Megaprosthesis use in Paprosky III/IV femoral defects in non-oncological patients: analysis of survival, clinical, and functional outcomes after an average follow-up of five years.

PURPOSE: To determine the survival and patient-reported outcomes in non-oncological patients treated with proximal femoral resection (PFR) using MEG for femoral reconstruction. MATERIALS AND METHODS: This retrospective study included 16 patients. Demographic variables and complications developed were analyzed. Clinical-functional outcomes were measured using the modified Harris score (mHSS), numeric Pain Rating Scale (NPRS) and Musculoskeletal Tumor Society (MSTS) score. MEG survival was estimated using a Kaplan-Meier survival analysis. RESULTS: Average follow-up was 5 years (range, 1-9). The 75% of patients were overweight and women with an average age of 74.2 ± 5.9-years (BMI of 28.5 ± 4.2 kg/m2). The main cause of MEG was periprosthetic infection (43.7%). The 50% of patients had post-surgical complications regarding with MEG, being the most frequent seromas and MEG dislocation. Implant survival was 93.4% and 80.9% at 3 and 7 years of follow-up, respectively. The functional results at the end of the follow-up with respect to the pre-surgical state improved from 9.5 ± 2.6 to 3 ± 0.9 mean NPRS and 26.5 ± 6.8 to 69.5 ± 13.5 mean mHHS, p < 0.001, respectively. The mean MSTS score was 68.1% that these results were considered excellent. CONCLUSIONS: The MEG for reconstruct III-IV femoral defects is a good therapeutic option that offers an acceptable clinical-functional result. Short-term and medium-term survival was greater than 80%. The most frequent complications are seromas and MEG dislocation. The use of constrained liner and abductor system reconstruction is essential to prevent the dislocation.

Unicompartmental knee arthroplasties: does the type of tibial component selected influence implant survival?

INTRODUCTION: Few information has been published on the survival of unicompartmental knee arthroplasty (UKA) and fixed-bearing tibial components. The aim of this study is to analyze if UKA survival varies according to UKA model used and to analyze the possible risk factors for UKA revision. MATERIALS AND METHODS: A retrospective study analyzing 301 UKAs (ACCURIS, all-polyethylene tibial component, 152; Triathlon PKR, metal-backed tibial component, 149) was performed. Demographic parameters as well as implant survival and cause of prosthetic revision were analyzed. The Kaplan-Meier survival analysis, the log-rank test and the Cox multiple regression were used for the analysis. RESULTS: Average follow-up was 8.1 ± 3.08-years. Average age was 68.1 ± 8.6-years; 70.4% of subjects were women. The ACCURIS UKA group had a UKA revision rate higher compared to the Triathlon PKR group (16/152, 10.6% vs 5/149, 3.4%, respectively; p < 0.001). The main cause of prosthetic revision was aseptic loosening (5/21, 23.8%). All aseptic loosening cases and tibial component collapse were reported with the ACCURIS UKA group. Overall UKA survival was 98.01% (95% CI 95.62-99.1) at 1-year, 94.27% (95% CI 90.95-96.4) at 5-years and 92.38% (95% CI 88.48-94.99) at 10-years' follow-up. There were no differences in the Kaplan-Meier survival curves regarding operated side or affected tibiofemoral compartment (log-rank test = 0.614 and 0.763, respectively). However, Kaplan-Meier survival curve according to UKA model used was different (log-rank test = 0.033). The metal-backed component appeared to be a protector factor for UKA revision when adjusted for age, sex, operated side, and affected tibiofemoral compartment (Hazard Ratio 0.32, p = 0.031). CONCLUSION: Fixed-bearing UKAs showed excellent mid- and long-term survival rates. Aseptic loosening is the main cause of implant failure. PKR group (metal-backed component) seem to be a protector factor to UKA revision when it was compared with ACCURIS UKA group (all-polyethylene tibial component).

Postnatal proteasome inhibition induces neurodegeneration and cognitive deficiencies in adult mice: a new model of neurodevelopment syndrome.

Defects in the ubiquitin-proteasome system have been related to aging and the development of neurodegenerative disease, although the effects of deficient proteasome activity during early postnatal development are poorly understood. Accordingly, we have assessed how proteasome dysfunction during early postnatal development, induced by administering proteasome inhibitors daily during the first 10 days of life, affects the behaviour of adult mice. We found that this regime of exposure to the proteasome inhibitors MG132 or lactacystin did not produce significant behavioural or morphological changes in the first 15 days of life. However, towards the end of the treatment with proteasome inhibitors, there was a loss of mitochondrial markers and activity, and an increase in DNA oxidation. On reaching adulthood, the memory of mice that were injected with proteasome inhibitors postnatally was impaired in hippocampal and amygdala-dependent tasks, and they suffered motor dysfunction and imbalance. These behavioural deficiencies were correlated with neuronal loss in the hippocampus, amygdala and brainstem, and with diminished adult neurogenesis. Accordingly, impairing proteasome activity at early postnatal ages appears to cause morphological and behavioural alterations in adult mice that resemble those associated with certain neurodegenerative diseases and/or syndromes of mental retardation.