Tumor necrosis factor-␣ (TNF-␣) plays a key role in inflammatory diseases such as rheumatoid arthritis and in postmenopausal osteoporosis. In various tissues, TNF-␣ action is mediated by a transcription factor, nuclear factor-kappa B (NF-B). However, little is known about how TNF-␣ exerts its action in osteoblasts. We thus examined the effect of TNF-␣ on the activation of NF-B in rat osteoblast-like osteosarcoma cells (ROS17/2.8). Electrophoretic mobility shift assay revealed that the activation of the p50-p65 heterodimer NF-B was induced by TNF-␣ as early as 15 minutes followed by a persistent activation for 48 h. When the binding activity of NF-B in cytosol was examined using detergents that dissociate NF-B from an inhibitory protein IB, it decreased during the initial 30 minutes and then increased to the unstimulated level. Northern blot analysis revealed a marked increase in the mRNA levels of p105,

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Tumor necrosis factor ␣ (TNF-␣) has been suggested to induce chondrocytic chondrolysis in both inflammatory and degenerative joint diseases. However, its intracellular signaling pathway leading to the chondrolysis has not been studied in detail. Thus, we investigated whether TNF-␣ activates a transcription factor nuclear factor B (

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Combinations of the C2C and KS as described here may offer greater ability to identify patients with early pre-radiographic high-grade cartilage damage compared to single clinical or biomarker parameters.