Inflammatory changes in synovial tissues occur commonly in knee osteoarthritis (OA) and are termed “inflammatory OA”. The pathogenic significance of this inflammatory OA is uncertain. It is also not known whether inflammatory changes in the synovial membrane are reflected in the synovial fluid (SF) and whether the SF contains a similar inflammatory cell infiltrate. This study examined 34 cases of knee joint OA and cytologically and immunohistochemically characterised inflammatory cells in the synovial membrane and SF. Specimens of SF and synovial membrane were taken at the time of knee arthroplasty. All cases of inflammatory OA synovium contained (CD68+) macrophages; several cases also contained a scattered, focally heavy (CD3+) lymphocytic infiltrate and occasional lymphoid aggregates. Inflammatory changes in OA SF reflected this cell composition with numerous CD68+ macrophages and CD3+ lymphocytes being noted in inflammatory OA cases. The SF volume was greater (>
5ml) in cases of inflammatory OA. Non-inflammatory OA knee joints contained very few inflammatory cells, which were mainly macrophages, in both the synovial membrane and SF. Our findings indicate that inflammatory changes in the synovial membrane of OA knee joints are reflected in the SF and that the volume of SF is commonly increased in cases of inflammatory OA. Both macrophages and lymphocytes in the inflammatory infiltrate of knee joint SF may contribute to joint destruction in OA by providing mononuclear phagocyte osteoclast precursors and the production of inflammatory cytokines and growth factors that promote osteoclastogenesis. In conclusion, the cytology of SF and synovitic membrane are similar in inflammatory OA. With knee effusions of greater than 5mls and inflammatory synovitic membrane consideration of total knee arthoplasty in the presence of single compartment disease should be considered because of the risk of further joint destruction.
Graf’s alpha angles and percentage cover were reviewed from the original ultrasounds, many of which were of poor quality. This demonstrated that there was less than 50% cover for 14/30 (47%) who were watched, for 6/9 (78%) who had arthrograms, for 1/1 (100%) treated by harness, for 4/5 (80%) treated with adductor tenotomy and hip spica and for 2/2 (100%) requiring surgery. Alpha angles less than 60 degrees did not predict the need for intervention. There were no late cases from the group that had X-rays classed as normal at 5 months.
Systemic embolic phenomena are well recognised during total knee replacement (TKR) and are widely believed to be the cause of intra-operative hypotension and reduced cardiac output, which may lead to circulatory collapse and sudden death. We undertook a prospective, double-blind, randomised study comparing the cardiac embolic load during computer-assisted and conventional (intramedullary-aligned) TKR, as measured by transoesophageal echocardiography. 26 consecutive procedures were performed by a single surgeon at a single site. Embolic load was scored using the modified Mayo grading system for echogenic emboli. Patients undergoing conventional TKR (n=12) had a mean embolic score of 6.15 (SD 0.83) on release of the tourniquet. Those undergoing computer-assisted TKR (n=14) had a mean embolic score of 4.89 (SD 1.10). Comparison of the groups using a two-tailed t-test confirmed a highly significant reduction (p=0.004) in embolic load when performing computer-assisted TKR. The groups were otherwise well matched and there were no complications. In conclusion, this study demonstrates that computer-assisted TKR results in the release of significantly fewer systemic emboli than conventional TKR using intra-medullary alignment. There is evidence that this should reduce perioperative morbidity and neurological dysfunction. This would appear to add to the ever-growing list of arguments in favour of computer-assisted total knee replacement.