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Letters to the Editor |
Orthopaedic Research Laboratory, Division of Orthopaedic Surgery, Royal Victoria Hospital, Rm L4.65, McGill University, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1. e-mail: gbaroud@orl.mcgill.ca
Paul Heini, MD
Spine Service, Department of Orthopaedic Surgery, Inselspital, University of Bern, Switzerland
James Nemes, PhD
Mechanical Engineering Department, McGill University, Montreal, Canada
Marc Bohner, PhD
Dr Robert Mathys Foundation, Bettlach, Switzerland
Stephen Ferguson, PhD
M. E. Müller Institute for Surgical Technology and Biomechanics, University of Bern, Switzerland
Thomas Steffen, MD, PhD, MBA
Orthopaedic Research Laboratory, Division of Orthopaedic Surgery, Royal Victoria Hospital, Rm L4.65, McGill University, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1*. e-mail: gbaroud@orl.mcgill.ca
Editor:
Dr Uppin and colleagues are to be commended on their article published in the January 2003 issue of Radiology (1). Many authors, as pointed out by Dr Uppin and colleagues, have referred to the phenomenon of adjacent fractures following vertebroplasty, but their article was among the first to focus on this complication clinically (13).
In the discussion section, the authors put forward some basic biomechanical explanations for adjacent fractures. Since the biomechanical aspects were beyond the scope of their study, they were not discussed in detail.
In our clinic, we also observed new compression fractures in vertebrae adjacent to augmented vertebrae (4). On the basis of our previous experience in arthroplasty and vertebroplasty, we hypothesized that an altered load transfer resulting from rigid cement fixation may induce degenerative changes in adjacent bone (5,6), especially because cement-filled bone is much stiffer than cancellous bone. In trying to explain adjacent fractures, we focused on the biomechanical aspects of vertebroplasty (59). In particular, we investigated the effect of the increased stiffness in the augmented vertebra on loading in the adjacent vertebrae by using theoretical and experimental models. Therefore, the purpose of this letter is to complement the article of Dr Uppin and colleagues by elaborating on the biomechanical effect of load shift and by discussing its clinical implications.
We developed (theoretical) finite-element models of a lumbar motion segment to examine the effect of rigid cement augmentation on the loading in adjacent vertebrae (68). The analysis of the model illustrated that the cement in the augmented vertebra acts as an upright pillar that reduces the physiologic inward bulging of the endplates of the augmented vertebra. As a result of this pillar effect, the pressure in the adjacent intervertebral disk increases substantially by approximately 19%. Subsequently, adjacent vertebrae experience a higher loading in the same range (68). On the basis of these results, we hypothesized that this shift in adjacent loading is the cause of adjacent fractures (67).
In an independent in vitro experimental study (9), the effect of cement augmentation on the failure load of adjacent vertebrae was examined. The results showed that the load of failure for a vertebra adjacent to an augmented vertebra was lower by about 17% compared with a vertebra adjacent to a nonaugmented vertebra. It was thus concluded that the load shift might provoke fractures in adjacent nonaugmented vertebrae.
Results of the theoretical and experimental models demonstrated that the increase in stiffness caused by bone cement induces a load shift that increases the risk of fractures in adjacent vertebrae. It is hypothesized that if the stiffness can be lowered by decreasing the amount of filling, the risk of adjacent fractures may also be reduced (57).
Currently, the predominant paradigm is maximum filling (4,10). For instance, in the study by Dr Uppin and colleagues, the vertebral body was filled as much as possible, and the average amount of polymethylmethacrylate injected per vertebral body was 9.14 mL (1). However, maximum filling may not be necessary for an effective vertebroplasty.
Results of in vitro studies on bone cement show that cement-filled bone is 36 times stronger than spinal cancellous bone (5,11). Since the load acting on the disk and on the spinal endplates measured in vivo is only in the range of 124 atm (12), this cement strengthening factor is probably unnecessarily large by at least a factor of 10. Therefore, reducing the filling or using softer materials than polymethylmethacrylate may not compromise the strength of the augmentation. Belkoff et al (13) demonstrated that only 2 mL of filling is sufficient for restoring the strength of an osteoporotic vertebra. Clinicians may therefore need to shift their paradigm from maximum filling to sufficient filling, but this is a question that needs further investigation.
This research has been supported in part by the Canadian Institute of Health Research grant no. MOP 57835. No benefits were or will be received from a commercial party related directly or indirectly to this study.
