Few studies have examined the prevalence of FCED on a large scale. First assessed in a clinical setting, Fuchs himself estimated the occurrence of dystrophia epithelialis corneae to be one in every 2000 patients; a rate that is likely reflective of those who progress to advanced disease. Cross-sectional studies suggest a relatively higher prevalence of disease in European countries relative to other areas of the world. Fuchs' dystrophy rarely affects individuals under 50 years of age.

CNV causes may be congenital in nature, such as with Aniridia, or acquired. Frequently, inflammatory, infectious, degenerative, traumatic and iatrogenic (from contact lenses) diseases are responsible for acquired CNV.

Some major associated, acquired inflammatory conditions include graft rejection following keratoplasty, graft or host diseases of the new tissue, atopic conjunctivitis, rosacea, ocular pemphigoid, Lyell's syndrome, and Steven's Johnson syndrome.

Infections responsible for CNV range from bacterial (chlamydia, syphilis, pseduomonas), Viral (herpes simplex and herpes zoster viruses), Fungal (candida, asperigillus, fusarium), and parasistic (onchocerca volvolus).

Degenerative diseases such as pterygiums, and terrien's marginal degeneration may be responsible.

Traumas frequently seen with CNV include ulceration, alkali burns, and stem cell deficiency.

One of the most common causes of corneal neovascularization is iastrogenic pathology from contact lens wear. This is especially true of lenses made with older hydrogel materials such as HEMA (2-hydroxyethyl methacrylate) for both daily and extended wear. Such older hydrogel materials have a relatively low oxygen transmissibility so the cornea becomes starved of oxygen leading to the ingress of blood capillaries into the clear cornea to satisfy that oxygen demand. Older estimates have 128,000 to 470,000 cases of lens-induced CNV each year, but this may be decreasing due to the increasing popularity of daily disposable lenses.

The risk for CNV is elevated in certain instances for patients following penetrating keratoplasty without active inflammation or epithelial defects. CNV is more likely to occur in those with active blepharitis, those who receive sutured knots in their host stromas, and those with a large recipient area.

A pinguecula is one of the differential diagnoses for a limbal nodule. It may have an increased prevalence in Gaucher's disease.

The incidence and prevalence of PMD are unknown, and no studies have yet investigated its prevalence or incidence. However, it is generally agreed that PMD is a very rare condition. Some uncertainty regarding the incidence of PMD may be attributed to its confusion with keratoconus. PMD is not linked to race or age, although most cases present early in life, between 20 and 40 years of age. While PMD is usually considered to affect men and women equally, some studies suggest that it may affect men more frequently.

Several diseases have been observed in patients with PMD. However, no causal relationships have been established between any of the associated diseases and the pathogenesis of PMD. Such diseases include: chronic open-angle glaucoma, retinitis pigmentosa, retinal lattice degeneration, scleroderma, kerato-conjunctivitis, eczema, and hyperthyroidism.

The National Eye Institute reports keratoconus is the most common corneal dystrophy in the United States, affecting about one in 2,000 Americans, but some reports place the figure as high as one in 500. The inconsistency may be due to variations in diagnostic criteria, with some cases of severe astigmatism interpreted as those of keratoconus, and" vice versa". A long-term study found a mean incidence rate of 2.0 new cases per 100,000 population per year. Some studies have suggested a higher prevalence amongst females, or that people of South Asian ethnicity are 4.4 times as likely to suffer from keratoconus as Caucasians, and are also more likely to be affected with the condition earlier.

Keratoconus is normally bilateral (affecting both eyes) although the distortion is usually asymmetric and is rarely completely identical in both corneas. Unilateral cases tend to be uncommon, and may in fact be very rare if a very mild condition in the better eye is simply below the limit of clinical detection. It is common for keratoconus to be diagnosed first in one eye and not until later in the other. As the condition then progresses in both eyes, the vision in the earlier-diagnosed eye will often remain poorer than that in its fellow.

Patients with keratoconus typically present initially with mild astigmatism and myopia, commonly at the onset of puberty, and are diagnosed by the late teenage years or early 20s. The disease can, however, present or progress at any age; in rare cases, keratoconus can present in children or not until later adulthood. A diagnosis of the disease at an early age may indicate a greater risk of severity in later life. Patients' vision will seem to fluctuate over a period of months, driving them to change lens prescriptions frequently, but as the condition worsens, contact lenses are required in the majority of cases. The course of the disorder can be quite variable, with some patients remaining stable for years or indefinitely, while others progress rapidly or experience occasional exacerbations over a long and otherwise steady course. Most commonly, keratoconus progresses for a period of 10 to 20 years before the course of the disease generally ceases in the third and fourth decades of life.

Treatment options include contact lenses and intrastromal corneal ring segments for correcting refractive errors caused by irregular corneal surface, corneal collagen cross-linking to strengthen a weak and ectatic cornea, or corneal transplant for advanced cases.

