Mild (not severe) disc degeneration is implicated in the progression of bilateral L5 spondylolysis to spondylolisthesis

Isthmic spondylolysis (or lytic defect) is characterised by a bony defect of the pars interarticularis and occurs most commonly as a bilateral defect in the L5 vertebra [1, 2]. The mechanism for the progression of the lytic defect to spondylolisthesis remains unclear despite viable qualitative theories supported with clinical radiographic evidence [3‐9].

Abnormal spinopelvic morphology and orientation measured through parameters such as pelvic incidence, sacral slope, pelvic tilt may create a biomechanical environment leading to the development of a pars defect and its progression to spondylolisthesis [3‐6, 9]. In children and adolescents, the progression of the defect to spondylolisthesis is attributed to growth plate injury which may perpetuate to epiphyseal ring separation [8, 10]. Slippage in skeletally immature spines is not attributed to any disc degeneration, but rather growth plate lesions [7].

Lytic spondylolisthesis is often associated with disc degeneration at the olisthetic segment; however, it is not clear whether disc degeneration is the cause or consequence of lytic spondylolisthesis [11]. Clinical evidence suggests that disc degeneration occurs more rapidly and prematurely in the presence of lytic spondylolisthesis [11, 12]. Szypryt et al. (1988) compared disc degeneration at the olisthetic segment in 40 consecutive patients with an age-and-sex matched control group of 40 asymptomatic volunteers. The authors observed that over the age of 25 years, the prevalence of disc degeneration was significantly higher in the spondylolytic group compared with the control group [11]. Seitsalo et al. (1997) in their long-term follow-up study of operatively and conservatively treated isthmic spondylolisthesis patients reported a strong correlation between the severity of disc degeneration and the degree of slippage in the conservatively treated cohort. Progression to spondylolisthesis in adults is almost always attributed to disc degeneration [11, 13]. Case studies, however, have cited the rare progression of pars defect to vertebral slippage in adults without any associated disc degeneration, adding to the ambiguity around the role of disc degeneration in the pathomechanism for slippage progression [14, 15].

The intervertebral disc plays an important role in resisting shear and torsional forces acting on the spinal column during physiological bending motions. Biomechanical studies on cadaveric lumbar spines with healthy intervertebral discs have shown increased kinematics at the index-level following a bilateral lytic defect [16‐18]. The loss of posterior tension band in the lumbar spine following the defect may redirect excessive shear and torsional forces on to the index-level disc, which may predispose the disc to accelerated or premature degeneration [19]. With progressive disc degeneration, the shear and torsional stiffness of the disc may get compromised, which in addition to the loss of posterior tension band, may perpetuate to spondylolisthesis. However, from a biomechanical standpoint, it remains unclear how different grades of disc degeneration may be implicated in the progression of a lytic defect to spondylolisthesis. Yong-Hing and Kirkaldy-Willis (1983) suggested that a degenerative progression occurs in the intervertebral disc from a state of hypermobility in the early stages of degeneration to hypomobility in the later stages [20]. Disc degeneration grades III and IV (Thomson’s grading) characterised by nuclear clefts, radial and concentric tears in the annulus fibrosus have been reported to cause kinematic instability in lumbar motion segments, whereas grade V degeneration characterised by disc height collapse and osteophyte formation resulted in biomechanical stability in the segments [21].

Here we use computed tomography (CT) data from a healthy human subject and nonlinear finite element modelling (FE) to assemble three-dimensional models of the lumbosacral spine to investigate the role of different grades of disc degeneration in the progression of a bilateral L5 lytic defect to spondylolisthesis. We hypothesised that a mildly degenerated disc is not able to arrest hypermobility following a bilateral lytic defect in the L5 vertebra and therefore the defect is disposed to progress to spondylolisthesis; however, in a severely degenerated disc, hypomobility is sufficient to stabilise the motion segment and limit the progression of the defect to spondylolisthesis.

All the results were analysed at peak Fx and Ex bending loads (10 Nm) in the five FE models.

The main objective of this biomechanical study was to examine the role of disc degeneration in the progression of a bilateral L5 spondylolytic defect to spondylolisthesis. The natural course of isthmic spondylolisthesis has been associated with disc degeneration and spontaneous stabilisation of the olisthetic segment, but the question whether disc degeneration is the cause or the consequence of vertebral slippage remains open [12].

