Long-term effects of vertebroplasty: adjacent vertebral fractures.
In today's aging population, osteoporosis-related fractures are an ever-growing concern. Vertebroplasty, a promising yet cost-effective treatment for vertebral compression fractures, has an increasing role. The first vertebroplasty procedures were reported by Deramond and Galibert in France in 1987, and international interest grew with continued development of clinical techniques and augmentation materials in Europe and the United States. Initial publications and presentations at peer review meetings demonstrated 60-90% success rates in providing immediate and significant pain relief. The objective of this review is to assemble experimental and computational biomechanical research whose goal is determining and preventing the negative long-term effects ofvertebroplasty, with a specific focus on adjacent vertebral fractures. Biomechanical studies using isolated cancellous bone cylinders have shown that osteoporotic cancellous bone samples augmented by the rigid bone cement were at least 12 times stiffer and 35 times stronger than the untreated osteoporotic cancellous bone samples. The biomechanical efficacy of the procedure to repair the fractured vertebrae and prevent further collapse is determined using single-vertebra models. The strength or load-bearing capacity of a single vertebra is significantly increased following augmentation when compared to the intact strength. However, there is no dear result regarding the overall stiffness of the single vertebra, with studies reporting contradictorily that the stiffness increases, decreases, or does not significantly alter following augmentation. The effects of vertebroplasty on adjacent structures are studied via multisegment models, whose results plainly oppose the findings of the single-vertebra and intravertebral models. Here, augmentation was shown to decrease the overall segment strength by 19% when compared to the matched controls. As well, there is a significant increase in disc pressure compared to the pre-augmentation measurements. This translates to a high hydrostatic pressure adjacent to the augmented vertebra, representing the first evidence of increased loading. Computational finite element (FE) models have found that the rigid cement augmentation results in an increase in loading in the structures adjacent to the augmented vertebra. The mechanism of the increase of the loading is predicted to be the pillar effect of the rigid cement. The cement inhibits the normal endplate bulge into the augmented vertebra and thus pressurizes the adjacent disc, which subsequently increases the loading of the untreated vertebra. The mechanism for adjacent vertebral fractures is still unclear, but from experimental and computational studies, it appears that the change in mechanical loading following augmentation is responsible. The pillar effect of injected cement is hypothesized to decrease the endplate bulge in the augmented vertebra causing an increase in adjacent disc pressure that is communicated to the adjacent vertebra. To confirm the viability of the pillar effect as the responsible mechanism, endplate bulge and disc pressure should be directly measured before and after augmentation. Future studies should be concerned with quantifying the current and ideal mechanical response of the spine and subsequently developing cements that can achieve this optimum response.
Baroud
Gamal
G
Laboratoire de biomécanique, Département de genie mécanique, Université de Sherbrooke, Sherbrooke, QC, Canada. Gamal.Baroud@USherbrooke.ca
Vant
Christianne
C
Wilcox
Ruth
R
D001696:Biomechanical Phenomena; D001843:Bone Cements / Q000627:therapeutic use*; D002484:Cementation / Q000009:adverse effects; D050815:Fractures, Compression / Q000503:physiopathology / Q000628:therapy*; D005598:Fractures, Spontaneous / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007267:Injections; D010024:Osteoporosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D011859:Radiography; D016103:Spinal Fractures / Q000503:physiopathology / Q000628:therapy*; D013131:Spine / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*
D001843:Bone Cements