Microproliferations in proliferative diabetic retinopathy and their relationship to the vitreous: corresponding light and electron microscopic studies

Faulborn, J.; Bowald, S.

doi:10.1007/bf02148888

Cited by 82 publications

(33 citation statements)

References 14 publications

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“…Conversely, 'complete' PVD protects against proliferative diabetic retinopathy, 51 because the newly formed blood vessels require the collagenous network of the cortical vitreous as a scaffold for growth and invasion. 52 In the presence of a PVD or following surgical vitrectomy, abortive neovascular outgrowths have been observed in the eyes of diabetic patients. 51 …”

Section: Morphology Of the Vitreousmentioning

confidence: 99%

Adult vitreous structure and postnatal changes

Goff

Bishop

2008

Eye

284

206

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This review will focus on the molecular organisation of the adult vitreous and how it undergoes ageing changes throughout life that result in vitreous liquefaction and a predisposition towards posterior vitreous detachment and retinal break formation. At birth, the vitreous humour is in a gel state due to the presence of a network of fine collagen fibrils. With ageing, these collagen fibrils progressively aggregate due to a loss of type IX collagen from their surfaces. The aggregation of collagen fibrils may cause vitreous liquefaction which, when combined with an age-related weakening of postbasal vitreoretinal adhesion, predisposes to posterior vitreous detachment. Throughout postnatal life, the posterior border of the vitreous base migrates posteriorly from the ora serrata into the peripheral retina. This is due to new collagen synthesis by the peripheral retina. This new collagen intertwines with pre-existing cortical vitreous collagen to create new adhesions and thereby extends the vitreous base posteriorly. If irregularities in the posterior border of the vitreous base arise from this process, there is a predisposition towards retinal break formation during posterior vitreous detachment and subsequent rhegmatogenous retinal detachment.

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Section: Morphology Of the Vitreousmentioning

confidence: 99%

Adult vitreous structure and postnatal changes

Goff

Bishop

2008

Eye

284

206

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“…These membranes are essentially neovascular in nature and their relationship to the ILM is impossible to assess on surgically excised membrane peel specimens. This issue has however been elegantly addressed on postmortem eyes by Faulborn et al 35 Their celloidin-embedded samples showed these vascular membranes present within the vitreous cortex. In our series, we were unable to identify ILM in any PDR cases.…”

Section: Cadaver Eyesmentioning

confidence: 99%

Pathological changes in the vitreoretinal junction 1: epiretinal membrane formation

Snead

James

Snead

2008

Eye

130

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Purpose/Background Epiretinal membrane (ERM) formation is a common change resulting in disturbance of macular vision and predisposing to rhegmatogenous retinal detachment. Current treatment strategies rely chiefly on surgical removal of the membranes from the surface of the retina, allowing the retina to remodel and reattach. Improved knowledge of the pathological process behind the formation of these membranes, particularly knowledge of the cell types involved in their formation, is likely to increase our understanding of the way this group of diseases behave and to improve treatment. Methods We reviewed the histological findings of 109 surgically removed specimens and correlated these to age-related changes seen in a 32 cadaver eyes studied after corneal harvesting. The samples were studied using light microscopy and immunocytochemistry. Results In all cases of idiopathic ERMs, including cellophane maculopathy, macular hole, and vitreomacular traction syndrome, laminocytes were the exclusive cell type present. In cases of macular pucker associated with retinal tears, the membranes contain variable cohesive groups of retinal pigment epithelial (RPE) cells in addition to laminocytes. In cases of proliferative diabetic retinopathy, membranes consist almost entirely of capillaries and hyaline stromal tissue, with or without haemosiderin pigment and RPE cells and in which laminocytes and ILM were not identified. In cadaver eyes PVD was seen in 17/32 (53%) of cases, and the vitreous was attached in 14/32 (43.7%) and in one case no vitreous was present. Isolated laminocytes were present on the retinal surface in 12/18 cases with detached vitreous and in 1/14 cases with attached vitreous. In all cases laminocytes were scanty and confined to the optic nerve head, macular or subjacent macular retina. Immunohistochemistry findings indicate that laminocytes are positive for glial fibrillary acidic protein (GFAP), cytokeratin marker AE1/AE3, type II collagen, and type IV collagen. In some cases novel basement membrane formation was seen. There was a tendency for increased positivity of GFAP and AE1/AE3 with increased cellularity, and where novel basement membrane formation was present. Conclusion Laminocytes are the fundamental cell type in idiopathic ERMs. These cells are frequently found in small and dispersed numbers in eyes containing a PVD. The presence of retinal pigment cells invariable indicates proliferative retinopathy and is only seen in association with a retinal detachment or tear. Diabetic membranes are composed of neovascular stromal tissue, which is most likely to be a response to retinal hypoxia.

