Journal of orthopaedic research : official publication of the Orthopaedic Research Society
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Clinical Trial
Postoperative serum attenuates LPS-induced release of TNF-alpha in orthopaedic surgery.
Studies with ex vivo stimulation of whole blood samples from injured patients have revealed a diminished production capacity for a broad range of secretory products, including inflammatory cytokines. Recent interest has focused on the release of mediators in serum that depress the cell-mediated immune response following trauma. The involvement of the lipid mediator prostaglandin E2 (PGE2) has been assumed because it is a potent endogenous immunosuppressor. ⋯ PGE2 was significantly (p = 0.008) increased in serum at postoperative day 6 as compared to preoperative levels. In conclusion, these data show that at day 6 after major orthopaedic surgery, the patient serum contained activity that inhibited ex vivo LPS-induced TNF-alpha release. The potent TNF-alpha inhibitory activity found at day 6 after injury correlated with increased levels of PGE2 and indicates cell-mediated hyporesponsiveness to a second stimulus.
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Patellofemoral complications following knee arthroplasty are a well-known problem. Patellar ischemia has been suspected to be causative for fracture, anterior knee pain, and patella component failure. The purpose of this study was to assess the influence of knee arthroplasty surgical dissection on patellar blood flow. ⋯ Flexion of the knee joint markedly reduced patellar perfusion. Standard medial parapatellar approach did not significantly change patellar blood flow. This study does not support the theory of postoperative patellar ischemia as a cause of anterior knee pain or patellofemoral problems.