Fig. 5

Treatment with monoclonal antibody (mAb) against receptor activator of nuclear factor κB ligand (anti-RANKL) leads to a small reduction in local and systemic inflammation and a pronounced reduction in osteoclastogenesis. Mice were treated with 500 μg of anti-RANKL mAb or isotype control in 200 μl of phosphate-buffered saline three times weekly from the time of immunization (day −7). a Paw (top panel) and ankle (bottom panel) swelling in mice treated with anti-RANKL or isotype control. The area under the curve (AUC) was calculated for individual mice for days 0–11 after arthritis induction, and data shown are mean ± standard error of the mean (SEM) (n = 10). *p < 0.05; **p < 0.01 (Student’s t test). b Serum levels (mean ± SEM, n = 10) of serum amyloid P component (SAP) and matrix metalloproteinase 3 (MMP3) measured on days 0, 7, and 11 after arthritis induction by enzyme-linked immunosorbent assay. *p < 0.05; **p < 0.01 (Student’s t test). Dashed line represents mean value of n = 10 naive mice. c Serum levels of tartrate-resistant acid phosphatase 5b (TRAP5b) and carboxy terminal telopeptide I (CTX-I) in serum measured on day 11 after arthritis induction. d Histochemical TRAP staining of paw sections from day 11 after arthritis induction from isotype and anti-RANKL-treated mice (two representative examples per treatment). Original magnification, ×100. DTHA delayed-type hypersensitivity arthritis