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Study Design: Microstructural investigation of compression-induced herniation of a lumbar disc held in a concordant complex posture.Objective: To explore the significance of loading rate in a highly asymmetric concordant posture, comparing the mechanisms of failure to an earlier study using a nonconcordant complex posture.Summary Of Background Data: A recent study with a nonconcordant complex posture (turning in the opposite direction to that which the load is applied) demonstrated the vulnerability of the disc to loading that is borne by one set of oblique-counter oblique fiber sets in the alternating lamellae of the annulus, and aggravated by an elevated loading rate. Given the strain rate-dependent properties of the disc it might be expected that the outcome differs if the posture is reversed.Methods: Forty-one motion segments from ovine 16 spines were split into two cohorts; adopting the previously employed low rate (40 mm/min) and surprise rate (400 mm/min) of loading. Both groups of damaged discs were then analyzed microstructurally.Results: With the lower rate loading the concordant posture significantly reduced the load required to cause disc failure than earlier described for nonconcordant posture (6.9 vs. 8.4 kN), with more direct tears and alternate lamella damage extending to the anterior disc. Contrary to this result, with a surprise rate, the load at failure was significantly increased with the concordant posture (8.08 vs. 6.96 kN), although remaining significantly less than that from a simple flexed posture (9.6 kN). Analysis of the damage modes and postures suggest facet engagement plays a significant role.Conclusion: This study confirms that adding shear to the posture lowers the load at failure, and causes alternate lamella rupture. Load at failure in a complex posture is not determined by loading rate alone. Rather, the strain rate-dependent properties of the disc influence which elements of the system are brought into play.Level Of Evidence: N/A. [ABSTRACT FROM AUTHOR]

Study Design: Microstructural investigation of low frequency cyclic loading and flexing of the lumbar disc.Objective: To explore micro-level structural damage in motion segments subjected to low frequency repetitive loading and flexing at sub-acute loads.Summary Of Background Data: Cumulative exposure to mechanical load has been implicated in low back pain and injury. The mechanical pathways by which cyclic loading physically affects spine tissues remain unclear, in part due to the absence of high quality microstructural evidence.Methods: The study utilized seven intact ovine lumbar spines and from each spine one motion segment was used as a control, two others were cyclically loaded. Ten motion segments were subjected to 5000 cycles at 0.5 Hz with a peak load corresponding to ∼30% of that required to achieve failure. An additional small group of segments subjected to 10,000 or 30,000 cycles was similarly analyzed. Following chemical fixation and decalcification samples were cryosectioned along one of the oblique fiber angles and imaged in their fully hydrated state using differential interference contrast optical microscopy. Structural damage obtained from the images was organized into an algebraic shell for analysis.Results: At 5000 cycles the disc damage was limited to inner wall distortions, evidence of stress concentrations at bridging-lamellae attachments, and small delaminations. The high-cycle discs tested exhibited significant mid-wall damage. There was no evidence of nuclear material being displaced.Conclusion: At this low frequency and without the application of sustained loading or a more severe loading regime, or maintaining a constant flexion with repetitive loading, it seems unlikely that actual nuclear migration occurs. It is possible that the inner-annular damage shown in the low dose group could disrupt pathways for nutrient diffusion leading to earlier cell death and matrix degradation, thus contributing to a cascade of degeneration.Level Of Evidence: N/A. [ABSTRACT FROM AUTHOR]

Study Design: Microstructural investigation of vibration-induced disruption of the flexed lumbar disc.Objective: The aim of the study was to explore micro-level structural damage in motion segments subjected to vibration at subcritical peak loads.Summary Of Background Data: Epidemiological evidence suggests that cumulative whole body vibration may damage the disc and thus play an important role in low back pain. In vitro investigations have produced herniations via cyclic loading (and cyclic with added vibrations as an exacerbating exposure), but offered only limited microstructural analysis.Methods: Twenty-nine healthy mature ovine lumbar motion segments flexed 7° and subjected to vibration loading (1300 ± 500 N) in a sinusoidal waveform at 5 Hz to simulate moderately severe physiologic exposure. Discs were tested either in the range of 20,000 to 48,000 cycles (medium dose) or 70,000 to 120,000 cycles (high dose). Damaged discs were analyzed microstructurally.Results: There was no large drop in displacement over the duration of both vibration doses indicating an absence of catastrophic failure in all tests. The tested discs experienced internal damage that included delamination and disruption to the inner and mid-annular layers as well as diffuse tracking of nucleus material, and involved both the posterior and anterior regions. Less frequent tearing between the inner disc and endplate was also observed. Annular distortions also progressed into a more severe form of damage, which included intralamellar tearing and buckling and obvious strain distortion around the bridging elements within the annular wall.Conclusion: Vibration loading causes delamination and disruption of the inner and mid-annular layers and limited diffuse tracking of nucleus material. These subtle levels of disruption could play a significant role in initiating the degenerative cascade via micro-level disruption leading to cell death and altered nutrient pathways.Level Of Evidence: 5. [ABSTRACT FROM AUTHOR]

