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Abnormal Spinal Anatomy in 27 Cases of Surgically Corrected Spondyloptosis: Proximal Sacral Endplate Damage as a Possible Cause of Spondyloptosis

Yue, Wai-Mun, MBBS, FRCSEd*†; Brodner, Wolfram, MD†‡; Gaines, Robert W., MD

doi: 10.1097/01.brs.0000155572.72287.92

Study Design. Retrospective review.

Objectives. To review the findings in the cases of spondyloptosis we have treated and to postulate on the possible cause of spondyloptosis.

Summary of Background Data. Spondyloptosis (Grade V spondylolisthesis) is rare, even though spondylolisthesis is a relatively common condition. While it is known that progression to spondyloptosis occurs in patients with developmental spondylolisthesis in their childhood and/or adolescent years, the precise factors leading to progression are not known.

Methods. Between 1979 and 2002, 27 patients with spondyloptosis were treated surgically with L5 resection and reduction of L4 onto S1. During the treatment process, detailed observations of the surgical findings were made through clinical and radiologic means. Six anatomic parameters (pars interarticularis defects, spina bifida of the L5 or sacral segments, dysplasia of the L5–S1 facet joints, L5–S1 disc degeneration, trapezoidal shape of L5, and rounding of the proximal end of the sacrum) were specifically studied.

Results. Pars interarticularis defects were present in 24 patients (88.9%), facet dysplasia in 16 patients (59.2%), spina bifida in 24 patients (88.9%), disc degeneration in 25 (92.6%), trapezoidal L5 in 20 patients (74.1%), and rounding of the proximal end of S1 in all 27 patients (100%).

Conclusions. Rounding of the proximal sacral endplate was the only constant abnormal anatomic feature in the patients. Damage to the proximal sacrum and sacral growth plate during late childhood and early adolescence, similar to the epiphyseal injury that produces Blount’s disease, and slipped capital femoral epiphysis seem to be key factors permitting the progression of developmental spondylolisthesis to spondyloptosis.

Local anatomic features were studied in 27 consecutive patients with surgically treated lumbosacral spondyloptosis. Rounding of the proximal sacrum was the only constant feature. Damage to the sacrum and proximal sacral growth seem to be key factors permitting the progression of developmental spondylolisthesis to spondyloptosis.

From the *Department of Orthopaedic Surgery, Singapore General Hospital, Singapore; †Columbia Orthopaedic Group, Columbia, MO; and ‡Department of Orthopaedics, Vienna General Hospital, Vienna, Austria.

Acknowledgment date: July 16, 2004. Acceptance date: December 22, 2004.

Study performed at the Columbia Orthopaedic Group, Columbia, MO.

The manuscript submitted does not contain information about medical device(s)/drug(s).

No funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript. Level of Evidence: Prognostic Studies, Level I.

Address correspondence and reprint requests to Robert W. Gaines, MD, Columbia Orthopaedic Group, 400 Keene Street, Columbia,MO 65203; E-mail:

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Lumbar spondylolysis occurs in the general population at the rate of around 5%, with racial and gender variations.1–5 The incidence of spondylolisthesis is less defined, with most studies indicating 3%,1,2 with higher values quoted when studied in the context of symptomatic patients or certain peculiar populations.3,5–7 However, spondylolysis is not the only cause of spondylolisthesis, only the most widely studied one. The most severe grades of spondylolisthesis often have dysplastic features in the lumbosacral region, especially in the proximal sacrum, although it has been said that progression beyond a 25% slip is not possible without a concomitant break in the pars interarticularis.4 Spondyloptosis or Grade V spondylolisthesis8 (defined as the entire vertebral body of L5 being inferior to a horizontal line tangential to the top of the sacrum on a standing lateral radiograph9) is exceedingly rare. Much effort has been made in the literature to identify the risk factors for progression of spondylolisthesis. The principal aim of these efforts is to be able to treat these patients early, before they progress. The treatment of spondylolisthesis, before it progresses to a high-grade lesion, is certainly simpler and less fraught with complications, compared with the treatment of spondyloptosis. Progression to spondyloptosis almost certainly occurs in the years of rapid growth, between the ages of 10 and 15 years, even for patients who present with spondyloptosis.1,10–12 The precise factors determining progression and its rate are still unknown.13

The senior author has the unique experience of treating 27 patients with spondyloptosis over a 23-year period. The aim of this study is to review the local anatomic findings in these cases and to see if light can be shed on the possible causes of spondyloptosis.

