OBJECTIVE: Loosening and pullout of pedicle screws are well-known problems in pedicle screw fixation surgery. Augmentation of pedicle screws with bone cement, first described as early as 1975, increases the pedicle-screw interface and pullout force in osteoporotic vertebrae. The aim of the present study was to identify cement leakage and pulmonary embolism rates in a large prospective single-center series of pedicle screw augmentations. METHODS: All patients who underwent cement-augmented pedicle screw placement between May 2006 and October 2010 at the authors' institution were included in this prospective cohort study. Perivertebral cement leakage and pulmonary cement embolism were evaluated with a CT scan of the area of operation and with a radiograph of the chest, respectively. RESULTS: A total of 98 patients underwent placement of cement-augmented pedicle screws; 474 augmented screws were inserted in 237 vertebrae. No symptomatic perivertebral cement leakage or symptomatic pulmonary cement embolism was observed, but asymptomatic perivertebral cement leakage was seen in 88 patients (93.6%) and in 165 augmented vertebrae (73.3%). Cement leakage most often occurred in the perivertebral venous system. Clinically asymptomatic pulmonary cement embolism was found in 4 patients (4.1%). CONCLUSIONS: Perivertebral cement leakage often occurs in pedicle screw augmentation, but in most cases, it is clinically asymptomatic. Cement augmentation should be performed under continuous fluoroscopy to avoid high-volume leakage. Alternative strategies, such as use of expandable screws, should be examined in more detail for patients at high risk of screw loosening.

The multifunctional sphingosine-1-phosphate (S1P) is a lipid signaling molecule and central regulator in the development of several cancer types. In recent years, intriguing information has become available regarding the role of S1P in the progression of Glioblastoma multiforme (GBM), the most aggressive and common brain tumor in adults. S1P modulates numerous cellular processes in GBM, such as oncogenesis, proliferation and survival, invasion, migration, metastasis and stem cell behavior. These processes are regulated via a family of five G-protein-coupled S1P receptors (S1PR1-5) and may involve mainly unknown intracellular targets. Distinct expression patterns and multiple intracellular signaling pathways of each S1PR subtype enable S1P to exert its pleiotropic cellular actions. Several studies have demonstrated alterations in S1P levels, the involvement of S1PRs and S1P metabolizing enzymes in GBM pathophysiology. While the tumorigenic actions of S1P involve the activation of several kinases and transcription factors, the specific G-protein (Gi, Gq, and G12/13)-coupled signaling pathways and downstream mediated effects in GBM remain to be elucidated in detail. This review summarizes the recent findings concerning the role of S1P and its receptors in GBM. We further highlight the current insights into the signaling pathways considered fundamental for regulating the cellular processes in GMB and ultimately patient prognosis.

Patients with glioblastoma multiforme (GBM) are at high risk to develop a relapse despite multimodal therapy. Assumedly, glioma stem cells (GSCs) are responsible for treatment resistance of GBM. Identification of specific GSC markers may help to develop targeted therapies. Here, we performed expression analyses of stem cell (ABCG2, CD44, CD95, CD133, ELF4, Nanog, and Nestin) as well as differentiation and microglia markers (GFAP, Iba1, and Sparc) in GBM compared to nonmalignant brain. Furthermore, the role of these proteins for patient survival and their expression in LN18 stem-like neurospheres was analyzed. At mRNA level, ABCG2 and CD95 were reduced, GFAP was unchanged; all other investigated markers were increased in GBM. At protein level, CD44, ELF4, Nanog, Nestin, and Sparc were elevated in GBM, but only CD133 and Nestin were strongly associated with survival time. In addition, ABCG2 and GFAP expression was decreased in LN18 neurospheres whereas CD44, CD95, CD133, ELF4, Nanog, Nestin, and Sparc were upregulated. Altogether only CD133 and Nestin were associated with survival rates. This raises concerns regarding the suitability of the other target structures as prognostic markers, but makes both CD133 and Nestin candidates for GBM therapy. Nevertheless, a search for more specific marker proteins is urgently needed.

The link between thrombocytosis and malignancy has been well known for many years and its associations with worse outcomes have been reported mainly for solid tumors. Besides measuring platelet count, it has become popular to assess platelet function in the context of malignant diseases during the last decade. Malignant gliomas differ tremendously from malignancies outside the central nervous system because they virtually never form distant metastases. This review summarizes the current understanding of the platelet–immune cell communication and its potential role in glioma resistance and progression. Particularly, we focus on platelet-derived proinflammatory modulators, such as sphingosine-1-phosphate (S1P). The multifaceted interaction with immune cells puts the platelet into an interesting perspective regarding the recent advances in immunotherapeutic approaches in malignant glioma.