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.

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.

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

FCED is a degenerative disease of the corneal endothelium with accumulation of focal outgrowths called guttae (drops) and thickening of Descemet's membrane, leading to corneal edema and loss of vision. The corneal endothelial cell layer and its basement membrane (Descemet's membrane) acts as a barrier to hydration of the corneal stroma by aqueous humor and are "pump" cells of the cornea that function to maintain hydration of the cornea at a specific level that maintains corneal stromal clarity through precise spatial arrangement of collagen fibers. In FED, Descemet's membrane is grossly thickened with accumulation of abnormal wide-spaced collagen and numerous guttae. Corneal endothelial cells in end-stage FED are reduced in number and appear attenuated, causing progressive stromal edema (swelling). Progressive endothelial cell loss causes relative influx of aqueous humor into the cornea, leading to swelling (corneal stromal edema), which results in blurred vision. Eventually, the epithelium also becomes edematous, resulting in more severe visual impairment. Focal blisters of epithelial edema ("bullae") may be particularly painful when they burst.

The inheritance of FCED is complex and polymorphic such that although inheritance is autosomal dominant there are genetic and environmental modifiers that determine the degree to which member of the same family express the disease. There is reasonable evidence of associations between transcription factor 4 (TCF4) genetic polymorphisms and risk of Fuchs' endothelial dystrophy (FED). Endothelial cell loss may be aggravated or accelerated by intraocular trauma or surgery. A common scenario involves prolonged corneal swelling or edema following cataract surgery or other types of ocular surgery. Hence, patients with a history of Fuchs' dystrophy may be at a greater risk of corneal edema after ocular surgery as they have fewer functioning endothelial cells.

FCED is classified into 4 stages, from early signs of guttae formation to end-stage subepithelial scarring. Diagnosis is made by biomicroscopic examination in the clinic. Other modalities, such as corneal thickness measurement (pachymetry), in-vivo confocal biomicroscopy, and specular microscopy can be used in conjunction.

Exact pathogenesis is unknown but factors include endothelial cell apoptosis, sex hormones, inflammation, and aqueous humor flow and composition. Mutations in collagen VIII, a major component of Descemet's membrane secreted by endothelial cells, have been linked to the early-onset FCED.

Genes include:

Reis-Bücklers corneal dystrophy is not associated with any systemic conditions.

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.

A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals.

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.

Corneal dystrophy is a group of rare hereditary disorders characterised by bilateral abnormal deposition of substances in the transparent front part of the eye called the cornea.

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.

A number of mutations causing this disease have been described in the M1S1 (TACSTD2) gene encoding "Tumor-associated calcium signal transducer 2", but not all patients have these mutations, suggesting involvement of other genes.

Several other corneal ectatic disorders also cause thinning of the cornea:

- Keratoglobus is a very rare condition that causes corneal thinning primarily at the margins, resulting in a spherical, slightly enlarged eye. It may be genetically related to keratoconus.

- Pellucid marginal degeneration causes thinning of a narrow (1–2 mm) band of the cornea, usually along the inferior corneal margin. It causes irregular astigmatism that, in the early stages of the disease can be corrected by spectacles. Differential diagnosis may be made by slit-lamp examination.

- Posterior keratoconus, a distinct disorder despite its similar name, is a rare abnormality, 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 is a complication of LASIK eye surgery.

The disease has been associated with mutations in TGFBI gene on chromosome 5q which encodes for keratoepithelin. The inheritance is autosomal dominant.

Posterior Polymorphous Corneal Dystrophy (PPCD; sometimes also "Schlichting dystrophy") is a type of corneal dystrophy, characterised by changes in Descemet's membrane and endothelial layer. Symptoms mainly consist of decreased vision due to corneal edema. In some cases they are present from birth, other patients are asymptomatic. Histopathological analysis shows that the cells of endothelium have some characteristics of epithelial cells and have become multilayered. The disease was first described in 1916 by Koeppe as "keratitis bullosa interna".

PPCD type 2 is linked to the mutations in COL8A2, and PPCD type 3 mutations in ZEB1 gene, but the underlying genetic disturbance in PPCD type 1 is unknown.

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.

Lattice corneal dystrophy has two types:

- type I: with no systemic association. It is caused by mutations in TGFBI gene encoding keratoepithelin, which maps to chromosome 5q.

- type II or Finnish type amyloidosis: associated with manifestations of systemic amyloidosis due to accumulation of gelsolin. Associated conditions may include cutis laxa and ataxia.

- type III is also described which has an onset at age 70 to 90 years and is not associated with systemic amyloidosis.

Epithelial basement membrane dystrophy (EBMD), also known as map-dot-fingerprint dystrophy and Cogans's microcystic dystrophy, is a disorder of the eye that can cause pain and dryness.

It is sometimes included in the group of corneal dystrophies. It diverges from the formal definition of corneal dystrophy in being in most cases non-familial. It also has a fluctuating course, while for a typical corneal dystrophy the course is progressive. When it is considered part of this group, it is the most common type of corneal dystrophy.

Phototherapeutic keratectomy (PTK) done by an ophthalmologist can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies including EBMD.

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.

Granular corneal dystrophy is a slowly progressive corneal dystrophy that most often begins in early childhood.

Granular corneal dystrophy has two types:

- Granular corneal dystrophy type I , also corneal dystrophy Groenouw type I, is a rare form of human corneal dystrophy. It was first described by German ophthalmologist Arthur Groenouw in 1890.

- Granular corneal dystrophy type II, also called Avellino corneal dystrophy or combined granular-lattice corneal dystrophy is also a rare form of corneal dystrophy. The disorder was first described by Folberg et al. in 1988. The name Avellino corneal dystrophy comes from the first four patients in the original study each tracing their family origin to the Italian province of Avellino.

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.

Familial transmission is now recognized in a small proportion of people with MacTel type 2; however, the nature of any related genetic defect or defects remains elusive. The MacTel genetic study team hopes that exome analysis in the affected population and relatives may be more successful in identifying related variants.

"Best disease" is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person has one parent with the condition.

The inheritance pattern of adult-onset vitelliform macular dystrophy is definitively autosomal dominant. Many affected people, however, have no history of the disorder in their family and only a small number of affected families have been reported. This is because the penetrance of the condition is incomplete; therefore, it is possible for an individual to have a copy of the mutant allele and not display the VMD phenotype. The ratio of males to females is approximately 1:1.

Vacuoles are demonstrated in the posterior parts of the cornea. The vesicles are located on the endothelial surface. The corneal endothelium is normally a single layer of cells that lose their mitotic potential after development is complete. In posterior polymorphous corneal dystrophy, the endothelium is often multilayered and has several other characteristics of an epithelium, including the presence of desmosomes, tonofilaments, and microvilli. These abnormal cells retain their ability to divide and extend onto the trabecular meshwork to cause glaucoma in up to 40% of cases.

A cone dystrophy is an inherited ocular disorder characterized by the loss of cone cells, the photoreceptors responsible for both central and color vision.