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PubMed · 2648555

[Corneal graft].

Abstract

As an architectonic, transparent and dioptric structure, the cornea plays an important role in the anatomy and physiology of the eye. Corneal grafting consists of replacing an irreversibly damaged cornea by a healthy cornea taken from a donor. Lamellar and transfixiant keratoplasty techniques are now well codified in their modus operandi and their indications. The marvellous and dramatic results achieved in some types of corneal lesions, such as keratoconus, stand in sharp contrast with the still mediocre results obtained in other lesions. Technical, surgical and above all biological research is therefore needed to improve our knowledge of rejection mechanisms and surgical failures.

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BibTeXRIS

L Durand, M F Dalmas. 1989-01-26. [Corneal graft].. https://pubmed.ncbi.nlm.nih.gov/2648555/

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The lattice corneal dystrophies (LCD) and granular corneal dystrophies (GCD) are autosomal dominant disorders of the corneal stroma. They are bilateral, progressive conditions characterized by the formation of opacities arising due to the deposition of insoluble material in the corneal stroma leading to visual impairment. The LCDs and GCDs are distinguished from each other and are divided into subtypes on the basis of the clinical appearance of the opacities, clinical features of the disease, and on histopathological staining properties of the deposits. The GCDs and most types of LCD arise from mutations in the transforming growth factor beta-induced (TGFBI) gene on chromosome 5q31. Over 30 mutations causing LCD and GCD have been identified so far in the TGFBI. There are two mutation hotspots corresponding to arginine residues at positions 124 and 555 of the transforming growth factor beta induced protein (TGFBIp) and they are the most frequent sites of mutation in various populations. Mutations at either of these two hotspots result in specific types of LCD or GCD. The majority of identified mutations involve residues in the fourth fasciclin-like domain of TGFBIp.

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