Epiretinal pathology of vitreomacular traction syndrome

Abstract

Aims: To investigate the ultrastructure of the vitreoretinal interface in patients with vitreomacular traction syndrome.

Methods: 14 patients with vitreomacular traction syndrome underwent standard pars plana vitrectomy. After induction of posterior vitreous detachment, epiretinal tissue and the inner limiting membrane (ILM) of the retina were removed, and processed for transmission electron microscopy.

Results: Ultrastructural analysis revealed two basic patterns of vitreoretinal pathology in eyes with vitreomacular traction syndrome. Seven specimens showed mostly single cells or a cellular monolayer covering closely the vitreal side of the ILM, not resulting in a biomicroscopically detectable epiretinal fibrocellular proliferation. The other seven specimens revealed premacular fibrocellular tissue which was separated from the ILM by a layer of native collagen, resembling the clinical features of idiopathic epiretinal membranes. In both groups of eyes, the myofibroblast was the predominant cell type. Fibrous astrocytes and fibrocytes were less frequent. Retinal pigment epithelial cells and macrophages were absent. Deposits of newly formed collagen were present only adjacent to fibrocellular multilayers.

Conclusions: There are two distinct clinicopathological features of vitreomacular traction syndrome which suggest different forms of epiretinal fibrocellular proliferation: (1) epiretinal membranes interposed in native vitreous collagen and (2) single cells or a cellular monolayer proliferating directly on the ILM. The presence of remnants of the cortical vitreous which remain attached to the ILM following posterior vitreous separation may determine the clinicopathological feature of the disease. The predominance of myofibroblasts may help to explain the high prevalence of cystoid macular oedema and progressive vitreomacular traction characteristic for this disorder.

Figure 1

Persistent attachment of the vitreous to the posterior pole defines vitreomacular traction syndrome. (A and B) Attachment of the hyaloid (asterisk) to a myofibroblast, characterised by aggregates of 5–7 nm subplasmalemmal cytoplasmic filaments with fusiform densities (arrowheads). (C and D) High magnification of the vitreous in the area of vitreocellular attachment demonstrates uniform collagen fibrils of 10–15 nm diameter, indicating the presence of native vitreous collagen on the vitreal side of the cell (C) and interposed between the cell and the inner limiting membrane (D). (A: 1800×; B: 4800×; C and D: 28 000×)

Figure 2

Epiretinal membrane located on a layer of native vitreous collagen. (A) The fibrocellular multilayer is situated on the vitreal side of a collagenous layer, which covers the ILM throughout the specimen. (B) A myofibroblast located on the collagenous layer. Arrowheads indicate aggregates of 5–7 nm subplasmalemmal cytoplasmic filaments with fusiform densities. (C) The cellular layer is composed of fibrous astrocytes and myofibroblasts. Note the wrinkled and distorted aspect of the ILM. (D) High magnification of (C). The collagenous layer consists of native vitreous collagen covering the ILM (asterisk). (E and F) Newly formed collagen is interposed between epiretinal cells and the layer of native vitreous collagen. (A, C: 1800×; B: 4800×; D, E: 28 000×; F: 60 000×)

Figure 3

Single cells and a cellular monolayer in close contact with the ILM. (A, B, C) A myofibroblast with aggregates of 5–7 nm subplasmalemmal cytoplasmic filaments with fusiform densities (arrowheads) firmly attached to the ILM (asterisk). Ring in (C) highlights the cellular attachment to the ILM. (D, E, F) A cellular monolayer situated on the vitreal side of the ILM. (F) Aggregates of 5–7 nm subplasmalemmal cytoplasmic filaments with fusiform densities (arrowheads) characteristic for myofibroblasts. Note the absence of collagen between the cells and the ILM in both specimens. (A and E: 4800×; B: 28 000×; C and F: 60 000×; D: 1800×).

Figure 4

A cellular multilayer covering the vitreal side of the ILM (asterisk). Preoperative biomicroscopy revealed cystoid macular oedema, but no detectable epiretinal tissue. (A) Note the slightly wrinkled aspect of the ILM. (B) The epiretinal tissue shows a three layered structure. (C) A cellular monolayer is located directly on the ILM. (D) Newly formed collagen is interposed between the monolayer and a multilayer. (E) The multilayer is composed of myofibroblasts and fibrous astrocytes characterised by masses of intracytoplasmic intermediate-type 10 nm filaments (F). (A: 1800×; B: 4800×; C and E: 9500×; D and F: 28 000×).