Key Takeaways

• Keratoconus is a progressive corneal disease where the cornea thins and bulges into a cone, causing blurred and distorted vision that glasses often can't fully correct.
• The old "non-inflammatory" label is outdated; tear and tissue studies repeatedly show elevated IL-6, TNF-α, and matrix metalloproteinases (MMP-9, MMP-13) plus high oxidative stress.
• Eye rubbing is the single most consistent modifiable risk factor and likely drives both mechanical damage and an inflammatory cascade in the cornea.
• Most cases begin in the teens or twenties and progress until the mid-to-late thirties, when the cornea naturally stiffens.
• Corneal cross-linking (CXL) is the only treatment proven to halt progression, and it works best when started early.
• Glasses help mild cases; rigid gas permeable and scleral lenses correct moderate disease; corneal transplant is reserved for advanced scarring.
• Keratoconus is strongly linked to allergy, atopic disease, asthma, eczema, Down syndrome, and connective tissue disorders.
• Corneal topography and tomography (such as Pentacam scanning) detect keratoconus years before vision changes appear.
• Oxidative stress depletes corneal antioxidant defenses, contributing to collagen breakdown and tissue weakening.
• Stopping eye rubbing, controlling allergies, and protecting sleep posture are practical steps that may slow progression alongside medical care.

Why does keratoconus matter, and who gets it?

Keratoconus matters because it strikes young people during their most visually demanding years and can quietly erode sight before anyone notices. It usually appears around puberty and worsens through the twenties and early thirties. Caught late, it can mean a corneal transplant; caught early, it can often be frozen in place with a single procedure.

The condition is more common than older estimates suggested. Classic textbooks cited roughly 1 in 2,000 people, but modern imaging-based studies report rates closer to 1 in 375 in some populations, and far higher in regions with strong sun exposure, high allergy rates, and consanguinity. Hot, dusty climates and atopic populations show some of the highest numbers worldwide.

Understanding keratoconus has shifted in two big ways. First, scanning technology now finds it early, before vision blurs. Second, lab research has dismantled the idea that keratoconus is purely mechanical and "non-inflammatory." This page explains what keratoconus is, why the inflammatory model has taken over, how it's diagnosed and treated, and what current evidence does — and doesn't — support.

Key Point: Keratoconus is no longer viewed as a simple structural defect. It's now understood as a disease where biochemical inflammation and oxidative stress weaken the cornea's collagen over time.

What exactly is keratoconus?

Keratoconus is a bilateral, progressive disorder in which the central or paracentral cornea thins and protrudes forward into a cone shape. That distortion creates irregular astigmatism — light entering the eye no longer focuses to a single point — so vision becomes blurred, smeared, and difficult to correct with ordinary glasses.

The cornea is the clear dome at the front of the eye and provides about two-thirds of the eye's focusing power. When it loses its smooth, regular curve, image quality collapses even if the rest of the eye is healthy. Patients often describe ghosting, streaking around lights, and a prescription that changes every few months.

The word comes from the Greek kerato (cornea) and konos (cone). It was first described in detail in the 19th century, but only in recent decades have imaging and molecular biology revealed how it actually develops.

How is the cornea built, and why does that matter here?

The cornea is a five-layer transparent tissue, and keratoconus mainly attacks the middle layer. Knowing the layers explains why the cornea thins, weakens, and scars in this disease.

From front to back, the cornea has the epithelium (surface skin), Bowman's layer (a tough membrane), the stroma (the thick collagen body, about 90% of corneal thickness), Descemet's membrane, and the endothelium (inner pump cells). The stroma's strength comes from precisely arranged collagen fibrils cross-linked together — a structure that keeps the cornea both clear and strong.

In keratoconus, this collagen architecture breaks down. Enzymes called matrix metalloproteinases digest collagen and the surrounding matrix faster than the cornea can rebuild it. Bowman's layer develops breaks, the stroma thins, and the weakened tissue bulges under normal eye pressure. In advanced disease, Descemet's membrane can split, allowing fluid to flood the cornea — a painful event called hydrops.

The cornea has no blood vessels; it gets oxygen directly from the air and nutrients from tears and the fluid behind it. This avascular setup means it relies heavily on its own antioxidant enzymes to handle oxidative stress. When those defenses are overwhelmed — a recurring theme in keratoconus — tissue damage accelerates.