The causes of TSPK are currently not yet well known.

However, there seem to be indications that dysfunctioning of the Meibomian gland can cause the condition. Inflammation of the meibomian glands (also known as meibomitis, meibomian gland dysfunction, or posterior blepharitis) causes the glands to be obstructed by thick waxy secretions. Besides leading to dry eyes, the obstructions can be degraded by bacterial lipases, resulting in the formation of free fatty acids, which irritate the eyes and sometimes cause punctate keratopathy.

Keratoconjunctivitis sicca is relatively common within the United States, especially so in older patients. Specifically, the persons most likely to be affected by dry eyes are those aged 40 or older. 10-20% of adults experience Keratoconjunctivitis sicca. Approximately 1 to 4 million adults (age 65-84) in the USA are effected.

While persons with autoimmune diseases have a high likelihood of having dry eyes, most persons with dry eyes do not have an autoimmune disease. Instances of Sjögren syndrome and keratoconjunctivitis sicca associated with it are present much more commonly in women, with a ratio of 9:1. In addition, milder forms of keratoconjunctivitis sicca also are more common in women. This is partly because hormonal changes, such as those that occur in pregnancy, menstruation, and menopause, can decrease tear production.

In areas of the world where malnutrition is common, vitamin A deficiency is a common cause. This is rare in the United States.

Racial predilections do not exist for this disease.

Before LASIK surgery, people must be examined for possible risk factors such as keratoconus.

Abnormal corneal topography compromises of keratoconus, pellucid marginal degeneration, or forme fruste keratoconus with an I-S value of 1.4 or more is the most significant risk factor. Low age, low residual stromal bed (RSB) thickness, low preoperative corneal thickness, and high myopia are other important risk factors.

The cornea, an avascular tissue, is among the most densely innervated structures of the human body. Corneal nerves are responsible for maintaining the anatomical and functional integrity of the cornea, conveying tactile, temperature and pain sensations, playing a role in the blink reflex, in wound healing and in the production and secretion of tears.

Most corneal nerve fibres are sensory in origin and are derived from the ophthalmic branch of the trigeminal nerve. Congenital or acquired ocular and systemic diseases can determine a lesion at different levels of the trigeminal nerve, which can lead to a reduction (hypoesthesia) or loss (anesthesia) of sensitivity of the cornea.

The most common causes of loss of corneal sensitivity are viral infections (herpes simplex and herpes zoster ophthalmicus), chemical burns, physical injuries, corneal surgery, neurosurgery, chronic use of topical medications, or chronic use of contact lenses.

Possible causes also include systemic diseases such as diabetes, multiple sclerosis or leprosy.

Other, albeit less frequent, potential causes of the disease are: intracranial space-occupying lesions such as neuroma, meningioma and aneurysms, which may compress the trigeminal nerve and reduce corneal sensitivity.

Conversely, congenital conditions that may lead to this disorder are very rare.

Recurrence within a few years occurs in all patients following corneal transplantation. Soft contact lenses are effective in decreasing recurrences.

Given that episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches to be taken to help prevent episodes include:

- Environmental:

- ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.

- use of protective glasses especially when gardening or playing with children.

- General personal measures:

- maintaining general hydration levels with adequate fluid intake.

- not sleeping-in late as the cornea tends to dry out the longer the eyelids are closed.

- Pre-bed routine:

- routine use of long-lasting eye ointments applied before going to bed.

- occasional use of the anti-inflammatory eyedrop FML (prescribed by an ophthalmologist or optometrist) before going to bed if the affected eye feels inflamed, dry or gritty

- use of a hyperosmotic (hypertonic) ointment before bed reduces the amount of water in the epithelium, strengthening its structure

- use the pressure patch as mentioned above.

- use surgical tape to keep the eye closed (if Nocturnal Lagophthalmos is a factor)

- Waking options:

- learn to wake with eyes closed and still and keeping artificial tear drops within reach so that they may be squirted under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.

- It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fingers, before trying to open them, or keeping the affected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.

Visual function declines as a result of the irregular corneal shape, resulting in astigmatism, and causing a distortion in vision. Deterioration can become severe over time.

Keratoconjunctivitis sicca is uncommon in cats. Most cases seem to be caused by chronic conjunctivitis, especially secondary to feline herpesvirus. Diagnosis, symptoms, and treatment are similar to those for dogs.

Lattice corneal dystrophy type, also known as Biber-Haab-Dimmer dystrophy, is a rare form of corneal dystrophy. It has no systemic manifestations, unlike the other type of the dystrophy, Lattice corneal dystrophy type II. Lattice corneal dystrophy was first described by Swiss ophthalmologist Hugo Biber in 1890.

Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma.

