Plasma cells promote osteoclastogenesis and periarticular bone loss in autoimmune arthritis

Periarticular Bone Loss in Antigen-Induced Arthritis

OBJECTIVE Bone loss in arthritis is a complex process characterized by bone erosions and periarticular and generalized bone loss. The antigen-induced arthritis (AIA) model is mainly used to study synovitis and joint destruction, including bone erosions; however, periarticular bone loss has been less extensively investigated. The objectives of this study were to characterize and establish AIA as...

Senescent T-Cells Promote Bone Loss in Rheumatoid Arthritis

Objective T-cells are critical players in the pathogenesis of osteoporosis in patients with rheumatoid arthritis (RA). Premature senescence of lymphocytes including the accumulation of senescent CD4+ T-cells is a hallmark feature of RA. Whether T-cell senescence is associated with bone loss in RA patients is elusive so far. Methods This includes a prospective study of consecutive patients wit...

Natural killer cells trigger osteoclastogenesis and bone destruction in arthritis.

Osteoclasts are bone-eroding cells that develop from monocytic precursor cells in the presence of receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). Osteoclasts are essential for physiological bone remodeling, but localized excessive osteoclast activity is responsible for the periarticular bone destruction that characteristically occurs in patients ...

Sclerostin inhibition reverses systemic, periarticular and local bone loss in arthritis

OBJECTIVE To test whether inhibition of sclerostin by a targeted monoclonal antibody (Scl-Ab) protects from bone and cartilage damage in inflammatory arthritis. Sclerostin is a potent inhibitor of bone formation and may be responsible for the low level of bone repair in patients with rheumatoid arthritis. METHODS Human tumour necrosis factor transgenic mice (hTNFtg mice) developing inflammato...

Siglec15 Mediates Periarticular Bone Loss But Not Joint Destruction In Murine Antigen induced Arthritis