Revision Surgery for Adjacent Segment Degeneration After Fusion for Lumbar Spondylolisthesis: Is there a Correlation with Roussouly Type?

STUDY DESIGN: Retrospective study. OBJECTIVE: The aim of this study was to investigate whether there is an association between revision surgery rates for adjacent segment degeneration (ASD) and Roussouly type after L4-5 transforaminal lumbar interbody fusion (TLIF) for spondylolisthesis. SUMMARY OF BACKGROUND DATA: Revision surgery for ASD is known to occur after spinal fusion; however, it is unclear whether rates of ASD are associated with certain Roussouly types. METHODS: Patients who underwent L4-5 TLIF for spondylolisthesis at the University of California San Francisco from January 2006 to December 2016 with minimum 2-year follow-up were retrospectively analyzed by Roussouly type. Revision surgery for ASD was noted and correlated by Roussouly type. Spinopelvic parameters were also measured for correlation. A value of P < 0.05 was significant. RESULTS: There were 174 patients who met inclusion criteria, (59 males and 115 females). The average age was 62.3 (25-80) years. A total of 132 patients had grade I spondylolisthesis, and 42 had grade II. Mean follow-up was 45.2 months (24-497). A total of 22 patients (12.6%) underwent revision surgery for ASD after L4-5 TLIF. When classified by Roussouly type, revision surgery rates for ASD were: 1, 14.3%; 2, 22.6%; 3, 4.9%; and 4, 15.6% (P = 0.013). Type 3 spines with normal PI-LL (8.85°â€Š±â€Š6.83°) had the lowest revision surgery rate (4.9%), and type 2 spines with PI-LL mismatch (11.06°â€Š±â€Š8.81°) had the highest revision surgery rate (22.6%), a four-fold difference (P = 0.013). The PI-LL mismatch did not change significantly in each type postoperatively (P > 0.05). CONCLUSION: We found that there may be a correlation between Roussouly type and revision surgery for ASD after L4-5 TLIF for spondylolisthesis, with type 2 spines having the highest rate. Spinopelvic parameters may also correlate with revision surgery for ASD after L4-5 TLIF.Level of Evidence: 4.

Predictors of the need for laminectomy after indirect decompression via initial anterior or lateral lumbar interbody fusion.

OBJECTIVE: The goal of this study was to evaluate factors that are associated with the need for additional posterior direct decompressive surgery after anterior lumbar interbody fusion (ALIF) or lateral lumbar interbody fusion (LLIF). METHODS: Eighty-six adult patients who underwent ALIF or LLIF for degenerative spondylolisthesis and foraminal stenosis were enrolled. Patient factors (age, sex, number of surgery levels, and visual analog scale [VAS] score for leg and back pain); procedure-related factors (cage height and lordosis); and radiographic measurements (disc height [DH]; foraminal height [FH], foraminal area [FA], central canal diameter [CCD], and facet joint degeneration [FD]) were analyzed. All patients underwent staged surgery on 2 different days, with the anterior portion first, followed by the posterior portion. RESULTS: Of 86 patients, 62 underwent posterior decompression and 24 had no posterior decompression. There were no significant differences between groups with regard to age, sex, preoperative VAS score for back pain, cage height, cage angulation, preoperative DH, FH, FA, CCD, and FD (p > 0.05). The group that underwent posterior decompression showed statistically different numbers of treated segments (1.92 vs 1.21, p < 0.01), preoperative VAS leg score (7.9 vs 6.3), symptom duration (14.2 months vs 9.4 months), postoperative DH improvement (61.3% vs 96.2%), postoperative FH improvement (21.5% vs 32.1%), postoperative FA improvement (24.1% vs 36.9%), and cage height minus preoperative DH (5.3 mm vs 7.5 mm) compared with the nondecompression group. CONCLUSIONS: There appears to be some correlation between the need for posterior decompression and the number of treated segments, VAS leg scores, symptom duration, FH, FA, and difference between the cage height and preoperative DH. In selected patients undergoing staged surgery, indirect decompression without direct decompression may be a reasonable option in treating degenerative spinal conditions.

