Zellen und Matrix im orthotop-homotransplantierten Epiphysenknorpel

1973; Elsevier BV; Volume: 149; Issue: 4 Linguagem: Inglês

10.1016/s0005-8165(73)80110-6

ISSN

0005-8165

Autores

U. N. Riede, J.M. Mihatsch,

Tópico(s)

Biopolymer Synthesis and Applications

Resumo

Introduction: The hyaline cartilage has a limited capacity of regeneration. Therefore, many attempts were made to replace destroyed cartilage by homotransplants. Surprisingly, the cartilage transplants were not infiltrated by lymphocytes 4 weeks after transplantation. Avoiding the avascularity of the hyaline cartilage, we transplanted in rachitic hosts. Material and Methods: The excised epiphyseal cartilage from juveniles Claxon-rats were transplanted in the epiphyseal plate of Fisher-rats after a four-week rachitogenous diet. 4 weeks after transplantation, the cartilage tissues were examined by electron microscopy. Prefixation in s-collidine-buffered glutardialdehyde (6.5%). Post-fixation in s-collidine buffered OsO4 (%). Embedding in epikote 812. Ruthenium red was used as a mucopolysaccharide staining. Results and Discussion: 4 weeks after transplantation, the cartilage homografts were vital and not infiltrated by lymphocytes. As responsible pathogenetic mechanisms were discussed: No or low antigenicy of the chondrocytes and/or the matrix. Retarded liberation of the antigens. Inhibited graft versus host reaction. The transplanted epiphyseal cartilage were resorbed at low rates compared with the controls. Furthermore, the cartilage matrix reveal atypic collagen fibres, and the chondrocytes show hypertrophic Golgi-apparatus and enormous dilated ergastoplasmic cisternae. These ultrastructural changes seem to be due to a false metabolic pathway of the overaged chondrocytes in cartilage homografts. With the surrounding of the cells with this atypical matrix, all phases of the cartilage rejection are retarded. 4 Wochen nach orthotoper Homotransplantation juvenilen Epiphysenknorpels ist das Knorpelgewebe vital und nicht durch Lymphozyten infiltriert. Als pathogenetische Mechanismen werden diskutiert: Keine oder nur geringe antigene Eigenschaft der Chondrozyten und/oder der Matrix. Verlangsamte Freisetzung der Antigene. Gestörte Antigen-Antikörper-Reaktion. Die transplantierten Epiphysenfugen werden verglichen mit den Kontrollen verlangsamt abgebaut. Auβerdem enthält die Knorpelmatrix atypische Kollagenfibrillen, und die Chondrozyten weisen einen hypertrophierten Golgi-Apparat und abnorm diktierte Ergasto-plasmazisternen auf. Diese ultrastrukturellen Veränderungen scheinen auf einem abwegigen Funktionsstoffwechsel der überalterten transplantierten Chondrozyten zu beruhen. Alle Phasen der Knorpeltransplantatverwerfung werden verlangsamt, weil die Zellen mit dieser atypischen Matrix umgeben sind.

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