经皮椎体后凸成形术骨水泥渗漏相关因素

目的分析经皮椎体后凸成形术(PKP)骨水泥渗漏的相关因素。方法回顾性分析采用PKP治疗的骨质疏松性压缩骨折患者102例183个椎体,根据术后椎体是否发生骨水泥渗漏,将压缩椎体分为渗漏组和非渗漏组,进而分析影响骨水泥渗漏的相关因素。结果术后患者视觉模拟评分(VAS评分)、Oswesty功能评分、Cobb角及椎体平均高度均较术前明显改善(P0.05)。183个椎体中共有21个椎体发生骨水泥渗漏。单因素分析显示:两组术前椎体高度、有无椎体周壁破坏及骨水泥注射剂量差异显著(P0.05);椎体后凸角度、骨折新鲜度、手术入路途径及骨折椎体部位比较无统计学差异。Logistic回归分析显示有无椎体周壁破坏及骨水泥注射剂量是与骨水泥渗漏发生的独立危险因素。结论有无椎体周壁破坏及骨水泥注射剂量与经皮椎体后凸成形术发生骨水泥渗漏密切相关,对此必须引起高度重视。     

吉莱骨粉强化术预防多个椎体成形术后邻近椎体再骨折的疗效

目的探讨吉莱骨粉(Gene X)可吸收骨水泥用于强化聚甲基丙烯酸甲酯骨水泥(polymethylmethacrylate,PMMA)成形椎体的邻近椎体,预防邻近椎体再骨折的临床效果。方法收集2010年11月至2011年11月在北京友谊医院骨科行多发椎体压缩骨折椎体成形术治疗的患者15例,使用Gene X对与填充PMMA椎体的相邻节段进行强化,观察术后强化椎体的高度变化及再骨折发生率。结果术后6个月、1年随访结果显示,强化椎体前、中、后部高度及Cobbs'角较术后即刻影像均未见明显差异,Gene X骨水泥吸收良好。再发椎体骨折1例,为非强化椎体。结论应用Gene X骨水泥对多发椎体压缩骨折手术椎体邻近椎体进行强化,术后高度保持良好,对椎体成形术后邻近椎体再骨折的预防具有一定临床意义。     

经皮穿刺椎体成形术中骨水泥的理化及生物力学性能回顾

经皮穿刺椎体成形术是治疗侵袭性椎体血管瘤、骨质疏松性椎体压缩性骨折、脊椎转移癌及多发性骨髓瘤的有效方法。自从20世纪60年代中期聚甲基丙烯酸甲酯（PMMA）用于临床以来，骨水泥在骨科的应用与日俱增。骨水泥潜在的用途导致新的经过修饰的骨水泥不断用于临床。应用骨水泥的合理性依赖于对它们性质的理解——包括其特点，抗菌效果及与周围骨组织的相互作用。     

骨质疏松性椎体骨折不同时期行经皮椎体成形术疗效比较

目的观察骨质疏松性椎体骨折(OVF)不同时期患者行经皮椎体成形术(PVP)治疗的临床效果。方法选择行PVP的OVF患者120例,根据损伤至手术时间不同分为损伤2周内手术(A组)65例、损伤第2~8周手术(B组)35例、损伤2个月后手术(C组)20例。比较三组患者术前、术后3 d、术后6个月时的疼痛视觉模拟评分(VAS)、欧洲骨质疏松症基金会生活质量问卷(QUALEFFO)评分;比较三组患者骨水泥分布情况、骨水泥注入量、骨水泥渗漏率。结果三组患者各组内比较,术后3 d的VAS均低于术前,术后6个月的VAS均低于术后3 d(P<0.05);术后6个月、术后3 d的QUALEFFO评分均低于术前(P<0.05)。三组同时点VAS、QUALEFFO评分差异均无统计学意义(P均>0.05)。三组骨水泥注入量、骨水泥渗漏率、骨水泥分布指数比较差异均有统计学意义(P均<0.05)。结论PVP在治疗不同时期OVF中均有良好效果。急性期骨水泥分布指数高,而在亚急性期、慢性期则分别存在骨水泥渗漏率较低、骨水泥注入量减少的情况。建议对于OVF患者应早期进行PVP治疗。     

CT引导PVP治疗椎体转移瘤疗效分析

目的观察CT引导经皮穿刺骨水泥注入椎体成形术（PVP）治疗椎体转移瘤的临床疗效。方法对25例椎体转移瘤患者在CT引导下穿刺针经皮穿刺进入椎体溶骨区注入骨水泥。结果25例手术顺利,术后疼痛即刻减轻17例,消失3例,3、7d后疼痛减轻各2例,无改善1例。未发生严重并发症。结论CT引导经皮穿刺PVP治疗椎体转移瘤安全、微创,疗效好。     

