Cell proliferation in osteoarthritic human cartilage

被引:18
|
作者
Pfander, D [1 ]
Körtje, D [1 ]
Weseloh, G [1 ]
Swoboda, B [1 ]
机构
[1] Univ Erlangen Nurnberg, Orthopad Klin & Poliklin, Abt Orthopad Rheumatol, D-91054 Erlangen, Germany
来源
ZEITSCHRIFT FUR ORTHOPADIE UND IHRE GRENZGEBIETE | 2001年 / 139卷 / 05期
关键词
cartilage; osteoarthritis; proliferation;
D O I
10.1055/s-2001-17977
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
Objective: Osteoarthritic (OA) cartilage is histologically characterized by the appearance of cell clusters, which are probably generated by mitotic cell division The aim of this study was to analyze the distribution and amount of proliferating chondrocytes in healthy and osteoarthritic cartilage systematically. Materials and methods: 6 normal and 43 osteoarthritic cartilage/bone samples were obtained during autopsies or total knee replacements. The cartilage specimens were stained with safranin-o and scored according to the Mankin-System. Proliferating chondrocytes were identified by immunohistochemical detection of the antigen PCNA. The number of proliferating chondrocytes was determined by counting 100 chondrocytes in each cartilage layer. Results: in normal and osteoarthritic human cartilage, proliferating chondrocytes were detected. The amount of proliferating chondrocytes increased during the progression of OA cartilage changes. Expression of PCNA was determined in single chondrocytes and clustered chondrocytes. Chondrocyte cell division was activated specifically in cartilage with severe OA changes. Conclusions. Osteoarthritic chondrocytes, which are known to increase the synthesis of different matrix proteins, show the phenomenon of mitotic cell division. Whether the increased amount of proliferating chondrocytes fails to compensate the rate of apoptotic chondrocytes, or whether the generation of cell clusters represents only a fruitless repair effort is a subject of recent research. However, the induction of chondrocyte proliferation is a potential target in the treatment of OA.
引用
收藏
页码:375 / 381
页数:7
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