Atherosclerosis research from past to present—on the track of two pathologists with opposing views, Carl von Rokitansky and Rudolf Virchow
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It is now clear that inflammation plays a key role in atherogenesis. As a matter of fact, signs of inflammation of atherosclerotic plaques have been observed for centuries and also constituted the basis for a fierce controversy in the 19th century between the prominent Austrian pathologist Carl von Rokitansky and his German counterpart, Rudolf Virchow. While the former attributed a secondary role to these inflammatory arterial changes, Virchow considered them to be of primary importance. We had the unique opportunity to address this controversy by investigating atherosclerotic specimens from autopsies performed by Carl von Rokitansky up to 178 years ago. Twelve atherosclerotic arteries originally collected between the years 1827 to 1885 were selected from the Collectio Rokitansky of the Federal Museum of Pathological Anatomy, Vienna Medical University. Using modern sophisticated immunohistochemical and immunofluorescence techniques, it was shown that various cellular intralesional components, as well as extracellular matrix proteins, were preserved in the historic atherosclerotic specimens. Most importantly, CD3 positive cells were abundant in early lesions, thus, rather supporting Virchows’s view, that inflammation is an initiating factor in atherogenesis. Furthermore, we hope to have opened a new and intriguing possibility to study various pathological conditions using valuable historical specimens.
KeywordsAtherosclerosis Inflammation Historical material
We want to thank Ruth Pfeilschifter-Resch and the medical technologists at the Department of Clinical Pathology in Vienna for preparing paraffin sections as well as Ilona Lengenfelder for assistance in the preparation of figures and Dr. Beatrix Patzak for consulting in sample selection. The Clinical Department of Plastic and Reconstructive Surgery, University Hospital Innsbruck, Austria and Dr. Felix Offner from the Department of Pathology, County Hospital Feldkirch, kindly provided recent control tissue. The authors want to acknowledge the Austrian Science Fund (FWF-project no.14741 to G.W.) and the European Union (Molecular basis of vascular events leading to thrombotic stroke, MOLSTROKE; LSHM-CT-2004-005206) for supporting the project.
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