经伤椎椎弓根自体骨植骨联合螺钉内固定术治疗腰椎压缩性骨折78例效果观察

目的探讨经伤椎椎弓根自体骨植骨联合螺钉内固定术治疗腰椎压缩性骨折的临床疗效。方法对78例腰椎压缩性骨折患者采用经伤椎椎弓根自体骨植骨联合螺钉内固定术治疗。于术前、术后1周、术后7个月对伤椎及上下椎体进行X线检查,计算伤椎前、中、后缘及伤椎高度值、伤椎Cobb’s角,观察伤椎愈合恢复及并发症情况,采用Frankel分级标准评定神经功能恢复情况。结果术后1周和7个月伤椎前中后三线高度较术前均有满意恢复,Cobb’s角无明显矫正丢失,无切口感染、神经症状加重、内固定松动及断裂。患者神经功能得到较好改善,不完全脊髓损伤均有1～2级神经功能改善。结论经伤椎椎弓根自体骨移植及螺钉内固定术治疗腰椎压缩性骨折临床效果确切,同时可防止骨折缺损及脊柱平背畸形等并发症的发生。     

生长激素与骨

本文简介生长激素（ＧＨ）直接或间接地影响骨及软骨的生长、分化及更新等的研究进展。一般认为，当机体ＧＨ水平异常时可引起骨代谢及骨量的改变。临床显示，使用ＧＨ对骨质疏松等有治疗作用。     

糖皮质激素与骨

糖皮质激素在临床上应用广泛,但所致的骨质流失、代谢失调等不良反应也限制了其使用.本文对糖皮质激素对骨及其细胞的生理和病理生理作用进行综述,并对其不良反应发生的分子机制进行讨论.     

生长激素与骨

本文简介生长激素（ＧＨ）直接或间接地影响骨及软骨的生长、分化及更新等的研究进展。一般认为，当机体ＧＨ水平异常时可引起骨代谢及骨量的改变。临床显示，使用ＧＨ对骨质疏松等有治疗作用。     

骨缺损的治疗研究进展

因创伤、感染、肿瘤切除或先天性疾病等造成的骨质局部缺失称为骨缺损。骨缺损治疗可采用骨移植、组织工程技术、膜引导性组织再生（MGTR）技术、基因疗法、生长因子等。其中应用组织工程技术和生长因子治疗骨缺损是目前研究的热点。现将骨缺损治疗的研究进展情况概述如下。     

骨填充材料在骨肿瘤缺损修复中的应用研究进展

骨填充材料既要满足骨缺损腔内充分植骨的需要,也要减少对骨膜及骨组织的损伤刺激。传统的自体骨和异体骨填充材料具有较好的临床疗效,但也具有一定的临床局限性。随着科技的不断进步创新,越来越多的骨填充材料被研究应用于骨肿瘤缺损修复。异种骨、生物陶瓷、骨水泥、高分子聚合物、胶原蛋白均是骨填充材料,不同的骨填充材料有着不同的优缺点。该文就骨填充材料在骨肿瘤缺损修复中的应用研究进展作一综述。     

肝性骨营养不良发病机制研究进展

肝性骨营养不良(hepatic osteodystrophy,HOD)是慢性肝病及原位肝移值(OLT)后的临床常见并发症,表现为骨质疏松(osteoporosis,OP)及骨质软化(osteomalacia,OM).胰岛素样生长因子-1(IGF-1)、性腺激素、护骨素(OPG)、IL-1、IL-6、TNF-α、维生素D受体基因(VDRG)多态性及OLT后免疫治疗在其发病机制中起重要作用.     

肝性骨营养不良发病机制研究进展

肝性骨营养不良(hepatic osteodystrophy，HOD)是慢性肝病及原位肝移值(OLT)后的临床常见并发症，表现为骨质疏松(osteoporosis，OP)及骨质软化(osteomalacia，OM)。胰岛素样生长因子-1(IGF-1)、性腺激素、护骨素(OPG)、IL-1、IL-6、TNF-α、维生素D受体基因(VDRG)多态性及OLT后免疫治疗在其发病机制中起重要作用。     

不同投氟方式对诱导性骨形成影响的实验研究

本文研究了不同投氟方式(连续、间断摄氟)对大鼠诱导性异位骨形成的影响。组织学及骨形态计量学研究结果显示:间断投予氟化钠(NaF)具有与持续投予 NaF 相同的刺激骨形成的作用,且诱导性骨质的结构为成熟的板层骨。即未观察到持续投氟组所出现的编织骨和类骨质。作者认为氟对骨细胞和骨质结构的影响主要取决于骨中氟积聚的程度。     

骨转换标志物临床应用研讨会议纪要

2013年6月21日,骨转换标志物临床应用研讨会在上海召开。来自美国新墨西哥大学医学院、新墨西哥阿尔伯克基临床研究及骨质疏松中心的迈克尔·莱维茨基(Michael Lewiecki)教授与国内多位骨质疏松治疗领域的知名专家齐聚一堂,共同对骨转换标志物的临床应用进展进行了深入探讨。1骨质疏松症的防治现状骨质疏松症是以骨量低下、骨微结构损坏,导致骨脆性增加、易发生骨折为特征的全身性骨病。如得不到及时治疗,将引起骨质疏松性骨折(多发于脊椎、髋部),给患者造成巨大危害。因此,骨质疏松症已成为我国重要的公共卫生问题之一。骨质疏松症的治疗是一个长期过程,至少需1年以上的治疗才能降低骨折风险。而临床治疗中,骨转换标志物检测在帮助临床快速监测骨质疏     

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.     

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.     

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.     

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.     

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.     

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).