The results from the present study confirm our hypothesis that in the presence of a bilateral L5 lytic defect, motion segments with a mildly degenerate index-level disc are at a greater risk for vertebral slippage compared to motion segments with a severely degenerate index-level disc. Compared with the baseline INTACT model, M-DEG LYTIC model experienced the greatest increase in kinematics (Fx ROM: 73% ↑; Fx IPT mid-discal projection: 53%↑), shear stresses in the annulus (Fx anteroposterior: 163%↑; Fx posteroanterior: 31%↑), and average strain in the ILL fibres (Fx: 90%↑). The S-COL LYTIC model experienced a decrease in mobility (Fx ROM: 48% ↓; Fx IPT mid-discal projection: 69%↓) and an increase in normal stresses in the annulus (Fx Tensile: 170%↑; Fx Compressive: 397%↑) compared with the INTACT model. The results are corroborated by previous clinical findings for conservatively treated L5-S1 lytic defect patients which revealed immobility of the motion segment with severe degeneration of the index-level disc [12]. In the light of Kirkaldy-Willis model for degenerative changes in the lumbar spine and results from the present study, we posit that severe disc degeneration of the index-level disc is one of the restabilisation mechanisms available to the L5-S1 motion segment in order to mitigate increased intervertebral motions and shear stresses due to a bilateral L5 lytic defect [28]. The results also indicate that the disc height collapse and not the degenerative changes in the stiffness properties of the disc per se, play a predominant role in the restabilisation of the L5-S1 segment. With a 50% loss in disc height, the L5-S1 segment became less mobile, offloaded the ILL fibres, and experienced lower shear stresses compared with the intact disc height models. No significant difference in results was noted between M-DEG-COL LYTIC and S-DEG-COL LYTIC models. The collapsed disc height models, however, experienced high normal stresses compared with the intact disc height models suggesting that loss in disc height redistributed loads within the motion segment, decreasing the shear component of the intradiscal forces and increasing the normal component.

Over the age of 25 years, the prevalence of index-level disc degeneration in lytic defect patients was found to be significantly greater compared with an age-and-sex matched control group [11]. Although progression of a lytic defect to spondylolisthesis in adults depends on numerous factors such as spinopelvic balance, lower-lumbar muscle strength, repetitive flexion-extension activities, strength of the iliolumbar ligament; the most important structure resisting the vertebral slippage is the index-level disc [4, 6, 29, 30]. The health (or lack thereof) of the index-level disc is therefore critical to resisting the vertebral slippage. Two distinct pathways may be available to a L5-S1 segment with a bilateral lytic defect and a mildly degenerate index-level disc:

From the onset of a bilateral L5 lytic defect, the exact duration of unstable and restabilisation phases may vary from patient to patient. Why some L5-S1 motion segments will adopt one pathway over the other may depend on genetic, anatomical, and lifestyle factors, and remains to be clinically explored. If the slippage progression is relatively rapid and intractable radicular pain associated with nerve root entrapment is evident, surgical intervention may be necessary to achieve biomechanical stability [12].

Progressive degeneration of the intervertebral disc is characterised by a cascade of cellular, biochemical, morphological, and functional changes. The sequence of these changes and the interplay between them are largely unknown. In the present study, a rather simplified approach was used to model progressive degeneration of the L5-S1 disc, altering only the structure (height) and material properties. The material properties of the AF and NP tissues were altered for different grades of disc degeneration in accordance with published data [25]. Whilst the shear modulus for the AF tissues was increased with progressive degeneration, Poisson’s ratio for the NP tissues was decreased to simulate the loss in incompressibility with progressive degeneration. [25] A 50% loss in mid-sagittal plane disc height was modelled to simulate a collapsed disc.

Some limitations to this study were noted. Poroelasticity and degeneration related structural defects (Schmorl’s node, annular tears, nuclear clefts, and rim lesions) in the disc were not modelled, which may have a bearing on the results. Instead of assembling multiple FE models representing a gradual change in the disc height, only a 50% collapse in disc height was modelled. The AF was modelled as a composite structure with only four concentric layers of collagen fibres (without translamellar bridges) embedded within a homogenous ground substance.

In the presence of a bilateral L5 spondylolytic defect, a mildly degenerate index-level disc experienced greater intervertebral motions and shear stresses compared with a severely degenerate index-level disc during flexion and extension bending. Disc height collapse, with or without severe degenerative changes in the stiffness properties of the disc, is one of the plausible restabilisation mechanism available to the L5-S1 motion segment to mitigate increased intervertebral motions and shear stresses due to a bilateral L5 lytic defect.