Incidence and Risk Factors of the Caudal Screw Loosening after Pelvic Fixation for Adult Spinal Deformity: A Systematic Review and Meta-analysis

Zhao Jian,Nie Zheng,Zhou Jiangjun,Liao Dongfa,Liu Da 대한척추외과학회 2024 Asian Spine Journal Vol.18 No.1

The purpose of this study was to assess the factors affecting caudal screw loosening after spinopelvic fixation for adult patients with spinal deformity. This meta-analysis calculated the weighted mean difference (WMD) and odds ratio (OR) using Review Manager ver. 5.3 (RevMan; Cochrane, London, UK). The loosening group was older than the control group (WMD, 2.17; 95% confidence interval [CI], 0.48–3.87; <i>p</i>=0.01). The S2 alar-iliac (S2AI) could prevent the caudal screw from loosening (OR, 0.43; 95% CI, 0.20–0.94; <i>p</i>=0.03). However, gender distribution (<i>p</i>=0.36), the number of fusion segments (<i>p</i>=0.24), rod breakage (<i>p</i>=0.97), T-score (<i>p</i>=0.10), and proximal junctional kyphosis (<i>p</i>=0.75) demonstrated no difference. Preoperatively, only pelvic incidence (PI) in the loosening group was higher (WMD, 5.08; 95% CI, 2.71–7.45; <i>p</i><0.01), while thoracic kyphosis (<i>p</i>=0.09), lumbar lordosis (LL) (<i>p</i>=0.69), pelvic tilt (PT) (<i>p</i>=0.31), pelvic incidence minus lumbar lordosis (PI–LL) (<i>p</i>=0.35), sagittal vertical axis (SVA) (<i>p</i>=0.27), and T1 pelvic angle (TPA) demonstrated no difference (<i>p</i>=0.10). PI–LL (WMD, 6.05; 95% CI, 0.96–11.14; <i>p</i>=0.02), PT (WMD, 4.12; 95% CI, 0.99–7.26; <i>p</i>=0.01), TPA (WMD, 4.72; 95% CI, 2.35–7.09; <i>p</i><0.01), and SVA (WMD, 13.35; 95% CI, 2.83–3.87; <i>p</i>=0.001) were higher in the screw loosening group immediately postoperatively. However, TK (<i>p</i>=0.24) and LL (<i>p</i>=0.44) demonstrated no difference. TPA (WMD, 8.38; 95% CI, 3.30–13.47; <i>p</i><0.01), PT (WMD, 6.01; 95% CI, 1.47–10.55; <i>p</i>=0.01), and SVA (WMD, 23.13; 95% CI, 12.06–34.21; <i>p</i><0.01) were higher in the screw loosening group at the final follow-up. However, PI–LL (<i>p</i>=0.17) demonstrated no significant difference. Elderly individuals were more susceptible to the caudal screw loosening, and the S2AI screw might better reduce the caudal screw loosening rate than the iliac screws. The lumbar lordosis and sagittal alignment should be reconstructed properly to prevent the caudal screw from loosening. Measures to block sagittal alignment deterioration could also prevent the caudal screw from loosening.

Multiple-Rod Constructs in Adult Spinal Deformity Surgery: A Systematic Review and Meta-Analysis

Zhao Jian,Nie Zheng,Zhang Zhengping,Liao Dongfa,Liu Da 대한척추외과학회 2023 Asian Spine Journal Vol.17 No.5

The purpose of this research was to compare the therapeutic efficacy of multiple-rod constructs vis-a-vis 2-rod constructs in the treatment of adult spinal deformity. A systematic review and meta-analysis were performed to determine whether the multiple-rod construct outperformed the 2-rod construct. We initially retrieved 357 papers, but only 12 were chosen for further meta-analysis. The rod breakage rates in the multiple-rod and the 2-rod groups were 10.66% and 29.87%, respectively. The multiple-rod construct inhibited rod breakage (odds ratio [OR], 0.28; 95% confidence interval [CI], 0.19–0.41; <i>p</i><0.001), pseudarthrosis (OR, 0.30; 95% CI, 0.18–0.50; <i>p</i><0.001) and rod fracture at the osteotomy site (OR, 0.34; 95% CI, 0.13–0.89; <i>p</i>=0.03). Furthermore, the multiple-rod construct reduces the risk of revision surgery (OR, 0.38; 95% CI, 0.20–0.73; <i>p</i>=0.04) as well as the revision risk of pseudarthrosis/rod fracture in the multiple- rod group (OR, 0.31; 95% CI, 0.18–0.52; <i>p</i><0.001), but increases the risk of caudal screw loosening (OR, 4.99; 95% CI, 1.87–13.30; <i>p</i>=0.001). There was no statistically significant difference in proximal junctional kyphosis (PJK) parameters (<i>p</i>=0.85), cerebrospinal fluid leakage (<i>p</i>=0.09), wound infection (p =0.71), age at surgery (<i>p</i>=0.62), gender distribution (<i>p</i>=0.93), body mass index (p =0.86), smoking status (<i>p</i>=0.05), hospital stay (<i>p</i>=0.09), osteoporosis (<i>p</i>=0.95), CoCr rod material (<i>p</i>=0.15), bone morphogenetic protein-2 (<i>p</i>=0.58), L5/S1 interbody fusion (<i>p</i>=0.07), high-grade osteotomies (<i>p</i>=0.07), the number of fusion levels (<i>p</i>=0.11), operation time (<i>p</i>=0.30), and blood loss volume (<i>p</i>=0.34). Regarding radiographic parameters, only preoperative sagittal vertical axis was found to be higher (weight means difference [WMD], 25.60; 95% CI, 15.43–35.77; <i>p</i><0.001) in the multiple-rod group. There was no difference in preoperative Oswestry Disability Index (ODI) (WMD, −3.32; 95% CI, −7.38 to 0.73; <i>p</i>=0.11), but the multiple-rod group had a lower ODI at follow-up (WMD, −7.71; 95% CI, −11.62 to −3.86; <i>p</i><0.001). Multiple-rod constructs could prevent rod breakage and pseudarthrosis while also lowering the revision rate, resulting in a better clinical outcome than the 2-rod construct. Nonetheless, due consideration should be given to PJK and screw loosening in multiple-rod constructs, possibly due to the increased stiffness caused by the multiple-rod structure.

