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The Pathogenesis of Giant Cell Arteritis: Morphological Aspects

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The Pathogenesis of Giant Cell Arteritis: Morphological Aspects The morphology of GCA / C. Nordborg et al. The pathogenesis of giant cell arteritis: Morphological aspects C. Nordborg1, E. Nordborg2, V. Petursdottir1 1Department of Pathology, 2Department of ABSTRACT in GCA. When studying V-beta families Rheumatology, Sahlgrenska University The light-microscopic, electron-micro- of the T-cell infiltrate with flow cyto- Hospital, Göteborg, Sweden. scopic and immunocytochemical charac- metry, Schaufelberger et al. found that These studies were supported by grants teristics of giant cell arteritis (GCA) the infiltrating lymphocytes are polyclo- from the Göteborg Medical Society, the have been investigated in a number of nal (3). On the other hand, Weyand et Swedish Heart-Lung Foundation, the studies on temporal arteries. Arterial al. (4) demonstrated the identical clonal Swedish Rheumatism Association, Rune atrophy and calcification of the internal expansion of a small proportion of the och Ulla Amlöfs Stiftelse and Syskonen elastic membrane appear to be prere- T-lymphocytes in separate segments of Holmströms Donationsfond. quisites for the evolution of the inflam- the same artery, which indicates antigen Please address correspondence and reprint matory process. Foreign body giant cells stimulation. A correlation between va- requests to: Claes Nordborg, Department form close to calcifications, apparently rious infections and the onset of GCA of Pathology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. without connection with other inflam- has been reported; it has been speculated E-mail: [email protected] matory cells and probably by the fusion that infectious disorders might trigger the of modified vascular smooth muscle inflammatory process (5). Zoster-vari- Clin Exp Rheumatol 2000: 18 (Suppl. 20): cells. The foreign body giant cells attack cella infection may induce granuloma- S18-S21. the calcifications. Lymphocytes accumu- tous angiitis. However, immunocyto- © Copyright CLINICAL AND EXPERIMENTAL late around them and may be found in chemistry or PCR did not reveal this type RHEUMATOLOGY 2000. pockets in their cell surface. of virus in inflamed temporal arterial tis- This focal reaction is found in atrophic, sue from 10 GCA patients (6). Key words: Giant cell arteritis, calcified arterial segments in a minority light microscopy, electron microscopy, of inflamed temporal artery biopsies. Atrophy and calcification of the morphometry, immunocytochemistry. More commonly seen is a diffuse mo- temporal artery nonuclear attack of the vessel wall in A previous morphometric study showed atrophic as well as non-atrophic seg- that asymmetric atrophy of the temporal ments which leads to severe arterial dila- artery media and an accompanying fo- tation. Langhans giant cells form by the cal calcification of the internal elastic fusion of macrophages in the diffuse membrane (IEM) are significantly more inflammatory infiltrate. pronounced in non-inflamed arterial seg- The fact that the diffusely inflamed arte- ments in polymyalgia rheumatica than ries are markedly widened compared to in controls (7). This type of atrophy the focally inflamed vessels suggests that should not be confused with post-inflam- the inflammatory process starts as a fo- matory scarring. The atrophic arteries cal foreign body giant cell reaction di- display an asymmetric reduction of the rected at calcifications which in turn ini- media, which may be lost in part of the tiates a more diffuse and widespread in- circumference but there is no fibroblastic flammation. or microvascular proliferation. More- over, morphometry showed that the Introduction atrophic, calcified arterial segments had Giant cell arteritis is a chronic form of a significantly smaller outer diameter vasculitis which predominantly affects than the inflamed vessels (7). This indi- women over 50 years of age. Its etiology cates that the atrophy and calcification and pathogenesis are incompletely are not the result of scarring after arteritic understood. Genetic factors are of rele- inflammation since arteries which are vance; the disease is more common in dilated due to a weakening of their wall Caucasians and in patients expressing the do not regain their original circumfer- histocompatibility antigen HLA-DR4 ence. Finally, the fact that the same type (1). Immunological analysis of the in- of calcification and media asymmetry flammatory infiltrate in the vessel wall may be seen in normal arterial aging, indicates the local activation of T-lym- although to a lesser extent, speaks in fa- phocytes (2), which supports the theory vour of a primary atrophy which is not that cell-mediated immunity is involved the result of previous inflammation. S-18 