Tissue-engineering strategies combining mesenchymal stem cells (MSCs) or extracellular vesicles (EVs) with bone-regenerative scaffolds may improve healing of critical-size bone defects, yet their comparative efficacy remains unclear. We systematically searched PubMed, Embase, Scopus, Web of Science, and ProQuest for animal studies published up to July 1, 2025. Risk of bias was assessed using the SYRCLE tool. New bone formation was synthesized as bone volume/total volume (BV/TV) using conventional meta-analysis and Bayesian network fixed/random-effects models, reported as standardized mean difference (SMD) with 95% confidence interval (CI)/credible interval (CrI). Subgroup analyses were conducted by MSC source, EV use, scaffold type, anatomical site, and follow-up duration, with sensitivity analyses and assessment of publication bias. In total, 207 studies across 7 animal models were included. MSC-loaded scaffolds significantly enhanced bone regeneration compared with no treatment or scaffold alone, showing a strong short-term effect and consistent benefits at medium and long follow-up. Bone marrow MSC (BMSC)-laden scaffolds underperformed adipose-derived MSC (ADSC)-laden scaffolds, and BMSC-derived EVs further improved outcomes compared with cell-free scaffolds. Calvarial defect models demonstrated greater gains than long-bone models. Network meta-analysis suggested multi-component composite scaffolds had the highest potential for new bone formation among cell-free designs. Overall, MSCs/EVs combined with supportive scaffolds markedly increase bone regeneration in preclinical models, but heterogeneity in models, biomaterials, dosing, and outcome reporting limits direct clinical translation, underscoring the need for standardized protocols and core outcome sets. STATEMENT OF SIGNIFICANCE: This comprehensive meta-analysis incorporated network comparisons across diverse mesenchymal stem cells (MSCs) or extracellular vesicles (EVs) sources and biomaterial categories. It reveals that MSC-EVs, particularly when combined with scaffolds or hydrogels, are the most effective in improving BV/TV ratio (bone volume/total volume) and histological outcomes in animal bone defect models. These data indicate that MSC or EV-enhanced biomaterial strategies may be leading candidates for repairing critical-sized defects and provide a standardized roadmap for transitioning preclinical success into clinical practice.

Inflammatory osteolysis arises from pro-inflammatory cytokine-driven osteoclast activation and disrupted bone remodeling equilibrium. The IRE1-XBP1s axis, a major unfolded protein response pathway, regulates cellular homeostasis, but its role in inflammatory osteoclastogenesis remained unexplored. Single-cell RNA-seq showed increased osteoclast precursor cells and activated IRE1-XBP1s in LPS-induced osteolysis. Inhibition of this axis reduced osteoclastogenesis and bone loss in vitro and in vivo. RNA-seq indicated that blocking IRE1-XBP1s suppressed Slc6a4 transcription, with gene set enrichment analysis confirming its role in 5-HT transport. Dual-luciferase assays and ChIP-PCR demonstrated XBP1s' direct transcriptional regulation targeting the Slc6a4 promoter. The 5-HT transporter inhibitor escitalopram also inhibited osteoclastogenesis, highlighting the IRE1-XBP1s-Slc6a4 axis's importance. Notably, untargeted metabolomics suggested 5-HT inhibited intracellular 3-methyladenine (3MA) metabolism, a compound previously considered unnatural. HPLC-MS confirmed the presence of 3MA metabolism in inflammatory osteoclasts, and 3MA supplementation attenuated 5-HT-induced autophagy and osteoclast differentiation. Blocking the IRE1-XBP1s-Slc6a4 axis reduced pro-osteoclastogenic effects in inflammatory bone disease patient-derived PBMCs. This study demonstrates that IRE1-XBP1s inhibition alleviates inflammatory osteoclastogenesis and osteolysis via a 5-HT-dependent anti-autophagy mechanism, proposing this pathway as a therapeutic target for inflammatory bone loss.

