It is therefore possible that elevated UPR may be involved in the increased RANKL and osteoclast number leading to bone loss in a variety of disorders, particularly those associated with inflammatory conditions like arthritis, orthopedic implant‐associated osteolysis, and periodontitis.6, 10 In summary, our findings together with these earlier reports set the stage for additional studies to investigate the role of the UPR in pathologic bone loss. This evidence concerns the gene TNFSF11 and arthritic joint disease.