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OBJECTIVES:To analyze the occurrence, risk factors, treatment and prognosis of postoperative pleural effusion after spinal deformity correction surgery. METHODS:The clinical and imaging data of 3325 patients undergoing spinal deformity correction were collected from the database of our hospital. We analyzed the therapeutic process of the 28 patients who had postoperative pleural effusion, and we identified the potential risk factors using logistic regression. RESULTS:Among the 28 patients with postoperative pleural effusion, 24 (85.7%) suffered from hemothorax, 2 (7.1%) from chylothorax, and 2 (7.1%) from subarachnoid-pleural fistula. The pleural effusion occurred on the convex side in 19 patients (67.9%), on the concave side in 4 patients (14.3%), and on both sides in 4 patients (14.3%). One patient with left hemothorax was diagnosed with kyphosis. The treatment included conservative clinical observation for 5 patients and chest tube drainage for 23 patients. One patient also underwent thoracic duct ligation and pleurodesis. All of these treatments were successful. Logistic regression analysis showed that adult patients(≥18 years old), congenital scoliosis, osteotomy and thoracoplasty were risk factors for postoperative pleural effusion in spinal deformity correction surgery. CONCLUSIONS:The incidence of postoperative pleural effusion in spinal deformity correction surgery was approximately 0.84% (28/3325), and hemothorax was the most common type. Chest tube drainage treatment was usually successful, and the prognosis was good. Adult patients(≥18 years old), congenital scoliosis, and had undergone osteotomy or surgery with thoracoplasty were more likely to suffer from postoperative pleural effusion.

The mechanistic basis of obesity-associated intervertebral disc degeneration (IDD) is unclear. Aberrant expression of aggrecan and its degrading enzymes ADAMTS-4 and ADAMTS-5 is implicated in the development of IDD. Here, we investigated the effect of leptin, a hormone with increased circulating levels in obesity, on the expression of aggrecan and ADAMTSs in primary human nucleus pulposus (NP) cells. Real-time PCR and Western blots showed that leptin increased the mRNA and protein expression of ADAMTS-4 and ADAMTS-5 and reduced the level of aggrecan in NP cells, accompanied by a prominent induction of p38 phosphorylation. Treatment of NP cells with SB203580 (a p38 inhibitor) abolished the regulation of aggrecan and ADAMTSs by leptin. Knockdown of ADAMTS-4 and ADAMTS-5 by siRNAs also attenuated the degradation of aggrecan in leptin-stimulated NP cells. To conclude, we demonstrated that leptin induces p38 to upregulate ADAMTSs and thereby promoting aggrecan degradation in human NP cells. These results provide a novel mechanistic insight into the molecular pathogenesis of obesity-associated IDD.

No recent studies have analyzed the rates of or reasons for unanticipated revision surgery within 30 days of primary surgery in spinal deformity patients. Our aim was to examine the incidence, characteristics, reasons, and risk factors for unplanned revision surgery in spinal deformity patients treated at one institution. All patients with a diagnosis of spinal deformity presenting for primary instrumented spinal fusion at a single institution from 1998 to 2012 were reviewed. All unplanned reoperations performed within 30 days after primary surgery were analyzed in terms of demographics, surgical data, and complications. Statistical analyses were performed to obtain correlations and risk factors for anticipated revision. Of 2758 patients [aged 16.07 years (range, 2-71), 69.8% female] who underwent spinal fusion surgery, 59 (2.1%) required reoperation within 30 days after primary surgery. The length of follow up for each patient was more than 30 days. Of those that required reoperation, 87.0% had posterior surgery only, 5.7% had anterior surgery, and 7.3% underwent an anteroposterior approach. The reasons for reoperation included implant failure (n = 20), wound infection (n = 12), neurologic deficit (n = 9), pulmonary complications (n = 17), and coronal plane imbalance (n = 1). The risk factors for reoperation were age, diagnosis, and surgical procedure with osteotomy.

