Anti-RANKL treatment inhibits erosive joint destruction and lowers inflammation but has no effect on bone formation in the delayed-type hypersensitivity arthritis (DTHA) model

Arthritis Research & Therapy
Sara Marie AtkinsonUta Syrbe

Abstract

The aims of the present study were to determine the relationship between bone destruction and bone formation in the delayed-type hypersensitivity arthritis (DTHA) model and to evaluate the effect of receptor activator of nuclear factor κB ligand (RANKL) blockade on severity of arthritis, bone destruction, and bone formation. DTHA was induced in C57BL/6 mice. Inflammation, erosive joint damage, and new bone formation were semiquantitatively scored by histology. Osteoclast activity was assessed in vivo, and messenger RNA (mRNA) expression of mediators of bone destruction and bone formation were analyzed by mRNA deep sequencing. Serum concentrations of tartrate-resistant acid phosphatase 5b, carboxy-terminal telopeptide I (CTX-I), matrix metalloproteinase 3 (MMP3), and serum amyloid P component (SAP) were determined by enzyme-linked immunosorbent assay. Anti-RANKL monoclonal antibody treatment was initiated at the time of immunization. Bone destruction (MMP3 serum levels, cathepsin B activity, and RANKL mRNA) peaked at day 3 after arthritis induction, followed by a peak in cartilage destruction and bone erosion on day 5 after arthritis induction. Periarticular bone formation was observed from day 10. Induction of new bone formatio...Continue Reading

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Citations

Aug 25, 2016·Basic & Clinical Pharmacology & Toxicology·Sara Marie Atkinson, Anneline Nansen
Feb 1, 2020·Expert Opinion on Pharmacotherapy·Sunny TrivediC Thomas Vangsness
Oct 27, 2017·Experimental and Therapeutic Medicine·Jianping FanMing Li

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Methods Mentioned

BETA
RNAseq
enzyme-linked immunosorbent assay

Software Mentioned

Ensembl
R
ShortRead
TopHat
Soft Imaging Software Cell
GraphPad
GraphPad Prism
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