Glaucoma-associated corneal endothelial cell damage: A review

Janson, Ben; Alward, Wallace L.M.; Kwon, Young H.; Bettis, Daniel I.; Fingert, John H.; Provencher, Lorraine M.; Goins, Kenneth M.; Wagoner, Michael D.; Greiner, Mark A.

doi:10.1016/j.survophthal.2017.11.002

Cited by 92 publications

(88 citation statements)

References 47 publications

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“…The material interaction of stainless steel with the corneal endothelium may also impact the extent of cell loss (and the critical contact pressure for maintenance of CEC viability) such that different results may be expected in fluid-mediated loading of the endothelium. Nevertheless, our finding that the critical contact pressure for CEC death due to indentation was 5.7 kPa (~43 mmHg) is consistent with decreased ECD measurements after documented episodes of IOP levels greater than 40 mmHg (such as those recorded in patients with primary angle closure glaucoma) (Janson et al, 2017; Olsen, 1980; Sihota et al, 2003; Tham et al, 2006). Whether hydrostatic fluid pressure (i.e., IOP) above 43 mmHg can cause CEC loss will be the topic of future investigations.…”

Section: Discussionsupporting

confidence: 86%

Vulnerability of corneal endothelial cells to mechanical trauma from indentation forces assessed using contact mechanics and fluorescence microscopy

Ramirez-Garcia

Khalifa

Buckley

2018

Experimental Eye Research

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Corneal endothelial cell (CEC) loss occurs from tissue manipulation during anterior segment surgery and corneal transplantation as well as from contact with synthetic materials like intraocular lenses and tube shunts. While several studies have quantified CEC loss for specific surgical steps, the vulnerability of CECs to isolated, controllable and measurable mechanical forces has not been assessed previously. The purpose of this study was to develop an experimental testing platform where the susceptibility of CECs to controlled mechanical trauma could be measured. The corneal endothelial surfaces of freshly dissected porcine corneas were subjected to a range of indentation forces via a spherical stainless steel bead. A cell viability assay in combination with high-resolution fluorescence microscopy was used to visualize and quantify injured/dead CEC densities before and after mechanical loading. In specimens subjected to an indentation force of 9 mN, the mean ± SD peak contact pressure P was 18.64 ± 3.59 kPa (139.81 ± 26.93 mmHg) in the center of indentation and decreased radially outward. Injured/dead CEC densities were significantly greater (p ≤ 0.001) after mechanical indentation of 9 mN (167 ± 97 cells/mm) compared to before indentation (39 ± 52 cells/mm) and compared to the sham group (34 ± 31 cells/mm). In specimens subjected to "contact only" - defined as an applied indentation force of 0.65 mN - the peak contact pressure P was 7.31 ± 1.5 kPa (54.83 ± 11.25 mmHg). In regions where the contact pressures was below 78% of P (<5.7 kPa or 42.75 mmHg), injured/dead CEC densities were within the range of CEC loss observed in the sham group, suggesting negligible cell death. These findings indicate that CECs are highly susceptible to mechanical trauma via indentation, supporting the established "no-touch" policy for ophthalmological procedures. While CECs can potentially remain viable below contact pressures of 5.7 kPa (42.75 mmHg), this low threshold suggests that prevention of indentation-associated CEC loss may be challenging.

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Section: Discussionsupporting

confidence: 86%

Vulnerability of corneal endothelial cells to mechanical trauma from indentation forces assessed using contact mechanics and fluorescence microscopy

Ramirez-Garcia

Khalifa

Buckley

2018

Experimental Eye Research

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“…18 Glaucoma and its treatment (medical and surgical) have deleterious effects on the corneal endothelium and can reduce the survival of corneal grafts. 19 , 20 …”

Section: Etiologiesmentioning

confidence: 99%

Corneal endothelial cell dysfunction: etiologies and management

Feizi

2018

Ophthalmol Eye Dis

118

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A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.

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“…Besides the neuroprotective effect of nicergoline there is a recent study that reported nicergoline among the drugs that are able to exert corneal protective action, improving corneal endothelial cells survival rate in increased oxidative stress conditions (29). The relationship between chronic glaucoma and corneal endothelial cells damage are still incomplete understood, but one of the theory is related to oxidative stress augmentation (30,31,32). By targeting the oxidative stress reduction and increasing the anti-oxidant capacity of plasma nicergoline can contribute as a therapy against optic nerve degeneration associated with chronic glaucoma.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress/antioxidant balance implication in reducing of intra-ocular pressure in patients with stroke, nicergoline therapy and open-angle glaucoma

Bulboacă

Nicula

Bulboacă

et al. 2019

BALNEO

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Background: The continue efforts for long term reducing of intraocular pressure (IOP) in patients with open angle glaucoma, focused the attention on those patients who received different therapies, other that topical drugs for IOP reduction, that can influence this parameter.. The aim of this study was to evaluate the IOP, total oxidative stress and anti-oxidant capacity of plasma before and after nicergoline therapy in patients with ischemic stroke and associated open angle glaucoma. Material and method: a group of 35 patients with ischemic stroke and chronic open angle glaucoma (under topical beta-blockers therapy) was studied regarding the values of IOP, total oxidative stress (TOS) and total antioxidant capacity (TAC) before (T1) and after 6 month (T2) of nicergoline therapy. Results: IOP values for both eyes were significantly reduced when the values of T1 examination were compared with those of T2 assessment. The total oxidative stress parameter was also significantly reduced after nicergoline therapy together with increasing of total antioxidant capacity of plasma. Conclusions: besides its positive effects on neuronal metabolism for ischemic stroke patients, nicergoline is able to influence the IOP in patients with open angle glaucoma and to improve the plasmatic oxidative stress/antioxidant balance. By this mechanism nicergoiline can contribute to a neuroprotection and better visual function preservation for these patients, improving their chances to neuro-motor rehabilitation and their quality of life.

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Glaucoma-associated corneal endothelial cell damage: A review

Cited by 92 publications

References 47 publications

Vulnerability of corneal endothelial cells to mechanical trauma from indentation forces assessed using contact mechanics and fluorescence microscopy

Vulnerability of corneal endothelial cells to mechanical trauma from indentation forces assessed using contact mechanics and fluorescence microscopy

Corneal endothelial cell dysfunction: etiologies and management

Oxidative stress/antioxidant balance implication in reducing of intra-ocular pressure in patients with stroke, nicergoline therapy and open-angle glaucoma

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