at 12 months, with 16.22% of subjects experiencing a reduction greater than -0.25 mm.4 Another large database study of 10,093 Chinese children found a median axial shortening of -0.19 mm, with individual reductions ranging from -0.10 to -0.73 mm; this was maintained from 1 year and up to 7 years in some cases.5 A separate study reported a mean axial shortening of −0.08 mm after one month of lens wear, followed by a rebound during the washout period, and a further −0.04 mm shortening upon re-wearing the lenses for a month then returning to baseline 7 months after recommencement of ortho-k.6

In a 2025 study of Japanese children (n=24) wearing SEED 1-day Pure EDOF soft contact lenses with a +1.50 add, axial length shortening of ≥-0.05 mm/year was observed in 20.8% of participants, with reductions ranging from −0.09 mm to −0.23 mm over one year.7

Axial length (AL) shortening has been observed in children undergoing repeated low-level red-light (RLRL) therapy, with reports from both retrospective and randomized controlled trials:In a retrospective multicentre study of 434 myopic children, AL shortening of ≥-0.05 mm/year was observed in 26.5% of participants, with 17.5% showing reductions of ≥-0.10 mm/year and 4.6% of  ≥-0.20 mm/year; the mean shortening among responders was −0.142 mm/year.8 A post hoc analysis of a randomized controlled trial (RCT) involving 264 children reported similar findings, with 21.85% experiencing AL shortening ≥−0.05 mm, 15.13% ≥−0.10 mm, and 5.88% ≥−0.20 mm at 12 months; the mean AL reduction in those with shortening was −0.156 mm, and the maximum individual reduction reached was −0.31 mm.9In a separate multicentre RCT of 202 children with high myopia (−6.00 D or higher), the average AL shortening was −0.11 mm after 12 months of RLRL therapy, with peak effect (-0.13 mm) observed at 9 months; 63% of participants showed reductions exceeding -0.05 mm.10Across the studies of various myopia control interventions, axial length shortening has been reported in the range of −0.009 mm to −0.73 mm, with the greatest individual reductions observed in orthokeratology and repeated low-level red-light therapy.

Axial length shortening appears to follow a treatment-dependent time course, with some interventions producing early, short-term changes and others showing more gradual but sustained effects. Shortening has been observed as early as 1 week with atropine and within 1 month of initiating orthokeratology or RLRL therapy.1-4,6,8-10 However, in some cases—such as with atropine and after ortho-k cessation—the initial shortening effect was not sustained and returned to baseline levels within months.1,6 In contrast, treatments like EDOF contact lenses and RLRL therapy have noted sustained AL shortening over 12 months; DIMS and HAL lenses have reported sustained axial shortening in a very small subset (2-3%) of patients over 24 months. RLRL therapy appeared to produce both early and enduring effects, with peak responses occurring between 6 to 9 months and persisting through 12 months in some participants. A summary of AL shortening of the different myopia control treatment modalities is provided in Table 1.

The mechanisms underlying axial length shortening in response to myopia control treatments are not yet fully understood, but possible theories involve a combination of transient physiological changes and perhaps longer-term structural remodelling:

• Choroidal thickening: Multiple studies suggest that choroidal thickening may contribute to short-term AL shortening by physically displacing the retinal pigment epithelium forward.1,4-6 In the post hoc analysis of an RLRL randomized trial, children who exhibited AL shortening showed an average choroidal thickening of 56 µm.9 
• Transient anterior segment changes: Although not the dominant explanation for sustained shortening, transient shifts in lens or vitreous chamber depth during accommodation have been reported in the literature as possible contributors to short-term AL changes.11 Orthokeratology can also cause central corneal thinning (~9 µm) which may contribute to temporarily reduce AL,12 but these effects rebound after cessation. 
• Diurnal variations: Axial length changes are also subject to diurnal variation, with a mean amplitude found in studies of between 0.032mm and 0.046mm.13,14 AL is longest during the day and typically shortest at night and may be due to normal biomechanical changes that occur in the eye. For example, the choroid is thicker at night and thinner during the day.14 AL changes may also partially be explained by IOP fluctuations—about 14% of AL variation was attributed to IOP changes, equating to around 18 μm change in AL from a 3.12 mmHg IOP variation.13 
• Posterior segment remodelling: One proposed mechanism regarding RLRL therapy is that it may improve circulation and metabolic function in the back of the eye, helping to alleviate scleral hypoxia. This enhanced environment could promote collagen production and structural remodelling of the posterior sclera, potentially leading to sustained axial length shortening.15-17

Mechanisms like choroidal thickening, anterior segment shifts, and diurnal variation may contribute to transient axial length changes, while posterior scleral remodelling may underlie more sustained effects. However, these proposed mechanisms remain theoretical and may not reflect true structural shortening of the eye. While the magnitude of axial length shortening observed in some studies suggests a complex interplay of physiological and structural processes, the exact nature and permanence of AL shortening remains uncertain and warrants further, longer-term investigation. 

Interpreting these small axial length changes also requires consideration of the precision of the measuring instrument. Modern optical biometers are highly precise, with axial length repeatability typically within ±0.04 mm.18,19 The OCULUS Myopia Master has a repeatability of 0.038 mm in adults and 0.057 mm in children.20 Figure 1 illustrates axial length reduction as displayed using Myopia software.

This level of repeatability is particularly important when interpreting small changes in axial length, such as those reported in studies on AL shortening. Any shortening data reported with A-scan ultrasound biometry would be a far less reliable measure of the effect.21

It’s essential to recognise that changes within the repeatability range of the instrument may not represent true anatomical change. In both clinical and research settings, axial length changes of less than 0.05 mm should be interpreted with caution, as they may fall within normal test–retest variability. Understanding the measurement limits of the device being used is critical to ensure accurate interpretation and to avoid overstating treatment effects.

While the documented magnitudes of axial length shortening across these studies are compelling, it would be premature to suggest that myopia—or axial elongation—can be truly reversed. The time course of this effect is not yet well established, and although some studies report sustained shortening over 12 months, others have shown that early reductions can rebound or return to baseline. As such, we should interpret these findings with caution. Rather than viewing axial shortening as a new goal for myopia management, it may instead serve as a biometric signal or predictor of treatment response. For example, the study on 1% atropine reported that axial shortening greater than −0.04 mm within the first two months was predictive of slower axial elongation over two years, effectively identifying likely responders to treatment.1 In this context, AL shortening may provide useful clinical insight—not necessarily as a marker of reversal, but as a potential indicator of treatment efficacy.

Axial length shortening challenges our traditional understanding of ocular growth and introduces new considerations in evaluating myopia control treatments. While the exact mechanisms and clinical significance of this phenomenon are still being explored, current evidence suggests that early AL shortening may offer valuable insight into treatment response. As research progresses, continued attention to measurement precision, treatment time course, and individual variability will be essential in translating these findings into meaningful clinical outcomes.