To investigate the relationship between bone destruction and new bone formation, as well as to clarify the impact of osteoclasts and specifically RANKL-dependent osteoclast activation and differentiation on arthritis severity, bone destruction, and new bone formation, we treated mice with an anti-RANKL mAb or an isotype control antibody from the time of mBSA immunization. This evidence concerns the gene TNFSF11 and arthritic joint disease.