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.
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
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).
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.
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.)
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.
- 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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Keywords:© 2005 Lippincott Williams & Wilkins, Inc.
spondyloptosis; etiology; sacral growth plate; epiphyseal injury