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Materials and Methods

Between 1979 and 2002, 27 consecutive patients with spondyloptosis were treated surgically by the senior author. All the patients had spondyloptosis or Grade V spondylolisthesis by the Meyerding classification.8 A brief summary of the operative procedure is provided here.9,14

The procedure was performed under general anesthesia in two stages. In the first stage, the lumbosacral spine is exposed either retroperitoneally or transperitoneally. The iliac vessels are mobilized laterally to enhance the exposure. Part of the anteroinferior corner of the L4 vertebral body may be excised to allow proper visualization of the L4–L5 intervertebral disc and the L5 vertebral body anteriorly. The L5 vertebral body, L4–L5 and L5–S1 intervertebral discs are excised. The inferior surface of L4 is completely denuded of disc and cartilage.

The second stage involves the midline approach to the lumbosacral spine. The posterior elements of L5 are completely excised and the L5 and S1 nerve roots are identified bilaterally and protected. The endplate of the sacrum is cleared of any remnant disc and cartilage before L4 is reduced onto the sacrum. With the L4, L5, and S1 nerve roots protected, instrumentation, reduction, and posterolateral fusion are then performed between L4 and the sacrum.

Records, including clinical photographs, plain radiographs, magnetic resonance image (MRI) scans, and operative findings, were meticulously kept by the senior author on all the patients. These were reviewed retrospectively by the other authors. Six local anatomic parameters were specifically studied for their presence or absence (Figure 1).

Figure 1

Figure 1

  1. Par interarticularis defect. Both frank lytic pars defects and elongation of the pars were included.
  2. Facet dysplasia of the L5–S1 facet joints.
  3. Evidence of spina bifida in the posterior elements of L5 and sacrum, including bifid spinous processes and laminar defects.

(For 1 to 3, these were suspected on preoperative radiographs and MRIs and confirmed during the posterior stage of the surgery when the posterior elements of L5 and the sacrum were exposed and the posterior elements of L5 were completely removed before reduction of L4 onto S1 was performed.)

  1. Evidence of disc degeneration of the L5–S1 intervertebral disc. These were graded as severe when the disc height was less than 25% of the L4–L5 intervertebral disc height in the same lateral radiograph or if the disc appeared uniformly dark on T2-weighted MRI scans; moderate when the disc height was between 25% and 75% of the L4–L5 intervertebral disc on the same lateral radiograph or if the disc had patchy signals on T2-weighted MRI scans; and absent if the disc height was greater than 75% of the L4–L5 intervertebral disc on the same lateral radiograph or if the disc appeared bright white on T2-weighted MRI scans.
  2. Trapezoidal L5 vertebral body. The lumbar index (LI)15 was used to define this. The L5 vertebral body was considered definitely trapezoidal if the LI was less than 80; borderline trapezoidal if the LI was between 80 and 90; and definitely normal if the LI was 90 or greater.1,16–18
  3. Rounding of the proximal sacral endplate. This is obvious on lateral radiographs, sagittal MRI scans, as well as during the second stage of the operative procedure.

All these findings are illustrated in Figure 1.

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In total, there were 27 patients who had the procedure done during a 23-year period, including 18 females and 9 males. The average age of patients during the time of the procedure was 30 years (range, 14–48 years).

The results are summarized in Table 1 and Figure 2.

Table 1

Table 1

Figure 2

Figure 2

In 21 patients (77.8%), there were actual defects in the pars interarticularis noted on both radiographs and intraoperative findings. Three patients (11.1%) had elongation of their pars interarticularis without lysis. However, in 3 patients (11.1%), an example of which is seen in Figure 3, there was neither a defect nor elongation present in the pars interarticularis.

Figure 3

Figure 3

The articular facets of the L5–S1 joints were dysplastic in only 16 patients (59.2%). None of the patients had a neural tube defect. However, spina bifida occulta was present in the L5 lamina in 4 patients (14.8%), and in the sacral segments and the L5 lamina in 20 patients (74.1%). The latter is probably more important as a risk factor for progression of spondylolisthesis.