骨水泥在骨质疏松性脊柱压缩骨折的应用与研究现状

骨水泥已广泛应用在脊柱外科领域。在椎体成形术和后凸成形术中应用的主要是三种骨水泥：聚甲基丙烯酸甲酯骨水泥（PMMA）;磷酸钙骨水泥（CPC）,硫酸钙骨水泥（CSC）;掺骨生长因子的其他可注射物。它们各有优缺点。随着骨水泥材料学、生物力学研究的进展,骨水泥的性能不断改进,在此基础上研究的新的骨水泥将能更好的用于脊柱骨折。     

经皮椎体成形术致骨水泥渗漏的原因分析

目的探讨经皮椎体成形术中骨水泥外渗原因及防范方法。方法 135例行经皮椎体成形术患者纳入本研究,共171个椎体。对患者进行术前VAS疼痛评分,根据Genant半量法对塌陷的椎体进行分级。按常规方法实施椎体成形术。结果 122例患者术后疼痛明显缓解。所有患者手术前、后疼痛评分分别为8.2±1.22和2.5±1.26。术中36例患者、共41个椎体出现骨水泥渗漏。在渗漏的41个椎体中,4个渗漏至椎管内,2个渗漏至神经根管周围,7个渗漏至椎旁或沿椎旁静脉扩散,9个渗漏至前纵韧带下及周围组织,17个渗漏至椎间隙,2个回渗至椎弓根。2例患者出现下肢神经症状,术后短期内恢复。骨水泥渗漏与总体疼痛缓解无明显相关性,但与术前椎体的压缩程度及手术技巧明显相关。结论椎体成形术是治疗某些椎体病损的有效方法,避免骨水泥渗漏的措施包括术前确认椎体的形态和穿刺技术等。     

骨水泥成形术与降钙素等药物治疗骨质疏松性椎体压缩骨折对比

目的 探讨骨水泥成形术及降钙素等药物治疗骨质疏松性椎体压缩骨折的临床疗效.材料与方法共68例患者,骨水泥成形术组46例,降钙素组22例.记录对比VAS及SF-12评分,记录骨水泥成形术组椎体高度变化和Cobb角改善情况,降钙素组骨密度变化情况,比较两组治疗用时及费用.结果 VAS评分及SF-12健康调查评分:降钙素组有波动,总体评分差于骨水泥成形术组.伤椎压缩恢复程度:椎体成形术组Cobb角平均改善11°,后凸成行术组Cobb角平均改善18°,椎体高度有所恢复.骨密度变化:降钙素组骨密度治疗后有提高.治疗用时及治疗费用:骨水泥成形术组治疗用时明显短于降钙素组,但治疗费用相对较高.结论 骨水泥成形术治疗骨质疏松性椎体压缩骨折能够迅速缓解疼痛,改善椎体高度和Cobb角,增加脊柱稳定性、提高患者生活质量;降钙素等药物治疗早期也可缓解疼痛,但止疼效果较骨水泥成形术滞后四周,长期应用止痛作用相对减弱,且其增加骨密度能力有限,治疗费用相比较低.     

经皮球囊椎体后凸成形术骨水泥渗漏分型及预防

目的探讨经皮球囊椎体后凸成形术治疗骨质疏松性胸腰椎压缩性骨折骨水泥渗漏的分型和预防措施。方法2005年6月-2008年2月施行经皮球囊椎体后凸成形术（percutaneous kyphoplasty,PKP）的患者81例临床资料全部随访,随访时间2个月～32个月,平均18．2个月。术前术后Denis腰痛分级,定期复查脊柱正侧位x光片,观察其疗效及骨水泥渗漏情况。结果术后腰背部疼痛均得到有效缓解,全组无死亡及脊髓神经损伤,伤口愈合好。术中发生骨水泥渗漏共有15例,男5例、女10例。年龄72-83岁,平均76．5岁。结论多种因素可以造成术中骨水泥的渗漏。而术前明确的诊断、硬件设施的完备及术者专业知识的系统地掌握与应用、手术器材的良好掌握与操作是可以避免或减少PMMA渗漏的发生的。     

高粘度骨水泥椎体成形术与普通粘度椎体后凸成形术治疗骨质疏松性椎体压缩性骨折的效果比较

目的对比高粘度骨水泥椎体成形术与普通粘度骨水泥椎体后凸成形术治疗骨质疏松性椎体压缩骨折(OVCF)的临床效果。方法选择27例OVCF患者,随机分为高粘度骨水泥椎体成形术组(高粘度骨水泥组14例)及普通粘度骨水泥椎体后凸成形术组(普通粘度骨水泥组13例),比较两组患者X线暴露时间、手术时间、骨水泥注射量、术后腰背部疼痛、腰背部功能、伤椎椎体高度%、伤椎后凸畸形角度及并发症发生情况。结果两组X线暴露时间及手术时间差异显著(P<0.05);骨水泥注射量无统计学差异(P>0.05)。两组术后疼痛明显缓解,视觉模拟疼痛评分(VAS)及ODI评分明显降低,伤椎椎体高度%及后凸畸形角度明显改善(P<0.05),但两组间比较无明显差异(P>0.05)。高粘度骨水泥组骨水泥渗漏率(14.3%)与普通骨水泥组(30.8%)比较无统计学差异(P>0.05)。结论采用高粘度骨水泥椎体成形术治疗OVCF,不仅可以达到与普通骨水泥椎体后凸成形术相同的临床效果,还可以一定程度上减少骨水泥渗漏,减少X线暴露时间及手术时间。     