Blocking fatty acid synthase inhibits tumor progression of human osteosarcoma by regulating the human epidermal growth factor receptor 2/phosphoinositide 3-kinase/protein kinase B signaling pathway in xenograft models.

Previous studies have demonstrated that fatty acid synthase (FASN) is overexpressed in osteosarcoma (OS) cells and tissues and, therefore, knockdown of FASN may inhibit OS cell proliferation, migration and invasion via regulation of the human epidermal growth factor receptor 2 (HER2)/phosphoinositide 3-kinase (PI3K)/protein kinase B(Akt) signaling pathway in vitro. However, the tumor microenvironment has a crucial role in the determination of tumor malignant phenotype. The aim of the present study was to investigate the effect of knockdown of FASN on OS progression and the potential molecular mechanism in nude mice with orthotopic tumor implants in vivo. Results demonstrated that the knockdown of FASN markedly suppressed the growth and metastasis of OS, at least partially, by blocking the HER2/PI3K/Akt signal pathway in mice with intratibial 143B OS xenografts. These results suggest that the FASN/HER2/PI3K/Akt signaling pathway may be a potential therapeutic target for OS management.

Chlorogenic Acid Prevents Osteoporosis by Shp2/PI3K/Akt Pathway in Ovariectomized Rats.

Cortex Eucommiae is used worldwide in traditional medicine, various constituents of Cortex Eucommiae, such as chlorogenic acid (CGA), has been reported to exert anti-osteoporosis activity in China, but the mechanism about their contribution to the overall activity is limited. The aims of this study were to determine whether chlorogenic acid can prevent estrogen deficiency-induced osteoporosis and to analyze the mechanism of CGA bioactivity. The effect of CGA on estrogen deficiency-induced osteoporosis was performed in vivo. Sixty female Sprague-Dawley rats were divided randomly among a sham-operated group and five ovariectomy (OVX) plus treatment subgroups: saline vehicle, 17α-ethinylestradiol (E2), or CGA at 9, 27, or 45 mg/kg/d. The rats' femoral metaphyses were evaluated by micro-computed tomography (µCT). The mechanism of CGA bioactivity was investigated in vitro. Bone mesenchymal stem cells (BMSCs) were treated with CGA, with or without phosphoinositide 3-kinase (PI3K) inhibitor LY294002. BMSCs proliferation and osteoblast differentiation were assessed with 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and alkaline phosphatase, with or without Shp2 interfering RNA (RNAi). The results display that CGA at 27 and 45 mg/kg/day inhibited the decrease of bone mineral density (BMD) that induced by OVX in femur (p< 0.01), significantly promoted the levels of bone turnover markers, and prevented bone volume fraction (BV/TV), connectivity density (CoonD), trabecular number (Tb.N), trabecular thickness (Tb.Th) (all p< 0.01) to decrease and prevented the trabecular separation (Tb.Sp), structure model index (SMI)(both p< 0.01) to increase. CGA at 1 or 10 µM enhanced BMSC proliferation in a dose-dependent manner. CGA at 0.1 to 10 µM increased phosphorylated Akt (p-Akt) and cyclin D1. These effects were reversed by LY294002. CGA at 1 or 10 µM increased BMSC differentiation to osteoblasts (p< 0.01), Shp2 RNAi suppressed CGA-induced osteoblast differentiation by decreasing Shp2, p-Akt, and cyclin D1. This study found that CGA improved the BMD and trabecular micro-architecture for the OVX-induced osteoporosis. Therefore, CGA might be an effective alternative treatment for postmenopausal osteoporosis. CGA promoted proliferation of osteoblast precursors and osteoblastic differentiation of BMSCs via the Shp2/PI3K/Akt/cyclin D1 pathway.