Functional outcomes of full-endoscopic spine surgery for high-grade migrated lumbar disc herniation: a prospective registry-based cohort study with more than 5 years of follow-up.

BACKGROUND: Full-endoscopic lumbar discectomy (FELD) is an alternative to posterior open surgery to treat a high-grade migrated herniated disc. However, because of the complexity of the surgery, success is dependent on the surgeon's skill. Therefore, patients are frequently treated using open discectomy. Anatomical constraints and technical difficulties can lead to the incomplete removal of high-grade migrated discs. METHODS: We retrospectively reviewed patients who had undergone FELD performed by a single surgeon between January 2010 and January 2014 from a prospective spine registry in an institute. Perioperative records and data of the Oswestry Disability Index, visual analog scale scores (preoperatively and 2 weeks, 6 weeks, 3 months, 6 months, 1 year, 2 years, and 5 years after the operation), and MacNab criteria were collected. RESULTS: Of 58 patients with a follow-up duration of > 5 years, (41 and 17 patients had undergone transforaminal endoscopic lumbar discectomy [TELD] and interlaminar endoscopic lumbar discectomy [IELD], respectively), the satisfaction rate was 87.8% (five unsatisfactory cases) for TELD and 100% for IELD. The overall percentage of patients with good to excellent results according to modified MacNab criteria was 91.3% (53/58 patients). Two patients had residual discs. Two patients needed an open discectomy due to recurrent disc herniation. One IELD patient received spinal fusion surgery due to segmental instability after 5 years. CONCLUSION: FELD has a high success rate for the management of high-grade migrated herniated discs. In patients with high-grade disc migration from L1 to L5, TELD is effective and safe. However, for L4-L5 and L5-S1 high-grade upward and downward disc migration, IELD is the favorable option and provides high patient satisfaction.

Leptin promotes VEGF-C production and induces lymphangiogenesis by suppressing miR-27b in human chondrosarcoma cells.

Chondrosarcoma is the second most frequently occurring type of bone malignancy that is characterized by the distant metastasis propensity. Vascular endothelial growth factor-C (VEGF-C) is the chief lymphangiogenic mediator, and makes crucial contributions to tumor lymphangiogenesis. Leptin is an adipocytokine and has been indicated to facilitate tumorigenesis, angiogenesis and metastasis. However, the effect of leptin on VEGF-C regulation and lymphangiogenesis in human chondrosarcoma has hugely remained a mystery. Our results showed a clinical correlation between leptin and VEGF-C as well as tumor stage in human chondrosarcoma tissues. We further demonstrated that leptin promoted VEGF-C production and secretion in human chondrosarcoma cells. The conditioned medium from leptin-treated chondrosarcoma cells induced lymphangiogenesis of human lymphatic endothelial cells. We also found that leptin-induced VEGF-C is mediated by the FAK, PI3K and Akt signaling pathway. Furthermore, the expression of microRNA-27b was negatively regulated by leptin via the FAK, PI3K and Akt cascade. Our study is the first to describe the mechanism of leptin-promoted lymphangiogenesis by upregulating VEGF-C expression in chondrosarcomas. Thus, leptin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

CCL3 promotes angiogenesis by dysregulation of miR-374b/ VEGF-A axis in human osteosarcoma cells.

Osteosarcoma is the most frequent bone tumor, characterized by a high metastatic potential. However, the crosstalk between chemokine (C-C motif) ligand 3 (CCL3), which facilitates tumor progression and metastasis. Vascular endothelial growth factor-A (VEGF-A), an angiogenesis inducer and a highly specific mitogen for endothelial cells, has not been well explored in human osteosarcoma. Here we demonstrate the correlation of CCL3 and VEGF-A expressions, quantified by immunohistochemistry, with the tumor stage of human osteosarcoma tissues. Furthermore, CCL3 promotes VEGF-A expression in human osteosarcoma cells that subsequently induces human endothelial progenitor cell (EPC) migration and tube formation. Phosphorylation of JNK, ERK, and p38 was found after CCL3 stimulation. In addition, JNK, ERK, and p38 inhibitors also abolished CCL3-induced VEGF-A expression and angiogenesis. We noted that CCL3 reduces the expression of miR-374b and miR-374b mimic by reversing CCL3-promoted VEGF-A expression and angiogenesis in vitro and in vivo. This study shows that CCL3 promotes VEGF-A expression and angiogenesis in human osteosarcoma cells by down-regulating miR-374b expression via JNK, ERK, and p38 signaling pathways. Thus, CCL3 may be a new molecular therapeutic target in osteosarcoma angiogenesis and metastasis.