Makrophagen in der Ultrastruktur der PDR- und AMD-Membranen – Potenzieller Einfluss auf Neoangiogenese?

Zusammenfassung

Hintergrund: Proliferative diabetische Retinopathie (PDR) und altersbedingte Makuladegeneration (AMD) sind Krankheiten, die sehr häufig auftreten und das Sehvermögen bedrohen. Ziel unserer Untersuchung ist es, die ultrastrukturellen Veränderungen in der Struktur proliferativer Membranen bei PDR mit denen bei AMD zu vergleichen.

Material und Methoden: Es wurden in dieser prospektiven Studie 24 PDR- und 11 AMD-Patienten einbezogen. Diese wurden nach dem allgemeingültigen Verfahren inklusive OCT untersucht. In allen Fällen wurde eine Vitrektomie durchgeführt und die proliferative Membranen direkt aus dem Augen entnommen. Die Membranen wurden ultrastrukturell im Transmissions- und Raster-Elektronen-Mikroskop und histochemisch mit Safranin O weiter analysiert.

Ergebnisse: In den proliferativen Membranen der PDR-Patienten fanden sich Fibroblasten und einige Makrophagen. Es fanden sich viele Kapillaren der neovaskulären Blutgefäße, die sich durch eine Schicht fenestrierter Endothelzellen, dünne Basalmembran und fehlende Perizyten auszeichneten. Die subretinalen Membranen der AMD-Patienten bestanden meistens aus Fibroblasten, einigen Pigmentepithelzellen und Blut-Bestandteilen. Zahlreiche Makrophagen und Leukozyten gruppiert oder einzeln umschlossen die Kapillaren der neugebildeten Gefäße. Einige Besonderheiten wie z. B reduzierte Anzahl von Pseudopodien, veränderte Form, gruppierte Zytofilamente in der Makrophagen-Zell-Peripherie wurden nachgewiesen. Die Zahl der Proteoglykane war deutlich erhöht.

Schlussfolgerung: Unsere Ergebnisse weisen darauf hin, dass Makrophagen in der Anordnung proliferativer Membranen der PDR und AMD eine wichtige Rolle spielen. Entzündung spielt in der Pathogenese von beiden Krankheiten eine Rolle. Vermutlich ist die Alterung der Makrophagen für die proangiogene Kaskade und Anordnung der neugebildeten Blutgefäße verantwortlich. Es zeigt sich, dass antientzündliche Medikamente für die Behandlung der beiden Krankheiten sinvoller erscheinen.

Abstract

Background and Purpose: Proliferative diabetic retinopathy (PDR) and age-related macular degeneration (AMD) are sight-threatening diseases with high social impact. The aim of our study is to compare the ultrastructure of PDR membranes and those in AMD with a special focus on the macrophages.

Material and Methods: In our study 24 PDR patients and 11 AMD patients were enrolled. They all underwent complete ophthalmological examination including OCT. In all cases pars plana vitrectomy with excision of epiretinal or subretinal membranes was performed. Proliferations taken directly from the eye have been studied by transmission and scanning electron microscopy and with safranin O.

Results: The fibrovascular proliferations in PDR consisted mostly of fibroblasts and occasional macrophages near the blood vessels. The prevailing type of blood vessels had one thin layer of endothelial cells, very thin basal membrane and no pericytes. Subretinal membranes in AMD patients consisted mainly of fibroblasts, isolated RPE cells and elements of the blood. Numerous macrophages and leukocytes in groups and clusters were found around the capillaries of subretinal blood vessels. The cells showed some peculiarities: diminished number of pseudopodia, altered shape. Groups of cytofilaments became visible in macrophages cell periphery. The number of proteoglycans in the matrix was increased.

Conclusion: Our results point out that macrophages play a key role in the formation of the fibrovascular proliferations in both PDR and AMD. Inflammation is assumed to act in the pathogenesis of both diseases. Probably the senescence of macrophages, which we found in our study, is responsible for their proangiogenic response and promotion of new vessel formation. It is reasonable to expect that anti-inflammatory therapy might be helpful in patients with AMD and PDR.

Schlüsselwörter

Pathologie - Retina - intraokulare Entzündungen

Key words

pathology - retina - intraocular inflammation

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