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  • 1
    ISSN: 1432-2307
    Keywords: Chondroblastoma ; Bone tumours ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical and morphological findings of 53 chondroblastomas in the files of the Bone Tumour Registry of Westphalia are presented. The mean age of all patients was 19.2 years. The male-to-female ratio was 1.5∶1. Forty-two of the tumours (79.8%) were located in the long tubular bones and short tubular bones of the hands and were closely related to the growth plate. Six cases (11.3%) were found in the flat bones, 4 cases (7.5%) in the tarsal bones and 1 case (1.9%) in the craniofacial bones. The characteristic radiological feature of 44 investigated lesions was a mostly eccentric radiolucency with a geographic pattern of bone destruction and matrix calcifications. Periosteal reaction was evident in 9% of the cases. Most tumours demonstrate the typical morphological features of chondroblastoma, but 3 cases resembled a giant cell tumour. In 2 cases a haemangio-pericytomalike growth pattern was observed. Nine of the tumours had an aneurysmal bone cyst-like component. Vascular invasion was seen in 1 case. Immunohistochemically most cells in 30 of the cases and fetal chondroblasts in 3 cases were strongly positive with vimentin and S-100 protein. Collagen type II was positive in the chondroid matrix of the tumours and in fetal cartilage tissue; collagen type VI was present focally around individual tumour cells and was always seen in the chondroid matrix of the lesions and in fetal cartilage. These findings support the cartilaginous nature of these tumours. In paraffin sections, 46.6% of the cases revealed a distinct positive reaction of some tumour cells with the monoclonal cytokeratin antibody KL1 (molecular weight 55–57 kDa). Only 4 of them demonstrated a coexpression with the other monoclonal cytokeratin anti-body CK (clone MNF 116, molecular weight 45–56.5 kDa). In paraffin sections all fetal chondroblasts were negative with both cytokeratin antibodies. Frozen sections of 3 tumours showed a strong positive reaction with both cytokeratin antibodies in many chondroblasts, indicating an “aberrant” cytokeratin expression. Osteoclast-like giant cells stained positive with leucocyte-common antigen (LCA) and with the macrophage-associated antibody KP1, but were negative with the other macrophage-associated antibody MAC 387. Recurrence rate was 10.7%. The clinical course of all tumours was benign.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 118 (1992), S. 152-156 
    ISSN: 1432-1335
    Keywords: Osteofibrous dysplasia ; Adamantinoma ; Cytokeratin ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The most controversial aspect of osteofibrous dysplasia (OFD) is its possible histogenetic relationship to adamantinoma of long bone. Evidence is recently beginning to accumulate that OFD may be a reactive process to regressive adamantinoma. To verify the concept, 13 lesions of OFD were studied again by immunohistochemistry for cytokeratins of different molecular masses, as well as by conventional stainings. In addition, 2 adamantinomas and 6 fibrous dysplasias of the tibia were studied for reference. A small number of spindle- or ovoid-shaped cells scattered individually in the fibro-osseous stroma showed positive reactions for cytokeratins of 55–57 kDa in 2 lesions, and for those of 45–56.5 kDa in 8 lesions of 13 OFDs, although no definite epithelial island could be detected even by immunohistochemistry. Adamantinomas also showed single cytokeratin-positive cells dispersed in fibroblastic stroma, in addition to epithelial islands positive for cytokeratins of both 55–57 kDa and 45–56,5 kDa. All cases of fibrous dysplasia were negative for cytokeratins. During the observation, no case of OFDs progressed to classic adamantinoma. The present study, demonstrating the existence of an intermediate stage between “differentiated adamantinoma” and total elimination of adamantinomatous components, gives further support for the concept that OFD is a secondary reactive process to adamantinomatous tissue. In practice, the existence of single scattered cytokeratin-immunoreactive cells in otherwise typical OFDs may not indicate the truly malignant behaviour of classic adamantinoma, unless discrete epithelioid cell nests are also found.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2307
    Keywords: Atherosclerosis ; Apolipoprotein A1, A2, B ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Atherosclerotic vessels were analysed histochemically for distribution, quantity, and composition of apolipoprotein (Apo) types in the vascular wall. The specimens comprised all stages of atherosclerosis, from very discrete intimal changes to complicated lesions. The vessel specimens were marked with antibodies against human Apo A1, A2, and B. Apo A1 can be demonstrated in even the earliest stage of atherosclerosis, and increases with the progression of the disease. In the initial stage, Apo A1 is found first in lumen-adjacent layers of the intima, and is evident in deeper layers of the wall as the disease progresses. Arteries of muscular type show accumulation of Apo in an earlier stage (or in greater quantity at the same stage) than arteries of elastic type. At all stages, the amount of Apo A1 always exceeds that of A2 and B. In the intima, Apo B is higher than Apo A2, the media contains hardly any Apo B, and the adventitia has less B than A2. Within the intimal layer, Apo A1 and A2 are found in an intracellular (mainly in foam cells) or in an extracellular location, according to the stage of atherosclerosis. Apo B is almost exclusively extracellular; only cases of advanced atherosclerosis show some intracellular localization (mostly in foam cells), visualized as electron dense lamellar organelles, probably of lysosomal origin. In the media, Apo A1 and A2 are accumulated in intracellular deposits, whereas the extracellular storage of Apo A1 A2 and B is observed only in cases with the most severe damage. Our investigations suggest that the accumulation of apolipoproteins in the vascular wall is effected not only by insudation from the plasma, but also by neosynthesis and/or metabolism by locally derived cells or cells immigrating in the process of atherosclerosis. The presence of Apo A1 and A2 in the vessel wall is now documented, and their role at this site apparently differs from that in the plasma.
    Type of Medium: Electronic Resource
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