Metabolic bone disease and bone quality

On the progress of study concerned with pathology of metabolic bone disease such as osteoporosis, it has been known that most of bone strength can be explained by bone volume. As bone volume can be determine by bone mineral density (BMD) with dual-energy X-ray absorptiometry (DXA), it has been widely used for diagnosis of osteoporosis or efficacy of treatment. However, with the advance of bone morphometry, decrease of bone strength or existence of insufficiency fracture is influenced by not only loss of BMD but also deterioration of bone quality especially bone microstructure. In this chapter, we will give an outline of change of bone quality in metabolic bone disease.     

Metabolic bone markers and bone cell biology

Various metabolic bone markers have been developed in order to analyze each process of bone resorption and bone formation. By evaluating the two processes using bone markers, an imbalance between bone resorption and formation can be estimated. Metabolic bone markers have already been in clinical use for the early diagnosis and the assessment of treatment efficacy in osteoporotic patients and for the diagnosis of cancer-induced bone diseases. Further elucidation of the mechanisms of formation and secretion, metabolic clearance, diurnal rhythm as well as their changes in various disorders should enable us to evaluate bone turnover at a real-time scale and to utilize for the diagnosis of a variety of metabolic bone diseases.     

Alcohol-induced bone loss and deficient bone repair

BACKGROUND: Chronic consumption of excessive alcohol eventually results in an osteopenic skeleton and increased risk for osteoporosis. Alcoholics experience not only increased incidence of fractures from falls, but also delays in fracture healing compared with non-alcoholics. In this review the term "alcohol-induced bone disease" is used to refer to these skeletal abnormalities. Alcohol-induced osteopenia is distinct from osteoporoses such as postmenopausal osteoporosis and disuse osteoporosis. Gonadal insufficiency increases the rate of bone remodeling, whereas alcohol decreases this rate. Thus, histomorphometric studies show different characteristics for the bone loss that occurs in these two disease states. In particular, alcohol-induced osteopenia results mainly from decreased bone formation rather than increased bone resorption. Human, animal and cell culture studies of the effects of alcohol on bone strongly suggest alcohol has a dose-dependent toxic effect on osteoblast activity. The capacity of bone marrow stromal cells to differentiate into osteoblasts has a critical role in the cellular processes involved in the maintenance of the adult human skeleton by bone remodeling. Chronic alcohol consumption suppresses osteoblastic differentiation of bone marrow cells and promotes adipogenesis. In fracture healing, the effect of alcohol is to suppress synthesis of an ossifiable matrix, possibly due to inhibition of cell proliferation and maldifferentiation of mesenchymal cells in the repair tissue. This results in the deficient bone repair observed in animal studies, characterized by repair tissue of lower stiffness, strength and mineral content. Current knowledge of cellular effects and molecular mechanisms involved in alcohol-induced bone disease is insufficient to develop interventional strategies for its prevention and treatment. OBJECTIVES: The objectives of this review are 1) to identify the characteristics of alcohol-induced bone loss and deficient bone repair as revealed in human and animal studies, 2) to determine the current understanding of the cellular effects underlying both skeletal abnormalities, and 3) to suggest directions for future studies to resolve current ambiguities regarding the cellular basis of alcohol-induced bone disease.     

Measurements of bone mass and bone density

X-ray-based procedures are available to measure bone mineral density in vitro at almost any skeletal site. These bone density measurements are not useful in the diagnosis of the cause of bone loss but at present are the only tests available for assessing bone mass prior to the occurrence of irreversible changes such as fractures or vertebral compression, which are easily recognizable on x-rays. When fractures are present, the severity of the bone loss and the risk for future fractures can be assessed. Repeated measurements permit estimation of the rate of bone loss, which gives useful information for monitoring treatment effect or course of the disease. Measurement of total body calcium is of less clinical importance because of the predominantly trabecular bone loss that generally occurs in metabolic bone disease. Dual-energy x-ray absorptiometry (DEXA) and quantitative computed tomography (QCT) of the spine are of about equal clinical value in the first approach to the patient with metabolic bone disease, although DEXA allows greater variety in sampling sites. For repeated measurements, DEXA provides better precision at significantly lower radiation burden. For bone mineral measurements, the lumbar spine appears to be the most sensitive skeletal site.     