Clinical Pearl: Because the stroma carries the cornea's structural load, even modest collagen loss there produces large optical distortions. This is why keratoconic vision degrades faster than the thinning alone might suggest.

What are the signs and symptoms by stage?

Keratoconus symptoms progress from mild blur to severe distortion, and the warning signs differ at each stage. Early disease is easy to miss; advanced disease can cause sudden, dramatic vision loss.

Key Point: Any teen or young adult whose astigmatism keeps worsening with each eye exam should be screened for keratoconus with corneal topography, even if vision still corrects to 20/20 with glasses.

A telltale clue is asymmetry: one eye is usually worse than the other. Patients may also notice that closing the better eye reveals how distorted the worse eye has become. Night driving often becomes the first real-world struggle because of glare and starbursting around headlights.

What causes keratoconus and who is at risk?

Keratoconus arises from a mix of genetic susceptibility and environmental triggers, with eye rubbing and atopic disease standing out as the strongest contributors. No single cause explains every case; it's a final common pathway reached by several routes.

Genetic and developmental factors

Family history raises risk, and keratoconus is more common in certain conditions. Down syndrome carries a markedly increased rate. Connective tissue disorders such as Ehlers-Danlos syndrome and Marfan syndrome, as well as Leber congenital amaurosis and floppy eyelid syndrome, are also associated. Multiple genes affecting collagen and oxidative regulation have been implicated, though no single "keratoconus gene" accounts for most cases.

Mechanical and behavioral factors

Eye rubbing is the most consistently reported modifiable risk factor across studies. Vigorous, habitual rubbing — often tied to allergy or eczema — physically stresses the cornea and triggers release of inflammatory mediators and tissue-digesting enzymes. Sleeping face-down or pressing on one eye may also contribute to asymmetry.

Inflammatory, allergic, and systemic factors

Atopy — the allergic tendency behind asthma, eczema, and hay fever — is strongly linked to keratoconus. Chronic allergic eye disease drives both itching (which provokes rubbing) and a baseline of inflammatory signaling at the ocular surface. Obstructive sleep apnea has also been associated, possibly through oxidative stress.

For more on the allergic-rubbing connection, see our allergic conjunctivitis and eye rubbing resource.

What's actually happening inside the cornea? The pathophysiology

Keratoconus develops when the cornea's collagen-building and collagen-destroying balance tips toward destruction, driven by inflammation, oxidative stress, mechanical injury, and enzyme imbalance. This is the core of why the modern "inflammatory disease in disguise" model has replaced the old non-inflammatory view.

Why are inflammatory molecules elevated if the eye isn't red?

Keratoconus involves low-grade, biochemical inflammation rather than the visible redness of classic eye infections. Multiple tear-film studies have found elevated pro-inflammatory cytokines in keratoconic eyes, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1 (IL-1). These molecules promote tissue remodeling and activate enzymes that degrade collagen.

The clinical consequence is that the cornea sits in a chronic, simmering inflammatory state that gradually weakens its structure. This is why the label "non-inflammatory" — repeated for generations — has been challenged by researchers who measure these markers directly. The inflammation is real; it's just subtle and biochemical rather than dramatic and visible.

Evidence Snapshot: Several studies, including work published in Investigative Ophthalmology & Visual Science and Experimental Eye Research, report higher tear levels of IL-6, TNF-α, and MMP-9 in keratoconus patients compared with healthy controls. The findings are consistent enough that inflammation is now considered part of the disease process, though it may not be the sole initiating cause.

How do matrix metalloproteinases break down the cornea?

Matrix metalloproteinases (MMPs) are enzymes that digest collagen and extracellular matrix, and in keratoconus they are overactive. MMP-9 and MMP-13 in particular are elevated in keratoconic tears and tissue. Normally these enzymes are kept in check by inhibitors called TIMPs (tissue inhibitors of metalloproteinases).

In keratoconus, the MMP-to-TIMP balance shifts toward degradation. The result is faster breakdown of the stromal collagen scaffold than the cornea can rebuild, leading to progressive thinning. Eye rubbing acutely spikes MMP-13 and IL-6 at the ocular surface, providing a direct mechanical-to-biochemical link.

What role does oxidative stress play?