Based on our criteria, the L5–S1 intervertebral disc was severely degenerate in 17 patients (63%) and moderately degenerate in another 8 patients (29.6%). The L5 vertebral body was definitely trapezoidal in 14 patients (51.9%), borderline trapezoidal in 6 patients (22.2%), and definitely normal in 7 patients (25.9%).

Rounding of the proximal sacrum was the only anatomic finding that was present in all 27 of the patients. All the sacra were severely rounded, definitely Grade III contours, by the criteria of Boxall et al.19

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Discussion and Conclusions

To date, to the best of the authors’ knowledge, there has not been a report of a patient who has been documented serially with radiographs to demonstrate the progressive change in position and form of the L5 vertebra and proximal sacrum during progression from low-grade lumbosacral spondylolisthesis to spondyloptosis. The etiologic and prognostic factors that reliably predict such progression are lacking. Suggestions have been made regarding the use of sacropelvic parameters such as the pelvic incidence “angle,” which has been proposed to be a constant in an individual, for such purposes.20,21 Curylo et al reported that the mean pelvic incidence angle in populations with high-grade spondylolisthesis is higher than that found in populations with low-grade spondylolisthesis as well as normal populations.22 Hanson et al found that the pelvic incidence angle for both low- and high-grade spondylolisthesis was higher than that of the normal population but did not differ between the two.23 Huang et al, on the other hand, found that the pelvic incidence angle cannot adequately predict the probability of spondylolisthetic progression.24 Considering the severe rounding and doming of the proximal sacrum found in our patients and the gross distortion of the entire sacrum (all 5 segments, not only the dome), we cannot see how it is possible to reliably make this measurement in a patient with spondyloptosis.

The use of commonly used classification schemes (either the Wiltse/Winter or Marchetti/Bartolozzi) categorizes patients into “isthmic/adult” or “congenital/dysplastic/developmental” categories. Neither of the commonly used classifications would describe all the spondyloptosis patients in our series. While many of the patients have isthmic defects, and spina bifida, and a few have small facets, 3 of these ptosis patients had none of these. Their ptosis was solely due to abnormal shape of the upper sacrum, the vertebral body of L5, and the L5–S1 disc. Therefore, the suggestion that merely classifying a patient will lead to an accurate prognosis and to proper clinical management seems certainly not to be true.

Figure 3 shows the surgical specimen from a ptosis patient, following the removal of the pedicle, and both facets from L5. The specimen clearly shows that her pars is intact and that both of her facets are totally normal. Her neural arch was also normal (Figure 3).

Spina bifida occulta has also been associated with the occurrence of spondylolisthesis.2,6,19,25 Dysplasia of the posterior elements of the proximal sacrum, especially of the facet joints, has also been identified as a risk factor for progression, contributing to a defective bony hook/catch mechanism of the posterior lumbosacral elements.10,16,22,26,27 The presence of pars interarticularis defects has been cited as a prerequisite for the development of high-grade spondylolisthesis, even in those patients with the dysplastic type of spondylolisthesis.4,16,19 Degeneration of the L5–S1 intervertebral disc is more commonly identified as an etiologic factor for progression of spondylolisthesis in adults.5,12,28 The wedging of the L5 vertebral body, in the form of the LI, has been cited both as a risk factor19,29 and as a secondary change for the progression of spondylolisthesis.1–4,6,11,12,30–32 From our study, while present in the majority of patients, none was constant features. We recognize these as possible contributory factors to the progression of spondylolisthesis to spondyloptosis.