Background Mesotherapy, a widely utilized minimally invasive cosmetic procedure, carries potential risks of adverse reactions due to non-standardized protocols and overuse. Delayed granulomatous reactions represent a chronic complication, imposing significant physical and psychological burdens on patients. Objective This case series aims to evaluate the efficacy and safety of tofacitinib in managing non-infectious granulomatous reactions following mesotherapy. Methods This retrospective analysis included six patients diagnosed with non-infectious granulomatous reactions post-mesotherapy, treated at Peking Union Medical College Hospital between October 2021 and April 2025. All patients received oral tofacitinib. Clinical outcomes, treatment regimens, and safety profiles were assessed. Results All six patients demonstrated significant improvement in skin lesion severity, with no treatment-related adverse events observed during follow-up. Conclusion Oral tofacitinib exhibits promising clinical efficacy and a favorable safety profile for non-infectious granulomatous reactions induced by mesotherapy, positioning it as a viable therapeutic option during the inflammatory phase.

Background Osteoclast-mediated bone resorption drives osteoporosis, a prevalent skeletal disorder with significant clinical and socioeconomic burden, yet the upstream molecular mechanisms controlling osteoclast differentiation remain incompletely defined. Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a known oncogenic regulator, but its role in bone metabolism and osteoclast biology has not been explored. Methods We used RANKL-induced mouse bone marrow macrophages (BMMs) to model osteoclast differentiation in vitro, with adenoviral-mediated gain- or loss-of-function of CIP2A. Mechanistic investigations included immunoprecipitation-mass spectrometry (IP-MS), co-immunoprecipitation (co-IP), ubiquitination assays, cycloheximide (CHX) chase analysis, RNA sequencing (RNA-seq), and chromatin immunoprecipitation sequencing (ChIP-seq). For translational assessment, in vivo, we employed an ovariectomy (OVX)-induced osteoporosis mouse model with systemic adeno-associated virus (AAV)-mediated gene manipulation as well as pharmacological inhibition using the CIP2A small-molecule inhibitor TD52. Results CIP2A expression was dynamically upregulated during RANKL-induced osteoclastogenesis. CIP2A promoted osteoclast formation, actin ring assembly, and bone resorptive activity in vitro, without affecting osteoblast differentiation. Mechanistically, CIP2A acted as a molecular scaffold that recruited the deubiquitinase OTUD4 to stabilize high mobility group A1 (HMGA1) by preventing its ubiquitination and proteasomal degradation. Stabilized HMGA1 translocated to the nucleus. Integrated multi-omics analyses (RNA-seq and HMGA1 ChIP-seq) identified c-Myc as a direct transcriptional target of HMGA1, which bound distal regulatory elements to enhance c-Myc transcription. Functional experiments further revealed that c-Myc formed a positive feedback loop with the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway, sustaining osteoclast activity. In OVX mice, c-Myc overexpression or AKT activation partially rescued the bone loss induced by CIP2A knockdown. Importantly, pharmacological inhibition of CIP2A with TD52 suppressed osteoclast differentiation and bone resorption both in vitro and in vivo, without causing major organ toxicity or affecting osteoblast function. Conclusions Our findings identify a novel CIP2A–OTUD4–HMGA1–c-Myc–PI3K/AKT regulatory axis that drives pathological osteoclastogenesis and bone loss. CIP2A represents a promising druggable target for osteoporosis and related osteolytic diseases. As a potential first-in-class CIP2A inhibitor, TD52 merits further preclinical development for the treatment of postmenopausal osteoporosis.

Osteoporosis is a systemic skeletal disorder characterized by reduced bone mass, compromised bone microstructure, and an increased risk of fractures, primarily due to excessive osteoclast-mediated bone resorption relative to osteoblast-mediated bone formation. While current anti-osteoporosis drugs, such as bisphosphonates and denosumab, predominantly focus on reducing bone resorption, osteoanabolic approaches are essential for restoring bone microarchitecture and ultimately reducing fracture risk. Traditional Chinese medicines (TCMs) and their active ingredients have long been used in China for osteoporosis prevention and treatment. This review provides a comprehensive evaluation of the effects and molecular mechanisms of 65 natural products across 24 categories on osteoblast-mediated bone formation. These compounds promote bone formation by regulating key transcription factors (RUNX2 and Osterix) and signaling pathways, including WNT/β-catenin, bone morphogenic protein (BMP), mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), oxidative stress, autophagy, and epigenetic regulation. Notably, certain natural products [e.g., icariin (ICA)] exert their effects through multiple targets and pathways. Many of these natural products have demonstrated significant therapeutic efficacy in animal models, such as ovariectomized (OVX) mice. Our findings suggest that natural products with kidney-tonifying, anti-inflammatory, and antioxidant properties, as well as those inhibiting adipocyte differentiation, may hold promise for osteoporosis treatment. Additionally, we highlight current research gaps and propose future directions, including high-throughput screening and validation in diverse animal models, development of novel bone-targeting delivery systems, and identification of natural compounds targeting osteocytes.

