You could be reading the full-text of this article now if you...

If you have access to this article through your institution,
you can view this article in

The Biomechanical Effects Of Spondylolysis and Its Treatment

Mihara, Hisanori MD*; Onari, Katsuhiro MD†; Cheng, Boyle C. PhD*; David, Stephen M. MD*; Zdeblick, Thomas A. MD*


Study Design. Biomechanical analysis of the level above pars defects was performed using calf lumbar spines.

Objectives. To evaluate whether complete spondylolysis contributes to the pathology of the upper adjacent motion segment to the pars defect.

Summary of Background Data. It is well recognized that patients with spondylolysis show a higher incidence of spondylolisthesis or degenerative disc changes at the level of the pars defects. However, some authors have referred to the fact that disc damage may occur at the level above the defect and give rise to symptoms. However, no previous studies have been directed to the kinematic influence on the upper adjacent segment to pars defects.

Methods. Nine fresh-frozen calf lumbar spines were used for this study. The bony defects were created on the L4 pars articularis bilaterally. Three linear extensometers and one specially designed angular extensometer were mounted across the L3–L4 and L4–L5 motion units. Nondestructive static loads, including axial compression, flexion–extension, and axial rotation, were applied on the specimens in four different conditions as follows: 1) intact spine; 2) bilateral pars defects on the L4 laminae; 3) pars defect repair with Buck technique; and 4) pedicle screw–rod fixation at L4–L5 after removal of the interarticular screws. Testing was performed on a material testing machine (MTS 858 Bionix test system, Minneapolis, MN), and load–displacement curves were recorded with the extensometers. Each test was performed for over five full sinusoidal loading cycles, and data from the fifth cycle were collected and analyzed.

Results. After creating the pars interarticularis defects at L4, mobility at both the L3–L4 and L4–L5 motion units were increased in all loading conditions. The normalized range of motion (% ROM) as compared with the intact specimens showed that the pars defects increased the mobility at the upper adjacent level (L3–L4) to 106.4% in flexion–extension and to 120.1% in axial rotation; the differences were significant (P < 0.01). Consequently, the increased mobility was stabilized by applying Buck screws through the defects on both sides; however, the effect was not statistically significant. Furthermore, pedicle screw–rod fixation applied at the L4–L5 segment increased the intervertebral motion at the upper adjacent level, and % ROM in axial rotation was significantly increased to 119.2% of the intact spine (P < 0.05). Comparing the treatments’ effects on the L3–L4 segment and that on L4–L5, the Buck screws restored the stability of both segments to the level of the intact spine, whereas the pedicle screw system limited the motion of L4–L5 motion and, on the contrary, increased the L3–L4 motion.

Conclusions. This biomechanical study exhibited that bilateral pars interarticularis defects increased the intervertebral mobility, not only at the involved level but also at the upper adjacent level to the lysis. The increased mobility at the upper segment was reduced by the Buck screw technique. However, this was increased again by the pedicle screw system applied on the involved segment. If clinically applicable, fixation of the pars defect alone appears to cause less adjacent level mechanical stress than pedicle screw–rod motion segment fixation.

Author Information

From the *Department of Orthopedics & Rehabilitation, University of Wisconsin Hospital, Madison, Wisconsin,

and the †Department of Orthopedic Surgery, Yokohama Minami Kyosai Hospital, Yokohama, Japan.

Acknowledgment date: January 15, 2002.

First revision date: May 6, 2002.

Acceptance date: July 9, 2002.

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.

Address correspondence to Thomas A. Zdeblick, MD, Department of Orthopedic Surgery, University of Wisconsin, Clinical Science Center, 600 Highland Avenue, Madison, WI 53792-7375, USA; E-mail:

© 2003 Lippincott Williams & Wilkins, Inc.