Comparison of two joint-preserving treatments for osteonecrosis of the femoral head: core decompression and core decompression with additional cancellous bone grafting.

Objective: Femoral head necrosis (FHN) affects mostly young and active people. The most common operative therapy is core decompression (CD) with optional cancellous bone grafting (CBG). Because little information is available on the long-term results of these procedures, we investigated the effectiveness of CD and CD + CBG in patients with ARCO stage II FHN in terms of postoperative pain, range of motion, patient-reported outcome measures (Harris Hip Score, Hip Disability and Osteoarthritis Outcome Score, EuroQol 5D, and Short Form 36 Questionnaire), and disease progression.

Avascular necrosis of the femoral head: three-dimensional measurement of drilling precision reveals high accuracy and no difference between fluoroscopically controlled core decompression and cancellous bone grafting.

Introduction: Avascular osteonecrosis of the femoral head (AVN) is a widespread disease affecting mostly young and active people, often exacerbating in progressive stages, ending in joint replacement. The most common joint preserving operative therapy for early stages is core decompression (CD), optional with cancellous bone grafting (CBG). For success it is vital that the necrotic area is hit and the sclerotic rim is broken by drilling into the defect zone to relieve intraosseous pressure.

Distinct histological alterations of cortical interneuron types in mouse models of Huntington's disease.

Huntington's disease (HD) is a debilitating hereditary motor disorder caused by an expansion of the CAG triplet repeat in the Huntingtin gene. HD causes neurodegeneration particularly in the basal ganglia and neocortex. In the cortex, glutamatergic pyramidal neurons are known to be severely affected by the disease, but the involvement of GABAergic interneurons remains unclear.

Fluc-EGFP reporter mice reveal differential alterations of neuronal proteostasis in aging and disease.

The cellular protein quality control machinery is important for preventing protein misfolding and aggregation. Declining protein homeostasis (proteostasis) is believed to play a crucial role in age-related neurodegenerative disorders. However, how neuronal proteostasis capacity changes in different diseases is not yet sufficiently understood, and progress in this area has been hampered by the lack of tools to monitor proteostasis in mammalian models.