REFERENCES
Department of Interventional Neuroradiology, Massachusetts General Hospital, Gray 289, Boston, MA 02214. e-mail: jahirsch@partners.org
We would like to thank Dr Baroud and colleagues for their comments and added insight on a probable mechanism underlying compression failure of vertebral segments adjacent to augmented vertebra. Dr Baroud and colleagues used both computational and experimental methods to investigate the effect of cement augmentation on the mechanical response of trabecular bone to axial compression. This relationship was then extended to investigate the effect of augmentation on the mechanical response of a partial lumbar spinal unittwo vertebral bodies and the intervening disk. Their findings indicated that the cement mass acted as a vertical "pillar" within the vertebral body, which resulted in a decrease in endplate deformation and a marked increase in the pressure within the disk. This increase then leads to an increase in the loading of the adjacent vertebrae, which was suggested to be a contributing factor in the observed decrease in the failure of adjacent vertebrae in vitro (1).
The authors clearly demonstrated the marked effect of full infiltration of the bone with cement, an ideal situation, on the strength of the new composite, with the composite showing an increase of up to 36 times that of bone alone. The process of cement infiltration within the vertebral bone is complex and necessitates the replacement of the bone marrow and/or fat with the injected cement. As demonstrated in our own in vitro study (2) and that of Berlemann et al (1), the injection of cement into the vertebrae is inversely related to the density of vertebral bone. At present, few data exist on the effect of the three-dimensional structure of trabecular bone on the process of cement infiltration during augmentation.
Furthermore, the existence of fault lines and/or discontinuities within this structural matrix, which are caused by the failure of the vertebra, is likely to alter this process, since it offers a path of least resistance. The latter can often be observed in cases of endplate fracture with the cement infiltrating the disk space. It is clear that the effectiveness of cement injection will depend on many factors, among which are the viscosity of cement, injection location and pressure of application, time to polymerization, composition of the vertebral bone marrow and the configuration of the vertebral fracture in particular, and the consolidation of vertebral bone.
Although clinically, a smaller increase in composite strength is to be expected, the work presented by Dr Baroud and colleagues highlights the need to clarify the interaction between the material properties of the cement chosen and the condition of the vertebra. With the increased emphasis on the development and use of new "biocompatible" cement formulation, the effort initiated by this group is to be applauded in trying to provide quantitative information as to the effect of augmentation on the response of vertebral bone. Such information is paramount for the future development and application of such materials for vertebral augmentation.
In their computational model, the authors suggested the cement mass altered the structural response of the vertebral body in which a reduction in the deformation of the endplate leads to increased pressure in the intervertebral disk, thus causing increased loading on the adjacent vertebrae. Although clearly informative and suggestive of a possible mechanism for early failure of adjacent segments, the marked increase in disk pressure (19%) may be masked by six- to eightfold increased propensity of fracture for patients who demonstrated existing fractures independent of density (3). In addition, interpretation of the results of this model is made difficult because of several limitations. The intervertebral disk was modeled as having a distinctive nucleus and annulus regions with elastic and mixed elastic and nonelastic formulation applied for the constitutive behavior of these respective tissues.
For the target population of this procedure, however, the intervertebral disk is likely to have lost the definition of these tissues, resulting in a more even deformation of the endplate, in effect, becoming more "cartilaginous" in nature. Furthermore, the degenerative process within the disk, which is associated with both mechanical damage to the disk tissue and increasing calcification of the endplates, is likely to result in a reduced bulging of the endplate and concomitant increase in the degree of radial bulging in the disk. Consequently, a reduced amount of increased deformation will be transmitted to the adjacent vertebrae, resulting in a smaller overall increase in stress. The lower vertebrae, L5, was modeled to be fully infiltrated with cement, despite the fact that even when a high volume of cement is used (up to 10 mL), this volume may correspond to less then 25% of the volume of the vertebra (1).
Indeed, our study results have demonstrated that the use of such quantities does little to affect the overall deformation pattern of the failed vertebra, since the cement cannot practically fill the whole volume without considerable leakage (4).
Moreover, the effectiveness of structural augmentation will critically depend on the type of fracture and the geometry of the fractured vertebra (5). In particular, we have demonstrated that the process of augmentation substantially alters the three-dimensional response of the vertebrae, which may be an additional contributing factor in the increased loading of the adjacent segments (2).
The present model proposed by Dr Baroud and colleagues represents an attempt to understand the complex interaction between the augmented vertebra and its adjacent segments. Their response to this clinical study highlights some of the effect and possible causes of adjacent vertebral failure phenomena. Through better understanding, the biomechanics of the procedure can ultimately be further improved.
REFERENCES
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