Oxidative stress damages corneal cells and collagen, and keratoconic corneas show reduced antioxidant defenses. The avascular cornea is constantly exposed to ultraviolet light and atmospheric oxygen, generating reactive oxygen species. Keratoconic tissue shows lower activity of protective enzymes like superoxide dismutase and increased markers of oxidative damage.

When antioxidant defenses fall behind, reactive oxygen species injure keratocytes (the cornea's repair cells) and trigger their death by apoptosis. Fewer healthy keratocytes means less collagen repair, compounding the structural loss. Oxidative stress and inflammation reinforce each other in a damaging loop.

How does eye rubbing tie it all together?

Eye rubbing connects the mechanical and biochemical pathways into one self-perpetuating cycle. Rubbing raises corneal temperature, applies repeated pressure, and acutely increases inflammatory cytokines and MMPs at the surface. In people who are already genetically and biochemically vulnerable, this repeated insult appears to accelerate the disease.

The cycle is vicious: allergy causes itching, itching causes rubbing, rubbing spikes inflammation and enzyme activity, and weakened cornea distorts vision. Breaking the rubbing habit is one of the few prevention levers patients directly control.

Clinical Pearl: Telling a keratoconus patient "stop rubbing your eyes" is not trivial advice — it may be one of the most impactful interventions available, especially in young patients before the cornea has stiffened with age.

How is keratoconus diagnosed?

Keratoconus is diagnosed through corneal imaging that maps the shape and thickness of the cornea, often before symptoms appear. A standard glasses exam can miss early disease, so dedicated scanning is essential.

The clinical workup starts with history — progressive astigmatism, eye rubbing, allergy, family history — and a slit-lamp exam. Doctors look for classic signs such as corneal thinning, a Fleischer ring (iron deposits around the cone base), Vogt's striae (stress lines in the stroma), and in advanced cases, Munson's sign (a V-shaped bulge of the lower lid when the patient looks down).

The cornerstone of diagnosis is imaging. Corneal topography maps the front surface curvature, while corneal tomography (such as Scheimpflug-based Pentacam scanning) maps the front and back surfaces plus thickness across the whole cornea. Back-surface and thickness changes often appear earliest, which is why tomography catches subtle disease.

Differential diagnosis includes pellucid marginal degeneration, keratoglobus, post-refractive-surgery ectasia, and contact-lens-induced corneal warpage. Distinguishing these matters because treatment differs. Learn more about screening on our corneal topography and imaging page.

Key Point: Anyone considering LASIK should be screened for early keratoconus first. Operating on a subtly weak cornea can trigger rapid ectasia — a major reason tomography is standard before refractive surgery.

How is keratoconus treated conventionally?

Conventional treatment has two goals: stop progression and restore clear vision. The right approach depends on disease severity, from glasses in mild cases to corneal transplant in advanced disease.

Corneal cross-linking (CXL)

Corneal cross-linking is the only treatment proven to halt keratoconus progression. The procedure applies riboflavin (vitamin B2) drops and ultraviolet-A light to the cornea, creating new chemical bonds between collagen fibers and stiffening the tissue. The landmark Dresden protocol and later trials, including the U.S. FDA approval trials, showed CXL stabilizes or flattens the cornea in most patients.

CXL doesn't usually reverse damage already done, so it works best caught early. Its main job is to freeze the disease in place before vision is lost. Side effects can include temporary discomfort, haze, and a small risk of infection during healing.

Vision correction options

Different lenses suit different stages of keratoconus. The progression typically moves from glasses to rigid lenses to scleral lenses as the cornea becomes more irregular.

Scleral lenses vault over the cone and rest on the white of the eye, creating a smooth optical surface with a tear-fluid reservoir. They've transformed comfort and vision for many advanced patients. When scarring is severe, a corneal transplant — deep anterior lamellar keratoplasty (DALK) or full-thickness penetrating keratoplasty (PK) — replaces the damaged tissue. See our scleral lens fitting and corneal transplant pages for details.

Evidence Snapshot: A 2017 systematic review and multiple randomized trials confirm that cross-linking significantly reduces the risk of keratoconus progression compared with no treatment. It is now a standard of care for documented progressive disease in many countries.

Why does keratoconus sometimes progress despite treatment?

Keratoconus can keep advancing even after treatment because cross-linking doesn't address every driver of the disease, and some patients continue the behaviors that fuel it. Treatment stabilizes structure but doesn't switch off the underlying biology.

