{"title":"The pathology of vascular grafts.","authors":"K M Müller, G Dasbach","doi":"10.1007/978-3-642-76846-0_7","DOIUrl":null,"url":null,"abstract":"<p><p>In order to analyse the incorporation pattern of synthetic prosthesis made of Teflon and Dacron in the arterial system, 21 prostheses removed surgically and seven prostheses obtained from autopsies were examined; the duration of the implantation periods ranged from 30 min up to 10 years. Essentially the early phase of prosthetic incorporation (phase I) includes exudative inflammatory reactions as part of acute inflammatory processes. The degree of order within the tissue architecture and the mutual influence of matrix and cells in the reaction appeared to be slight. The cellular infiltrate found on the outer prosthetic surface is of local origin whereas the inner prosthetic lining contains cells of haematogenous origin. The organisation phase (phase II), which is comparable to the reparative-proliferative phase of an inflammatory reaction, showed activation of the reticulo-endothelial system together with the start of phagocytosis and a thinning of the prosthetic structures. Collagen type I and type III and fibronectin served both as a guidance and a growth tract for the cells during the cellular permeation of the prosthesis. Fibronectin and collagen type III have a special \"catalytic\" function. Collagen type I causes the firm anchoring of the vascular prosthesis in the periprosthetic tissue. The loss of stability of the prosthesis due to phagocytosis of fibres is balanced by the newly formed connective tissue within the wall of the vessel. The fibroblasts involved in the organisation must be derived from the flowing blood and from local mesenchymal cells. A chronic inflammatory reaction persisted during the late phase. In some cases increased proliferation of the inner mesenchymal lining of the prosthesis was observed together with regressive changes. The lack of a continuous surrounding stromal architecture on the luminal side of the vessel can be regarded as the main reason for this proliferation. Transformation of haematogenous cells into angioblasts or endothelial cells was not seen. Small endothelialised areas were only seen in the vicinity of anastomoses and following transprosthetic permeation by capillaries.</p>","PeriodicalId":75767,"journal":{"name":"Current topics in pathology. Ergebnisse der Pathologie","volume":"86 ","pages":"273-306"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"31","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current topics in pathology. Ergebnisse der Pathologie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-642-76846-0_7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31
Abstract
In order to analyse the incorporation pattern of synthetic prosthesis made of Teflon and Dacron in the arterial system, 21 prostheses removed surgically and seven prostheses obtained from autopsies were examined; the duration of the implantation periods ranged from 30 min up to 10 years. Essentially the early phase of prosthetic incorporation (phase I) includes exudative inflammatory reactions as part of acute inflammatory processes. The degree of order within the tissue architecture and the mutual influence of matrix and cells in the reaction appeared to be slight. The cellular infiltrate found on the outer prosthetic surface is of local origin whereas the inner prosthetic lining contains cells of haematogenous origin. The organisation phase (phase II), which is comparable to the reparative-proliferative phase of an inflammatory reaction, showed activation of the reticulo-endothelial system together with the start of phagocytosis and a thinning of the prosthetic structures. Collagen type I and type III and fibronectin served both as a guidance and a growth tract for the cells during the cellular permeation of the prosthesis. Fibronectin and collagen type III have a special "catalytic" function. Collagen type I causes the firm anchoring of the vascular prosthesis in the periprosthetic tissue. The loss of stability of the prosthesis due to phagocytosis of fibres is balanced by the newly formed connective tissue within the wall of the vessel. The fibroblasts involved in the organisation must be derived from the flowing blood and from local mesenchymal cells. A chronic inflammatory reaction persisted during the late phase. In some cases increased proliferation of the inner mesenchymal lining of the prosthesis was observed together with regressive changes. The lack of a continuous surrounding stromal architecture on the luminal side of the vessel can be regarded as the main reason for this proliferation. Transformation of haematogenous cells into angioblasts or endothelial cells was not seen. Small endothelialised areas were only seen in the vicinity of anastomoses and following transprosthetic permeation by capillaries.