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“…Several clinical and experimental studies have demonstrated that the vitreous plays a primary role in the pathogenesis of PDVR. The studies have shown the presence of new vessels microproliferating inside the vitreous cavity, indicating the vitreous to be active in the angiogenesis process [34]. There is also evidence that epiretinal membranes in the vitreous of patients with PDVR produce a high amount of growth factors as the retinal cells do [43, 44, 46, 79].…”

Section: Hypothetical Pathogenesis Of Pdvrmentioning

confidence: 99%

“…The instability of the vitreous resulting from this loss of the gel state without dehiscence at the vitreoretinal interface may also induce traction on the retina, which in turn might not only lead to retinal tears but can also contribute to the neovascular process itself. Thus, in addition to providing a scaffold for retinal capillary endothelial and other vasoproliferative cells as postulated by Faulborn and Bowald in 1985 [34], the vitreous may aggravate the process of neovascularization because of changes in the rheologic state.…”

Section: Hypothetical Pathogenesis Of Pdvrmentioning

confidence: 99%

“…For example, one growth factor may have a direct effect and it may stimulate a second mediator, which potentiates or inhibits its effect. Some authors postulated the importance of a combination of advanced glycosylated end products and accumulation of vascular endothelial growth factor (VEGF) at the vitreous as a trigger mechanism for initiation of the proliferative stage of diabetic vitreoretinopathy [34, 72, 83]. The biochemical mechanisms of pathogenesis of diabetic retinopathy and PDVR may be separated into those caused by hyperglycemia and those related to hypoxia.…”

Section: Hypothetical Pathogenesis Of Pdvrmentioning

confidence: 99%

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Pathogenesis and Classification of Proliferative Diabetic Vitreoretinopathy

Kroll¹,

Rodrigues²,

Hoerle³

2007

Ophthalmologica

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Purpose: To review the current knowledge regarding the pathogenesis of proliferative diabetic vitreoretinopathy (PDVR) and to present recommendations for its clinical staging. Design: Focused literature review and authors’ clinical experience. Results: Although several biochemical mediators may be responsible for the pathogenesis of PDVR, no common biochemical pathway exists. Of those mediators, vascular endothelial growth factor is the one most studied so far. However, since in proliferative diabetic retinopathy (PDR) the thickened posterior vitreous cortex is one of the main factors in the development of proliferations, a consequent shrinkage of the posterior vitreous cortex leads to hemorrhages and tractive retinal detachments. Therefore, PDR should be called PDVR. In consequence, the authors present a new morphological classification of PDVR. Conclusions: There is no consensus about the biochemical pathway responsible for the progression of PDVR. Although several classifications are described in the literature, the classification suggested here is important in the judgment of, the communication about and the therapy of diabetic retinopathy. Furthermore, it is the only reliable classification for predicting the surgical outcome in diabetics.

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Microproliferations in proliferative diabetic retinopathy and their relationship to the vitreous: corresponding light and electron microscopic studies

Cited by 82 publications

References 14 publications

Adult vitreous structure and postnatal changes

Adult vitreous structure and postnatal changes

Pathological changes in the vitreoretinal junction 1: epiretinal membrane formation

Pathogenesis and Classification of Proliferative Diabetic Vitreoretinopathy

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