The relationship between the spinopelvic balance and the incidence of adjacent vertebral fractures following percutaneous vertebroplasty.

UNLABELLED: We evaluated the relationship between sagittal spinopelvic parameters and the occurrence of adjacent vertebral fractures (AVF) and determined the possible risk factor. The most important factors for AVFs are the degree of osteoporosis and altered biomechanics due to the spinopelvic imbalance in the fractured area of the spine. INTRODUCTION: We intend to evaluate the relationship between sagittal spinopelvic parameters and the occurrence of adjacent vertebral fractures following the initial compression fracture and to determine the possible dominant risk factor associated with new compression fractures. METHODS: From March 2010 to May 2012, 240 consecutive patients with painful vertebral compression fractures (VCFs) were enrolled in a retrospective study. Ninety-one patients with VCFs underwent percutaneous vertebroplasty (VP) at 112 levels. The sagittal vertical axis (SVA), thoracic kyphosis (TK), lumbar lordosis (LL), sacral slope (SS), pelvic tilt (PT), pelvic incidence (PI), and segmental kyphotic angle on sagittal standing radiographs were used to evaluate radiologic outcomes. RESULTS: In 2 years, 15 out of 134 patients (11.1%) treated with conservative treatment, and 12 out of 91 patients (13.1%) treated with VP sustained adjacent level fracture. More patients with the BMD higher or equal to 3.0 experienced a new fracture than those with a BMD less than 3.0 (p = 0.019), and the risk for adjacent level fractures decreased significantly when segmental kyphotic angle was less than 11° (p = 0.001), SVA was less than 6 cm (p = 0.001), SS was higher or equal to 25° (p = 0.004), and LL was higher or equal to 25° (p = 0.020). CONCLUSIONS: The most important factors for new VCFs after the initial compression fractures are the degree of osteoporosis and altered biomechanics due to the spinopelvic imbalance in the fractured area of the spine. Regarding the spinopelvic alignment to investigate the relationship with a subsequent AVF, segmental kyphotic angle, SS, LL, and SVA may be a potential predictor.

The water extract of Samultang protects the lipopolysaccharide (LPS)/phorbol 12-myristate 13-acetate (PMA)-induced damage and nitric oxide production of C6 glial cells via down-regulation of NF-kappaB.

Samultang has been traditionally used for treatment of ischemic heart and brain diseases in oriental medicine. However, little is known about the mechanism by which Samultang rescues the myocardial and neuronal cells from ischemic damage. This study was designed to evaluate whether the water extract of Samultang may modulate the production of nitric oxide (NO) in LPS and PMA treated-C6 glial cells to protect the cells from NO-induced cytotoxicity. C6 glial cells treated with both LPS and PMA significantly produced a large amount of NO compared to untreated, PMA, or LPS-treated cells. In parallel with NO production, cotreatment of LPS and PMA induced the severe apoptotic death of C6 glial cells. However, Samultang significantly reduced both cell death and NO production by LPS/PMA in a dose-dependent manner. In addition, the modulatory effects of Samultang on LPS/PMA-induced cytotoxicity and NO production could be mimicked by exogenous treatments of N(G)MMA, a nitric oxide synthase (NOS) inhibitor, and pyrrolidine dithiocarbamate (PDTC), a strong NF-kappaB inhibitor. Treatment of C6-glial cells with LPS/PMA induced the transcriptional activation of NF-kappaB, which was markedly inhibited by Samultang. Taken together, we suggest that the protective effects of Samultang against LPS/PMA-induced cytotoxicity may be mediated by the suppression of NO synthesis via down-regulation of NF-kappaB activation.