Abstract There is accumulating evidence that osteoclasts, the primary cells responsible for bone resorption, are involved in bone and joint destruction in rheumatoid arthritis (RA). Recent progress in bone cell biology has revealed the molecular mechanism of osteoclast differentiation and bone resorption by mature osteoclasts. We here highlight the potential role of RANKL-RANK pathways in bone destruction in RA. We also describe our recent trials on gene therapy of arthritic joint disease targeting osteoclasts by regulating Src kinase activity in the cells.
Key words
Key words Adenovirus ・ C-terminus Src family kinase (Csk) ・ Osteoclast recepter activator of NF-&kgr;B ligand (RANKL) ・ Src
