Cartilage and bone markers and inflammatory cytokines are increased in synovial fluid in the acute phase of knee injury (hemarthrosis) – a cross-sectional analysis

Abstract

Our results suggest that an acute knee injury is associated with an instant local biochemical response to the trauma, which may affect cartilage and bone as well as the inflammatory activity.

A clinically realistic large animal model of intra-articular fracture that progresses to post-traumatic osteoarthritis

“…While fracture-related increases in minipig IL1b and TNFa concentrations did not maintain statistical significance, it is possible that their peak values were not captured at our 3-day and 1-week sampling times. Sward et al reported maximum levels of these cytokines in human patients 1 day after injury, which began to resolve within 2e3 days after injury 34 . The significantly increased IL6 values at our sampling time points may be a result of upregulation caused by previous increases in IL1b that had begun to resolve by 3 days post injury.…”

Post-operative bracing after ACL reconstruction has no effect on knee joint effusion. A prospective, randomized study

“…In addition, three months after ACL reconstruction (ACLR), reconstructed knees were observed to have three times the amount of joint effusion as studied by MRI, compared to knees with ACL injury alone [7]. Excessive knee joint effusion, in itself, may be part of the process of joint cartilage degradation after joint trauma and surgery [8,9].…”

Inflammatory Cytokines and Biomarkers of Cartilage Metabolism 8 Years After Anterior Cruciate Ligament Reconstruction

“…At the time of injury, there is a large increase in inflammatory cytokines and cartilage degradation products in the synovial fluid. 35,36 The postinjury duration of these elevated levels has not been fully established, and the mechanisms of PTA have not been elucidated. One theory is that inflammatory cells that are present in high concentrations acutely remain in the joint on a chronic long-term basis and cause ongoing joint degradation.…”

“…In rheumatoid arthritis, interleukin (IL)-1b, IL-6, and tumor necrosis factor (TNF)-a act as major inflammatory mediators, 3,23 and it has been suggested that the same cytokines mediate the cartilage loss in posttraumatic OA. 11 Only a few studies 8,15,22,36 have examined the role of these cytokines in knees with ACL injuries.…”