A soluble bone morphogenetic protein type IA receptor increases bone mass and bone strength

Diseases such as osteoporosis are associated with reduced bone mass. Therapies to prevent bone loss exist, but there are few that stimulate bone formation and restore bone mass. Bone morphogenetic proteins (BMPs) are members of the TGFβ superfamily, which act as pleiotropic regulators of skeletal organogenesis and bone homeostasis. Ablation of the BMPR1A receptor in osteoblasts increases bone mass, suggesting that inhibition of BMPR1A signaling may have therapeutic benefit. The aim of this study was to determine the skeletal effects of systemic administration of a soluble BMPR1A fusion protein (mBMPR1A-mFc) in vivo. mBMPR1A-mFc was shown to bind BMP2/4 specifically and with high affinity and prevent downstream signaling. mBMPR1A-mFc treatment of immature and mature mice increased bone mineral density, cortical thickness, trabecular bone volume, thickness and number, and decreased trabecular separation. The increase in bone mass was due to an early increase in osteoblast number and bone formation rate, mediated by a suppression of Dickkopf-1 expression. This was followed by a decrease in osteoclast number and eroded surface, which was associated with a decrease in receptor activator of NF-κB ligand (RANKL) production, an increase in osteoprotegerin expression, and a decrease in serum tartrate-resistant acid phosphatase (TRAP5b) concentration. mBMPR1A treatment also increased bone mass and strength in mice with bone loss due to estrogen deficiency. In conclusion, mBMPR1A-mFc stimulates osteoblastic bone formation and decreases bone resorption, which leads to an increase in bone mass, and offers a promising unique alternative for the treatment of bone-related disorders.     

Histomorphometric analysis of bone in metabolic bone disease

Most of the tools necessary for a detailed study of bone remodeling are now available. These methods will enable us to substitute simple surface-based histomorphometry with pertinent derived variables that reveal more information about the processes going on. Because of the inherent variability of the methods, bone histomorphometry is less well suited for investigations in single individuals. However, in terms of basic investigations of cell and tissue activity in grouped materials of patients with metabolic bone disease and the evaluation of treatment regimens in these materials, bone histomorphometric investigations still yield the most detailed analyses.     

Aseptic bone/bone marrow necrosis in leukaemia

Aseptic (avascular) bone/bone marrow necrosis (ABN) was found in 21 leukaemic patients during a period of 14 yr, with a frequency of 6.5% in autopsied leukaemic patients, and with the highest frequency in ALL. 8 patients (38%) complained of bone pain. X-ray examination was carried out in 7 of these with a positive result in 3 (43%). Only 1 patient had elevated S-Alkaline phosphatase. Leucocytosis was found in 12 patients. Only 1 patient (ALL) received steroid in a rather high dose during 6 weeks. At autopsy ABN was found localized to the femur in all patients and 2 patients also had ABN in other bones. Post-mortem X-ray examination demonstrated changes in 8 of 15 cases (53%), with osteolysis in 6 and sclerosis in 2. 19 patients had had recent ABN with some fibroblast proliferation. In 4 of these, appositional bone formation had started. 2 patients had sclerosis as the only change. The pathogenesis of ABN is not known; an important factor, however, may be ischaemia due to vascular obstruction.     

Injectable bone

Tissue engineering applies the principles of biology and engineering to the development of functional substitutes,for example 1) cells, 2) scaffolds, 3) some cytokines, for lost tissues. The meaning of this bone regeneration is that it decreases the needed tissues and burden of patients. In this time, we applied to mesenchymal stem cells (MSCs) from the own bone marrow as cell sources. MSCs are thought to be multipotent cells that can replicate. And we also used a beta-tricalcium phosphate (beta-TCP) as a scaffold and fibrin glue as materials to regenerate a injectable bone and we injected into the subcutaneous space on the dorsum of the rat. After 8 weeks of implantation, it could be confirmed newly formed bone and fibrin glue functioned as a injectable materials without loosing the cell activity and the proliferation of MSCs. Next we applied Platelet Rich Plasma (PRP) to improve the ability of osteogenesis. PRP contains some cytokines and are expected to promote the increase of osteogenesis. The merit is not immunity rejection from autologous blood collected in the immediate preoperative period. The admixtures of PRP or fibrin glue have fluidity and gel-like consistency as the thrombin mixing. They can be injected with a syringe in tissues. We named this "Injectable Bone". According to the histological observations, the MSCs with PRP were well formed mature bone and neovascularization compared with control (defect only) after 8 weeks implantation. These results demonstrated that the mixture of MSCs and PRP were useful as injectable bone substitute and its ability of bone regeneration is almost equal to autogenous particulate cancellous bone and marrow (PCBM).