Extensive research has underscored the pivotal role of DNA methylation in the development of various diseases, including osteoarthritis (OA). DNA methylation is regulated by methylation writers, readers, and erasers. As a crucial methylation reader, methyl-CpG-binding domain2 (MBD2) has been implicated in modulating the occurrence and progression of multiple inflammatory diseases. This study aims to investigate whether MBD2 contributes to the pathogenesis of OA through its regulation of DNA methylation. Our study confirmed that MBD2 was increased in OA cartilage tissues from humans as well as mice with destabilization of the medial meniscus, despite a reduction in its nuclear import. Specific knockout of Mbd2 in cartilage exacerbated cartilage degradation and accelerated OA progression. Mechanistically, RNA sequencing studies demonstrated that the deletion of MBD2 induced ferroptosis in chondrocytes. Subsequent CUT&Tag and reduced representation bisulfite sequencing analyses revealed that MBD2 binds to the Steap3 promoter region and modulates its methylation state in chondrocytes. STEAP3 catalyzes the reduction of ferric iron (Fe3+) to ferrous iron (Fe2+), contributing to the induction of ferroptosis. The administration of a ferroptosis inhibitor and adeno-associated virus-mediated Steap3 knockdown alleviated OA induced by MBD2 deletion. Adeno-associated virus-mediated overexpression of Mbd2 partially mitigated destabilization of the medial meniscus-induced OA. Our findings provide evidence linking DNA methylation readers to OA development, and targeting MBD2 may offer a promising therapeutic strategy for OA treatment.

Abstract Epidural fibrosis (EF) is a frequent and debilitating complication that impairs recovery following spinal surgery, yet effective targeted therapies are lacking. Here we observe enrichment of FAP⁺ fibroblasts at surgical sites in patients after laminectomy. To therapeutically target this subset, we develop bispecific antibody–decorated extracellular vesicles (BsAb EVs), which redirect endogenous T cells to eliminate FAP⁺ fibroblasts in situ. In a preclinical model, BsAb EVs selectively eliminate pathogenic fibroblasts, reduce fibrotic collagen accumulation, and prevent the development of postoperative epidural fibrosis without detectable systemic toxicity under the tested conditions. Single-cell RNA sequencing reveals that FAP⁺ fibroblasts represent a transcriptionally distinct subset from α-SMA⁺ myofibroblasts, characterized by enhanced extracellular matrix remodeling and TGF-β production. Together, these findings highlight a critical stromal subset in EF pathogenesis and position BsAb EVs as a promising immunotherapeutic strategy for targeting pathogenic stromal cells in fibrotic and tissue-remodeling disorders.

CONTEXT:Emerging observational evidence has suggested a comorbidity between type 1 diabetes (T1D) and juvenile idiopathic arthritis (JIA). OBJECTIVE:The study aimed to evaluate the causal effect of T1D on JIA, explore the mediating role of circulating immune cells, and verify the causal relationship in mouse models. METHODS:We first assessed the genetic correlation using linkage disequilibrium score regression. We then evaluated the causal relationship through Mendelian randomization and subsequently conducted in vivo investigations using nonobese diabetic (NOD) mice, streptozotocin (STZ)-induced diabetic mice, and mannan-induced arthritic mice. RESULTS:Our analysis confirmed a strong, positive genetic correlation between these 2 diseases and identified a robust positive causal effect of T1D on JIA. Next, the mediation analysis indicated that CD8+ natural killer T (NKT) absolute count had a significant mediating effect and accounted for 32.5% of the increased risk of JIA attributable to T1D. Furthermore, in vivo experiments revealed that young NOD mice spontaneously developed mild osteoarthritis and progressive synovitis, along with systemic inflammation. In contrast, no signs of osteoarthritis or synovitis were detected in young STZ-induced diabetic mice. Additionally, the CD8+ NKT cell count was negatively associated with the development of mannan-induced arthritis in SKG mice. CONCLUSION:The study confirmed a significant causal effect of T1D on JIA from a genetic perspective, revealed CD8+ NKT cells as a pivotal mediating factor in this causal pathway, and verified a predisposition to inflammatory arthritis in young NOD mice.

