The PVP is an effective treatment for vertebral compression fractures. However, unexpected vertebral fractures commonly occur after PVP, and these require additional PVP as a part of the treatment process. A number of studies have reported the incidence of serial vertebral fractures after PVP from 12% to 52%11,18,25,27,28)
. The cause and development of newly formed vertebral fractures were reviewed in several articles, but it is uncertain whether the PVP itself works as a cause of the fracture or not3,20,21)
. Therefore, we aimed to estimate the relationship of vertebral fracture with risk factors, and ways to reduce the fractures through the analysis of patterns of newly formed vertebral fractures.
In general, it is known that the degree of osteoporosis is risk factor for subsequent fracture24,25)
. However, there have been few reports about the effect of constitutional factors on the development of subsequent spinal fracture after vertebroplasty. As a result of univariate analysis and multivariate analysis in our study, lower BMD is an important constitutional factor of subsequent fractures after PVP. Spinal BMD in the new VCFs group was -3 in average, while it was -2.5 in the no VCFs group (p
<0.05). The comparisons of lower BMD between nonadjacent fractures group and no VCFs group were significantly different. This result suggests spinal degenerative change as an important risk factor, in addition to the increased risk of fractures after procedures like PVP. Uppin et al.28)
noted that when osteoporosis worsens, patients easily develop new fractures in adjacent vertebrae. Belkoff et al.5)
reported that cement augmentation increases the strength and stiffness of the individual fractured vertebral bodies, which may place greater stress on the adjacent vertebrae. However, this study did not show significant differences in BMD between adjacent fractures group and no VCFs group. On the other hand, the initial fracture level of T-L junction was greater in adjacent fractures group than the nonadjacent fractures group, which suggested higher BMD, adjacent fractures after PVP can be explained since T-L junction has higher dynamic motility. In T-L junction level vertebral fractures, the increase in adjacent nucleus pulposus and endplate pressure change of untreated adjacent vertebra is caused by dynamic motility of this level although BMD is higher, leading to the development of fractures.
In addition to BMD, the cement leakage to the disk space can also be a risk factor of newly formed VCFs. We verified this result; the risk of new VCF in patients with cement leakage is 4.6 times higher than in patients without the cement leakage17)
. This study revealed intradiscal cement leakage as important risk factors, but there was no significant difference between no fractures group and adjacent fractures group. Many studies report that intradiscal cement leakage increases risk of new VCFs at the adjacent regions of PVP after new VCFs18,25)
. They reported that the intradiscal cement leakage increased the newly formed VCFs in an already weak disc or discs weakened by intradiscal leakage. These biomechanical changes caused by intradiscal cement leakage may affect new VCFs formation. Unlike such hypothesis, this study demonstrated intradiscal cement leakage to be a significant risk factor in nonadjacent fractures group. This may support the study of Ahn et al.1)
, which demonstrated the mechanism of nonadjacent-segment fracture after initial PVP. If the adjacent segment is already rigid, the pillar effect is not prominent through the adjacent segment. In that case, the augmentation strength may affect a mobile remote segment. The mobility gradient between a rigid adjacent segment and a relatively mobile remote segment may cause a subsequent fracture. By this mechanism, intradiscal cement leakage can works as factor that increase augmentation strength that affecting mobile remote segment. In addition, increased anterior vertebral height restoration is one of the well-known risk factor of VCFs. In particular, it increases the risk of the newly formed VCFs because of the restoration of vertebral height, and greater loading of adjacent vertebra16)
. Although this study did not showe significant differences between the no fractures group and adjacent fractures group, the fracture can increase due to the dynamic hammer effect in the same mechanism with cement intradiscal leakage, since the anterior vertebral restoration affect the development of remote segmental fractures in the comparison with nonadjacent fractures group. In conclusion, remote vertebra with lower BMD increases intradiscal cement leakage and an anterior vertebral body height, which enhances the stiffness and the strength gradient and caused environmental basement of the new VCFs formation in remote vertebral segment.
Elderly patients with a severely collapsed or deformed fracture at the T-L junction were at high risk of developing a non-union of the fracture22)
. In our study, new VCFs pattern showed that adjacent fracture occurred more frequently, if the initial fracture level is at the T-L junction, in comparison between the subgroups of new VCFs group, the adjacent fracture group, and the nonadjacent fracture group. In general, the T-L junction is the most dynamic in the flexion and extension of the spine23)
. Thus new VCFs occurrence was higher in an adjacent location, due to high dynamic motility in T-L junction. Also, new VCFs had lower BMD in a nonadjacent location (). The fracture that appears at a nonadjacent level can be explained by the vertebral body's disease activity, which develops through the degenerative change of the spine itself, due to lower BMD than an adjacent level.
The cement volume is the one of the major concerns regarding vertebroplasty. A large volume of cement is injected increasing stress on adjacent vertebra, raising risk of subsequent fracture. Many researchers have studied such problem, and found higher instances of fractures related to large volume of cement injection4,6,25)
. However, others insisted that there is no specific association between cement volume and consequent fractures13,15)
. In this review, PMMA volume and subsequent vertebral fractures not related.
Low BMI and low body weight are known to increase the risk of recurrent fracture on the spine or the hip8,26)
. In one study, lower BMI caused direct pillar effect on the adjacent vertebra and the weakened vertebra1)
. In another study, authors reported that patients with BMI less than 22 kg/m2
had a significantly greater chance of developing new VCFs after vertebroplasty19)
. The results of this study showed that comparison of weight, height and mean BMI of the adjacent and nonadjacent fracture groups did not result in statistically significant differences. Further, the age and gender was not significantly different between these groups.
In summary, the significant predictive factors for the post-PVP development of new VCFs were lower BMD, intradiscal cement leakage, anterior body restoration. Also, the comparison between no fractures group with nonadjacent fractures group and subgroups of new fractures group, may support the dynamic hammer effect explained by Ahn et al.1)
in the case of nonadjacent segmental fracture.
Differences between our study and others could be because our study is a retrospective review, performed in only one institution and included only patients who underwent repeated intervention, not those patients with subsequent fracture treated with conservative management. In addition, the efficacy of the PVP, the degree of pain relief, medical treatment, physical activity, acquisition of follow up images of the patients after PVP were not reviewed. This review included patients who underwent repeated vertebroplasty, not conservative treatment. This limited our estimates of prevalence of subsequent vertebral fracture. However, our study also has considerable validity. The patients of each study group were compared under strict inclusion criteria, and the cases were selected from a relatively large patient population (365 consecutive patients). Further multi-institutional, prospective randomized controlled studies to determine the real risks with greater accuracy for future studies are required.