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Comparative Anatomy and Physiology of the Mammalian Eye
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
The mammalian cornea is a transparent, avascular structure that functions to transmit and refract light, and as a protective barrier for the internal ocular contents. In general, the cornea of various species is remarkably similar, differing in thickness, curvature, and shape only. The cornea is thickest peripherally and its thickness increases during sleep.2 The histologic layers of the cornea, from the outside in, are the epithelium, stroma, Descemet’s membrane, and endothelium (Figure 2). In addition in humans, primates, and cattle a layer beneath the epithelium, Bowman’s layer, is present under light microscopy, but disappears under electron microscopy.2,3
Therapeutic Approach in Fungal Keratitis
Published in Mahendra Rai, Marcelo Luís Occhiutto, Mycotic Keratitis, 2019
Victoria Díaz-Tome, María Teresa-Rodríguez Ares, Rubén Varela-Fernández, Rosario Touriño-Peralba, Miguel González-Barcia, Laura Martínez-Pérez, María Jesús Lamas, Francisco J. Otero-Espinar, Anxo Fernández-Ferreiro
The type of surgical intervention depends on the microorganism, location and affected area by the keratitis. When the infection is limited to the corneal surface, lamellar keratoplasty may be performed to eliminate lesions. Deep Anterior Lamellar Keratoplasty (DALK) eliminates all the corneal stroma to Descemet’s membrane and does not penetrate the anterior chamber, minimizing the risk of endothelial rejection (Sabatino et al. 2017).
Collagens of the Disc
Published in Peter Ghosh, The Biology of the Intervertebral Disc, 2019
This protein, originally identified as a product of bovine aortic endothelial cells25 and rabbit corneal endothelial cells26 in culture, is a structural component of Descemet’s membrane27 and perhaps of other endothelial basal laminae. Recent data point to a molecule consisting of a triple-helix that is about half the length of that in types I, II, and III collagens.7
Rho-kinase inhibitors: Role in corneal endothelial disorders
Published in Seminars in Ophthalmology, 2023
Nimish Kumar Singh, Srikant Kumar Sahu
Corneal endothelium which is present on the inner surface of cornea plays a major role in maintaining corneal transparency through the endothelial pump mechanism. The endothelial cells do not have regenerative capacity and any loss in their number is compensated by migration of adjoining cells thereby decreasing their average density. Normal adult endothelial density ranges from 2000 to 2500 cells/mm.2 Decrease in endothelial density below 500–1000 cells/mm,2 due to various reasons, results in corneal edema and decompensation.4 Currently, posterior lamellar keratoplasties like Descemet stripping Endothelial Keratoplasty (DSEK) and Descemet Membrane Endothelial Keratoplasty (DMEK) are the only treatment options available for endothelial decompensation. Scarcity of appropriate donor cornea, perpetual risk of rejection, infection and side-effects of long-term corticosteroid use pose considerable hindrance in making these modalities available for all despite their high success rate.4 In such a scenario, the possible role of rho-kinase (ROCK) inhibitors in the treatment of endothelial disease can be a major breakthrough for restoring corneal transparency in such cases.
Graft Size and Double Scroll Formation Rate in Descemet Membrane Endothelial Keratoplasty
Published in Current Eye Research, 2022
Hiroshi Matsumae, Takefumi Yamaguchi, Yuki Kusano, Shigeto Shimmura, Akira Kobayashi, Yuki Morizane, Jun Shimazaki
Descemet membrane endothelial keratoplasty (DMEK) is currently the standard surgical procedure for bullous keratopathy and Fuchs endothelial corneal dystrophy (FECD) owing to less irregular astigmatism in the posterior corneal surface, faster visual recovery, less graft rejection, and superior overall visual outcomes compared to penetrating keratoplasty and Descemet stripping automated endothelial keratoplasty.1–3 However, DMEK surgery is technically challenging and requires experience in graft preparation, donor insertion, and graft unfolding. To overcome these issues, Fogla et al.4 developed a novel surgical technique of intentional double scroll formation of donor Descemet membrane (DM) within a glass tube inserter for donor insertion and unfolding in DMEK (hereafter referred to as the Fogla technique), which allows controlled delivery of donor DM scroll into the anterior chamber (AC) and assists in maintaining its correct orientation for atraumatic unfolding using minimal donor manipulation. After adopting this technique in our DMEK procedure, we noted that while some of the donor DMs easily formed a double scroll configuration, some did not. In the current study, we evaluated the success rate and usefulness of the Fogla technique in the DMEK procedure. Moreover, the association of the DM graft characteristics and the tendency to form a double scroll configuration within a glass tube and unfolding time was evaluated comparing single and double scroll configurations in both clinical setings and ex vivo experiments.
Endothelial Cell Viability after DMEK Graft Preparation
Published in Current Eye Research, 2021
Alina Miron, Anita Sajet, Esther A. Groeneveld–van Beek, Jet S. Kok, Mehtap Dedeci, Maloeke de Jong, Vicky Amo-Addae, Gerrit R. J. Melles, Silke Oellerich, Jacqueline van der Wees
Descemet membrane endothelial keratoplasty (DMEK) is an increasingly popular treatment option for patients with corneal endothelial dysfunction, optimizing visual outcomes, recovery time, and rejection risk relative to previous generation of corneal transplantation, such as penetrating keratoplasty (PK) and Descemet stripping (automated) endothelial keratoplasty (DSAEK). Typical endothelial cell loss rates within the first 6 months after DMEK are reported to be 25–40%, followed by a slower decrease thereafter.1–5 The majority of the observed cell loss after DMEK, however, actually occurs within the first week after DMEK.6 At the same time, it was shown that endothelial cell loss after DMEK showed a high degree of variability between patients. Several studies tried to identify donor, recipient and surgery-related risk factors for endothelial cell loss after DMEK, with no consistent results so far.5,7–10