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Evaluation of nucleus pulposus fluid velocity and pressure alteration induced by cartilage endplate sclerosis using a poro-elastic finite element analysis.

ABSTRACT: The nucleus pulposus (NP) in the intervertebral disk (IVD) depends on diffusive fluid transport for nutrients through the cartilage endplate (CEP). Disruption in fluid exchange of the NP is considered a cause of IVD degeneration. Furthermore, CEP calcification and sclerosis are hypothesized to restrict fluid flow between the NP and CEP by decreasing permeability and porosity of the CEP matrix. We performed a finite element analysis of an L3-L4 lumbar functional spine unit with poro-elastic constitutive equations. The aim of the study was to predict changes in the solid and fluid parameters of the IVD and CEP under structural changes in CEP. A compressive load of 500 N was applied followed by a 10 Nm moment in extension, flexion, lateral bending, and axial rotation to the L3-L4 model with fully saturated IVD, CEP, and cancellous bone. A healthy case of L3-L4 physiology was then compared to two cases of CEP sclerosis: a calcified cartilage endplate and a fluid constricted sclerotic cartilage endplate. Predicted NP fluid velocity increased for the calcified CEP and decreased for the calcified + less permeable CEP. Decreased NP fluid velocity was prominent in the axial direction through the CEP due to a less permeable path available for fluid flux. Fluid pressure and maximum principal stress in the NP were predicted to increase in both cases of CEP sclerosis compared to the healthy case. The porous medium predictions of this analysis agree with the hypothesis that CEP sclerosis decreases fluid flow out of the NP, builds up fluid pressure in the NP, and increases the stress concentrations in the NP solid matrix.

SUBMITTER: Hassan CR

PROVIDER: S-EPMC7897237 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundIn the follow-up after internal fixation of thoracolumbar fractures, the imaging of some patients shows "crater-like" collapse of the superior endplate of the injured vertebra, with variable collapse area and depth, even involving the anterior edge of the vertebral body. Though many papers had described the phenomenon, but nearly no one did biomechanical research about this. So we did this research in a creative way by using finite element model.MethodsA healthy male volunteer was selected. The 64-slice thin-section spiral computed tomography images at the level of T11-L3 were collected. Data were imported into Mimics 15.0 medical image processing software to establish three-dimensional finite element skeletal models of T11 to L3 containing only three-dimensional surface elements without entities. The model was assigned values and verified. Then the pedicle screw-rod system was added to this model, and five models containing the screw-rod system with different defect sizes as well as five models that simulated the removal of the screw-rod system were derived at the same time (the defect volume was 1/5, 2/5, 3/5, 4/5, or 5/5 of the anterior vertebral column, respectively). Biomechanical analysis was then performed on this basis.ResultsAfter the removal of the internal fixator, as defect volume increased, the stress difference between the 4/5 defect group and the 5/5 defect group had the greatest magnitude of combined stress under the seven working conditions. When the volume of the collapse defect reached 4/5 of the anterior column of the vertebral body, the concentration of stress increased significantly, suggesting that the risk of continued compression or even refracture of the injured vertebra increased if the internal fixator was removed at that time.ConclusionsWhen the volume of the defect in the superior endplate of the injured vertebra reaches 4/5 of the anterior column, the removal of the internal fixator should be carefully considered to avoid refracture of the anterior column of the injured vertebra.

Project description:To investigate the regulatory effect of carbohydrate sulfotransferase 3 (CHST3) in cartilage endplate-derived stem cells (CESCs) on the molecular mechanism of intervertebral disc degeneration after nucleus pulposus repair in rats. We performed GO and KEGG analysis of GSE15227 database to select the differential genes CHST3 and CSPG4 in grade Ⅱ, Ⅲ and Ⅳ intervertebral disc degeneration, IHC and WB to detect the protein profile of CHST3 and CSPG4, Co-IP for the interaction between CHST3 and CSPG4. Then, immunofluorescence was applied to measure the level of CD90 and CD105, and flow cytometry indicated the level of CD73, CD90 and CD105 in CESCs. Next, Alizarin red staining, Alcian blue staining and TEM were performed to evaluate the effects of CESCs into osteoblasts and chondroblasts, respectively, CCK8 for the cell proliferation of osteoblasts and chondroblasts after induction for different times; cell cycle of osteoblasts or chondroblasts was measured by flow cytometry after induction, and WB for the measurement of specific biomarkers of OC and RUNX in osteoblasts and aggrecan, collagen II in chondroblasts. Finally, colony formation was applied to measure the cell proliferation of CESCs transfected with ov-CHST3 or sh-CHST3 when cocultured with bone marrow cells, WB for the protein expression of CHST3, CSPG4 and ELAVL1 in CSECs, transwell assay for the migration of CESCs to bone marrow cells, TEM image for the cellular characteristics of bone marrow cells, and WB for the protein profile of VCAN, VASP, NCAN and OFD1 in bone marrow cells. CHST3 and CSPG4 were differentially expressed and interacted in grade Ⅱ, Ⅲ and Ⅳ intervertebral disc degeneration; CD73, CD90 and CD105 were lowly expressed in CESCs, osteogenic or chondroblastic induction changed the characteristics, proliferation, cell cycle and specific biomarkers of osteoblasts and chondroblasts after 14 or 21 days,; CHST3 affected the cell proliferation, protein profile, migration and cellular features of cocultured CESCs or bone marrow cells. CHST3 overexpression promoted CESCs to regulate bone marrow cells through interaction with CSPG4 to repair the grade Ⅱ, Ⅲ and Ⅳ intervertebral disc degeneration.

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Evaluation of nucleus pulposus fluid velocity and pressure alteration induced by cartilage endplate sclerosis using a poro-elastic finite element analysis.

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