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Interface tissues and pseudocapsules from loose total hip replacements were removed during revision of 11 cases and were investigated for the plasminogen activation system and IL-1beta. Control samples of synovium were taken during knee arthroscopy (n 8), and from the hip joint during primary total hip replacement (n 5). The concentrations of urokinase plasminogen activator (uPA), tissue type plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) and interleukin 1beta were all found to be significantly different in interfaces and in pseudocapsules, compared to controls. Immunohistochemistry disclosed localization in periprosthetic tissues of uPA, uPA-receptor and tPA in macrophages with phagocytosed metal, polyethylene, cement particles or accompanying pieces of necrotic bone. PAI-1 staining was present in the neighboring areas that stained for uPA or tPA, but PAI-1 staining was also found overlapping and outside these areas. These findings suggest a role for the uPA/uPA- receptor and PAI-1 in activation and focalization of extracellular matrix degradation in periprosthetic tissues. The expression of the plasminogen activation system by macrophages containing phagocytosed material suggests undegradable microdebris as a possible initiating and perpetuating stimulus for a proteolytic activation cascade, which may contribute to loosening of the prosthesis.

We analyzed the fibrinolytic system in patients with chronic low back pain using a venous occlusion test to stimulate fibrinolysis, and we subsequently determined the levels of tissue plasminogen activator (TPA) and fast-acting inhibitor of TPA (PAI). There were 20 patients with a mean age of 50 years. Two thirds had radiographically spinal stenosis. Scar tissue around the spinal nerves was seen in 11 cases. Thirteen patients had undergone back surgery, whereas 21 healthy subjects served as controls. In the basal samples, TPA activity was decreased in the patients while TPA antigen level was increased compared with the controls. No clear explanation for this defective function of TPA in the patients was obtained, because no difference was seen in PAI level in basal samples. After the venous occlusion, no difference was observed in TPA activity between the two groups excluding the constitutionally defective fibrinolytic system in the patients. However, our results confirm low basal fibrinolytic activity in patients with chronic low back pain with manifest spinal pathology.