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Corneal Epithelial Autograft for LSCD

2017-07-17 09:53:52 | BioPortfolio

Summary

The purpose of the study is to explore whether femtosecond laser-assisted corneal epithelial autograft is more effective than limbal conjunctival autograft for ocular surface reconstruction in patients with limbal stem cell deficiency (LSCD).

Study Design

Conditions

Limbal Stem Cell Deficiency

Intervention

Corneal epithelial autograft, Limbal conjunctival autograft

Status

Not yet recruiting

Source

Sun Yat-sen University

Results (where available)

View Results

Links

Published on BioPortfolio: 2017-07-17T09:53:52-0400

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PubMed Articles [6079 Associated PubMed Articles listed on BioPortfolio]

Combined Conjunctival Limbal Autografts and Living-Related Conjunctival Limbal Allografts for Severe Unilateral Ocular Surface Failure.

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Optimizing the role of limbal explant size and source in determining the outcomes of limbal transplantation: An in vitro study.

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Medical and Biotech [MESH] Definitions

Corneal and conjunctival dryness due to deficient tear production, predominantly in menopausal and post-menopausal women. Filamentary keratitis or erosion of the conjunctival and corneal epithelium may be caused by these disorders. Sensation of the presence of a foreign body in the eye and burning of the eyes may occur.

Fixation of the ANTERIOR CRUCIATE LIGAMENT, during surgical reconstruction, by the use of a bone- patellar tendon autograft.

A type I keratin that is found associated with the KERATIN-3 in the CORNEA and is regarded as a marker for corneal-type epithelial differentiation. Mutations in the gene for keratin-12 have been associated with MEESMANN CORNEAL EPITHELIAL DYSTROPHY.

A type II keratin that is found associated with the KERATIN-12 in the CORNEA and is regarded as a marker for corneal-type epithelial differentiation. Mutations in the gene for keratin-3 have been associated with MEESMANN CORNEAL EPITHELIAL DYSTROPHY.

An autosomal dominant form of hereditary corneal dystrophy due to a defect in cornea-specific KERATIN formation. Mutations in the genes that encode KERATIN-3 and KERATIN-12 have been linked to this disorder.

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