Xerophthalmia usually affects children under nine years old and "accounts for 20,000-100,000 new cases of childhood blindness each year in the developing countries." The disease is largely found in developing countries like many of those in Africa and Southern Asia. The condition is not congenital and develops over the course of a few months as the lacrimal glands fail to produce tears. Other conditions involved in the progression already stated include the appearance of Bitot's spots, which are clumps of keratin debris that build up inside the conjunctiva and night blindness, which precedes corneal ulceration and total blindness.

Corneal ectatic disorders or corneal ectasia are a group of uncommon, noninflammatory, eye disorders characterised by bilateral thinning of the central, paracentral, or peripheral cornea.

- Keratoconus, a progressive, noninflammatory, bilateral, asymmetric disease, characterized by paraxial stromal thinning and weakening that leads to corneal surface distortion.

- Keratoglobus, a rare noninflammatory corneal thinning disorder, characterised by generalised thinning and globular protrusion of the cornea.

- Pellucid marginal degeneration, a bilateral, noninflammatory disorder, characterized by a peripheral band of thinning of the inferior cornea.

- Posterior keratoconus, a rare condition, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia, a complication of LASIK eye surgery.

- Terrien's marginal degeneration, a painless, noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.

Some infections may scar the cornea to limit vision. Others may result in perforation of the cornea, (an infection inside the eye), or even loss of the eye. With proper medical attention, infections can usually be successfully treated without long-term visual loss.

It is a much rarer condition than keratoconus, which is the most common of the cornea. Similar to keratoconus it is typically diagnosed in the patient's adolescent years and attains its most severe state in the twenties and thirties.

Treatment options include contact lenses, intrastromal corneal ring segments, corneal collagen cross-linking, or corneal transplant.

When cross-linking is performed only after the cornea becomes distorted, vision remains blurry even though the disease is stabilised. As a result, combining corneal collagen cross-linking with LASIK ('LASIK Xtra') aims to strengthen the cornea at the point of surgery and may be useful in cases where a very thin cornea is expected after the LASIK procedure. This would include cases of high spectacle power and people with thin corneas before surgery. Definitive evidence that the procedure can reduce the risk of corneal ectasia will only become available a number of years later as corneal ectasia, if it happens, usually occurs in the late post-operative period. Some study show that combining LASIK with cross-linking adds refractive stability to hyperopic treatments and may also do the same for very high myopic treatments.

In 2016, the FDA approved the KXL system and two photoenhancers for the treatment of corneal ectasia following refractive surgery.

Corneal perforation is an anomaly in the cornea resulting from damage to the corneal surface. A corneal perforation means that the cornea has been penetrated, thus leaving the cornea damaged.

The cornea is a clear part of the eye which controls and focuses the entry of light into the eye. Damage to the cornea due to corneal perforation can cause decreased visual acuity.

Corneal abrasions are generally a result of trauma to the surface of the eye. Common causes include being poked by a finger, walking into a tree branch, and wearing old contact lenses. A foreign body in the eye may also cause a scratch if the eye is rubbed.

Injuries can also be incurred by "hard" or "soft" contact lenses that have been left in too long. Damage may result when the lenses are removed, rather than when the lens is still in contact with the eye. In addition, if the cornea becomes excessively dry, it may become more brittle and easily damaged by movement across the surface. Soft contact lens wear overnight has been extensively linked to gram negative keratitis (infection of the cornea) particularly by a bacterium known as "Pseudomonas aeruginosa" which forms in the eye's biofilm as a result of extended soft contact lens wear. When a corneal abrasion occurs either from the contact lens itself or another source, the injured cornea is much more susceptible to this type of bacterial infection than a non-contact lens user's would be. This is an optical emergency as it is sight (in some cases eye) threatening. Contact lens wearers who present with corneal abrasions should never be pressure patched because it has been shown through clinical studies that patching creates a warm, moist dark environment that can cause the cornea to become infected or cause an existing infection to be greatly accelerated on its destructive path.

Corneal abrasions are also a common and recurrent feature in people who suffer specific types of corneal dystrophy, such as lattice corneal dystrophy. Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. In some people, these abnormal protein fibers can accumulate under the cornea's outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions: (1) Alter the cornea's normal curvature, resulting in temporary vision problems; and (2) Expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful.

Boehm Syndrome defines erosion events that occur only during periods of sleep.

Keratopathy is common in older people. Keratopathy occurs after cataract surgery, its incidence has decreased since the advent of intraoperative viscoelastic agents that protect the endothelium.

Thygeson's superficial punctate keratopathy (TSPK; also "Thygeson Superficial Punctate Keratitis") is a disease of the eyes. The causes of TSPK are not currently known, but details of the disease were first published in the Journal of the American Medical Association in 1950 by the renowned American Ophthalmologist, Phillips Thygeson (1903–2002) - after whom it is named.