Ultrastructure of vitreomacular traction syndrome associated with persistent hyaloid artery

Gandorfer, Arnd; Rohleder, Matthias; Charteris, David G.; Luthert, Philip J.

doi:10.1038/sj.eye.6701459

Cited by 12 publications

(12 citation statements)

References 9 publications

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“…Most importantly, we observed an extra layer of cells adjacent to the pericytes having morphology distinct from either endothelial cells or pericytes. These cells showed an abundant rough endoplasmic reticulum, were rich in mitochondria, and contained cytoplasmic microfilaments, which are defining features of fibroblast or myofibroblast (12,15). Figure 8C shows a representative micrograph demonstrating the ultrastructural changes between endothelial cells at the PAFinduced peak Lp on day 4 vessels.…”

Section: Resultsmentioning

confidence: 99%

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

Dong

2012

Journal of Applied Physiology

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Section: Resultsmentioning

confidence: 99%

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

Dong

2012

Journal of Applied Physiology

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“…1 Anteroposterior vitreoretinal traction is caused by persistent vitreoretinal adhesions because of an incomplete posterior vitreous detachment (PVD), whereas tangential traction is caused by contractive ERMs as a result of progressive fibrocellular proliferation at the vitreal side of the ILM. [2][3][4][5][6] Removal of the vitreous and epiretinal tissue is the principal goal of vitreoretinal surgery in MP and VMTS because ERMs represent the morphological correlate of typical symptoms found in these diseases, such as reduction in visual acuity and metamorphopsia. 3,7 The concept of peeling off the ILM and epiretinal tissue in eyes with traction maculopathies is supported by numerous studies reporting on improved functional and anatomical outcomes.…”

mentioning

confidence: 99%

“…[2][3][4][5][6] Removal of the vitreous and epiretinal tissue is the principal goal of vitreoretinal surgery in MP and VMTS because ERMs represent the morphological From the…”

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confidence: 99%

Epiretinal Cell Proliferation in Macular Pucker and Vitreomacular Traction Syndrome

Zhao

Gandorfer

Haritoglou

et al. 2013

Retina

127

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Purpose: To describe new details of epiretinal cell proliferation in flat-mounted internal limiting membrane specimens.Methods: One hundred nineteen internal limiting membrane specimens were removed en bloc with epiretinal membranes from 79 eyes with macular pucker (MP) and 40 eyes with vitreomacular traction syndrome. Intraoperatively, posterior vitreous detachment was assessed as complete or incomplete. Whole specimens were flat-mounted on glass slides and processed for interference and phase-contrast microscopy, cell viability assay, and immunocytochemistry.Results: Mean cell viability percentage was higher in MP than in vitreomacular traction syndrome. Two cell distribution patterns were found. Anti-CD163 labeling presented predominantly in MP with complete posterior vitreous detachment. CD45 expression was similar in all groups of diagnosis. Anti-glial fibrillary acidic protein (GFAP) labeling was found in MP irrespective of the extent of posterior vitreous detachment. Alpha-SMA (a-smooth muscle actin) labeling was mainly presented in MP with incomplete posterior vitreous detachment and in vitreomacular traction syndrome. Simultaneous antibody labeling included GFAP/CD45, GFAP/CD163, CD163/CD45, and CD163/a-SMA.Conclusion: Hyalocytes constitute a major cell type of epiretinal cell proliferation in eyes with MP and vitreomacular traction syndrome. Glial cells, notably retinal Muller cells, are involved as well. It appears that transdifferentiation of cells in vitreomacular traction might be more frequent than previously thought and that those cells possess a greater variability of immunocytochemical properties than expected.RETINA 33:77-88, 2013 E piretinal gliosis, such as macular pucker (MP), and vitreomacular traction syndrome (VMTS) are traction vitreoretinopathies that develop at the vitreoretinal interface of the macular area. The major component of the vitreoretinal interface is the internal limiting membrane (ILM) that has attracted enormous interest for decades. The ILM is the site of epiretinal membrane (ERM) formation, and it mediates tractional forces from the vitreous to retinal layers. There is general consent that vitreoretinal traction plays a crucial role in the pathogenesis and the clinical course of MP and VMTS.1 Anteroposterior vitreoretinal traction is caused by persistent vitreoretinal adhesions because of an incomplete posterior vitreous detachment (PVD), whereas tangential traction is caused by contractive ERMs as a result of progressive fibrocellular proliferation at the vitreal side of the ILM. [2][3][4][5][6] Removal of the vitreous and epiretinal tissue is the principal goal of vitreoretinal surgery in MP and VMTS because ERMs represent the morphological From the

