Fuchs Endothelial Corneal Dystrophy

Elhalis, Hussain; Azizi, Behrooz; Jurkunas, Ula V.

doi:10.1016/s1542-0124(12)70232-x

Cited by 185 publications

(197 citation statements)

References 88 publications

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“…the above equation implies that any increase in permeability, described by L i , that is not balanced with a compensatory increase in ionic pump function, described by J ai , will result in stromal swelling and eventually clinical oedema [54]. The permeability and pumping rates have been estimated via transient swelling experiments [55,56], but these are not relevant for equilibrium conditions.…”

Section: Model Calibration From Imbibition Pressurementioning

confidence: 99%

A structural model for thein vivohuman cornea including collagen-swelling interaction

Cheng

Petsche

Pinsky

2015

J. R. Soc. Interface.

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A structural model of the in vivo cornea, which accounts for tissue swelling behaviour, for the three-dimensional organization of stromal fibres and for collagen-swelling interaction, is proposed. Modelled as a binary electrolyte gel in thermodynamic equilibrium, the stromal electrostatic free energy is based on the mean-field approximation. To account for active endothelial ionic transport in the in vivo cornea, which modulates osmotic pressure and hydration, stromal mobile ions are shown to satisfy a modified Boltzmann distribution. The elasticity of the stromal collagen network is modelled based on three-dimensional collagen orientation probability distributions for every point in the stroma obtained by synthesizing X-ray diffraction data for azimuthal angle distributions and second harmonicgenerated image processing for inclination angle distributions. The model is implemented in a finite-element framework and employed to predict free and confined swelling of stroma in an ionic bath. For the in vivo cornea, the model is used to predict corneal swelling due to increasing intraocular pressure (IOP) and is adapted to model swelling in Fuchs' corneal dystrophy. The biomechanical response of the in vivo cornea to a typical LASIK surgery for myopia is analysed, including tissue fluid pressure and swelling responses. The model provides a new interpretation of the corneal active hydration control (pump-leak) mechanism based on osmotic pressure modulation. The results also illustrate the structural necessity of fibre inclination in stabilizing the corneal refractive surface with respect to changes in tissue hydration and IOP.

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Section: Model Calibration From Imbibition Pressurementioning

confidence: 99%

A structural model for thein vivohuman cornea including collagen-swelling interaction

Cheng

Petsche

Pinsky

2015

J. R. Soc. Interface.

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“…Although not much is known about the pathological mechanism behind FECD, it is suspected that genetic mutations and environmental factors, and possibly their interactions, 11,12 lie at the root of the disease. When we take a look at what is currently known about the genetic background of FECD, mutated genes have only been found in inherited cases and some sporadic cases.…”

Section: Pathophysiology Of Fecdmentioning

confidence: 99%

“…This idea is based on recent clinical observations showing the important role of the 'dystrophic' host endothelium in corneal clearance after endothelial keratoplasty, [8][9][10] and current knowledge regarding the pathophysiology of FECD. 11,12 More detailed knowledge of FECD etiology might even open the door to the development of new, less invasive treatment modalities, and have far reaching consequences for patients, corneal surgeons, and eye banks. Clinical observations after Descemet membrane endothelial keratoplasty suggesting a role for the 'dystrophic' recipient endothelium in corneal clearance Corneal endothelial cells are considered to be 'dystrophic' and have limited to no regenerative capacity in vivo.…”

Section: Introductionmentioning

confidence: 99%

What does the future hold for the treatment of Fuchs endothelial dystrophy; will ‘keratoplasty’ still be a valid procedure?

Bruinsma

Tong

Melles

2013

Eye

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Fuchs endothelial corneal dystrophy (FECD) is a well recognized corneal disorder characterized by the presence of collagenous warts extending from Descemet membrane (guttae) and endothelial cellular dysfunction due to cell loss and/or degeneration. Because of the characteristic abnormal cell morphology as seen with specular microscopy as well as the limited regenerative capacity in vivo, the endothelial cells were considered to be 'dystrophic'. Hence, FECD is commonly managed by replacement of the endothelium with donor tissue by means of a penetrating or endothelial keratoplasty. The latter procedure has now been refined to the isolated transplantation of a donor Descemet membrane and its endothelium, referred to as Descemet membrane endothelial keratoplasty (DMEK). Unexpectedly, clinical observation made after DMEK seemed to challenge the current concept of the state of the endothelium in FECD; we actually observed an important role for the 'dystrophic' host endothelium in reendothelialization of the denuded DM, and subsequent corneal clearance. In addition, recent studies regarding the pathophysiology of FECD made us realize that the endothelial cells are not 'dystrophic' per se, but in the course of time may have acquired a dysfunction instead. This paper describes the rationale behind this new concept and based on this, discusses the possibilities for future, less invasive treatment modalities for FECD.

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“…This work focuses on late-onset FECD, which is the most common variant and affects approximately 4% of the population over the age of 40 in the United States [1]. FECD is the second most common indication for corneal transplantation performed in the elderly [2]. The prevalence of FECD and the need for donor corneas are expected to rise with aging of the population [3], hence the importance to identify molecular targets for drug therapy.…”

Section: Introductionmentioning

confidence: 99%

“…The prevalence of FECD and the need for donor corneas are expected to rise with aging of the population [3], hence the importance to identify molecular targets for drug therapy. So far, many factors have been found to contribute to the pathophysiology of FECD [4], such as oxidative stress [2], but a unifying theory and tangible drug targets are lacking.…”

Section: Introductionmentioning

confidence: 99%

Automated detection and classification of nuclei in immunohistochemical stainings for Fuchs' endothelial corneal dystrophy

Janssens

Roo

Foets

et al. 2014

Proceedings of the Ophthalmic Medical Image Analysis First International Workshop

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Abstract. Fuchs' endothelial corneal dystrophy (FECD) is a degenerative disease that affects the elderly population, and which lacks a unifying pathogenic theory and tangible drug targets. Immunohistochemical stainings can be used to identify proteins involved in the pathogenesis of FECD. We introduce a method for the automatic quantification of the ratio of stained cells starting from full high-resolution cornea images. First, the endothelium is extracted using entropy information in a low-resolution resampling. Then, within the endothelium, we heuristically detect and classify nuclei based on their size, color, and the color of the surrounding cytoplasm. This method achieves comparable results to manual evaluation in a set of corneas of patients with and without FECD.

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Fuchs Endothelial Corneal Dystrophy

Cited by 185 publications

References 88 publications

A structural model for thein vivohuman cornea including collagen-swelling interaction

A structural model for thein vivohuman cornea including collagen-swelling interaction

What does the future hold for the treatment of Fuchs endothelial dystrophy; will ‘keratoplasty’ still be a valid procedure?

Automated detection and classification of nuclei in immunohistochemical stainings for Fuchs' endothelial corneal dystrophy

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