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.

Contralateral anterior cruciate ligament (ACL) injuries are together with the risk of developing osteoarthritis of the knee and the risk of re-rupture/graft failure important aspects to consider after an ACL injury. The aim of this review was to perform a critical analysis of the literature on the risk factors associated with a contralateral ACL injury. A better understanding of these risk factors will help in the treatment of patients with unilateral ACL injuries and in the development of interventions designed to prevent contralateral ACL injuries. A Medline search was conducted to find studies investigating risk factors for a contralateral ACL injury, as well as studies where a contralateral ACL injury was the outcome of the study. Twenty studies describing the risk of a contralateral ACL rupture, or specific risk factors for a contralateral ACL injury, were found and systematically reviewed. In 13 of these studies, patients were followed prospectively after a unilateral ACL injury. The evidence presented in the literature shows that the risk of sustaining a contralateral ACL injury is greater than the risk of sustaining a first time ACL injury. Return to a high activity level after a unilateral ACL injury was the most important risk factor of sustaining a contralateral ACL injury. There was inconclusive evidence of the relevance of factors such as female gender, family history of ACL injuries, and a narrow intercondylar notch, as risk factors for a contralateral ACL injury. Risk factors acquired secondary to the ACL injury, such as altered biomechanics and altered neuromuscular function, affecting both the injured and the contralateral leg, most likely, further increase the risk of a contralateral ACL injury. This literature review indicates that the increased risk of sustaining a contralateral ACL injury should be contemplated, when considering the return to a high level of activity after an ACL injury.

No abstract

BackgroundThe complement system is suggested to be involved in the pathogenesis of osteoarthritis (OA), and proinflammatory cytokines may play a role in OA development by inducing proteases. The association between complement factors, cytokines and OA has not been investigated. The aim of the present study was to explore the involvement of the complement system after knee trauma and in OA.MethodsC4d, C3bBbP and soluble terminal complement complex (sTCC) resulting from complement activation were immunoassayed in synovial fluid from subjects with healthy knees (reference), OA, rheumatoid arthritis (RA; positive control), pyrophosphate arthritis (PPA; positive control) and knee injury; other biomarkers were previously assessed. Magnetic resonance imaging was used to assess joint injuries.ResultsCompared with levels in the reference group, the median concentrations of C4d, C3bBbP and sTCC in the OA, RA, PPA and knee injury groups were 2- to 34-fold increased (p < 0.001 to p = 0.044). For the knee injury group, the median concentrations of C4d, C3bBbP and sTCC were 5- to 12-fold increased (p < 0.001) at the day of injury; after 3–12 weeks, C3bBbP and sTCC concentrations were similar to reference levels; and C4d was still increased several years after injury. In the 0–12 weeks period after injury, the concentrations of C4d, C3bBbP and sTCC correlated positively with levels of interleukin (IL)-1β, IL-6 and tumour necrosis factor α (r s range 0.232–0.547); none of the measured complement factors correlated with proteolytic fragments of aggrecan or cartilage oligomeric matrix protein. Knees with osteochondral fracture, with or without disrupted cortical bone, had higher concentrations of C4d (p = 0.014, p = 0.004) and sTCC (p = 0.004, p < 0.001) compared with knees without fractures.ConclusionsThe complement system is activated in OA and after knee injury. Following knee injury, this activation is instant and associated with inflammation as well as with the presence of osteochondral fractures.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1123-x) contains supplementary material, which is available to authorized users.