BACKGROUND:Tuberculosis is among the most devastating infectious diseases worldwide. Spinal tuberculosis is not easy to detect at an early stage, which without effective treatment often leads to spinal deformity and spinal cord damage which in turn cause complications such as paraplegia and quadriplegia. In this study, we established a model using three concentrations of bacteria and carried out a comprehensive evaluation of the model by imaging, general observations, and histopathological and bacteriological studies. AIM:To establish a rabbit model of spinal tuberculosis and examine the effect on the model's efficacy using different concentrations of Mycobacterium tuberculosis (M. tuberculosis) inoculum. METHODS:New Zealand rabbits were randomly divided into experimental, control and blank groups. The experimental and control animals were sensitized with complete Freund's adjuvant, a hole was drilled beneath the upper endplate of the L6 vertebral body and filled with gelfoam sponge. The experimental group was divided into three subgroups (experimental 1, experimental 2, experimental 3) and infused with M. tuberculosis suspension at various concentrations. The control group was inoculated with saline and the blank group received no treatment. The 12-week post-operative survival rates were 100%, 80% and 30% in the experimental groups inoculated with concentrations of 106, 107 and 108 CFU/mL bacteria, respectively. RESULTS:The survival rate of the control and blank groups was 100%. Vertebral body destruction at 8 weeks in the three experimental groups as determined by X-ray analysis was 33.3%, 62.5% and 66.7%, and by computed tomography (CT) and 3-dimensional CT 44.4%, 75% and 100%, respectively. At 12 weeks, the figures were 44.4%, 75% and 100% by X-ray analysis and 44.4%, 100% and 100% by CT and 3-dimensional CT, respectively. All surviving rabbits of the experimental groups had vertebral destruction. The positive bacterial culture rates were 22.2%, 75% and 66.7%, respectively, in the experimental groups. After being sensitized with complete Freund's adjuvant, large differences were observed in the extent of spinal tuberculosis after inoculation of the rabbits with different concentrations of H37RV standard M. tuberculosis. CONCLUSION:The experimental 1 had a low success rate at establishing an infection. The experimental 3 resulted in high mortality and complication rates. The experimental 2 was optimum for establishing a spinal tuberculosis model based on the high level of symptoms observed and the low rabbit mortality.

There is a positive causality between coffee consumption and osteoarthritis (OA); however, whether gut microbiota is involved needs to be discussed. Here, we observed that in caffeine consumers, fecal Prevotella copri abundance was positively correlated with subchondral bone mass, serum caffeine concentration was negatively correlated with bone mass, and fecal P. copri was negatively correlated with serum caffeine. In the OA model, caffeine intake aggravated articular cartilage destruction, bone mass loss, and intestinal barrier damage; on the contrary, paraxanthine intake reversed the above lesions. Importantly, after the intestinal P. copri supplement, caffeine-induced lesions in OA mice were effectively alleviated. Mechanically, P. copri has the potential to metabolize caffeine into paraxanthine, and this effect could alleviate the ferroptosis of osteoblast in the OA model. This study screened out that P. copri, an endogenous bacteria, has the ability to metabolize caffeine and revealed its effects on OA progression.IMPORTANCEThere is positive causality between coffee consumption and osteoarthritis (OA). Caffeine exposure is responsible for the reduction of bone mass and restrained osteoblast function. Prevotella copri abundance is exhausted in gut and positively correlated with subchondral bone mass in coffee consumption patients with OA. Supplement of intestinal P. copri alleviates caffeine-induced subchondral bone loss. P. copri has the potential to metabolize caffeine into paraxanthine, and this effect alleviates ferroptosis of osteoblast. Our study illustrated that intestinal P. copri possibly serves as a novel promising treatment for coffee consumers with OA.