Aberrant proliferation of nucleus pulposus cell is implicated in the pathogenesis of intervertebral disc degeneration. Recent findings revealed that microRNAs, a class of small noncoding RNAs, could regulate cell proliferation in many pathological conditions. Here, we showed that miR-10b was dramatically upregulated in degenerative nucleus pulposus tissues when compared with nucleus pulposus tissues isolated from patients with idiopathic scoliosis. Moreover, miR-10b levels were associated with disc degeneration grade and downregulation of HOXD10. In cultured nucleus pulposus cells, miR-10b overexpression stimulated cell proliferation with concomitant translational inhibition of HOXD10 whereas restored expression of HOXD10 reversed the mitogenic effect of miR-10b. MiR-10b-mediated downregulation of HOXD10 led to increased RhoC expression and Akt phosphorylation. Either knockdown of RhoC or inhibition of Akt abolished the effect of miR-10b on nucleus pulposus cell proliferation. Taken together, aberrant miR-10b upregulation in intervertebral disc degeneration could contribute to abnormal nucleus pulposus cell proliferation through derepressing the RhoC-Akt pathway by targeting HOXD10. Our study also underscores the potential of miR-10b and the RhoC-Akt pathway as novel therapeutic targets in intervertebral disc degeneration.

Increasing evidence suggests that obesity and aberrant proliferation of nucleus pulposus (NP) cells are associated with intervertebral disc degeneration. Leptin, a hormone with increased circulating level in obesity, has been shown to stimulate cell proliferation in a tissue-dependent manner. Nevertheless, the effect of leptin on the proliferation of human NP cells has not yet been demonstrated. Here, we show that leptin induced the proliferation of primary cultured human NP cells, which expressed the leptin receptors OBRa and OBRb. Induction of NP cell proliferation was confirmed by CCK8 assay and immunocytochemistry and Real-time PCR for PCNA and Ki-67. Mechanistically, leptin induced the phosphorylation of STAT3, Akt and ERK1/2 accompanied by the upregulation of cyclin D1. Pharmacological inhibition of JAK/STAT3, PI3K/Akt or MEK/ERK signaling by AG490, Wortmannin or U0126, respectively, reduced leptin-induced cyclin D1 expression and NP cell proliferation. These experiments also revealed an intricate crosstalk among these signaling pathways in mediating the action of leptin. Taken together, we show that leptin induces human NP cell cyclin D1 expression and proliferation via activation of JAK/STAT3, PI3K/Akt or MEK/ERK signaling. Our findings may provide a novel molecular mechanism that explains the association between obesity and intervertebral disc degeneration.

Most cases of congenital spinal deformities were sporadic and without strong evidence of heritability. The etiology of congenital spinal deformities is still elusive and assumed to be multi-factorial. The current study seeks to elucidate the effect of maternal vitamin A deficiency and the production of congenital spinal deformities in the offsping. Thirty two female rats were randomized into two groups: control group, which was fed a normal diet; vitamin A deficient group, which were given vitamin A-deficient diet from at least 2 weeks before mating till delivery. Three random neonatal rats from each group were killed the next day of parturition. Female rats were fed an AIN-93G diet sufficient in vitamin A to feed the rest of neonates for two weeks until euthanasia. Serum levels of vitamin A were assessed in the adult and filial rats. Anteroposterior (AP) spine radiographs were obtained at week 2 after delivery to evaluate the presence of the skeletal abnormalities especially of spinal deformities. Liver and vertebral body expression of retinaldehyde dehydrogenase (RALDHs) and RARs mRNA was assessed by reverse transcription-real time PCR. VAD neonates displayed many skeletal malformations in the cervical, thoracic, the pelvic and sacral and limbs regions. The incidence of congenital scoliosis was 13.79% (8/58) in the filial rats of vitamin A deficiency group and 0% in the control group. Furthermore, vitamin A deficiency negatively regulate the liver and verterbral body mRNA levels of RALDH1, RALDH2, RALDH3, RAR-α, RAR-β and RAR-γ. Vitamin A deficiency in pregnancy may induce congenital spinal deformities in the postnatal rats. The decreases of RALDHs and RARs mRNA expression induced by vitamin A deprivation suggest that vertebral birth defects may be caused by a defect in RA signaling pathway during somitogenesis.