Several factors explain ongoing progression. Cross-linking may be incomplete in very thin corneas, where safety limits how much UV energy can be applied. Continued eye rubbing keeps spiking inflammatory cytokines and MMPs. Uncontrolled allergy maintains surface inflammation. And in younger patients, the disease is simply more aggressive because the cornea hasn't naturally stiffened with age yet.

Clinical Pearl: Progression after CXL should prompt a hard look at modifiable factors — especially rubbing and allergy control — before assuming the procedure failed. Sometimes the biology is being re-triggered daily.

This is where the inflammatory model has practical value. If inflammation and oxidative stress contribute to progression, then controlling allergy, stopping rubbing, supporting antioxidant defenses, and protecting the ocular surface become logical adjuncts to structural treatment — not replacements for it.

What emerging therapies are being studied?

Researchers are exploring treatments that target the biology of keratoconus, not just its shape, though most remain early-stage. Honest evidence labeling matters here: some approaches are promising in the lab but unproven in patients.

• Customized and accelerated cross-linking (moderate evidence): Newer CXL protocols aim to treat thinner corneas and shorten procedure time while preserving effectiveness.
• Anti-inflammatory and anti-MMP therapy (emerging): Topical agents that lower MMP activity or cytokines are under investigation as add-ons, given the inflammatory model.
• Corneal tissue addition / customized lenticules (emerging): Adding tissue to thicken and reshape the cornea is being explored in early studies.
• Gene and molecular studies (preclinical): Identifying genetic and oxidative pathways may eventually guide targeted therapy, but this is research-stage only.
• Antioxidant strategies (emerging): Because oxidative stress is implicated, supporting antioxidant defenses is being studied, though strong clinical proof is still lacking.

Research Update: The inflammatory and oxidative-stress understanding of keratoconus has shifted research toward biological adjuncts. As of now, corneal cross-linking remains the only intervention with solid evidence for halting progression; the rest are investigational.

What does integrative ophthalmology add?

Integrative approaches focus on reducing inflammation, oxidative stress, and rubbing through lifestyle and nutrition, supporting — never replacing — standard care. The rationale is mechanistic, and the evidence is still developing.

The strongest integrative lever is allergy and rubbing control. Treating allergic conjunctivitis with appropriate antihistamine or mast-cell-stabilizer drops, managing eczema and asthma, and consciously breaking the rubbing habit address documented disease drivers. This is mainstream advice grounded in the inflammatory model.

Nutrition and antioxidant support draw on the oxidative-stress findings. A diet rich in antioxidants — vegetables, fruits, omega-3 sources — and good sleep and stress management are reasonable general eye-health measures. However, no specific supplement has proven to stop keratoconus, so these should be framed as supportive, not curative.

Where does Netra Restoration Therapy fit?

Netra Restoration Therapy is positioned as a complement to standard keratoconus care, focusing on the biological terrain — inflammation, oxidative stress, and ocular surface health — rather than the corneal shape itself. It does not replace cross-linking, specialty lenses, or surgery, and it promises no specific outcome.

The proposed mechanisms align with the disease biology now described in the literature: reducing oxidative stress on corneal cells, supporting healthy inflammatory regulation at the ocular surface, encouraging better tear-film and surface health, and reinforcing the behavioral basics (rubbing avoidance, allergy control, sleep). These are framed around mechanisms, not guarantees.

Key Point: Research into the inflammatory and oxidative drivers of keratoconus is still evolving. Any integrative or restoration-focused approach should be used alongside — and never instead of — evidence-based treatment like corneal cross-linking and proper vision correction.

Patients interested in this approach should continue regular monitoring with corneal imaging so that any progression is caught and treated promptly with proven methods. Learn more on our Netra Restoration Therapy overview.

What does the clinical evidence actually show?

The evidence is strongest for cross-linking and for the presence of inflammatory and oxidative markers; it's weaker for biological add-on therapies. Here's an honest summary.

Evidence Snapshot: The biochemical inflammation in keratoconus is well-documented in laboratory studies, but whether it initiates the disease or results from mechanical injury (like rubbing) is still debated. Both likely interact.

Common myths about keratoconus

Misunderstandings about keratoconus are common and can delay care. Here are the facts behind the most frequent myths.

