- Paper Report
- Open Access
OSM-induced periosteal bone apposition
- Riako Masuda1
© Biomed Central Ltd 2002
- Received: 27 June 2002
- Accepted: 15 August 2002
- Published: 15 August 2002
- Bone apposition
- Oncostatin M
Oncostatin M (OSM) is a member of the interleukin (IL)-6 family and induces the expression of IL-6. Since the level of OSM is elevated in the synovial fluid, but not in the serum, in RA, OSM is considered to play a role in the local inflammation seen in RA. To elucidate the influence of OSM on joint inflammation, the authors induced inflammation in wild-type and IL-6 deficient mice using an injection of adenoviral vector expressing murine OSM (AdmuOSM).
In spite of OSM inducing the expression of IL-6, histological scoring of joint inflammation showed no difference between wild-type and IL-6 deficient mice. Moreover, periosteal bone apposition (the formation of layers of osteoblast-like cells and the deposition of new bone) occurred in the injected joints of both strains. These results suggest that these effects of OSM are not mediated by IL-6. Using murine osteoblast cell lines, the authors showed that new formation of bone is caused by the interaction of OSM with other bone-forming factors such as BMP-2. At sites of bone apposition, RANK (receptor activator of nuclear factor-κB) and RANKL (RANK ligand) were also expressed but no osteoclasts could be detected. In addition, the authors that showed overexpression of OSM induced the expression of RANKL inhibitor osteoprotegerin (OPG), which might control bone resorption.
Adenoviral transfer, ALP, ALP assay, IL-6 deficient mice, immunohistochemistry, semiquantitative RT-PCR, TRAP, Von Kossa and Goldner's Trichrome staining.
- de Hooge ASK, van de Loo FAJ, Bennink MB, de Jong DS, Arntz OJ, Lubberts E, Richards CD, van den Berg WB: Adenoviral transfer of murine Oncostatin M elicits periosteal bone apposition in knee joints of mice, despite synovial inflammation and up-regulated expression of interleukin-6 and receptor activator of nuclear factor-κB ligand. Am J Pathol . 2002, 160: 1733-1743.PubMedPubMed CentralView ArticleGoogle Scholar