No abstract

In the year 2000 the rate of infection after arthroplasty in our hospital was 9.75% and methicillinresistant Staphylococcus aureus (MRSA) was the organism in 33% of the infected joints. In an attempt to overcome this unacceptable situation, we changed our prophylaxis regime over a period of 6 months. This involved modifying the precautionary measures for preventing surgical infections, active prophylaxis against any nasal reservoir of infection in joint implant patients, the control of health care personnel, the strict application of standard and contact precautions in all patients with MRSA, and the use of teicoplanin as prophylaxis during this 6-month period. This resulted in a definite decrease in the incidence of orthopaedic wound infections by MRSA, while the level of MRSA infection elsewhere in the hospital remained constant. Only one infection was detected during this 6-month trial, and this beneficial effect was maintained during the following 6 months. Since then, only sporadic new infections have been detected. Patients with arthroplasties performed during the study were followed for 12 months, and no new cases of MRSA infection were detected.Résumé Dans l'année 2000 le taux d'infection après arthroplastie dans notre Hôpital fût de 9.75% et le Staphylocoque aureus methicilline -résistant (MRSA) était le germe en cause dans 33% des articulations infectées. Dans le but d'améliorer cette situation inacceptable nous avons changé notre méthode de prophylaxie pendant une période de 6 mois. Cela a impliqué de modifier les mesures pour prévenir les infections chirurgicales : prophylaxie active contre tout réservoir nasal d'infection chez les

Our results show a decreased cell population, with low COMP and altered matrix organization in osteoarthritis menisci that suggest an altered meniscal scaffold and potential impairment of meniscal function. These meniscal changes may be associated with the development of knee osteoarthritis.

The etiology of Perthes' disease is unclear. Recent reports have suggested that inheritable thrombophilic disorders may be one of its pathogenetic causes. The G20210A prothrombin gene, factor V Leiden, and MTHFR C677T mutations have been identified as predisposing genetic factors for thrombosis. Ninety children diagnosed with Perthes' disease were studied. A family history of thrombosis and any other personal thromboembolic events were researched. PCR and endonuclease digestion were used to analyze factor V Leiden, prothrombin G20210A, and MTHFR C677T. Two hundred healthy donors were included as a control group. No patient had a family or personal history of early thrombotic events. Four children with Perthes' disease (4.4%) were heterozygous for G20210A polymorphism compared with controls (odds ratio: 2.07; 95% confidence interval: 0.40-8.46). No association between factor V Leiden and Perthes' disease was observed. Three patients (3.33%) were heterozygous for factor V Leiden (odds ratio: 1.36; 95% confidence interval: 0.32-5.84). The prevalence of different genotypes of C677T MTHFR did not show statistical differences compared with controls. Eleven patients were homozygous for this polymorphism (odds ratio: 1.02; 95% confidence interval: 0.42-2.44). This study does not support the screening of this group of polymorphism in patients with Perthes' disease.