OBJECTIVE: As giant cell arteritis (GCA) progresses, newly formed microvessels are one of the main sites of leukocyte-endothelial cell interaction. Our aim was to stereologically map the distribution of microvessels in the temporal arterial wall and to assess their relationship to the degree of inflammation in GCA. METHODS: Inflamed temporal arteries from 21 patients who fulfilled the American College of Rheumatology criteria for GCA were analyzed. Paraffin sections, stained with an antibody directed at vascular endothelium, were analyzed stereologically. The degree of inflammation and the surface of microvascular endothelium per volume (microm2/microm3) were assessed in 4 different layers of the arterial wall. RESULTS: The degree of inflammation and of vascularization was greatest in the adventitia, smaller in the media, and smallest in the intima. A significant positive relationship was observed between the degree of inflammation and the degree of vascularization in the media and in the outer and inner layers of the intima. In 8 biopsies, the microvessels formed a prominent plexus in the intima without apparent connection with microvessels in the adventitia/media, and there were no signs of endothelial budding from the arterial lumen. CONCLUSION: Our results confirm that inflammation is a major determinant in neovascularization in GCA. Some new microvessels are formed by the budding of the adventitial vasa vasorum. The presence of intimal microvascular networks without apparent connection with microvessels in the media might indicate additional influence on neovascularization.
OBJECTIVE: As giant cell arteritis (GCA) progresses, newly formed microvessels are one of the main sites of leukocyte-endothelial cell interaction. Our aim was to stereologically map the distribution of microvessels in the temporal arterial wall and to assess their relationship to the degree of inflammation in GCA. METHODS: Inflamed temporal arteries from 21 patients who fulfilled the American College of Rheumatology criteria for GCA were analyzed. Paraffin sections, stained with an antibody directed at vascular endothelium, were analyzed stereologically. The degree of inflammation and the surface of microvascular endothelium per volume (microm2/microm3) were assessed in 4 different layers of the arterial wall. RESULTS: The degree of inflammation and of vascularization was greatest in the adventitia, smaller in the media, and smallest in the intima. A significant positive relationship was observed between the degree of inflammation and the degree of vascularization in the media and in the outer and inner layers of the intima. In 8 biopsies, the microvessels formed a prominent plexus in the intima without apparent connection with microvessels in the adventitia/media, and there were no signs of endothelial budding from the arterial lumen. CONCLUSION: Our results confirm that inflammation is a major determinant in neovascularization in GCA. Some new microvessels are formed by the budding of the adventitial vasa vasorum. The presence of intimal microvascular networks without apparent connection with microvessels in the media might indicate additional influence on neovascularization.
Authors: Jiusheng Deng; Brian R Younge; Richard A Olshen; Jörg J Goronzy; Cornelia M Weyand Journal: Circulation Date: 2010-02-08 Impact factor: 29.690
Authors: Jiusheng Deng; Wei Ma-Krupa; Andrew T Gewirtz; Brian R Younge; Jörg J Goronzy; Cornelia M Weyand Journal: Circ Res Date: 2009-01-15 Impact factor: 17.367
Authors: Marc Corbera-Bellalta; Roser Alba-Rovira; Sujatha Muralidharan; Georgina Espígol-Frigolé; Roberto Ríos-Garcés; Javier Marco-Hernández; Amanda Denuc; Farah Kamberovic; Patricia Pérez-Galán; Alexandra Joseph; Annalisa D'Andrea; Kent Bondensgaard; Maria C Cid; John F Paolini Journal: Ann Rheum Dis Date: 2022-01-19 Impact factor: 19.103