Kinematics analyses of the spine have been recognized as an effective method for functional analysis of the spine. CT is suitable for obtaining bony geometry of the vertebrae but radiation is a clinical concern. MRI is noninvasive but it is difficult to detect bone edges especially at endplates and processes where soft tissues attach. Kinematics analyses require tracking of solid bodies; therefore, bony geometry is not always necessary for kinematics analysis of the spine. This study aimed to develop a reliable and robust method for kinematics analysis of the spine using an innovative MRI-based 3D bone-marrow model. This IRB-approved study recruited 17 patients undergoing lumbar decompression surgery to treat a single-level symptomatic herniation as part of a clinical trial for a new dynamic stabilization device. T1 & T2 sagittal MRI scans were acquired as part of the pre-operative evaluation in three positions: supine and with the shoulders rotated 45° to the left and right to induce torsion of the lumbar spine. 3D bone-marrow models of L5 and S1 at the neutral and rotated positions were created by selecting a threshold level of the bone-marrow intensity at bone-marrow/bone interface. Validated 3D-3D registration techniques were used to track movements of L5 and S1. Segmental movements at L5/S1 during torsion were calculated.Introduction
Materials and Methods
The morbidity associated with tendinopathy is a costly burden on our health system. Recent investigations in our laboratory have shown that alterations in mechanical stress cause significant changes in tendon expression of key matrix molecules and proteolytic enzymes including the aggrecanase molecules, (e.g. ADAMTS-5). Here, we investigate the biomechanical consequences of such altered tensile stress in tail tendons from mice with and without deletion of the ADAMTS-5 gene. Tail tendons from 12 week old C57BL6 wild type and ADAMTS-5 knock-out mice were immediately snap frozen (ex vivo), or cultured stress deprived for 120 hours in DMEM/10% FCS (eight tendons per group). Material properties including maximum stress, strain and elastic modulus were determined for each tendon in uniaxial tension to failure at a constant strain rate of 1.0 mm/second (10% strain/second) on an Instron 8874 servo-hydraulic testing apparatus. Significant differences between groups were determined with Kruskal-Wallis one-way analysis of variance, followed by Mann-Whitney U test with Benjamini-Hochberg post-hoc corrections for multiple comparisons. Stress deprivation for 120 hours led to a significant increase in maximum stress for both the wild type (~150% increase, p = 0.0008) and ADAMTS-5 deficient (~100%, p = 0.0033) mice when compared to ex vivo tendon. Stress deprivation led to a 100% increase in elastic modulus compared to ex vivo for the wild type tendons (p = 0.0033) but failed to increase this parameter in the ADAMTS-5 deficient mice. When the effect of stress deprivation of the ADAMTS-5 deficient mice was directly compared to the wild type stress deprived tendons, a 35% decrease in elastic modulus was found (p = 0.021). We have shown for the first time that deletion of an aggrecanase molecule significantly decreases the material properties of tendon. Alterations in the expression of the aggrecanase molecules may play a role in the development and progression of tendinopathy through their ability to modulate the metabolism of aggrecan [
