gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Exudative AMD caused by an inflammatory process?

Meeting Abstract

  • corresponding author P. Hermans - Ophtha-Lab, St. Franziskus-Hospital, Münster
  • K.-D. Müller - Ophtha-Lab, St. Franziskus-Hospital, Münster
  • N. Bornfeld - Ophtha-Lab, St. Franziskus-Hospital, Münster
  • D. Pauleikhoff - Ophtha-Lab, St. Franziskus-Hospital, Münster

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogDO.17.10

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Veröffentlicht: 22. September 2004

© 2004 Hermans et al.
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In the pathogenesis of age-related macular degeneration (AMD) seems an low-grade inflammatory process to be involved. The aim of the study was to determine presence and distribution of inflammatory markers in normal macula specimen and age related deposits sub RPE, to correlate the normal situation with results from AMD tissues.


An immunhistological investigation of 30 donor macula specimen (60-97years) as well as sub RPE lokalized diffuse deposits (basal laminar deposits, BLD) from 30 CNV was performed. Antibodies against proteins of the complement system C3 and C5b-9 were used. Although an CD68 antibody for macrophages and HLA-DR antibody to detect antigen presenting cells were used.


The results in the 30 specimen were homogenous. The terminal complement complex C5b-9 was found in Bruch´s membrane (BM), while the early complement protein C3 was absent. Macrophages and antigen presenting cells were found numerous in the choroidea, but not in BM (30/30). In contrast in all investigated BLD the early complement protein C3 as well as the terminal membrane attacking complex C5b-9 were found. In addition some Macrophages were found in BLD, too.


An low-grade inflammatory process seems to be absent in BM of normal donors >60y. But an activation of the complementsystems seems to be possible in BM. Than in BLD the presence of the early complement protein C3 and C5b-9 indicates that complement activation occurs in BLD more often. In addition the accumulation/ over production of extracellular matrix proteins especially vitronectin in BLD indicates a defense system to scavenge the cytotoxic membrane attacking complex C5b-9. Because active complement and macrophages can induce angiogenesis it seems to be likely that an low-grade inflammatory process is involved in CNV genesis.