Rounding of the proximal sacrum has also been proposed as a risk factor for progression by some authors,7,19,29,33 while others regard it as a secondary phenomenon.1,4,6,11,24,30,31,34,35 Our findings suggest that rounding of the proximal sacrum plays a central rather than a secondary role in severe spondylolisthesis. Takahashi et al also noticed that, on magnetic resonance scanning, patients with severe spondylolisthesis demonstrate defects in the anterosuperior portion of the sacrum and suggest that this is a key pathology to the disorder.36

Farfan et al first hypothesized that the pathology of spondylolisthesis may involve an epiphyseal slip at the superior sacrum.37 Ikata et al noted that, in adolescents with sports-related spondylolisthesis, there is evidence on radiographs of L5 wedging and sacral rounding with increasing slippage.34 In addition, on magnetic resonance imaging, endplate lesions between the growth plate and osseous endplate occur more commonly in those patients with spondylolisthesis. Further observations made by Sairyo et al in adolescents showed that progression of slippage occurred most commonly in the most immature stage of lumbosacral spine development (cartilaginous stage), less commonly in the next stage (apophyseal stage) and none in the mature epiphyseal stage.35 They suggested that the biomechanical weakness of the vertebral endplate against an anterior shear force may play an important role in the progression of slippage in the immature spine, with higher risk for progression in the weaker, more immature stages. In human cadaveric studies, Karlsson et al showed that, in adolescents, the weakest part of the functional spinal unit to an axial compression force was the growth plate.38

Sakamaki et al demonstrated that, after posterior destabilization of the lumbar spine, slippage and destabilization occur in young rats but not in old rats.39 Histologic examination of those rats that developed spondylolisthesis revealed vertebral growth plate impairment of the superior endplate of the caudal vertebral body (Figure 4).

Figure 4

Figure 4

Animal studies in immature calf spines by Sairyo et al demonstrated that failure occurred at the superior growth plate of the caudal vertebral body when bilateral pars defects were created in the rostral vertebra and the spine then subjected to loading40 (Figure 5). They further postulated that, in the pediatric lumbar spine with pars defects, slippage might occur between the growth plate and osseous endplate. This may also result in rounding of the S1 vertebra. The same study also showed that there was no difference in the loads required to produce failure between the group with intact intervertebral discs and those with intervertebral discs damaged by dissection. Kajiura et al, using immature calf spines, also showed that, in the presence of pars defects, the growth plate was the site of failure when subjected to an anterior shearing force.41 They further showed that, with greater immaturity, less load is required to produce failure. With an immature baboon model, using both in vitro and finite element analysis, Konz et al were able to demonstrate that the weakest link during an anterior-posterior shear load was the growth plate, between the cartilaginous and osseous endplate.42 They also suggested that the presence of a more sagittally oriented facets and/or a pars fracture are prerequisites for spondylolisthesis to occur.

Figure 5

Figure 5

From the finding of our study that proximal sacral rounding was the only constant feature in 27 consecutive cases of spondyloptosis, and the clinical and experimental observations made in the aforementioned studies, we postulate that severe endplate and growth plate damage in the immature proximal sacrum, either manifesting as a growth disturbance or an epiphyseal slippage, is the central etiologic factor that allows the severe deformity of spondyloptosis to occur. This would be akin to either Blount’s disease of the proximal tibia or slipped capital femoral epiphysis. It is interesting to note that Newman first noted a similarity in the gender and age distribution of spondylolisthesis and slipped capital femoral epiphysis, although no further pursuit of this association has been made since.43 A number of predisposing factors lead to this damage in some patients, just as in Blount’s disease and slipped capital femoral epiphysis, and we have identified some of them in the current study. In addition, we propose that, once initiated, the extent of its propagation determines the progression of the translation and rotation of the L5 vertebra, which ultimately results in spondyloptosis (Figure 6). (A video illustrating this mechanism is available on ArticlePlus.)

Figure 6

Figure 6

Other features, such as dysplastic L5–S1 facet joints, disc degeneration, trapezoidal L5 vertebral body, spina bifida, and pars interarticularis defects, are facilitating developmental predispositions, which permit spondyloptosis to develop.

We reiterate, however, that 3 of our patients had no predisposing factors in the posterior elements. Their spondyloptosis developed entirely because of damage to the sacrum and its growth during adolescence and late childhood.

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Key Points

  • Rounding of the proximal sacrum was the only constant anatomic feature in 27 cases of surgically treated spondyloptosis.
  • Severe growth plate damage in the immature proximal sacrum seems to be the central etiologic factor that allows the severe deformity of spondyloptosis to occur.
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spondyloptosis; etiology; sacral growth plate; epiphyseal injury

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