BackgroundWe compared the perioperative results and complications associated with PLIF and TLIF, and collected evidence for choosing the better fusion method.MethodsA literature survey of the MEDLINE and EMBASE databases identified 7 comparative observational studies that met our inclusion criteria. Checklists by Cowley were used to evaluate the risk of bias of the included studies. A database including patient demographic information, perioperative results, and complications was established. The summary odds ratio and weighed mean difference with 95% confidence interval were calculated with a random-effects model.ResultsWe found that PLIF had a higher complication rate (P <0.00001), and TLIF reduced the rate of durotomy (P = 0.01). No statistical difference was found between the two groups with regard to clinical satisfaction (P = 0.54), blood loss (P = 0.14), vertebral root injury (P = 0.08), graft malposition (P = 0.06), infection (P = 0.36), or rate of radiographic fusion (P = 0.27). The evidence indicated that PLIF required longer operative time (P = 0.03).ConclusionsThe evidence indicated that TLIF could reduce the complication rate and durotomy. Neither TLIP nor PLIF was found superior in terms of clinical satisfaction or radiographic fusion rate. PLIF might result in longer time in surgery.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2474-15-367) contains supplementary material, which is available to authorized users.
The transcriptional repressor Bmi‐1 is involved in cell‐cycle regulation and cell senescence, the deficiency of which has been shown to cause oxidative stress. This study investigated whether Bmi‐1 deficiency plays a role in promoting disc degeneration and the effect of treatment with antioxidant N‐acetylcysteine (NAC) on intervertebral disc degeneration. Bmi‐1 −/− mice were treated with the antioxidant NAC, supplied in drinking water (Bmi‐1 −/− +NAC). For in vitro experiments, mouse intervertebral discs were cultured under low oxygen tension and serum‐limiting conditions in the presence of tumour necrosis factor α and interleukin 1β in order to mimic degenerative insult. Disc metabolism parameters in these in vitro and in vivo studies were evaluated by histopathological, immunohistochemical and molecular methods. Bmi‐1 −/− mice showed lower collagen Ⅱ and aggrecan levels and higher collagen Ⅹ levels than wild‐type and Bmi‐1 −/− +NAC mice. Bmi‐1 −/− mice showed significantly lower superoxide dismutase (SOD)‐1, SOD‐2, glutathione peroxidase (GPX)‐1 and GPX‐3 levels than their wild‐type littermates and Bmi‐1 −/− + NAC mice. Relative to Bmi‐1 −/− mice, the control and Bmi‐1 −/− +NAC mice showed significantly lower p16, p21, and p53 levels. These results demonstrate that Bmi‐1 plays an important role in attenuating intervertebral disc degeneration in mice by inhibiting oxidative stress and cell apoptosis.
In the present study, we investigated whether high dietary Ca and exogenous parathyroid hormone 1–34 fragments (PTH 1–34) have synergistic effects on bone formation in adult mice, and explored the related mechanisms. Adult male mice were fed a normal diet, a high-Ca diet, a PTH-treated diet, or a high-Ca diet combined with subcutaneously injected PTH 1–34 (80 μg/kg per d) for 4 weeks. Bone mineral density, trabecular bone volume, osteoblast number, alkaline phosphatase (ALP)- and type I collagen-positive areas, and the expression levels of osteoblastic bone formation-related genes and proteins were increased significantly in mice fed the high-Ca diet, the PTH-treated diet, and, even more dramatically, the high-Ca diet combined with PTH. Osteoclast number and surface and the ratio of receptor activator for nuclear factor-κB ligand (RANKL):osteoprotegerin (OPG) were decreased in the high-Ca diet treatment group, increased in the PTH treatment group, but not in the combined treatment group. Furthermore, third-passage osteoblasts were treated with high Ca (5 mm), PTH 1–34 (10− 8 m) or high Ca combined with PTH 1–34. Osteoblast viability and ALP activity were increased in either the high Ca-treated or PTH-treated cultures and, even more dramatically, in the cultures treated with high Ca plus PTH, with consistent up-regulation of the expression levels of osteoblast proliferation and differentiation-related genes and proteins. These results indicate that dietary Ca and PTH play synergistic roles in promoting osteoblastic bone formation by stimulating osteoblast proliferation and differentiation.
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