Complement C3 deficiency inhibits osteoclast differentiation and prevents ovariectomy-induced osteoporosis.

The pathomechanistic role of the complement system is well recognized in various pathological conditions affecting bone tissues and the bone microenvironment, including rheumatoid arthritis, osteoarthritis, bone fractures, and periodontitis. The homeostasis of the bone is maintained by continuous remodeling, in which bone-resorbing or demineralizing osteoclast cells remove bone calcification, and osteoblast cells deposit new bone matrix. Major complement protein C3 is reported to control endochondral ossification, cartilage-to-bone transition, and longitudinal bone growth.