[Ultrastructural studies on the articular cartilage of spontaneous osteoarthritis in C 57 black mice].
In order to clarify the cause and mechanism of joint degeneration in osteoarthritis (OA), a histopathological study and ultrastructural-histochemical analysis were performed on the articular cartilage of the C57 Black mouse, a model of spontaneous osteoarthritis. Using transmission electron microscopy (TEM), in all stages of light microscopically recognized OA, we found that Golgi apparatus++ were poorly developed, intracellular microfilaments markedly increased, proteoglycan granules decreased and collagen networks broken. Observing histologically normal models of different ages by TEM, we found Golgi apparatus++ and other organelles to be well developed regardless of age. Many proteoglycan granules were seen, mainly consisting of keratan sulphate in the later months. Collagen networks were maintained. These results suggest that disturbed protein transport and sugar synthesis in chondrocytes due to the deficient development of Golgi apparatus++ caused the degenerative change in articular cartilage and that, with aging, the structure and function of the matrix were maintained mainly due to the continued presence of keratan sulphate.
Yamamoto
K
K
Department of Orthopaedic Surgery, Tokyo Medical College, Japan.
D000375:Aging / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002358:Cartilage, Articular / Q000378:metabolism / Q000648:ultrastructure*; D005260:Female; D006056:Golgi Apparatus / Q000378:metabolism / Q000648:ultrastructure; D007632:Keratan Sulfate / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron; D010003:Osteoarthritis / Q000378:metabolism / Q000473:pathology*; D011509:Proteoglycans / Q000378:metabolism
D011509:Proteoglycans; D007632:Keratan Sulfate