10 key recommendations for diagnosis of knee OA were developed using both research evidence and expert consensus. Although there is no agreed reference standard, thorough clinical assessment alone can provide a confident rule-in diagnosis.

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Summary. Background: Activation of coagulation and ®brino-lysis play a role in the pathophysiology of experimental arthritis. Objective: To determine the extent of activation of the coagulation and ®brinolytic pathways in different joint diseases in humans and to ascertain the factors that may in¯uence ®brin deposition within the joint. Methods: Plasma from normal subjects (controls, n 21) and plasma and synovial¯uid samples from patients with rheumatoid arthritis (RA; n 64), osteoarthritis (OA; n 29), spondyloarthropathy (SpA; n 22) and crystal arthritis (CA; n 25) were analyzed for the levels of TF (tissue factor) and tissue factor pathway inhibitor (TFPI) activities, thrombin±antithrombin III (TAT) complexes, and F1 2 (thrombin fragment), ®brin D-dimer and thrombin-activated ®brinolysis inhibitor (TAFI) antigenic levels. The measurements were analyzed by pairwise correlation with each other as well as with standard parameters of in¯ammation [C-reactive protein (CRP), joint leukocyte count]. Inter-group comparisons were performed to look for diseasespeci®c differences. Results: Compared with healthy controls, patients with joint diseases had higher levels of TAT, F1 2 and D-dimers in their plasma. In the synovial¯uid, TF activity, TAT, D-dimers, and TAFI were signi®cantly higher in in¯ammatory arthritides than in OA. The levels were highest in RA patients. In the plasma, TF activity was correlated with TAT and D-dimer levels with CRP, TFPI, and TAT. In the synovial¯uid, TF activity correlated with plasma CRP levels, synovial¯uid leukocyte count, and synovial TAT and TAFI levels. In addition, synovial D-dimers correlated with CRP, and synovial TAFI levels were correlated with synovial F1 2 and TAT. Conclusions: Activation of the coagulation and ®brinolytic cascades in the joint and in the circulation is evident in both in¯ammatory and degenerative joint diseases. Within the joint, in¯ammatory mechanisms leading to TF-mediated activation of the coagulation pathway and subsequent ®brin deposition is the most likely explanation for the observed ®ndings. In the plasma, the link between in¯ammation (CRP increase) and TF activation is weak, and a non-TF-mediated mechanism of coagulation activation could explain these ®ndings. RA is characterized by signi®cantly higher levels of TAT in the synovial¯uid and plasma than other arthritides. Although ®brinolytic activity is linked to in¯ammation, the increased amounts of TAFI in the joint, particularly in RA, may explain why ®brin formation is so prominent in this condition compared with other joint diseases.