Medial opening wedge high tibial osteotmy (HTO) is often used to treat varus gonarthrosis in young, active, highly demanding patients, although it has many pitfalls, which were evaluated in a consecutive cohort of patients. A retrospective analysis of a consecutive series of 45 patients with 49 medial opening HTO for varus gonarthrosis using a spacer plate (Puddu I, Arthrex, USA) were included. A Chi square test was used to study the effect between the wedge size and complications. Complications occurred in 22 knees (45%). There was no significant difference between groups for individual complications; however, when combined, there were significantly more complications in the >10 mm wedge group (Chi square p=0.05). The overall complication rate in this series was 45%. The majority were related to intrinsic instability at the osteotomy site (24%) and surgical technique (20%). The evaluated spacer provided inadequate stability.

SUMMARYProteolytic joint destruction in inflammatory and non-inflammatory arthropathy is believed to be mediated, at least in part, by the plasminogen activation (PA) system. To further investigate possible involvement of the PA system, we qiu immunoreactive urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), both plasminogen activator inhibitors (PAI-1 and PAI-2) and u-PA-receptor (u-PAR) in synovial tissue extracts of 14 patients with rheumatoid arthritis (RA) and 12 with osteoarthritis (OA). u-PA, PAI-1, PAI-2 and u-PAR concentrations were significantly higher in RA than in OA patients. t-PA antigen levels were significantly lower in RA than in OA synovial tissue extracts. Immunohistochemistry was performed to compare the distribution and staining intensity of these components in samples of RA and OA synovial tissue. Intense immunostaining of u-PA, u-PAR, PAI-1 and, to a lesser degree, PAI-2 was observed predominantly in the synovial lining of RA patients. In OA patients, u-PA, PAI-1, PAI-2 and u-PAR were barely detectable. t-PA immunostaining was restricted to the endothelial side of vascular walls in both groups. We conclude that the observed increase of u-PA, u-PAR and PAI expression, distributed mainly in the synovial lining area of proliferative and invasively growing synovia] tissue in RA patients, supports a pathogenic role for the PA system in destructive arthritis. Depressed t-PA-mediated plasminogen activation might contribute to delayed intra-articular fibrin removal.K e y w o rd s : Urokinase, Plasminogen activation, Immunohistochemistry, Rheumatoid arthritis. Osteoarthritis.R h e u m a t o id arthritis (RA) is a chronic inflammatory disease, characterized by the destruction of articular cartilage and bone. Proteolytic degradation of the extracellular matrix in inflammatory arthritis is considered to be mediated by proteinases like aspartic, serine, cysteine and metalloproteinases [1], Hyper plastic inflamed synovial tissue overgrows and invades the articular cartilage, and may be involved in the destruction of bone, tendons and ligaments by the production of proteolytic enzymes [2,3].Several studies suggest an important pathogenic role of the plasminogen activation (PA) system in destructive joint disease [4][5][6], but detailed knowledge of the mechanism and components involved is lacking. The central enzyme, plasmin, is a broad-spectrum serine protease, involved in fibrinolysis and thrombo lysis as well as in the degradation of extracellular matrix that is required for normal and pathological forms of cellular invasiveness [7]. Plasmin is able to degrade extracellular matrix directly [8] and by activation of latent matrix metalloproteinases [9,10]. It is produced as inactive plasminogen which is converted into its active form by limited proteolysis of a single peptide bond by plasminogen activators. Two types of plasminogen activators have been characterized: tissue-type plasminogen activator (t-PA), generally viewed as being important in fibrin dissolution, a...

The OHS proves to be an appropriate instrument for assessment of the outcome of total hip replacement from the patient's perspective. Together with the judgement of the surgeon, it provides useful insights into the question of whether this operation has been a success or not.

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Purpose Head-neck modularity was introduced into total hip arthroplasty to provide more intraoperative surgical options. However, modularity led to new problems, such as trunnionosis and fractures of the femoral prosthesis neck. The purpose of this study was to identify risk factors for hip neck fractures and to provide recommendations to prevent damage and fractures of the neck. Methods A systematic review of the literature was performed according to the PRISMA guidelines. Results Thirty-three case studies were included. Methodologically, most included studies were of moderate or good quality. The 80 neck fractures included in the review took place, on average, 7 years after stem placement. Male gender, high body weight, obesity, previous revision surgery, mixing components from different manufacturers, use of long skirted heads, cobalt-chromium (large size) heads were identified as potential risk factors. Conclusion Hip neck fractures occur on average 7 years after stem placement. The etiology of hip neck fractures is multifactorial. This review revealed several preventable implant- and surgeon-related risk factors.