Clinical and radiographic evaluation of sagittal imbalance: a new radiographic assessment.

In this article, we describe a case series study involving a new radiologic evaluation of sagittal imbalance. We review the current radiologic assessment of sagittal imbalance and introduce a new radiologic evaluation that helps in ruling out hip flexion contracture as the primary cause of sagittal imbalance and the type and level of spinal osteotomy required to regain sagittal balance. Sagittal imbalance is important in spinal deformity assessment. Studies have confirmed that overall clinical outcomes and patient satisfaction with surgery were best in cases that resulted in an increase in lumbar lordosis. For this study, radiologic assessment of sagittal imbalance was conducted on a long, 14 × 51-inch upright lateral plain radiograph that included the proximal femur and the entire spine. The radiograph was taken with the arms at 45° forward flexion and the hips and knees fully extended. The femoral axis line was drawn and extended cephalad. The C7 offset, the perpendicular distance between the femoral axis line and the center of C7, represented the degree of sagittal imbalance. The angle between the femoral axis line and a line extending from the center of C7 to the vertebra at the level of the proposed osteotomy--the Seattle angle--predicted how much correction was required to bring the C7 plumb in line with the femoral axis and to decrease the C7 offset, thus regaining sagittal balance. The proposed method was used to evaluate 10 consecutive patients who required spinal osteotomies to regain sagittal balance. Preoperative and postoperative plain radiographs were assessed twice, at a 6-week interval, by an independent spine surgeon and a musculoskeletal radiologist. Cohen κ correlation coefficients were used to calculate intraobserver and interobserver reliability. The 2 reviewers' intraobserver reliability was excellent (κs = 0.98, 0.93). Interobserver reliability was lower but good (κ = 0.76). Inclusion of the proximal femur on the long upright lateral plain radiograph of the entire spine and identification of the relation between the femoral axis line and the center of C7 are important in evaluating sagittal imbalance. Excellent intraobserver reliability, coupled with good interobserver reliability, suggest that this new radiologic assessment method can be helpful in preoperative assessment of sagittal imbalance.

Effect of zoledronic acid in an L6-L7 rabbit spine fusion model.

Previous studies have shown that zoledronic acid administration can increase mineral content and strength in distraction osteogenesis. Of the few studies that have examined the use of bisphosphonates in spinal arthrodesis, none have assessed the effect of single dose treatment. The objective of this study was to evaluate the feasibility of enhancing spinal fusion rate using single dose zoledronic acid (ZA) to increase fusion-mass size and mineral density. Forty-eight New Zealand white rabbits underwent an L6-L7 intertransverse process fusion. The L6-L7 model is more challenging than the more commonly used level of L5-L6. Animals were randomly allocated to one of three groups, one received iliac crest bone graft alone, one group received iliac crest bone graft with locally administered zoledronic acid, 20 microg, and one group received iliac crest bone graft with a single dose of systemically administered zoledronic acid, 0.1 mg/kg. ZA doses were administered at the time of surgery. Twenty-four rabbits were culled at 6 weeks and 24 rabbits were culled at 12 weeks. Success of spinal fusion was determined by manual palpation. Specimens were evaluated radiographically, underwent quantitative computerised tomography analysis and were tested biomechanically in flexion and extension. In the six-week group, only five of the 24 spines fused with no noticeable trend with respect to treatment. In the 12-week group there was a trend toward increased fusion in the systemically administered ZA group (63%) versus the other two groups (25%) but was not statistically significant (p = 0.15). Radiographically, the local ZA treatment group showed a delay in remodelling with the presence of unremodelled bone chips. The 12-week systemic ZA group exhibited an 86% increase in BMC, a 31% increase in vBMD and a 41% increase in the volume of the fusion-mass (p < 0.05). The 12-week local ZA group also showed significant increases in BMC (69%), vBMD (31%) and total fusion-mass volume (29%) (p < 0.05). Biomechanical testing showed that the range of motion in flexion decreased to 4.5 (+/-2.5) degrees and 4.8 (+/-4.7) degrees for the local and systemic groups respectively compared to 9.6 (+/-4.9) degrees for the control group (p < 0.05). This study has shown that zoledronic acid increased fusion-mass size and bone mineral content. Systemic ZA led to an increased fusion rate; however the fusion rate remained below 100%. We suggest that bisphosphonate treatment may require an anabolic conjunctive therapy to ensure enhanced successful fusion.

Manipulation of the anabolic and catabolic responses with OP-1 and zoledronic acid in a rat critical defect model.

UNLABELLED: Bone repair involves both anabolic and catabolic responses. We hypothesized that anabolic treatment with OP-1 (BMP-7) and anti-catabolic treatment with zoledronic acid could be synergistic. In a rat critical defect, this combination therapy produced significant increases in new bone volume and strength. INTRODUCTION: When used to augment bone healing, osteogenic protein 1 (OP-1/BMP-7) and other BMPs stimulate the anabolic response, inducing osteoblast recruitment, differentiation, and bone production. However, BMPs can also upregulate catabolism by direct stimulation of osteoclasts and indirectly by osteoblasts through RANKL/RANK. We hypothesized that if such osteoclastic upregulation were modulated by zoledronic acid (ZA), the combination of OP-1 and ZA should produce increased new bone over OP-1 alone. MATERIALS AND METHODS: Rats with a surgically induced 6-mm femoral critical size defect were separated into five dosing groups: Carrier, Carrier + ZA, OP-1, OP-1 + ZA, and OP-1 + ZA administered 2 weeks after surgery (2W). Carrier +/- 50 microg OP-1 was placed in the defect, and 0.1 mg/kg ZA or saline was administered subcutaneously. Bone repair was analyzed by radiographs, QCT, mechanical testing, histology, and histomorphometry. RESULTS: Carrier alone and Carrier ZA groups did not unite by 8 weeks. Radiological union occurred in all OP-1 groups but was tenuous in some animals treated with OP-1 alone. BMC was increased by 45% in the OP-1 ZA group and 96% in the OP-1 ZA 2W group over OP-1 alone (p < 0.01). Callus volume increased over OP-1 alone by 45% and 86% in the OP-1 ZA and OP-1 ZA 2W groups, respectively (p < 0.01). The increased callus volume in the OP-1 ZA 2W group translated to increases in strength of 107% and stiffness of 148% (p < 0.05). BFR was not significantly different between OP-1 groups regardless of ZA treatment. CONCLUSIONS: ZA treatment significantly increased the BMC, volume, and strength of OP-1-mediated callus in a critical size defect in rats at 8 weeks. Thus, modulation of both anabolic and catabolic responses may optimize the amount and mineral content of callus produced, which could be of clinical benefit in obtaining bone union.