In addition to the role in fracture healing, the effect of complement activation on cartilage destruction after joint injuries has been discussed in recent years [130] . Gene expression analyses demonstrated that chondrocytes express a broad range of complement components and complement regulatory proteins [145] [146] [147] . The origin of complement components in the synovial fluid remains a topic of debate [130, 148] . Aside from chondrocyte-induced biosynthesis, it appears that multiple other non-cartilaginous sources contribute to complement release in the inflamed joint, including synovial cells and infiltrating leukocytes [130] . We recently hypothesized that chondrocytes may release pro-inflammatory cytokines, express neoantigens and undergo enhanced apoptosis after cartilage injury [130] . However, until present, the involvement of the complement system in posttraumatic joint inflammation and the development of posttraumatic osteoarthritis remains poorly understood, and requires further research.