Ultrastructural investigation of amyloidosis. Pathogenesis of systemic amyloidosis.
Three types of ultrastructural changes in the cell membrane observed in the formation and accumulation of amyloid fibrils in systemic amyloidosis were described: in type I change (contact loss type), unusual dilatation of the intercellular gaps accompanied by occasional disappearance of the tight junction and desmosomes appeared. Type II change (indentation or cystic invagination type) showed cone-shaped indentations or cave-like cystic invaginations. Type III change (surface fold type) consisted of newly developed or inherent surface folds. The widened intercellular gaps of type I, advanced indentation or invagination of type II and the disrupted surface folds of type III resulted in atrophy of the cells and final replacement by amyloid. The author believes that amyloid fibrils are produced by many cells, not by a certain specific cell, extracellularly.
D000682:Amyloid / Q000378:metabolism; D000686:Amyloidosis / Q000209:etiology / Q000473:pathology*; D002199:Capillary Permeability; D002462:Cell Membrane / Q000378:metabolism / Q000648:ultrastructure; D006651:Histocytochemistry; D006801:Humans; D007365:Intercellular Junctions / Q000378:metabolism / Q000648:ultrastructure; D008854:Microscopy, Electron; D011498:Protein Precursors / Q000378:metabolism
D000682:Amyloid; D011498:Protein Precursors