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It involves excising a damaged section of cornea, and replacing it with a section (or "flap") of the patient's own conjunctiva. [ 1 ] It is named for Trygve Gundersen (1902 – February 24, 1987), an American ophthalmologist of Scandinavian descent, who first described the procedure in 1958 at the Massachusetts Eye and Ear Infirmary .
BCEM, also referred to as conjunctival hypermelanosis, complexion-associated melanosis, or racial melanosis, is a non-cancerous lesion of the conjunctiva that is more commonly found in dark-skinned individuals (over 90% of lesions are found in black persons and around 5% in white persons). [1]
Corneal opacification is a term used when the human cornea loses its transparency. The term corneal opacity is used particularly for the loss of transparency of cornea due to scarring. Transparency of the cornea is dependent on the uniform diameter and the regular spacing and arrangement of the collagen fibrils within the stroma.
Anterior segment mesenchymal dysgenesis, or simply anterior segment dysgenesis, is a failure of the normal development of the tissues of the anterior segment of the eye. It leads to anomalies in the structure of the mature anterior segment, associated with an increased risk of glaucoma and corneal opacity .
The anterior corneal epithelium also becomes fragile. This usually affects both eyes rather than a single eye and worsens over time. There are two phenotypes, Meesmann corneal dystrophy 1 (MECD1) and Meesmann corneal dystrophy 2 (MECD2), which affect the genes KRT3 and KRT12, respectively. A heterozygous mutation in either of these genes will ...
Corneal opacities (scarring of the cornea that creates an opaque or semi-transparent area on the eye) may be caused by leucoma, keratitis or cataracts. [1] Such opacities can be cosmetically disruptive for patients in their everyday lives. Tattooing the cornea can alter a discoloration, blending an opacity into the normal eye color.
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. [1] Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma.
These burns cause a ring of constriction on the peripheral cornea causing the cornea to steepen making the eye focus better at near. This procedure may regress somewhat over time. It is similar to the conductive keratoplasty (CK) procedure where a micro-needle high frequency probe is used to make a ring of corneal burns in a similar fashion.