Biomechanical Role of the Thoracolumbar Ligaments of the Posterior Ligamentous Complex: A Finite Element Study.

OBJECTIVES: To investigate the effect of sequential ligament failure on the range of motion (ROM) and location of the instantaneous axes of rotation (IAR) of the thoracolumbar spine (T12-L1) finite element (FE) model, and to verify the role of the supraspinous ligament (SSL) in maintaining the stability of the injured thoracolumbar spine. METHODS: An FE model of the fractured thoracolumbar spine was developed and validated against published data. The posterior ligamentous complex (PLC) in the fractured T12-L1 segment was then reduced in a sequential manner from the facet capsular ligament (FCL), part of the interspinous ligament (ISL), SSL, and entire ISL, to the ligamentum flavum (LF). The ROM and IAR of the T12-L1 segment were measured at the fracture and at each reduced ligament step under 4 directions of flexion, extension, lateral bending, and rotation, and 4 bending motions of 1.5, 3.0, 4.5, 6.0 Nm. RESULTS: The FE model showed a consistent increase in the ROM and location of the IAR as the ligaments were removed sequentially. Furthermore, failure of the SSL had the most significant influence on the change in the ROM and IAR in flexion. In extension, removal of the FCL caused the largest shift. CONCLUSIONS: The SSL is a significant ligament that allows the PLC to maintain the stability of the thoracolumbar spine during injury.

Risk Factor of Failed Reduction of Posterior Ligamentatoxis Reduction Instrumentation in Managing Thoracolumbar Burst Fractures: A Retrospective Study.

OBJECTIVE: To determine whether radiographic findings associated with thoracolumbar burst fractures could be predictors of failure of short-segment posterior instrumentation with insertion screw at the fracture level (SSPI-f). METHODS: Seventy-five patients with thoracolumbar burst fracture surgically treated by SSPI-f were enrolled in the study and divided into 2 groups: a reduction group (n = 46) and a failed-reduction group (n = 29). Radiographic data including local kyphosis, Cobb angle, anterior vertebral height, posterior vertebral height (PVH), anterior/posterior vertebral height ratio, interpedicle distance (IPD), bony compress area, bony fracture area, and compress-fracture area of the fractured vertebra and clinical data including age and neurologic function were also analyzed. t test, Pearson χ2 test, and binary logistic regression were performed to compare the values. RESULTS: The PVH in the failed-reduction group was smaller than that of the reduction group (83.5% ± 7.2% and 89.1% ± 5.4%, respectively) (P = 0.001). The IPD differed between the reduction and failed-reduction group (18.0% ± 4.1% and 25.8% ± 7.1%, respectively) (P < 0.001). There was a statistical difference between the 2 groups in delayed time before surgery (P = 0.008). There was a significant difference of bony fracture area and compress-fracture area of the fractured vertebra between the failed-reduction and reduction group (both P < 0.001). Binary logistic regression showed that IPD was a risk factor of reduction failure of SSPI-f (P = 0.001). CONCLUSIONS: These results showed that increased IPD was a risk factor of failed-reduction of SSPI-f in managing thoracolumbar burst fractures, particularly for patients with neurologic deficit, whereas local kyphosis, Cobb angle, anterior vertebral height, PVH, anterior/posterior vertebral height ratio, bony compress area, bony fracture area, and compress-fracture area of the fractured vertebra were not.

Sirt6 overexpression suppresses senescence and apoptosis of nucleus pulposus cells by inducing autophagy in a model of intervertebral disc degeneration.

Treatment of intervertebral disc degeneration (IDD) seeks to prevent senescence and death of nucleus pulposus (NP) cells. Previous studies have shown that sirt6 exerts potent anti-senescent and anti-apoptotic effects in models of age-related degenerative disease. However, it is not known whether sirt6 protects against IDD. Here, we explored whether sirt6 influenced IDD. The sirt6 level was reduced in senescent human NP cells. Sirt6 overexpression protected against apoptosis and both replicative and stress-induced premature senescence. Sirt6 also activated NP cell autophagy both in vivo and in vitro. 3-methyladenine (3-MA) and chloroquine (CQ)-mediated inhibition of autophagy partially reversed the anti-senescent and anti-apoptotic effects of sirt6, which regulated the expression of degeneration-associated proteins. In vivo, sirt6 overexpression attenuated IDD. Together, the data showed that sirt6 attenuated cell senescence, and reduced apoptosis, by triggering autophagy that ultimately ameliorated IDD. Thus, sirt6 may be a novel therapeutic target for IDD treatment.