Study Design. Microstructural investigation of compressioninduced herniation of the flexed lumbar disc. Objective. To provide a microstructural analysis of the mechanisms of annular wall failure in healthy discs subjected to flexion and a rate of compression comparable with the maximum rate at which the muscles of the spinal column can generate a force. Summary of Background Data. Clinical evidence indicates the involvement of the endplate in herniation. It is known that both an elevated rate of compression and a flexed posture are necessary to cause disc failure either within the midspan of the annulus or at the annular-endplate interface. However, the question of what effect a sudden or "surprise" loading might have on the mode of failure is, as yet, unanswered. Methods. Twenty-four healthy mature ovine lumbar motion segments were compressed to failure in high physiological flexion (10º). This occurred over approximately 5 mm of crosshead displacement in 0.75 seconds that resulted in a displacement rate of 400 mm/min (defined as a "surprise" rate) and was intended to simulate the maximum rate at which the muscles of the spinal column can generate a force. The damaged discs were then analyzed microstructurally. Results. Fifty-eight percent of discs suffered annular-endplate junction rupture, 25% suffered midspan annular rupture, and the balance of 17% endplate fracture. Microstructural analysis indicated that annular rupture initiated at the endplate apical ridge in the mid-to-outer region of the annulus in both annular-endplate and midspan annulus rupture. Conclusion. Motion segments subjected to a "surprise" loading rate are likely to fail via some form of annular rupture. Failure under such sudden loading occurs mostly via rupture of the annularendplate junction and is thought to arise from a rate-induced mechanostructural imbalance between the annulus and the endplate. [ABSTRACT FROM AUTHOR]

STUDY DESIGN: Microstructural investigation of compression-induced disruption of the flexed lumbar disc. OBJECTIVE: To provide a microstructural analysis of the mechanisms of annular wall failure in healthy discs subjected to flexion and an elevated rate of compression. SUMMARY OF BACKGROUND DATA: At the level of the motion segment failure of the disc in compression has been extensively studied. However, at the microstructural level the exact mechanisms of disc failure are still poorly understood, especially in relation to loading posture and rate. METHODS: Seventy-two healthy mature ovine lumbar motion segments were compressed to failure in either a neutral posture or in high physiological flexion (10°) at a displacement rate of either 2 mm/min (low) or 40 mm/min (high). Testing at the high rate was terminated at stages ranging from initial wall tearing through to facet fracture so as to capture the evolution of failure up to full herniation. The damaged discs were then analyzed microstructurally. RESULTS: Approximately, 50% of the motion segments compressed in flexion at the high rate experienced annulus or annulus-endplate junction failure, the remainder failed via endplate fracture with no detectable wall damage. The average load to induce disc failure in flexion was 18% lower (P < 0.05) than that required to induce endplate fracture. Microstructural analysis indicated that wall rupture occurred first in the posterior mid-then-outer annulus. CONCLUSION: Disc wall failure in healthy motion segments requires both flexion and an elevated rate of compression. Damage is initiated in the mid-then-outer annular fibers, this a likely consequence of the higher strain burden in these same fibers arising from endplate curvature. Given the similarity in geometry between ovine and human endplates, it is proposed that comparable mechanisms of damage initiation and herniation occur in human lumbar discs.Level of Evidence: N/A. [ABSTRACT FROM AUTHOR]

The article discusses a study which investigated the existence of structural integration between the nucleus and the inner annulus. The study used ten millimeter-thick sagittal slabs which were cut from the central region of ovine lumbar discs. It isolated the annulus-nucleus transition region and the resulting samples subjected to transverse tensile loading up to failure. It found that the annulus-nucleus boundary could support an average load of 5.7 N.

The authors respond to a comment on their article which deals with a microstructural investigation of compression-induced disruption of the flexed lumbar disc in sheep during flexion and compression loading. They explain the basis for the major findings of their article. They discuss the reason for limiting their article to herniation in healthy discs. They also argue that the ovine and human endplates have the same geometries.