Nitric oxide protects osteoblasts from oxidative stress-induced apoptotic insults via a mitochondria-dependent mechanism.

Nitric oxide (NO) contributes to the regulation of osteoblast activities. In this study, we evaluated the protective effects of NO pretreatment on oxidative stress-induced osteoblast apoptosis and its possible mechanism using neonatal rat calvarial osteoblasts as the experimental model. Exposure of osteoblasts to sodium nitroprusside (SNP) at a low concentration of 0.3 mM significantly increased cellular NO levels without affecting cell viability. However, when the concentration reached a high concentration of 2 mM, SNP increased the levels of intracellular reactive oxygen species and induced osteoblast injuries. Thus, administration of 0.3 and 2 mM SNP in osteoblasts were respectively used as sources of NO and oxidative stress. Pretreatment with NO for 24 h significantly ameliorated the oxidative stress-caused morphological alterations and decreases in alkaline phosphatase activity, and reduced cell death. Oxidative stress induced osteoblast death via an apoptotic mechanism, but NO pretreatment protected osteoblasts against the toxic effects. The mitochondrial membrane potential was significantly reduced following exposure to the oxidative stress. However, pretreatment with NO significantly lowered the suppressive effects. Oxidative stress increased cellular Bax protein production and cytochrome c release from mitochondria. Pretreatment with NO significantly decreased oxidative stress-caused augmentation of Bax and cytochrome c protein levels. In parallel with cytochrome c release, oxidative stress induced caspase-3 activation and DNA fragmentation. Pretreatment with NO significantly reduced the oxidative stress-enhanced caspase-3 activation and DNA damage. Results of this study show that NO pretreatment can protect osteoblasts from oxidative stress-induced apoptotic insults. The protective action involves a mitochondria-dependent mechanism.

Double-bundle posterior cruciate ligament reconstruction using inlay technique with quadriceps tendon-bone autograft.

Surgical reconstruction of the posterior cruciate ligament (PCL) is indicated in a PCL-deficient knee with symptomatic instability and multiple ligament injuries. The results of the traditional tunnel method for PCL reconstruction remain uncertain. The tibial inlay method offers the benefit of preventing the acute-turn associated with transtibial reconstruction. Additionally, the double-bundled graft appears to restore normal knee laxity across the full range of flexion. This study presents an inlay technique for arthroscopic PCL reconstruction with double-bundled quadriceps tendon-patellar bone autograft. This technique offers a reasonable alternative for PCL reconstruction.

Clavicular hook plate may induce subacromial shoulder impingement and rotator cuff lesion--dynamic sonographic evaluation.

BACKGROUND: Clavicular hook plates are effective fixation devices for distal clavicle fractures and severe acromioclavicular joint dislocations. However, increasing number of studies has revealed that subacromial portion of the hook may induce acromial bony erosion, shoulder impingement, or even rotator cuff damage. By sonographic evaluation, we thus intended to determine whether the presence of hook plate may induce subacromial shoulder impingement and its relationship relative to surrounding subacromial structures. METHODS: We prospectively followed 40 patients with either distal clavicle fracture or acromioclavicular joint dislocation that had surgery using the Arbeitsgemeinschaft für Osteosynthesefragen (AO) clavicular hook plate. All patients were evaluated by monthly clinical and radiographic examinations. Static and dynamic musculoskeletal sonography examinations were performed at final follow-up before implant removal. Clinical results for pain, shoulder function, and range of motion were evaluated using Constant-Murley and Disability of Arm, Shoulder, and Hand (DASH) scores. RESULTS: Clinically, 15 out of 40 patients (37.5%) presented with subacromial impingement syndrome and their functional scores were poorer than the non-impinged patients. Among them, six patients were noted to have rotator cuff lesion. Acromial erosion caused by hook pressure developed in 20 patients (50%). CONCLUSIONS: We demonstrated by musculoskeletal sonography that clavicular hook plate caused subacromial shoulder impingement and rotator cuff lesion. The data also suggest an association between hardware-induced impingement and poorer functional scores. To our knowledge, the only solution is removal of the implant after bony consolidation/ligamentous healing has taken place. Thus, we advocate the removal of the implant as soon as bony union and/or ligamentous healing is achieved.