Annulus Fibrosus Can Strip Hyaline Cartilage End Plate from Subchondral Bone: A Study of the Intervertebral Disk in Tension

Abstract

Study Design Biomechanical study on cadaveric spines. Objective Spinal bending causes the annulus to pull vertically (axially) on the end plate, but failure mechanisms in response to this type of loading are poorly understood. Therefore, the objective of this study was to identify the weak point of the intervertebral disk in tension. Methods Cadaveric motion segments (aged 79 to 88 years) were dissected to create midsagittal blocks of tissue, with ∼10 mm of bone superior and inferior to the disk. From these blocks, 14 bone–disk–bone slices (average 4.8 mm thick) were cut in the frontal plane. Each slice was gripped by its bony ends and stretched to failure at 1 mm/s. Mode of failure was recorded using a digital camera. Results Of the 14 slices, 10 failed by the hyaline cartilage being peeled off the subchondral bone, with the failure starting opposite the lateral annulus and proceeding medially. Two slices failed by rupturing of the trabecular bone, and a further two failed in the annulus. Conclusions The hyaline cartilage–bone junction is the disk's weak link in tension. These findings provide a plausible mechanism for the appearance of bone and cartilage fragments in herniated material. Stripping cartilage from the bony end plate would result in the herniated mass containing relatively stiff cartilage that does not easily resorb.

Structure‐function relationships at the human spinal disc‐vertebra interface

“…33 Failure stresses and failure locations measured in the current study were consistent with those found in previous human disc-bone tensile tests. Our measured failure stresses (range: 0.22-0.93 MPa) were within the range of those reported by Balkovec et al 11 (range: 0.14-2.8 MPa) and lower than those found by Green et al 18 (average 1.7 MPa for posterior and 3.8 MPa for AA), presumably because we cut our specimens smaller to isolate more specific regions, thus disrupting the collagen network mid-fiber due to the angled orientation of annulus fibers. The higher modulus of the PA compared to the AA may help to resist forward bending movements, but the lower extensibility may put weak EPJs at risk for herniation.…”

“…Historical data suggest structural weakness at the cartilage-vertebral EPJ, as supported by recent work showing this location as the weak link of the disc-vertebra interface. 11 …”

“…Historical data suggest structural weakness at the cartilage-vertebral EPJ, as supported by recent work showing this location as the weak link of the disc-vertebra interface. 11 The architectural features and biomechanical behavior of other hard-soft tissue interfaces in the body inform hypotheses about structural properties of the disc-vertebra attachment. For example, functional grading of material properties (i.e., mineralization and collagen fiber organization) enables effective stress transfer and decreases stress concentrations across tendon-bone interfaces, 5,6,12 while collagen fiber anchoring of articular cartilage to bone enhances the integrity of attachment.…”

Staying connected: structural integration at the intervertebral disc–vertebra interface of human lumbar spines

“…Our preliminary findings suggest that lack of integration, especially at the CEP-VEP interface, is associated with IVD degeneration and adds to the current knowledge within the field, whereby lack of structural integrity at the CEP-VEP junction is increasingly being implicated in the aetiology of herniations [31], [20], [40], [16], [3]. Possible reasons for reduced connectivity at the CEP-VEP junction may be either an increase in marrow spaces abutting this interface [18], so reducing locations where fibre integration is possible or retention of discontinuities in the endplate following insufficient retraction of the notochord during spinal development [8].…”

“…Possible reasons for reduced connectivity at the CEP-VEP junction may be either an increase in marrow spaces abutting this interface [18], so reducing locations where fibre integration is possible or retention of discontinuities in the endplate following insufficient retraction of the notochord during spinal development [8]. A further reason could be due to actual physical disruption, as has been described in a recent biomechanical study in which the IVD was subjected to loading in tension such as might be experienced during spinal bending [3]. Indeed, the mechanism by which these two tissues are secured together may be more reliant on the rigid inorganic fraction present in the tissues instead of the soft non-mineralised organic fraction.…”