Abnormal spinal anatomy in 27 cases of surgically corrected spondyloptosis: proximal sacral endplate damage as a possible cause of spondyloptosis.

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.