Pedicle Involvement on MR Imaging Is Common in Osteoporotic Compression Fractures

Discussion

Differentiating benign osteoporotic compression fractures from malignant pathologic fractures is clinically important because both occur frequently in elderly patients. For many years, various diagnostic signs on CT and MR imaging have been considered useful for such evaluation.^1–12

Morphologic changes suggest malignancy when a convex posterior cortex of the vertebral body is seen due to a mass effect or epidural and/or paravertebral masses.^1–4,8 Among these signs, the presence of an epidural mass has been reported as both specific and sensitive. Pedicle involvement has also been described as specific for malignant lesions.³ In addition, findings such as destruction of anterolateral or posterior cortical bone of the vertebral body or the pedicle on CT have been reported to suggest a malignant process.²

On the other hand, benign osteoporotic compression fractures show various signal-intensity patterns on MR imaging. Early-phase fractures typically show a bandlike low signal intensity on T1WI, which is localized adjacent to the collapsed endplate. In most cases, signal-intensity changes are focal, and normal marrow is preserved in at least 1 area of the vertebral body.³ An intravertebral cleft including fluid or gas and a linear signal-intensity hyperintensity on STIR are significantly associated with osteoporotic fractures.⁶ These are believed to reflect avascular necrosis or a nonunionized bony gap with pseudoarthrosis. In addition, retropulsion of a posterior bone fragment is considered both sensitive and specific for osteoporotic fractures.²

The usefulness of diffusion-weighted MR imaging or chemical shift MR imaging in differentiating benign and malignant vertebral lesions has been reported recently, but the results are controversial.^13,14

Correct diagnosis can be made in most cases of osteoporotic compression fracture because the useful signs mentioned above usually coexist in the collapsed vertebrae. However, in our experience, imaging features mimic malignant compression fractures in acute osteoporotic compression fractures, when the height of the vertebral body is preserved and diffuse signal-intensity changes are seen on T1WI, STIR, and Gd-T1WI. In such cases, a differential diagnosis is not always easy.

Because pedicle involvement is a common notion suggesting a malignant nature, we tend to diagnose malignant compression fracture when pedicle involvement is the only sign (Fig 1). We always evaluate the pedicle with CT and MR imaging before PV, because fracture or abnormal signal-intensity changes of the pedicle may be the source of pain and instability. In such cases, pediculoplasty may be beneficial to relieve the pain.^15–18 From our experience, abnormal signals of the pedicle are frequently seen on MR imaging with osteoporotic compression fractures, particularly in the early phase, and fracture of the pedicle is seen in approximately one-third of our patients.

As described in the “Results” section, abnormal signal intensity and contrast enhancement were seen in the pedicle in 64% of benign compression fractures and 84.2% of malignant pathologic fractures, with no significant difference between groups. This suggests that pedicle involvement is also common in benign osteoporotic compression fractures. These results differ from those of previous articles.

Yuh et al¹ compared MR imaging findings between 84 benign fractures and 25 malignant fractures on T1WI and T2WI. They reported pedicle involvement in 22 of the 25 patients with malignant compression fractures but in none of 52 nontraumatic compression fractures, contrasting starkly with our observations. They did not perform STIR or Gd-T1WI, which could have demonstrated subtle pathologic abnormalities in the pedicle. The results might, thus, have differed if these sequences had been used. Moreover, onset of fracture and duration of pain were not described. The prevalence of pedicle involvement varies depending on the age of the fracture. Tumor involvement usually remains for a long duration if untreated, but signal intensity abnormality of the pedicle may disappear after healing of a benign compression fracture.

Cuenod et al³ compared MR imaging findings between 63 osteoporotic fractures and 30 malignant compression fractures in the acute phase (<2 months). The MR imaging protocol included T1WI, T2WI, T2*WI, and Gd-T1WI without fat suppression. Pedicle involvement was seen in 24 malignant fractures and 4 benign fractures, and sensitivity and specificity for malignancy were 80% and 94%, respectively, suggesting pedicle involvement as a specific sign for malignancy. They did not use a fat-suppression technique, which might be the reason for the low detectability of pedicle involvement in their patients with osteoporosis. Generally, detection of pedicle involvement by tumor is not difficult due to the presence of homogeneous diffuse signal-intensity changes or a mass effect, but signal-intensity changes in osteoporotic fractures are sometimes difficult to recognize because they are often focal and inhomogeneous. Bone marrow is almost completely replaced with fatty tissue in elderly patients, so fat suppression is considered necessary for the evaluation of diseased vertebrae.

