Morphology of partial-thickness macular defects: presumed roles of M\xfcller cells and tissue layer interfaces of low mechanical stability

Andreas Bringmann,Jan Darius Unterlauft,Matus Rehak,Peter Wiedemann,Renate Wiedemann

doi:10.1186/s40942-020-00232-1

Andreas Bringmann, Jan Darius Unterlauft + Show 3 more

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https://doi.org/10.1186/s40942-020-00232-1

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Abstract

BackgroundThe pathogenesis of partial-thickness macular defects and the role of Müller glial cells in the development of such defects are not well understood. We document the morphological characteristics of various types of partial-thickness macular defects using spectral-domain optical coherence tomography, with the focus on tractional and degenerative lamellar holes, and discuss possible pathogenic mechanisms.MethodsA retrospective case series of 61 eyes of 61 patients with different types of partial-thickness macular defects is described.ResultsPartial-thickness macular defects are caused by anteroposterior or tangential traction onto the fovea exerted by the partially detached posterior hyaloid and epiretinal membranes, respectively. Tractional elevation of the inner Müller cell layer of the foveola—without (outer lamellar holes, foveal pseudocysts) or with a disruption of this layer (tractional lamellar holes, macular pseudoholes)—produces an elevation of the inner layers of the foveal walls (nerve fiber layer to outer plexiform layer [OPL]) and a schisis between the OPL and Henle fiber layer (HFL). With the exception of outer lamellar holes, the (outer part of the) central outer nuclear layer and the external limiting membrane remain nondisrupted in the various types of partial-thickness defects. Degenerative lamellar holes are characterized by cavitations between the inner plexiform layer and HFL of the foveal walls; many cases have lamellar hole-associated epiretinal proliferation (LHEP). Proliferating cells of the disrupted Müller cell cone may contribute to the development of LHEP and fill the spaces left by degenerated photoreceptors in the foveal center.ConclusionsIt is suggested that morphological characteristics of partial-thickness macular defects can be explained by the disruption of the (stalk of the) Müller cell cone in the foveola and the location of tissue layer interfaces with low mechanical stability: the boundary with no cellular connections between both Müller cell populations in the foveola, and the interface between the OPL and HFL in the foveal walls and parafovea. We propose that the development of the cavitations in degenerative lamellar holes is initiated by traction which produces a schisis between the OPL and HFL, and enlarged by a slow and chronic degeneration of Henle fibers and bipolar cells.Trial registration retrospectively registered, #143/20-ek, 04/03/2020

Highlights

The pathogenesis of partial-thickness macular defects and the role of Müller glial cells in the development of such defects are not well understood
Schistic tissue splitting in tractional lamellar holes Tractional lamellar holes are characterized by a disruption of the Müller cell cone in the foveola and an elevation of the inner layers of the foveal walls (NFL to outer plexiform layer (OPL)) which causes a schistic splitting of the foveal walls and parafovea between the OPL and Henle fiber layer (HFL); obliquely arranged bundles of Henle fibers traverse the schistic cavities (Fig. 1a, b)
Thereafter, tangential traction exerted by epiretinal membranes (ERM) caused a further elevation of the inner layers of the foveal walls which was associated with a schistic tissue splitting between the OPL and HFL

Summary

Introduction

The pathogenesis of partial-thickness macular defects and the role of Müller glial cells in the development of such defects are not well understood. The Müller cell cone provides critical structural support for the fovea and increases the resistance of the tissue against mechanical stress resulting from anteroposterior and tangential tractions which may occur, for example, in cystoid macular edema and after partial detachment of the posterior vitreous [1, 3, 5]. (ii) Müller cells of the foveal walls and parafovea have a characteristic z-shape because their outer processes run horizontally or obliquely through the Henle fiber layer (HFL) towards the foveal center; the Henle fibers, which are composed of photoreceptor axons surrounded by Müller cell processes, compensate the spatial shift between the inner and outer layers of the foveal tissue [4, 5]. The Müller cell cone maintains the integrity of the foveal walls while the structural stability of the outer layers of the fovea is mainly provided by the Müller cells of the foveal walls [1]

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