Fas receptor induces apoptosis of synovial bone and cartilage progenitor populations and promotes bone loss in antigen-induced arthritis

What is it about?

Rheumatoid arthritis is a chronic immune system-mediated joint inflammation, whose most important feature is development of progressive joint deformities. These deformities, along corresponding joint pain, lead to permanent disability and significantly decrease patients' overall quality of life. Deformities develop as a result of bone damage. It is well known that inflammation promotes resorption of bone tissue by specific bone resorbing cells, osteoclasts, and prevent regeneration of bone tissue by specific bone forming cells, osteoblasts. _x000D_ The mechanisms involved in the transmission of inflammatory signals to bone cells are not yet completely understood. Some types of joint diseases with intensive joint inflammation often lack bone damage, and vice versa, mild inflammation, may be accompanied by underlying bone destruction. _x000D_ This study is important because it reveals important influence of immune-related receptor Fas, on regulating the death and survival of local precursors of bone forming osteoblasts in the affected joints, and therefore directly affecting bone regeneration during arthritis. Arthritis induced in mice without Fas shows less inflammation and preserved bone mass and architecture. Further studies on the effects of Fas on osteoblast precursors have a potential to reveal new promising targets to block inflammation-induced suppression of bone formation and better prevent and treat deformities.

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