Intraoperative kinematic analysis of posterior stabilized total knee arthroplasty with asymmetric helical post-cam design.

PURPOSE: To investigate intraoperative kinematics during passive flexion using a surgical navigation system for knees undergoing posterior stabilized (PS) total knee arthroplasty (TKA) with an asymmetric helical post-cam design using navigation system. METHODS: In total, 45 knees with both pre- and postoperative kinematic data available were included in the study. Intraoperative kinematic measurements were performed during the course of surgery using the software incorporated in the navigation system. Measurements were performed at the following two time points: (1) before TKA procedure and (2) after TKA implantation. Among the kinematic parameters studied, anterior/posterior translation and axial rotation during flexion were subjected to the analysis. RESULTS: Before surgery, physiologic anterior/posterior translational pattern of the tibia during flexion (rollback of the femur) was found in only 15.6% of the knees. After TKA implantation, postoperative kinematic measurement showed no significant change in the tibial translational during knee flexion. Similarly, with regard to rotation, non-physiologic external tibial rotation in early flexion was observed in the majority of the knees before surgery, and this abnormal kinematic pattern remained after the TKA procedure. CONCLUSIONS: The intraoperative three-dimensional motion analysis using a navigation system showed that the physiologic kinematic pattern (anterior translation and internal rotation of the tibia during flexion) of the knee was distorted in osteoarthritic knees undergoing TKA. The abnormal kinematic pattern before surgery was not fully corrected even after implantation of the PS TKA designed to induce natural knee motion; however, no clear relationship between the intraoperative kinematic pattern and knee flexion angle at one year was demonstrated, and the effect of knee kinematics on postoperative knee function and patient's satisfaction is still unclear.

Local Infiltration Analgesia Versus Continuous Femoral Nerve Block in Pain Relief After Total Knee Arthroplasty: A Randomized Controlled Trial.

BACKGROUND: Although both local infiltration analgesia (LIA) and continuous femoral nerve block (FNB) are common analgesic modalities for pain relief after total knee arthroplasty (TKA), we are aware of no parallel-group, randomized controlled trial that has solely compared the efficacy of LIA and continuous FNB. METHODS: We conducted a prospective, 2-arm, parallel-group, randomized controlled trial involving patients scheduled for TKA. A total of 45 patients were randomly assigned to either the LIA or the continuous FNB group. Except for the analgesic modality, perioperative managements were identical in both groups. The primary outcome was postoperative pain score at rest 1 day after surgery, measured using a 100-mm visual analog scale. RESULTS: Patients in the LIA group had a significantly lower visual analog scale score at rest 1 day after surgery than those in the continuous FNB group (34 ± 10 vs 42 ± 13 mm; P = .028). The opioid consumption during the initial 24 hours was significantly lower in the LIA group (12 ± 4 vs 16 ± 7 mg; P = .031). There were no differences in the rate of complications between the groups. CONCLUSION: LIA was associated with better pain relief with a comparable complications rate for patients undergoing TKA than FNB. We recommend LIA for pain relief after TKA.

Double threaded screw fixation for bilateral stress fracture of the medial malleolus.

An 18-year-old college basketball player presented with continued ankle pain. A radiographic examination showed bilateral medial malleolus stress fractures. Considering the prolonged history and refractory nature of this injury, surgery was adopted as a treatment option. At surgery, the fracture site was percutaneously fixed using two cannulated double threaded screws. Surgery for each side was sequentially performed two months apart. Prompt bony healing was attained after surgery, and the patient could return to his previous sports level six months after the first surgery without subsequent recurrence.

Mechanical injury suppresses autophagy regulators and pharmacologic activation of autophagy results in chondroprotection.

