Introduction: Endplate fractures are clinically important. They are very common, are associated with an increased risk of back pain, and can probably lead on to intervertebral disc degeneration. However, such fractures tend to damage the cranial endplate much more often than the caudal. In this study, we test the hypothesis that the vulnerability of cranial endplates arises from an underlying structural asymmetry in cortical and cancellous bone.

Methods: Sixty-two “motion segments” (two vertebrae and the intervening disc and ligaments) were obtained post-mortem from human spines aged 48–92 yrs. All levels were represented, from T8–9 to L4–L5. Specimens were compressed to failure while positioned in 2–6o of flexion, and the resulting damage characterised from radiographs and at dissection. 2mm-thick slices of 94 vertebral bodies (at least one from each motion segment) were cut in the mid-sagittal plane, and in a para-sagittal plane through the pedicles. Microradiographs of the slices were subjected to image analysis to determine the thickness of each endplate at 10 locations, and to measure the optical density of the endplates and adjacent trabecular bone. Comparisons between measurements obtained in cranial and caudal regions, and in mid-sagittal and pedicle slices, were made using repeated measures ANOVA, with age, level and gender as between-subject factors. Linear regression was used to determine significant predictors of compressive strength (yield stress).

Results: Fracture affected the cranial endplate in 55 specimens and caudal endplate in 2 specimens. Endplate thickness was low centrally and higher towards the periphery. Cranial endplates were thinner than caudal, by 14% and 11% in mid-sagittal and pedicle slices respectively (p=0.003). Differences were greater in central and posterior regions. Cranial endplates were supported by trabecular bone with 6% less optical density (p=0.004) with this difference also being greatest posteriorly. Caudal but not cranial endplates were thicker at lower spinal levels (p=0.01). Vertebral yield stress (mean 2.21 MPa, SD 0.78 MPa) was best predicted by the density of trabecular bone underlying the cranial endplate in the mid-sagittal slices of the fractured vertebral bodies (r2 = 0.67, p=0.0006).

Conclusions: When vertebrae are compressed by adjacent discs, cranial endplates usually fail before caudal endplates because they are thinner and supported by less dense trabecular bone. These asymmetries in vertebral structure may be explained by the location of back muscle attachments to vertebrae, and by the nutritional requirements of adjacent intervertebral discs.

Introduction: When the spine is subjected to compressive loading in-vivo and ex-vivo, there appears to be a predisposition for the cranial endplates to fracture before the caudal. We hypothesise that this fracture pattern arises from an underlying structural asymmetry. Endplate damage is common in elderly people, and closely related to disc degeneration and pain.

Methods: 47 human thoracolumbar motion segments aged 62–90 yrs were compressed to failure while positioned in moderate flexion. Damage was assessed from radiographs and at dissection. Two 2mm-thick slices were obtained from each vertebral body in the sagittal plane. Microradiographs were analysed to yield the following: thickness and image greyscale density (IGD) of the cranial and caudal cortex at 10 locations (94 vertebrae), and IGD of the cancellous bone in three regions adjacent to each endplate (34 vertebrae).

Results: Endplate damage occurred cranially in 39/47 vertebrae, and caudally in 4/47. Mean thickness of cranial and caudal endplates was 0.77mm (SD 0.27) and 0.90mm (SD 0.29) respectively (p=0.01). Thinnest regions were located centrally on cranial endplates. Endplate thickness increased at lower spinal levels for caudal (p< 0.01) but not cranial endplates. IGD was similar in cranial and caudal endplates, but IGD of trabecular bone adjacent to the endplate was 3–8% lower cranially than caudally (P< 0.01).

Discussion: In elderly spines, cranial endplates fracture more readily because they are thinner and supported by less dense trabecular bone. Endplate thickness may be minimised by the need to allow nutritional access to adjacent discs, and the vulnerability of cranial endplates may be associated with asymmetries in blood supply, or proximity to the pedicles.

Introduction : We have shown previously that, in the presence of severe disc degeneration, the neural arch can resist up to 80% of the compressive force acting on the spine. We hypothesise that the inferior articular processes can then act as a “pivot” during backward and lateral bending movements.

Materials and Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate flexion, extension and lateral bending, while vertebral movements were tracked using an optical MacReflex system. The varying position of the centre of rotation (CoR) during these movements was calculated. Experiments were repeated after a treatment designed to simulate two effects of severe disc degeneration: creep loading to dehydrate the disc, and compressive overload to fracture a vertebral endplate and decompress the nucleus.

Results: In flexion, the CoR was usually located just below the inferior endplate of the disc, close to the antero-posterior midline, and in extension it moved an average 4.6 mm posteriorly. The additional “disc degeneration” treatment increased the variability of the CoR within and between specimens. It also moved the CoR an average 10.7mm posteriorly during extension movements (P< 0.001), so that in some specimens it was near the tip of the inferior articular processes.

Discussion: Severe disc decompression and narrowing increase translational (gliding) movements between adjacent vertebrae so that the effective CoR becomes more variable. During extension movements, the CoR can move so far posteriorly that the vertebrae can effectively “pivot” about the inferior articular processes.

Introduction: We hypothesise that disc degeneration is a major cause of segmental instability in elderly spines. Accordingly, we simulated two mechanical features of disc degeneration on cadaveric spines, and measured their effects on spinal movements.

Methods: Twenty-one motion segments (T8–9 to L4–5) were obtained from spines aged 48–90yrs. Specimens were loaded rapidly to simulate full spinal bending movements in vivo, while vertebral movements were tracked using an optical MacReflex system. Intradiscal stresses were investigated using “stress profilometry”. Experiments were repeated following compressive creep loading (which reduced disc water content by an amount similar to the aging process) and again following a compressive overload cycle which fractured a vertebral endplate and decompressed the nucleus. MacReflex data were used to quantify the neutral-zone (NZ), the range of motion (ROM), and the range of translational (gliding) movements.

Results Creep and endplate fracture both reduced disc height, and generated stress concentrations within the posterior annulus. Both treatments increased NZ, ROM and translational movements in flexion and lateral bending, but not in extension. Endplate fracture markedly increased the “instability index” (NZ/ROM) in flexion.

Discussion Disc “degeneration” increased all measures of spinal instability during flexion and lateral bending. Disc decompression in particular created a large NZ in which the spine had negligible resistance to bending. In life, muscle action would prevent the spine “wobbling” within this range of movement. Results in extension suggest impaction between the neural arches. Back pain associated with spinal instability could arise from stress concentrations in the annulus and neural arches, or from abnormal muscle activity.