A distinguishing feature of older mesenchymal stem cells (MSCs) from bone marrow (BM) is the transition in their differentiation capabilities from osteoblasts to adipocytes. However, the mechanisms underlying these cellular events during the aging process remain unclear. We identified angiopoietin-like protein 8 (ANGPTL8), an adipokine implicated in lipid metabolism, that influenced the fate of MSCs in BM during skeletal aging. Our studies revealed that ANGPTL8 steered MSCs toward adipogenic differentiation, overshadowing osteoblastogenesis. Mice with overexpressed ANGPTL8 exhibited reduced bone mass and increased BM adiposity, while those with transgenic depletion of ANGPTL8 showed lowered bone loss and less accumulation of BM fat. ANGPTL8 influenced the BM niche of MSCs by inhibiting the Wnt/β-catenin signaling pathway. Partial inhibition of PPARγ rescued some aspects of the phenotype in MSCs with ANGPTL8 overexpression. Furthermore, treatment with an Angptl8 antisense oligonucleotide improved the phenotype of aging mice. Our research suggests that ANGPTL8 is a crucial regulator of senesence-related changes in the BM niche and the cell-fate switch of MSCs.

Iron overload and related oxidative damage are seen in many rare diseases, due to mutation of iron homeostasis-related genes. As a core regulator on cellular antioxidant reaction, Nrf2 can also decrease systemic and cellular iron levels by regulating iron-related genes and pathways, making Nrf2 activators very good candidates for the treatment of iron overload disorders. Successful examples include the clinical use of omaveloxolone for Friedreich's Ataxia and dimethyl fumarate for relapsing-remitting multiple sclerosis. Despite these uses, the therapeutic potentials of Nrf2 activators for iron overload disorders may be overlooked in clinical practice. Therefore, this study talks about the potential use, possible mechanisms, and precautions of Nrf2 activators in treating rare iron overload diseases. In addition, a combination therapy with Nrf2 activators and iron chelators is proposed for clinical reference, aiming to facilitate the clinical use of Nrf2 activators for more iron overload disorders.

AIMS:This study aimed to test the hypothesis that nuclear factor of activated T cells 1 (NFAT1) signaling contributes to bone cancer pain by regulating interleukin (IL)-18 expression in spinal microglia. METHODS:This study was performed on male mice using a Lewis lung carcinoma-induced bone cancer pain model. Nociceptive behaviors were evaluated by measuring mechanical allodynia, thermal hyperalgesia, and spontaneous pain. Expression levels were measured via real-time quantitative polymerase chain reaction, western blotting, and immunofluorescence analysis. The effect of pharmacologic intervention of spinal NFAT1/IL-18 signaling on bone cancer pain was the primary outcome. RESULTS:NFAT1 expression was upregulated in the spinal microglia after tumor inoculation. Pharmacological inhibition of NFAT1 upregulation prevented and reversed bone cancer-related pain behaviors. In spinal microglia, NFAT1 inhibition decreased p38 MAPK phosphorylation and IL-18 production. Blocking NFAT1 signaling suppressed tumor-induced neuronal sensitization and microglial activation as well as activation of the N-methyl-D-aspartate receptor and the subsequent Ca2+-dependent signaling. CONCLUSION:Microglia NFAT1-p38 signaling contributes to bone cancer pain through IL-18-mediated central sensitization in spinal microglia. NFAT1 could be a potential target for therapeutic intervention to prevent bone cancer pain.