OBJECTIVE: Mechanical injury induces cell death in cartilage and triggers a remodeling process that ultimately can manifest as osteoarthritis. Autophagy is a process for turnover of intracellular organelles and macromolecules that protects cells during stress responses. This study was undertaken to determine changes in and functions of autophagy following mechanical injury to cartilage. METHODS: Bovine and human cartilage explants were subjected to mechanical impact (40% strain for 500 msec). Cell viability, sulfated glycosaminoglycan (sGAG) release, and changes in the levels of the autophagy markers ULK1, beclin 1, and microtubule-associated protein 1 light chain 3 (LC3) were evaluated. Cartilage explants were treated with the mammalian target of rapamycin complex 1 (mTORC-1) inhibitor and the autophagy inducer rapamycin and tested for protective effects against mechanical injury. Explants were also treated with the cell death inducers nitric oxide and tumor necrosis factor α (TNFα) plus actinomycin D, and the proinflammatory cytokine interleukin-1α (IL-1α). RESULTS: Mechanical injury induced cell death and loss of sGAG in a time-dependent manner. This was associated with significantly decreased ULK1, beclin 1, and LC3 expression in the cartilage superficial zone (P < 0.05) 48 hours after injury. The levels of LC3-II were increased 24 hours after injury but decreased at 48 and 96 hours. Rapamycin enhanced expression of autophagy regulators and prevented cell death and sGAG loss in mechanically injured explants. Rapamycin also protected against cell death induced by sodium nitroprusside and TNFα plus actinomycin D and prevented sGAG loss induced by IL-1α. CONCLUSION: Our findings indicate that mechanical injury leads to suppression of autophagy, predominantly in the superficial zone where most of the cell death occurs. Pharmacologic inhibition of mTORC-1, at least in part by enhancement of autophagy, prevents cell and matrix damage, suggesting a novel approach for chondroprotection.

The role of ERK signaling and the P2X receptor on mechanical pain evoked by movement of inflamed knee joint.

Pain during inflammatory joint diseases is enhanced by the generation of hypersensitivity in nociceptive neurons in the peripheral nervous system. To explore the signaling mechanisms of mechanical hypersensitivity during joint inflammation, experimental arthritis was induced by injection of complete Freund's adjuvant (CFA) into the synovial cavity of rat knee joints. As a pain index, the struggle threshold of the knee extension angle was measured. In rats with arthritis, the phosphorylation of extracellular signal-regulated kinase (ERK), induced by passive joint movement, increased significantly in dorsal root ganglion (DRG) neurons innervating the knee joint compared to the naïve rats that received the same movement. The intrathecal injection of a MEK inhibitor, U0126, reduced the phosphorylation of ERK in DRG neurons and alleviated the struggle behavior elicited by the passive movement of the joint. In addition, the injection of U0126 into the joint also reduced the struggle behavior. These findings indicate that the ERK signaling is activated in both cell bodies in DRG neurons and peripheral nerve fibers and may be involved in the mechanical sensitivity of the inflamed joint. Furthermore, the phosphorylated ERK-positive neurons co-expressed the P2X3 receptor, and the injection of TNP-ATP, which antagonizes P2X receptors, into the inflamed joint reduced the phosphorylated ERK and the struggle behavior. Thus, it is suggested that the activation of the P2X3 receptor is involved in the phosphorylation of ERK in DRG neurons and the mechanical hypersensitivity of the inflamed knee joint.

Plasma membrane calcium ATPase expression in the rat spinal cord.

Plasma membrane Ca2+-ATPase (PMCA) is a calcium pump that exists on the plasma membrane and has a role in keeping the intracellular Ca2+ concentration low. In the current study, the expression of PMCA isoforms in spinal cord tissues was investigated in detail and the changes of the expression was examined after contusion injury. Rats received a weight drop on the thoracic spinal cord as the injury or they received a sham surgery as a control. Three or twenty-four hours after spinal cord injury (SCI), the spinal cord was removed and processed for in situ hybridization, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. PMCA1-4 mRNAs were expressed in neurons in the control spinal cord. Each isoform of the PMCA proteins showed distinct expression patterns in the spinal cord. PMCA1 and PMCA3 were expressed in all of the layers of gray matter. PMCA2 was also abundant in gray matter, except laminae I and II, while PMCA4 expression was restricted to the superficial layers of the dorsal horn. Distinct expression patterns of the PMCA isoforms suggest differential functions of each isoform in the spinal cord. After spinal cord injury, the expression of PMCA2 was decreased; however, the change in expression of other isoforms showed a tendency of decrease but did not reach a statistically significant level. The decrease in PMCA expression may contribute to the increase in intracellular Ca2+ concentration and PMCA may have a role in secondary injury following spinal cord injury.