Binding Immunoglobulin Protein (BIP) Inhibits TNF‐α–Induced Osteoclast Differentiation and Systemic Bone Loss in an Erosive Arthritis Model

Objective The association between inflammation and dysregulated bone remodeling is apparent in rheumatoid arthritis and is recapitulated in the human tumor necrosis factor transgenic (hTNFtg) mouse model. We investigated whether extracellular binding immunoglobulin protein (BiP) would protect the hTNFtg mouse from both inflammatory arthritis as well as extensive systemic bone loss and whether BiP had direct antiosteoclast properties in vitro.