OBJECTIVE:To investigate the feasibility of prepsoas oblique lumbar interbody fusion (OLIF) at L5-S1 level and propose a new practical framework for approach selection of OLIF51. METHODS:The feasibility of left-sided and right-sided prepsoas approaches was graded as easy, advanced, and difficult depending on retraction distance and perivascular adipose tissue in the radiographic study. The classification results were summarized, and the OLIF51 approach selection framework was proposed to guide the subsequent clinical research. The clinical outcomes and incidence of complications were compared between two groups in which the inpatients underwent OLIF51 from 2019 to 2022. RESULTS:Among the 200 consecutive randomized outpatients who met the inclusion criteria, the easy, advanced, and difficult cases of left-sided prepsoas were 19, 158, and 23, respectively, with right-sided prepsoas (40, 160, 0). Guided by the proposed framework, 65 inpatients who underwent left-sided prepsoas OLIF51 were enrolled in group A and 71 inpatients who underwent right-sided prepsoas OLIF51 were enrolled in group B. There was no significant difference in demographic and preoperative follow-up results. The operation time for OLIF51 alone was shorter in group B than in group A. Operations were successfully completed in all patients of group B. In group A, sufficient exposure was not achieved in four patients (6.2%). Ligation of the iliolumbar vein was needed for adequate exposure in 16 (24.6%) patients from group A and 14 (19.7%) from group B. Postoperative clinical outcomes were improved and not significantly different between the two groups. CONCLUSIONS:Prepsoas OLIF51 is feasible, which can serve as alternative approaches for anterior interbody fusion of L5-S1 according to preoperative imaging evaluation. Although there is no difference in the therapeutic effect between the two groups, the right-sided prepsoas approach was preferred with its greater feasibility and advantages.

Tumor necrosis factor receptor-associated factor 1 (TRAF1) is a crucial signaling adaptor involved in multiple cellular events. However, its role in regulating osteoclastogenesis and energy metabolism remains unclear. Here, we report that TRAF1 promotes osteoclastogenesis and oxidative phosphorylation (OXPHOS). Employing RNA sequencing, we found that TRAF1 is markedly upregulated during osteoclastogenesis and is positively associated with osteoporosis. TRAF1 knockout inhibits osteoclastogenesis and increases bone mass in both normal and ovariectomized adult mice without affecting bone mass in childhood. Furthermore, TRAF1 promotes osteoclast OXPHOS by increasing the phosphorylation level of AKT. Mechanistically, TRAF1 functions to inhibit TRAF2-induced ubiquitination of Gβl, a known activator of AKT, and further upregulates AKT phosphorylation. Rescue experiments revealed that the inhibitory effects of TRAF1 knockout on osteoclastogenesis, OXPHOS, and bone mass are dependent on AKT. Collectively, our findings uncover a previously unrecognized function of TRAF1 in regulating osteoclastogenesis and energy metabolism, and establish a novel TRAF1-AKT-OXPHOS axis in osteoclasts.

BACKGROUND:The presence of bone invasion in aggressive pituitary adenoma (PA) was found in our previous study, suggesting that PA cells may be involved in the process of osteoclastogenesis. miR-19a (as a key member of the miR-17-92 cluster) has been reported to activate the nuclear factor-кB (NF-кB) pathway and promote inflammation, which could be involved in the process of the bone invasion of pituitary adenoma. METHODS:In this work, FISH was applied to detect miR-19a distribution in tissues from patients with PA. A model of bone invasion in PA was established, GH3 cells were transfected with miR-19a mimic, and the grade of osteoclastosis was detected by HE staining. qPCR was performed to determine the expression of miR-19a throughout the course of RANKL-induced osteoclastogenesis. After transfected with a miR-19a mimic, BMMs were treated with RANKL for the indicated time, and the osteoclast marker genes were detected by qPCR and Western Blot. Pit formation and F-actin ring assay were used to evaluate the function of osteoclast. The TargetScan database and GSEA were used to find the potential downstream of miR-19a, which was verified by Co-IP, Western Blot, and EMSA. RESULTS:Here, we found that miR-19a expression levels were significantly correlated with the bone invasion of PA, both in clinical samples and animal models. The osteoclast formation prior to bone resorption was dramatically enhanced by miR-19, which was mediated by decreased cylindromatosis (CYLD) expression, increasing the K63 ubiquitination of tumor necrosis factor receptor-associated factor 6 (TRAF6). Consequently, miR-19a promotes osteoclastogenesis by the activation of the downstream NF-кB and mitogen-activated protein kinase (MAPK) pathways. CONCLUSIONS:To summarize, the results of this study indicate that PA-derived miR-19a promotes osteoclastogenesis by inhibiting CYLD expression and enhancing the activation of the NF-кB and MAPK pathways.

