Influence of asymmetric tether on the macroscopic permeability of the vertebral end plate.

摘要

We implemented an experimental model of asymmetrical compression loading of the vertebral end plate (VEP) in vivo. The macroscopic permeability of the VEP was measured. We hypothesized that static asymmetrical loading on vertebrae altered the macroscopic permeability of the VEP. In scoliosis, solute transport to and from the disc is dramatically decreased especially at the apical intervertebral disc. The decrease in permeability could be induced by mechanical stress. Nine skeletally immature pigs were instrumented with left pedicle screws and compression rod at the T5/T6 and L1/L2 levels. After 3 months, three cylindrical specimens of the VEP were obtained from each of the tethered levels. A previously validated method for measuring permeability, based on the relaxation pressure due to a transient-flow rate was used. A pistoning device generated a fluid flow that fully saturated the cylindrical specimen. The decrease in upstream pressure was measured using a pressure transducer, which allowed the macroscopic permeability to be derived. A microscopic study completed the approach. Overall macroscopic permeability was lower for the tethered VEPs than for the VEPs of the control group, respectively -47 for flow-in (p = 0.0001) and -46 for flow-out (p = 0.0001). In the tethered group, macroscopic permeability of the specimens from the tethered side was lower than macroscopic permeability of those from the non-tethered side, -39 for flow-out (p = 0.024) and -47 for flow-in (p = 0.13). In the control group, the macroscopic permeability was greater in the center of the VEP than in its lateral parts for flow-out (p = 0.004). Macroscopic permeability of the center of the VEPs was greater for flow-out than for flow-in (p = 0.02). There was no significant difference between thoracic and lumbar. This study demonstrated that compression loading applied to a growing spine results in decreased permeability of the VEP. This result could be explained by local remodeling, such as calcification of the cartilage end plate or sclerosis of the underlying bone.