Frequently asked questions

Is keratoconus really an inflammatory disease?

Increasingly, yes — at least partly. The old textbook label was "non-inflammatory," but modern tear and tissue studies consistently find elevated inflammatory molecules like IL-6, TNF-α, and matrix metalloproteinases, plus signs of oxidative stress. The inflammation is low-grade and biochemical rather than visibly red and swollen, which is why it was missed for so long.

Can eye rubbing cause keratoconus?

Eye rubbing is the strongest modifiable risk factor and can both trigger and worsen keratoconus in susceptible people. Vigorous rubbing physically stresses the cornea and acutely raises inflammatory enzymes that break down collagen. If you have keratoconus or are at risk, stopping rubbing is one of the most important things you can do.

At what age does keratoconus usually start?

It typically begins around puberty and progresses through the twenties and early thirties. Progression usually slows by the mid-to-late thirties as the cornea naturally stiffens with age. Because younger patients tend to progress faster, early diagnosis and treatment are especially important in teens.

Will I go blind from keratoconus?

Total blindness from keratoconus is rare. With modern treatment — cross-linking to halt progression and specialty lenses or transplant to restore vision — most patients keep functional sight. The key is catching it early and preventing progression rather than waiting until vision is severely distorted.

Does keratoconus affect both eyes?

Almost always, though usually unequally. One eye is typically worse than the other, and the second eye may lag in severity. Even if only one eye seems affected at diagnosis, doctors monitor both because the disease is fundamentally bilateral.

What is corneal cross-linking and does it hurt?

Cross-linking is a procedure that strengthens the cornea using riboflavin drops and UV light to stiffen collagen. It's the only treatment proven to stop progression. There's usually some discomfort and light sensitivity for a few days afterward, managed with drops and sometimes a bandage contact lens, but the procedure itself is done under numbing drops.

Can keratoconus be cured?

There's no cure that reverses keratoconus, but it can be effectively managed and stopped. Cross-linking halts progression, and lenses or surgery restore vision. Think of it as a controllable chronic condition rather than something that's permanently fixed in one step.

Can I still wear contact lenses with keratoconus?

Yes — in fact, specialty contacts are a mainstay of treatment. Rigid gas permeable lenses and scleral lenses create a smooth optical surface over the irregular cornea, often giving much sharper vision than glasses. A skilled fitter is essential because the fit is more complex than for a normal eye.

Is keratoconus hereditary?

Genetics play a role, and having a family member with keratoconus raises your risk. However, most people with keratoconus have no known family history, so it's not a simple inherited trait. It results from a combination of genetic susceptibility and triggers like rubbing and allergy.

Can LASIK fix keratoconus?

No — and LASIK is generally avoided in keratoconus because it removes corneal tissue and can dangerously weaken an already thin cornea, accelerating the disease. This is why everyone is screened with corneal imaging before refractive surgery to rule out early keratoconus.

Does allergy make keratoconus worse?

Allergy is strongly linked to keratoconus, mainly because itchy eyes lead to rubbing, and allergic inflammation raises surface cytokines. Controlling allergies with appropriate drops and managing conditions like eczema and asthma is a practical way to reduce two known disease drivers at once.

What is corneal hydrops?

Hydrops is a sudden complication of advanced keratoconus where the inner membrane of the cornea splits and fluid floods the tissue, causing pain, redness, and a rapid drop in vision. It usually heals over weeks but can leave scarring. It needs prompt evaluation by an eye specialist.

How fast does keratoconus progress?

Progression varies widely. Some people change slowly over years; younger patients and those who rub their eyes or have uncontrolled allergies can progress quickly over months. Because the rate is unpredictable, regular corneal imaging is used to catch and treat progression early.

Can diet help keratoconus?

A healthy, antioxidant-rich diet supports overall eye health and may help counter the oxidative stress involved in keratoconus, but no diet or supplement has been proven to stop the disease. Diet should be seen as supportive alongside proven treatments like cross-linking, not as a substitute.

Why does my glasses prescription keep changing?

Rapidly shifting astigmatism is a classic early sign of keratoconus, especially in teens and young adults. As the cornea steepens and distorts, the refraction changes. If your prescription keeps changing significantly, ask for corneal topography to check for keratoconus.

Is scleral lens wear safe long-term?

