These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Metabolic activation of chondrocytes in human osteoarthritis. Expression of type II collagen].
    Author: Pullig O, Kladny B, Weseloh G, Swoboda B.
    Journal: Z Orthop Ihre Grenzgeb; 1999; 137(1):67-75. PubMed ID: 10327565.
    Abstract:
    OBJECTIVE/METHODS: Type II collagen is the dominating collagen in articular cartilage. It is essential for the structural integrity and the biomechanical properties of cartilage. Using immunohistology and in situ hybridization we systematically analyzed the protein and mRNA-expression of type II collagen in cartilage/bone sections without any signs of osteoarthritis and osteoarthritic samples with various degrees of osteoarthritis. RESULTS: In normal articular cartilage without any histologic signs of osteoarthritis type II collagen was distributed homogeneously. An expression of the type II collagen-mRNA was not detectable in any of these samples. In cartilage sections with a roughening of the cartilage surface and a superficial loss of the safranin O staining as early histologic signs of osteoarthritis the immunohistologic staining for type II collagen was reduced in the deep cartilage zone. An expression of the type II collagen-mRNA was found in 19 of 35 preparations. This expression, however, was restricted to the middle 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 of chondrocytes in osteoarthritic cartilage are important to characterize certain stages of osteoarthritis and thus identify new prognostic factors. Increasing knowledge of the factors regulating the matrix synthesis and degradation in cartilage will provide the basis for new disease modifying therapies in osteoarthritis.
    [Abstract] [Full Text] [Related] [New Search]