Objective: To investigate the improvement of spinopelvic parameters and therapeutic efficacy in the treatment of complex degenerative lumbar spondylolisthesis (CDLS) after oblique lumbar interbody fusion (OLIF) and transforaminal lumbar interbody fusion (TLIF). Methods: From January 2018 to December 2020, 71 patients with CDLS underwent OLIF or TLIF at the same hospital: 31 in the OLIF group and 40 in the TLIF group. The spinopelvic parameters, perioperative data, and clinical outcomes were elected and compared between the 2 groups. Results: There were no statistic differences in demographic perioperative complication rates and preoperative spinopelvic parameters between the two groups. OLIF group showed lower serum C-reactive protein in the early postoperative stage, shorter length of stay, less estimated blood loss and larger slippage correction rate (88.05 vs. 62.37%) (all P < 0.05). There was no significant difference in the visual analog scale and Oswestry disability index scores before operation and three and six months after surgery, but OLIF group was better in the long-term with visual analog scale and Oswestry disability index (1.7/13.2 vs. 2.3/16.5). And it was significantly different in the lumbar lordosis angle, segmental lordosis angle, pelvic tilt, sacral slope (46.0 degrees/9.3 degrees/18.2 degrees/35.9 degrees vs. 40.4 degrees/7.2 degrees/23.9 degrees/31.1 degrees), and sagittal vertical axis (21.6 vs. 31.7mm) after surgery between OLIF and TLIF groups (all P < 0.05). Conclusions: In the therapy of CDLS, OLIF can better reduce pelvic tilt, L1 axis S1 distance, and sagittal vertical axis, and increase lumbar lordosis angle and sacral slope, showing advantages over TLIF in improving and maintaining spinopelvic parameters. Although there was no difference in complication rates between OLIF and TLIF, OLIF was more minimally invasive, had less tissue damage, had faster recovery, and had better long-term outcomes.

OBJECTIVE The goal of this study was to evaluate the feasibility of the fractured vertebra antedisplacement reconstruction technique for the treatment of posttraumatic thoracolumbar kyphosis (PTK). METHODS A total of 22 patients with PTK who were treated with the fractured vertebra antedisplacement reconstruction technique were retrospectively analyzed. The radiological evaluation included global kyphosis, thoracolumbar angle, and sagittal vertical axis. The clinical evaluation included visual analog scale pain score, Oswestry Disability Index score, SF-12 Health Survey score, and American Spinal Injury Association grade. The complications were recorded. RESULTS The mean global kyphosis was 55.0° ± 12.6° preoperatively, 8.5° ± 5.0° postoperatively, and 10.3° ± 4.8° at the latest follow-up (p < 0.001). The average total kyphosis correction achieved was 44.7° ± 14.2°, with a range of 23.4°–79.4°, indicating a mean final correction of 80.1%. The mean thoracolumbar angle was 46.2° ± 13.2° preoperatively, 6.6° ± 4.5° postoperatively, and 7.6° ± 4.2° at the latest follow-up (p < 0.001). The mean sagittal vertical axis was improved significantly, from 51.1 ± 24.2 mm preoperatively to 28.5 ± 17.4 mm at the latest follow-up (p = 0.001). One patient (4.5%) experienced single intervertebral fusion nonunion, and 1 patient (4.5%) experienced distal screw loosening. No patients experienced any neurological deterioration. The visual analog scale pain score, Oswestry Disability Index score, SF-12 Health Survey score, and American Spinal Injury Association grade achieved significant improvement at the latest follow-up. CONCLUSIONS Fractured vertebra antedisplacement reconstruction technique can effectively correct kyphosis, reconstruct spinal stability, and improve the patient’s symptoms and neurological function. This technique is safer, minimally traumatic, and less technically demanding to avoid osteotomy-related complications. It is a feasible treatment choice for PTK.

Retraction: "(2R,3R)Dihydromyricetin inhibits osteoclastogenesis and bone loss through scavenging LPS-induced oxidative stress and NF-kappa B and MAPKs pathways activating," by Xuejun Zhang, Xin Li, Jianguo Fang, Xiaolong Hou, Huang Fang, Fengjing Guo, Feng Li, Anmin Chen, Shilong Huang, J Cell Biochem 2018, 119: 8981-8995. The above article, published online on 4 August 2018 in Wiley Online Library () has been retracted by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by third parties. During the investigation, several flaws and inconsistencies were found within the data presented. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the retraction but were not available for a final confirmation.