Metabolic activation of chondrocytes in human osteoarthritis - Expression of type II collagen

Citation
O. Pullig et al., Metabolic activation of chondrocytes in human osteoarthritis - Expression of type II collagen, Z ORTHOP GR, 137(1), 1999, pp. 67-75
Citations number
30
Categorie Soggetti
Ortopedics, Rehabilitation & Sport Medicine
Journal title
ZEITSCHRIFT FUR ORTHOPADIE UND IHRE GRENZGEBIETE
ISSN journal
00443220 → ACNP
Volume
137
Issue
1
Year of publication
1999
Pages
67 - 75
Database
ISI
SICI code
0044-3220(199901/02)137:1<67:MAOCIH>2.0.ZU;2-5
Abstract
Objective/Methods: Type II collagen is the dominating collagen in articular cartilage. It is essential for the structural integrity and the biomechani cal properties of cartilage. Using immunohistology and in situ hybridizatio n we systematically analyzed the protein and mRNA-expression of type II col lagen in cartilage/bone sections without any signs of osteoarthritis and os teoarthritic samples with various degrees of osteoarthritis. Results: In normal articular cartilage without any histologic signs of oste oarthritis type II collagen was distributed homogeneously. An expression of the type II collagen-mRNA was not detectable in any of these samples. In c artilage sections with a roughening of the cartilage surface and a superfic ial loss of the safranin O staining as early histologic signs of osteoarthr itis the immunohistologic staining for type II collagen was reduced in the deep cartilage zone. An expression of the type II collagen-mRNA was found i n 19 of 35 preparations. This expression, however, was restricted to the mi ddle and deep zone of cartilage. A good and reproducible correlation of the specific gene and protein expression was found in samples with more severe osteoarthritic lesions. Conclusions: Detailed information on metabolic changes and the activation o f chondrocytes in osteoarthritic cartilage are important to characterize ce rtain stages of osteoarthritis and thus identify new prognostic factors. In creasing knowledge of the factors regulating the matrix synthesis and degra dation in cartilage will provide the basis for new disease modifying therap ies in osteoarthritis.