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“…Postoji svega nekoliko saopštenja o krvarenjima u staklastom telu i trakcionim ablacijama retine povezanim sa perzistentnom hialoidnom arterijom [4,10,11]. Svega je 20 pacijenata sa perzistentnom hialoidnom arterijom prijavljeno u literaturi [ 12].…”

Section: Introductionunclassified

“…Nepotpuna regresija embrionalnog vitreusa sa PHA može uzrokovati ablaciju zadnjeg vitreusa oko optičkog diska, što može uzrokovati vitrealnu trakciju, kao i pojavu vitrealnih traka i makularne trakcije ili razvoj epimakularne membrane [12].…”

Section: Introductionunclassified

Bilateral persistent hyaloid artery in the adult patient

Trenkic-Božinović¹,

Novak²,

Radenković³

et al. 2015

Tim Med Glas

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Sažetak:Uvod: Hialoidna arterija se pojavljuje u trećoj nedelji gestacije kod embriona i doseže do sočiva u četvrtoj ili petoj nedelji gestacije da bi formirala tunicu vasculosu lentis. Atrofija hialoidne arterije uglavnom se završava pre rođenja. Postojanje hialoidne arterije sa aktivnim krvnim protokom se retko sreće, naročito ako je bilateralno. Postoji nekoliko saopštenja o vitrealnim hemoragijama (spontanim i traumatskim) i trakcionim ablacijama retine koje su u vezi sa perzistentnom hialoidnom arterijom. Pacijent i metode: Pacijent 25 godina starosti javio se oftalmologu zbog subjektivnih smetnji smanjenja vida. Vidna oštrina na oba oka bila je 1,0 određena po Snellenu, intraokularni pritisak 12mmHg. Refraktometrija je pokazala ROD +1,50 DSph/ +0,25DCyl (103°), ROS +1,50DSph / +0,50DCyl (38°). Pregledom na biomikroskopu viđena je obostrana opalescencija u prostoru staklastog tela iza providnog sočiva. Pregled očnog dna pokazao je da su obe papile vidnog živca velike i sa velikim centralnim kolobomom. Takođe je uočena a. hyaloidea persistens, koja polazi sa optičkog diska, okružena primarnim vitreusom na prednjem kraju, vidljivim kao zamućenje staklastog tela iza sočiva. B-scan je potvrdio ehogeno vidljivu linearnu strukturu srednje do više reflektivnosti u zadnjem delu staklastog tela koja polazi sa papile vidnog živca i proteže se ka sočivu (a. hyaloidea persistens). Dodatno je urađena fluoresceinska angiografija koja je pokazala usporeno i odloženo punjenje uske perzistentne hialoidne arterije. Kompjuterizovana perimetrija je pokazala obostrano proširenje slepe mrlje. Optička koherentna tomografija papile vidnog živca oba oka je pokazala tubularnu strukturu na papili vidnog živca sa hiporeflektivnom unutrašnjosti. Zaključak: Perzistentna hialoidna arterija se mora smatrati mogućim etiološkim faktorom za krvarenja u staklastom telu, naročito kod zdravih, mladih ljudi. Njeno prisustvo mozě da nas upozori na mogucé komplikacije tokom operacije katarakte i drugih hirursǩih intervencija. Ultrazvuk obezbeđuje esencijalne informacije pri postavljanju dijagnoze, određuje prisustvo lezije, njeno pružanje i zahvaćenost retine i glave optičkog diska. U pregled bi trebalo uvrstiti i fluoresceinsku angiografiju i optičku koherentnu tomografiju. Ključne reči: perzistentna hialoidna arterija, kolobom papile, vidni živac, oct, ultrazvuk. Summary:Introduction: Hyaloid artery occurs in the third week of gestation and reaches the lens in the fourth or fifth week of gestation to form the tunica vasculosa lentis. Atrophy of the hyaloid artery usually ends before birth. The existence of the hyaloid artery with the active blood flow is rare, especially if bilateral. There are several reports about vitreous hemorrhages (spontaneous and traumatic) and tractional retinal detachments that are associated with persistent hyaloid artery. Patient and Methods: A male patient, aging 25, reported to an ophthalmologist because of subjective complaints of visual impairment. Visual acuity in both eyes was 1.0 determined by Snellen, intraocu...

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Ultrastructure of vitreomacular traction syndrome associated with persistent hyaloid artery

Cited by 12 publications

References 9 publications

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

Vascular remodeling alters adhesion protein and cytoskeleton reactions to inflammatory stimuli resulting in enhanced permeability increases in rat venules

Epiretinal Cell Proliferation in Macular Pucker and Vitreomacular Traction Syndrome

Bilateral persistent hyaloid artery in the adult patient

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