It is currently estimated that approximately 36% of the world’s population is myopic, and this may rise to 50%, with 10% affected by high myopia.1 Myopia, or shortsightedness, is the most common refractive error and has been described as a global epidemic.
Myopia has become a major public health concern due to the increased risk of vision-threatening complications such as myopic maculopathy, retinal detachment, cataract, and glaucoma.2 These complications are more common with increasing axial length and severity of myopia.
Axial elongation in myopia
One of the main structural changes seen in myopia is increased axial length due to elongation of the globe. High myopia is defined as an axial length greater than 26mm or a spherical equivalent refractive error equal to or greater than −6.00D.
Axial elongation primarily occurs due to biomechanical remodeling of the sclera, driven by visual signals that originate in the retina and are transmitted through the retinal pigment epithelium (RPE) and choroid.3
This signaling cascade alters the extracellular matrix composition and reduces scleral stiffness, ultimately promoting elongation. Growth factors such as vascular endothelial growth factor (VEGF) and TGF-β play a role in this process, highlighting the choroid as a mediator between retinal visual stimuli and scleral response.4
There is now emerging research highlighting the role of the choroid as a key player in myopia development and progression.
Choroidal anatomy and function
The choroid is a highly vascularized tissue located between the RPE and sclera. It forms part of the uveal tract along with the iris and ciliary body. It extends from the ora serrata anteriorly to the optic nerve posteriorly.
Structurally, the choroid consists of five layers arranged from innermost to outermost:4
- Bruch’s membrane
- Choriocapillaris
- Sattler’s layer (medium-sized vessels)
- Haller’s layer (large vessels)
- Suprachoroid adjacent to the sclera
In addition to its primary role of supplying oxygen and nutrients to the outer retina, the choroid also contributes to thermoregulation, intraocular pressure modulation, and light absorption.
The choroid exhibits dynamic behavior in response to visual and retinal changes by modulating its perfusion, thickness, and the secretion of growth-regulating factors that influence scleral structure and ocular elongation.3
Choroidal thinning, myopia, and axial length
A thinner choroid layer is seen in myopic eyes compared to emmetropic and hyperopic eyes.5 Marked thinning of the choroid was seen in children with myopia, and this thinning increased during myopia development, whereas children without myopia showed an increase in choroidal thickness.5
A more recent study showed a decrease in choroidal thickness in new-onset myopia compared to children with persistent non-myopia and persistent myopia, suggesting that choroidal thinning is an active process in early myopia progression.3
Choroidal thinning is strongly associated with axial elongation, suggesting mechanical stretching and structural remodeling of the choroid. Before the onset of myopia, rapid axial elongation may be linked to reduced choroidal blood flow, contributing to scleral ischemia and hypoxia, which further leads to thinning and weakening of the sclera, promoting elongation.3
This thinning is most pronounced subfoveally and in the peripapillary region—two areas with the highest metabolic demand and structural remodeling during ocular growth. Clinically, as axial length increases, mechanical stretching contributes to a visibly thinner choroid, which can be appreciated during fundus examination in moderate to high myopia.
Characteristic fundus findings include:6
- Increased visibility of underlying sclera and choroidal vessels
- Temporal crescent formation
- Tilted or obliquely inserted optic discs
- Posterior staphylomas
Choroidal imaging and visualization
The choroid can be visualized in high-resolution cross-sectional imaging using enhanced depth imaging optical coherence tomography (EDI-OCT) and swept-source optical coherence tomography (SS-OCT). The Spectralis OCT (Heidelberg Engineering) uses EDI technology, providing excellent contrast for choroidal thickness measurements with built-in calipers.
The Triton OCT (Topcon) utilizes SS-OCT, which penetrates deeper into tissue with a longer wavelength light source, offering clearer visualization of the choroid-sclera interface and allowing choroidal thickness maps. Blood flow can also be visualized with OCT angiography (OCTA) to provide analysis of retinal and choriocapillaris microvasculature.
