Deep vein thrombosis (DVT) is common seen in patients undergoing spine surgery. However, its prevalence and associated risk factors have not been well understood yet. This retrospective case-cohort study was designed to investigate risk factors for postoperative DVT using retrospectively collected data from department of spine surgery between 07/2013 and 07/2014. Univariate analysis and binary logistic regression analysis were used to determine risk factors for DVT. A total of 861 patients were admitted into DVT-associated analyses, including 410 males and 451 females, aged from 15 to 87 years old (median 54, IQR 18). Of them, 147 cases (17%) sustained postoperative DVT. DVT incidence was 15.9% in patients undergoing lumbar interbody fusion, 13.5% in patients treated by low-molecular-weight heparin (LMWH), while only 8.1% in patients without LMWH. However, it revealed no significant difference between LMWH group and non-LMWH group (χ2 = 1.933, p = 0.164). Logistic regression equation was logit P = −4.09 + 0.05*X1 − 0.55*X2 + 0.41*X3 + 1.41*X7, (X1 = age; X2 = regions; X3 = hypertension; X7 = D-dimer). In this study, LMWH prophylaxis after spine surgery proved ineffective. Advanced age, D-dimer and hypertension have proved to be the risk factors for postoperative DVT in patients undergoing spine surgery.

In our previous study, 17β-estradiol was proved to protect rat annulus fibrosus cells against apoptosis induced by interleukin-1β (IL-1β). However, whether 17β-estradiol has protective effect on rat nucleus pulposus cells remains unclear. The purpose of this study was to further explore the effects of 17β-estradiol on rat nucleus pulposus cells based on IL-1β-induced apoptosis. TUNEL assay and Annexin V/PI double staining were used to detect apoptosis and revealed that IL-1β induced notable apoptosis, which was reversed by 17β-estradiol. Meanwhile, cell viability and binding ability were decreased by IL-1β, but activated caspase-3 was increased. However, all of the detected effects of IL-1β were eliminated by 17β-estradiol. Furthermore, real-time quantitative RT-PCR was used to further find that IL-1β downregulated expression level of type II collagen, aggrecan, tissue inhibitor of matrix metalloproteinase (TIMP)-1, while upregulated matrix metalloproteinase (MMP)-3, MMP-13 and Bcl-2, which was further confirmed by western blot. Finally, 17β-estradiol was proved to abolish the above negative effects of IL-1β. In summary, this work presented that IL-1β maybe induced apoptosis of rat nucleus pulposus cells, which was resisted by 17β-estradiol by down-regulating MMP-3 and MMP-13 via a mitochondrial pathway. This research provides a novel insight into the anti-apoptotic effect of 17β-estradiol on IL-1β-induced cytotoxicity, and may potentially lead to a better understanding of the clinical effects of 17β-estradiol, especially in terms of intervertebral disc degeneration.

Levofloxacin has been reported to have cytotoxicity to chondrocytes in vitro. And 17β-estradiol has been widely studied for its protective effects against cell apoptosis. Based on apoptotic cell model induced by levofloxacin, the purpose of this study was to explore the mechanism by which 17β-estradiol protects rat nucleus pulposus cells from apoptosis. Inverted phase-contrast microscopy, flow cytometry, and caspase-3 activity assay were used to find that levofloxacin induced marked apoptosis, which was abolished by 17β-estradiol. Interestingly, estrogen receptor antagonist, ICI182780, and functional blocking antibody to α2β1 integrin, both prohibited the effect of 17β-estradiol. Simultaneously, levofloxacin decreased cellular binding ability to type II collagen, which was also reversed by 17β-estradiol. Furthermore, western blot and real-time quantitative PCR were used to find that integrin α2β1 was responsible for estrogen-dependent anti-apoptosis, which was time-response and dose-response effect. 17β-estradiol was proved for the first time to protect rat nucleus pulposus cells against levofloxacin-induced apoptosis by upregulating integrin α2β1 signal pathway.

The prevalence of MCs in patients with DLS was significantly higher than that of patients without DLS. Most of them were type 2 and usually located on the concave side of apex vertebrae. MCs were significantly associated with intervertebral disc degeneration and lumbar scoliosis.