Shih et al⁴ examined MR imaging findings for 37 patients with single-level vertebral compression fractures, including 21 patients with benign causes and 16 patients with malignancy. The imaging protocols included T1WI, T2WI with fat suppression, and Gd-T1WI with fat suppression, similar to those in the present study. They identified pedicle involvement in 6 vertebrae with benign fractures (28.6%) and 11 vertebrae with malignant fractures (68.8%), showing a clearly higher prevalence of pedicle involvement in benign compression fractures compared with those in the other studies mentioned above.^1,11 This higher rate of pedicle involvement in osteoporotic compression fractures compared with other studies is probably due to the use of fat-suppression techniques. However, a difference from our study is seen in patient selection. They selected patients with solitary vertebral collapse as the only inclusion criterion. Symptoms of patients were not mentioned in that investigation, while we analyzed patients with acute-to-chronic painful fractures. Signal-intensity changes are commonly seen in unhealed painful fractures and presumably contributed to the difference from our results.

To the best of our knowledge, no previous reports have identified correlations between the findings of pedicle involvement on MR imaging and CT. We investigated CT findings of the pedicle with or without pedicle involvement on MR imaging. Pedicle involvement in osteoporotic compression fractures exhibited 3 morphologic patterns on CT in this study: fracture, sclerotic change, and no abnormality. Fracture and sclerotic change of the pedicle were noted in 31% and 38.2% of vertebrae, respectively, in which MR imaging showed signal-intensity abnormality. Laredo et al² compared CT findings of 34 benign osteoporotic fractures with those of 32 malignant acute vertebral compression fractures. They found pedicle fracture in 3 vertebrae with osteoporotic fractures (8.8%). That prevalence was significantly lower than that found in the present study. The reason is unclear but may be attributable to differences in the CT imager and imaging protocol because they evaluated by using axial images alone. We analyzed images with reconstructed axial, sagittal, and coronal planes with 3-mm section thickness obtained by using 16- or 64-detector row CT, which seems likely to have contributed to the higher detectability of abnormal findings in the pedicle in our series compared with that of Laredo et al.²

Sclerosis of the pedicle appears to represent reactive change or the healing process of microfracture. Signal-intensity changes on MR imaging are considered to represent the inflammatory process, including exudation, inflammatory cell infiltration, granulation tissue, or fibrosis.

In our study, 30% of vertebrae in which abnormal signals were seen in the pedicle on MR imaging showed no obvious abnormality on CT. In those cases, the fractured vertebral body showed low signal intensity on T1WI and high signal intensity on STIR and Gd-T1WI, indicating edema and inflammatory changes. These changes presumably extended posterior to the pedicle. Our results show that abnormal signals can be seen more frequently in the pedicle with early-phase fractures than with chronic fractures. Such signal-intensity changes are likely to disappear when the healing process is completed, as with fractures in other locations; however, a long period may be required for complete healing.

The present study had some limitations. First, diagnosis of benign or malignant fracture was mainly made on the basis of patient history and clinical presentation, and biopsy was performed in only selected patients. Some patients diagnosed with benign fracture thus could possibly have had malignant compression fractures. However, we believe such cases were unlikely and would have had little influence on the study result because no new malignancies were found in any patients at 3-month and 1-year follow-ups after PV.

Second, our study had a selection bias. We included only patients who underwent PV. It is possible that patients included had a higher likelihood of pedicle involvement than the general population because we performed PV for patients who had some signal-intensity changes on MR imaging in fractured vertebrae. So, this result may not be applicable to the larger population.

Third, due to time constraints, the MR imaging protocol for PV at our institution included only sagittal images, and we could not assess axial images in any except a few patients. Axial imaging may thus yield some additional information.