S20_7

The pathogenesis of giant cell arteritis: Morphological aspects

C. Nordborg¹, E. Nordborg², V. Petursdottir¹

¹Department of Pathology, ²Department of Rheumatology, Sahlgrenska University Hospital, Göteborg, Sweden.

ABSTRACT
The light-microscopic, electron-microscopic and immunocytochemical characteristics of giant cell arteritis (GCA) have been invesernal elastic membrane appear to be prerequisites for the evolution of the inflammatory process. Foreign body giant cells form close to calcifications, apparently without connection with other inflammatory cells and probably by the fusion of modified vascular smooth muscle cells. The foreign body giant cells attack the calcifications. Lymphocytes accumulate around them and may be found in pockets in their cell surface.
This focal reaction is found in atrophic, calcified arterial segments in a minority of inflamed temporal artery biopsies. More commonly seen is a diffuse mononuclear attack of the vessel wall in atrophic as well as non-atrophic segments which leads to severe arterial dilatation. Langhans giant cells form by the fusion of macrophages in the diffuse inflammatory infiltrate.
The fact that the diffusely inflamed arteries are markedly widened compared to the focally inflamed vessels suggests that the inflammatory process starts as a focal foreign body giant cell reaction directed at calcifications which in turn initiates a more diffuse and widespread inflammation.

Key words
Giant cell arteritis, light microscopy, electron microscopy, morphometry, immunocytochemistry.

These studies were supported by grants from the Göteborg Medical Society, the Swedish Heart-Lung Foundation, the Swedish Rheumatism Association, Rune och Ulla Amlöfs Stiftelse and Syskonen Holmströms Donationsfond.

Please address correspondence and reprint requests to: Claes Nordborg, Department of Pathology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden.
E-mail: claes.nordborg@path.gu.se