Scleral lenses are generally safe and well-tolerated long-term when fitted and maintained properly. They vault over the cornea and rest on the white of the eye. Proper hygiene, regular follow-up, and good fitting reduce risks like infection or oxygen-related corneal stress.

Can keratoconus come back after a transplant?

Keratoconus can sometimes recur in the transplanted tissue many years later, though it's uncommon. The same drivers — especially eye rubbing — should still be controlled after surgery. Lifelong follow-up helps catch any recurrence or graft issues early.

Should my children be screened if I have keratoconus?

Yes — children of people with keratoconus benefit from screening, especially around puberty, since early disease is detectable with corneal imaging before vision changes. Catching it early allows cross-linking to halt progression before significant damage occurs.

Does keratoconus cause pain?

Usually not. Keratoconus is typically painless and shows up as blurred, distorted vision. The main exception is hydrops, the acute fluid-flooding complication of advanced disease, which can cause sudden pain, redness, and watering and needs prompt care.

Can stress or lack of sleep affect keratoconus?

Stress and poor sleep don't directly cause keratoconus, but they may raise systemic inflammation and worsen allergies and rubbing habits. Good sleep and stress management are reasonable supportive measures, and sleep posture that avoids pressing on the eye may help reduce asymmetry.

Is cross-linking suitable for everyone?

Not always. Cross-linking requires a minimum corneal thickness for safety, so very thin or heavily scarred corneas may not be candidates for the standard protocol. Your eye doctor uses corneal imaging to decide, and newer protocols are expanding who can be treated.

What's the difference between topography and tomography?

Topography maps only the front surface of the cornea, while tomography maps both front and back surfaces plus thickness across the whole cornea. Tomography catches keratoconus earlier because back-surface and thickness changes often appear before front-surface ones.

Can I exercise or play sports with keratoconus?

Yes, keratoconus doesn't limit physical activity. Just protect your eyes from injury and avoid rubbing them, even when sweaty or irritated. If you wear scleral or rigid lenses, sports goggles can help keep them secure and your eyes protected.

Will keratoconus stop on its own?

It often stabilizes naturally by the mid-to-late thirties as the cornea stiffens with age, but waiting and hoping is risky because damage done before then is permanent. If imaging shows active progression, treatment like cross-linking is recommended rather than simply waiting it out.

Glossary

• Cornea: The clear front dome of the eye that focuses light.
• Keratoconus: Progressive thinning and cone-shaped bulging of the cornea.
• Stroma: The thick collagen middle layer of the cornea.
• Astigmatism: Blurred vision from an unevenly curved cornea.
• Corneal cross-linking (CXL): Treatment using riboflavin and UV light to stiffen the cornea.
• Topography: A map of the cornea's front-surface curvature.
• Tomography: A map of front and back corneal surfaces plus thickness.
• Matrix metalloproteinases (MMPs): Enzymes that break down collagen and matrix.
• Cytokines: Signaling molecules that drive inflammation (e.g., IL-6, TNF-α).
• Oxidative stress: Cell damage from reactive oxygen molecules outpacing antioxidant defenses.
• Hydrops: Sudden corneal swelling from a break in the inner membrane.
• Scleral lens: A large rigid lens that vaults over the cornea onto the white of the eye.
• Atopy: The allergic tendency underlying asthma, eczema, and hay fever.

Summary

Keratoconus is a progressive disease where the cornea thins and bulges into a cone, distorting vision. The long-standing "non-inflammatory" label has given way to a model in which low-grade inflammation, elevated matrix metalloproteinases, and oxidative stress weaken the corneal collagen — often driven by eye rubbing and allergy in genetically susceptible people.

It usually starts in adolescence and slows by the late thirties. Diagnosis relies on corneal topography and tomography, which detect the disease early. Corneal cross-linking is the only proven way to halt progression, while specialty lenses and, in advanced cases, transplant restore vision. Controlling rubbing and allergy, supporting antioxidant defenses, and protecting the ocular surface are sensible adjuncts that fit the inflammatory model — used alongside, never instead of, proven medical care.

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Author: Netra Eye Institute Editorial Team. Medically reviewed by an ophthalmologist. Review date: June 2024. Medical Disclaimer: This article is for educational purposes only and does not replace personalized medical advice. If you have or suspect keratoconus, consult a qualified eye care professional for diagnosis and treatment tailored to your eyes.