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

Abstract

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 V1_strain > V3_strain > V2_strain. 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 V2_strain > V1_strain > V3_strain (V2_strain⪢V3_strain). 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.

Introduction

Vertebral compression fractures (VCFs) are a common clinical problem. They may occur after trauma or may be pathological resulting from decreased bone integrity from tumor or metabolic bone disease. Osteoporosis is a “systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture” [1]. Osteoporosis is a silent disease often detected after fractures have already occurred. Approximately 2.5 million osteoporotic fractures occur worldwide annually, usually involving the vertebrae, wrist and hip. Vertebral fractures are the most common osteoporotic fractures and may be associated with significant and progressive physiologic and functional limitations [2]. In the United States about 1.5 million osteoporotic fractures occur annually of which 700,000 are VCFs [3]. The acute pain of the fracture may improve over a few weeks, but more than 30% go on to chronic pain. As height is lost, the patients develop restrictive lung disease and become vulnerable to pneumonia. They also develop a protruberant abdomen causing early satiety on eating and resultant malnutrition. VCFs lead to poor posture, functional impairment, disability and subsequent economic burden [4]. Women with VCF have been found to increase mortality from pulmonary disease [5].

The greatest long-term consequence of VCF is secondary fracture [4], which occurs more frequently after an index VCF [3], [4], [6]. Low bone mineral density (BMD) and previous fracture are strong predictors of new VCF and even better predictors when combined together. A probable reason for this is that the prevalent deformity may increase or alter the load distribution on other vertebrae [7]. The increased risk of fracture in women with an index VCF extends beyond the vertebrae above and below it to distant vertebrae. This may be the result of a combination of altered biomechanics and reduced bone architectural integrity [8].

The load carried by the vertebral body is shared between the trabecular centrum and the peripheral cortex. Osteoporosis reduces the load-carrying ability of the vertebral body through a reduction primarily in trabecular strength [9]. Osteoporotic wedge compression fractures of the spine affect the anterior cortex by increasing the stress concentration to the point of failure. Deformation of cortical bone has been measured with strain gauges, measuring elements bonded to the bone, that through a change in resistance detect a change in length. Determination of bone strain is an important aspect of biomechanics research [10]. Surface strain distribution in lumbar vertebrae was studied by Shah et al. [11] using the techniques of brittlecoat and photoelastic analysis and the principal strain components determined on lumbar vertebrae. These findings were confirmed by a subsequent strain gauge study, and strain was found to be directly proportional to compressive load [12]. Hongo et al. [13] studied the mechanism of burst fracture initiation using strain gauges based on the study findings of Shah et al. [12]. Hongo et al. [13] used the greatest strain distribution as an indicator of the region where the fracture initiates. Other biomechanical studies have used strain gauges to study strain and stress in the spine [14], [15], [16], [17], [18].

The objective of this study was to determine the distribution of anterior cortical strain in thoracic spinal subsegments before and after the evolution of an experimentally created VCF to determine the vertebra at highest risk for secondary fracture.