Peroxisome Proliferator-Activated Receptor α Facilitates Osteogenic Differentiation in MC3T3-E1 Cells via the Sirtuin 1-Dependent Signaling Pathway

Kai Gong,Bo Qu,Cairu Wang,Jingsong Zhou,Dongfa Liao,Wei Zheng,Xianming Pan 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.6

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by lack of insulin and high glucose levels. T2DM can cause bone loss and fracture, thus leading to diabetic osteoporosis. Promoting osteogenic differentiation of osteoblasts may effectively treat diabetic osteoporosis. We previously reported that Sirtuin 1 (Sirt1), a NAD+-dependent deacetylase, promotes osteogenic differentiation through downregulation of peroxisome proliferator-activated receptor (PPAR) γ. We also found that miR-132 regulates osteogenic differentiation by downregulating Sirt1 in a PPAR /δ-dependent manner. The ligand-activated transcription factor, PPAR , is another isotype of the peroxisome proliferator-activated receptor family that helps maintain bone homeostasis and promot bone formation. Whether the regulatory role of PPAR in osteogenic differentiation is mediated via Sirt1 remains unclear. In the present study, we aimed to de-termine this role and the underlying mechanism by using high glucose (HG) and free fatty acids (FFA) to mimic T2DM in MC3T3-E1 cells. The results showed that HG-FFA significantly inhibited expression of PPAR , Sirt1 and osteogenic differentiation, but these effects were markedly reversed by PPAR overexpression. Moreover, siSirt1 attenuated the positive effects of PPAR on osteogenic differentiation, suggesting that PPAR promotes osteogenic differentiation in a Sirt1-dependent manner. Luciferase activity assay confirmed interactions between PPAR and Sirt1. These findings indicate that PPAR promotes osteogenic differentiation via the Sirt1-dependent signaling pathway.

Peroxisome Proliferator-Activated Receptor α Facilitates Osteogenic Differentiation in MC3T3-E1 Cells via the Sirtuin 1-Dependent Signaling Pathway

Gong, Kai,Qu, Bo,Wang, Cairu,Zhou, Jingsong,Liao, Dongfa,Zheng, Wei,Pan, Xianming Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.6

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by lack of insulin and high glucose levels. T2DM can cause bone loss and fracture, thus leading to diabetic osteoporosis. Promoting osteogenic differentiation of osteoblasts may effectively treat diabetic osteoporosis. We previously reported that Sirtuin 1 (Sirt1), a $NAD^+$-dependent deacetylase, promotes osteogenic differentiation through downregulation of peroxisome proliferator-activated receptor (PPAR) ${\gamma}$. We also found that miR-132 regulates osteogenic differentiation by downregulating Sirt1 in a $PPAR{\beta}/{\delta}$-dependent manner. The ligand-activated transcription factor, $PPAR{\alpha}$, is another isotype of the peroxisome proliferator-activated receptor family that helps maintain bone homeostasis and promot bone formation. Whether the regulatory role of $PPAR{\alpha}$ in osteogenic differentiation is mediated via Sirt1 remains unclear. In the present study, we aimed to determine this role and the underlying mechanism by using high glucose (HG) and free fatty acids (FFA) to mimic T2DM in MC3T3-E1 cells. The results showed that HG-FFA significantly inhibited expression of $PPAR{\alpha}$, Sirt1 and osteogenic differentiation, but these effects were markedly reversed by $PPAR{\alpha}$ overexpression. Moreover, siSirt1 attenuated the positive effects of $PPAR{\alpha}$ on osteogenic differentiation, suggesting that $PPAR{\alpha}$ promotes osteogenic differentiation in a Sirt1-dependent manner. Luciferase activity assay confirmed interactions between $PPAR{\alpha}$ and Sirt1. These findings indicate that $PPAR{\alpha}$ promotes osteogenic differentiation via the Sirt1-dependent signaling pathway.