Rope Jumping−Induced Traumatic Compression Fractures: the Underestimated Danger of Repetitive Axial Load Forces

Highlights

• The danger of repetitive subpathologic axial load forces in the setting of traumatic spinal injuries is oftentimes underestimated.

• Experimental and clinical evidence suggests that, at least in the scenario of repetitive axial load, unmitigated propagation of trabecular microscopic cracks through the vertebral bone marrow precedes end plate fractures.

• In the context of stress traumatic compression fractures, MRI abnormalities may constitute a surrogate marker of trabecular microfractures rather than “benign” interstitial edema secondary to vertebral end plate fractures.

A non-osteoporotic adult presented with multilevel compression fractures at the apex of the thoracic kyphosis after strenuous rope jumping. Magnetic resonance imaging demonstrated diffuse bone marrow changes in the vertebral bodies with only a small unilateral endplate fracture. Besides highlighting the oftentimes neglected role of repetitive subpathological axial load forces in traumatic spinal injuries, the observed imaging pattern substantiates previous experimental studies which demonstrated that under cyclic axial loading the initial damage occurs in the cancellous regions of the bone (with observation of cracks with average length between 50−100 μM), ultimately leading to a reduction in its elastic modulus. This pathophysiological mechanism, in which unmitigated propagation of trabecular microscopic cracks through the vertebral bone marrow precedes endplate fractures, may provide a rationale for recent proposals of targeted cement-augmentation in traumatic compression fractures with cement injection directed toward the regions of bone marrow changes.

Introduction

A healthy, 34-year-old, non-osteoporotic male (W: 185 lb/H: 6′2″/body mass index: 23.8) presented with sudden onset of mechanical axial pain in the apex of the thoracic kyphosis after an intensive training protocol of rope jumping consisting of 20 modules of 30 consecutive jumps, with an interval of 30 seconds between the modules, for a total exercise time of 15 minutes. Magnetic resonance imaging of the thoracic spine revealed diffuse bone marrow changes in the T8 vertebral body, as revealed by T2−short tau inversion recovery sequence hyperintensity (Figure 1A) and T1 hypointensity (Figure 1B), with only a mild unilateral superior endplate fracture (Figure 1C). There were also bone marrow changes in the anteroinferior portion of the T7 vertebral body; however, without any evidence of underlying endplate fracture. The patient was successfully treated with a thoracolumbar orthosis brace and reduction in the level of physical activities. Besides highlighting the oftentimes neglected role of repetitive subpathological axial load forces in traumatic spinal injuries, the imaging pattern observed in this case substantiates previous experimental studies suggesting that, under cyclic axial loading, the initial damage occurs in the cancellous regions of the bone (with observation of cracks with average length between 50−100 μM), ultimately leading to a reduction in its elastic modulus, which further increases the chances of propagation of such trabecular microfractures.¹ In the specific context of spinal pathologies, Kummari et al² have similarly demonstrated in a rat model that under cyclic overloading such microscopic cracks precede cortical shell failure. This pathophysiological mechanism, in which unmitigated propagation of trabecular microfractures through the vertebral bone marrow precedes endplate fractures, provides a strong rationale for recent proposals of targeted cement-augmentation in traumatic compression fractures,3, 4 with cement injection directed toward the region of bone marrow abnormalities as observed on magnetic resonance imaging. Although further experimental and clinical studies are warranted in order to validate such a hypothesis, it is likely that, at least in the context of stress compression fractures related to repetitive axial load, such magnetic resonance imaging abnormalities may constitute surrogate markers of trabecular microfractures rather than “benign” interstitial edema secondary to vertebral endplate fractures as commonly believed.