Distribution of anterior cortical shear strain after a thoracic wedge compression fracture.

Background Context: Vertebral compression fractures (VCFs) are a common clinical problem and may follow trauma or be pathological. Osteoporosis increases susceptibility to fracture by reducing bone mass and weakening bone architecture. Approximately 2.5 million osteoporotic fractures occur worldwide annually, usually involving the vertebrae, wrist and hip. In the United States 700,000 VCFs occur annually, causing significant morbidity, mortality and economic burden. An initial VCF often leads to subsequent VCFs. The strain distribution along the anterior cortex, the major load-bearing pathway in flexion, may be predictive of impending VCF. Regions of high strain distribution are likely to experience secondary fracture.

Purpose: To investigate the distribution of anterior cortical strain at, above and below an experimentally created index VCF to determine the vertebral body at risk of secondary fracture.

Study Design: In vitro experimental study using cadaveric thoracic spinal segments.

Methods: Seventeen thoracic spines underwent dual-energy X-ray absorptiometry (DEXA) to assess bone mineral density and were divided into T1-T3 (Subsegment 1), T4-T6 (Subsegment 2), T7-T9 (Subsegment 3) and T10-T12 (Subsegment 4). Rectangular rosette strain gauges were applied to the anterior cortices of the vertebrae of each subsegment (vertebrae in each specimen were denoted V1-superior, V2-intermediate and V3-inferior). V1 and V3 were partially embedded into polyester resin blocks, which were used to mount the specimens in a materials testing machine. Nondestructive predefect testing was performed in compression at 125 N and 250 N, followed by flexion at 1.25 Nm and 2.5 Nm. To ensure fracture reproducibility, V2 of each specimen had a trabecular defect created to a volume of 21.3+/-4.4% of the V2 centrum. Postdefect nondestructive compression and flexion were then performed in a manner similar to the predefect tests, followed by destructive testing in flexion. Anterior cortical shear strain on V1, V2 and V3, applied moments and applied flexion angle were all measured and analyzed.

Results: A VCF occurred in 55 of the 59 subsegments. Fifty-one VCF (93%) were seen in V2 and 4 VCF (7%) were seen in V1. After the creation of the trabecular defect, the shear strain on V2 increased, but a comparison of the postdefect with the predefect nondestructive tests showed no significant differences. The pre- and postdefect shear strain distribution in compression and flexion was V1strain>V3strain>V2strain. Shear strain at failure was highest on V2, and in all subsegments there were significant differences between V2 and V3 (p<.05). In all subsegments there were no significant differences between V2 and V1 (p>.05) at failure with the exception of Subsegment 1 where V2 and V1 were significantly different (p<.05). The predominant strain pattern at failure was (V2strain>V1strain>V3strain V2strain>>V3strain). Using shear strain as the codeterminant of peak moment with bending stiffness and applied angle at failure, the strain on V1 was the greatest predictor (p=.0084; R2=0.78). These findings suggest that the events leading to a secondary fracture probably start before the index VCF occurs and continue with loading beyond the index VCF.

Conclusion: Anterior cortical strain is concentrated at the apex of a thoracic kyphotic curve. The vertebral body immediately above the index VCF has the next highest amount of strain and therefore the highest risk of secondary fracture.