Age-related choroidal changes
Choroidal thickness also decreases with age, even in non-myopic eyes, reflecting ongoing structural and vascular changes. EDI-OCT studies have shown a decline in choroidal thickness of 15 to 30µm per decade, with the greatest thinning seen subfoveally.7
Reduced choroidal blood flow, vascular dropout, and atrophy—each contributing to decreased ocular perfusion—are believed to be the primary mechanisms. These vascular changes not only contribute to age-related thinning but may also be linked to retinal conditions such as age-related macular degeneration (AMD) and myopic degeneration.4
The role of blood flow in choroidal thickness
Blood flow is a central topic when discussing the choroid, as it is a highly vascular structure capable of rapidly altering its perfusion. It is thought that changes in choroidal blood flow are the main driver of thickness changes.3
Several studies have shown reduced blood flow in myopic eyes due to delayed choroidal filling, narrowed vessel diameter, increased vascular stiffness, and thinning of the choroidal vasculature.3
Since the choroid is the main source of oxygen and nourishment for the outer retina, reduced blood flow creates a hypoxic environment that may initiate or exacerbate scleral remodeling and axial elongation in myopia.
Short-term choroidal thickness as a biomarker for myopia
Short-term modulation of choroidal thickness has emerged as a potential biomarker in myopia management, reflecting the choroid’s dynamic role in eye growth. Experimental animal studies have shown that myopic defocus leads to significant choroidal thickening, while hyperopic defocus induces thinning, often followed by axial elongation.8
Even brief periods of optical defocus in children have been shown to alter choroidal thickness.8 Accommodation studies have demonstrated that near work causes transient choroidal thinning, which may also contribute to the link between excessive near work and myopia.9
Pharmacologically, dopamine agonists and muscarinic antagonists like atropine have also shown choroidal thickening. Environmental stimuli such as increased light exposure have also been shown to increase choroidal thickness. Bright light exposure can lead to thickening, supporting the theory that dopamine released by the retina in response to light inhibits eye growth.10
These findings show that the choroid responds rapidly to various stimuli and alters its thickness. As some of these functional changes may occur before structural changes like axial elongation, short-term modulation of choroidal thickness is a promising biomarker for monitoring myopia onset, progression, and treatment response.
With standard OCT and advanced forms of OCT widely available in clinical practice, these choroidal changes should be monitored, making choroidal thickness a valuable tool in myopia care.
Interventions targeting choroidal thickness
Many current myopia control interventions show modulation of choroidal thickness, which may play a part in some of the effects of reducing axial elongation.
Orthokeratology lenses, which flatten the central cornea and steepen the mid-periphery, create a peripheral myopic defocus that slows axial elongation. MiSight (CooperVision) daily soft contact lenses utilize concentric rings of myopic defocus to achieve a similar effect. Spectacle lens designs like Stellest (Essilor) and Miyosmart (HOYA) also generate myopic defocus to reduce axial elongation.11
Low-dose atropine (0.01 to 0.05%) drops, often used in myopia control, inhibit muscarinic receptors in the retina and sclera, reducing axial elongation.8 It has been shown to induce mild choroidal thickening, likely through modulation of blood flow and retinal neuromodulation.8
Outdoor time is frequently recommended to pediatric patients, not only to reduce near work but to increase retinal dopamine and light exposure—both of which show a thicker, more perfused choroid.
Finally, low-level red light therapy (LLLT) using wavelengths around 650nm is an emerging option. Early trials have shown significant reductions in axial length progression and modest increases in choroidal thickness.11
In summary
Previous anatomical research and experimental models of myopia have laid the groundwork for identifying the choroid as a dynamic structure involved in myopic development and progression.
Additionally, advances in imaging—particularly OCT, now widely available in clinical practice—allow for direct in vivo visualization of the choroid, bringing lab research into primary eyecare.
With myopia rising at epidemic levels and myopia control becoming a major focus of eyecare, future treatments may directly modulate the choroid as both a biomarker and interventional therapeutic target for myopia control.