Hypothalamus-pituitary-adrenocortical and -gonadal axis in RA / M. Cutolo The morphology of GCA / C. EDITORIALNordborg et al. The morphology of the inflamma- Once widened by the weakening of their is rarely seen before the age of 50 be re- tory process wall, arteries do never regain their ori- lated to differences in sex hormone me- According to a light-microscopic exami- ginal outer diameter. tabolism ? The estrogen production of nation of semi-thin plastic sections, for- pre-menopausal women is cyclic, with eign-body giant cells form focally Giant cell aortitis a higher secretion rate than in men. around the calcifications in atrophic seg- Morphological and morphometric ana- Moreover, menopause implies a major ments of the temporal artery. Serial sec- lyses thus indicate that atrophy and calci- change in estrogen metabolism. A recent tioning revealed giant cells in segments fication are a prerequisite for the initia- epidemiologic study indicates that for- which were devoid of other inflamma- tion of the inflammatory process in tem- mer pregnancies may be a protective fac- tory cells (7). The immuno-phenotype poral arteries. Analogously, the aortic tor against GCA (14), which supports the and ultrastructure of the foreign-body inflammatory reaction in GCA is related contention that GCA may be related to giant cells and the polygonal cells with to smooth muscle atrophy and calcifica- estrogen metabolism. Theoretically, it which they fuse indicate that they might tion. Petursdottir et al. (10) showed la- could influence the pathogenesis of GCA be formed by the fusion of modified ar- minar smooth muscle atrophy and calci- in several ways. Functioning estrogen terial smooth muscle cells (7, 8). The in- fication in the aortic media from patients receptors have been detected in cultured duction of this fusion, which always with GCA. The inflammatory reaction human vascular smooth muscle cells, takes place close to calcifications, needs and the breakdown of elastic lamellae indicating that estrogen may be involved further clarification. was confined to the borders of such atro- in vessel wall metabolism. Moreover, a Mononuclear cells accumulate around phic lesions. The findings support the number of studies suggest that estrogen the foreign-body giant cells; some lym- contention that atrophy and calcification plays an important role in immunology. phocytes may even be found in shallow preceed the inflammatory reaction which In a recent immunocytochemical study pockets in the giant cell surface. It re- is, in fact, primarily directed at calcified we found that the inflamed arteries in mains to be shown whether the foreign- tissue. Moreover, the coupling to arte- GCA expressed distinct cytoplasmic body giant cells present antigen to these rial atrophy and calcification may ex- immunoreactivity to estrogen receptor surrounding lymphocytes, thereby initi- plain why GCA is a disorder of elderly alpha (ERa ) in activated mononuclear ating T-cell activation. An association be- people. inflammatory cells and in giant cells tween the foreign-body giant cell reac- (15). Furthermore, biopsies from GCA tion and T-cell activation has previously The origin of the inflammatory patients and from non-GCA controls dis- been suggested around silicone gel breast infiltrate played cytoplasmic immunopositivity in implants (9). The distribution of inflammatory cells in smooth muscle cells. Western blot ana- The fact that the foreign-body giant cell the arterial wall indicates that the ma- lysis revealed a band corresponding to granuloma, in its pure form, is only found jority of the invading cells are recruited the wild type ERa in inflamed arteries in a minority of temporal artery biopsies from microvessels in the adventitia, and in controls and RT-PCR analysis re- may be due to its focality but may also whereas a minority seem to emanate vealed a strong band corresponding to indicate that it is a short-lasting reaction from the lumen of the inflamed artery approximately 670 bp, as expected (15). which is soon replaced by a diffuse (11, 12). One evidence of cellular migra- These findings justify further studies re- mononuclear cell invasion. In most biop- tion from the adventitia into the vessel garding the roles of estrogen metabolism sies the mononuclear infiltration is more wall is the crowding of inflammatory in vascular aging and GCA. widespread, involving the whole circum- cells at the outer margin of the media, as ference of the artery in atrophic as well would be expected if cells were migra- Hypothesis as non-atrophic arterial segments. Lang- ting from the loose adventital connec- Based on our morphological observa- hans giant cells form in the diffuse in- tive tissue into the tighter smooth mus- tions we have formed the following hy- flammatory infiltrate by the fusion of cle layer. Within the intima, the inflam- pothesis
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