珍珠层人工骨促进成骨细胞的体外成骨能力

目的:研究珍珠层人工骨对人成骨细胞体外成骨能力的影响。方法:将珍珠层人工骨、聚乳酸(对照组)与人成骨细胞共同培养,观察细胞形态、细胞活性、碱性磷酸酶(ALP)活性和基质钙化情况。结果:实验组在细胞形态、细胞活性等指标与对照组相比差异无显著性;实验组在培养7d及14d后ALP阳性细胞数多于对照组;培养21d后可观察到骨结节,对照组没有骨结节产生。结论:珍珠层人工骨可促进成骨细胞的体外成骨能力。     

珍珠层人工骨促进成骨细胞的体外成骨能力

目的:研究珍珠层人工骨对人成骨细胞体外成骨能力的影响.方法:将珍珠层人工骨、聚乳酸(对照组)与人成骨细胞共同培养,观察细胞形态、细胞活性、碱性磷酸酶(ALP)活性和基质钙化情况.结果:实验组在细胞形态、细胞活性等指标与对照组相比差异无显著性;实验组在培养7d及14d后ALP阳性细胞数多于对照组;培养21d后可观察到骨结节,对照组没有骨结节产生.结论:珍珠层人工骨可促进成骨细胞的体外成骨能力.     

珍珠层人工骨促进成骨细胞的体外成骨能力

目的：研究珍珠层人工骨对人成骨细胞体外成骨能力的影响。方法：将珍珠层人工骨、聚乳酸（对照组）与人成骨细胞共同培养，观察细胞形态、细胞活性、碱性磷酸酶（ALP）活性和基质钙化情况。结果：实验组在细胞形态、细胞活性等指标与对照组相比差异无显著性；实验组在培养7d及14d后ALP阳性细胞数多于对照组；培养21d后可观察到骨结节，对照组没有骨结节产生。结论：珍珠层人工骨可促进成骨细胞的体外成骨能力。     

调节破骨细胞功能的相关信号分子的研究进展

破骨细胞(osteoclast,OC)蚀骨能力是骨骼发育和骨骼重塑的重要细胞功能。大多数病理性骨病,如骨质疏松症,反映出破骨细胞数量、活性和骨吸收能力增加。由于破骨细胞数量和活性的增加会导致骨结构受损和骨量降低,这是骨质疏松症等骨疾病的共同特征,因此抑制破骨细胞分化是预防和/或治疗骨疾病及相关骨折的治疗策略之一。阐明破骨细胞诱导骨吸收的分子机制以及调节破骨细胞活性的信号分子,将为通过抑制骨吸收改善病理性骨疾病的药物开发提供参考。本文就破骨细胞的分化、活性和吸收功能信号分子的近期研究进展作一综述。     

H型血管在骨质疏松症中的研究进展

骨质疏松症是一种全身性骨病,具有骨微结构退化、骨密度低的特点,在世界范围内发病率较高。随着我国人口逐渐进入老龄化,骨质疏松症的发病率日益上升,已经成为威胁老年人群生活质量的重要因素,给公共卫生系统带来了难以预料的挑战。近年来,许多文献报道骨内特殊型血管——H型血管生成与骨生成之间存在耦合,为骨质疏松症的治疗提供了新的研究目标。本文就H型血管的结构及功能、参与H型血管生成与成骨的细胞因子以及其他因素做一综述。     

成骨过程中细胞内能量代谢研究进展

骨质疏松症是一种全身性代谢性骨病,是由于破骨细胞介导的骨吸收和成骨细胞介导的骨形成之间失衡引起的。近年来骨骼细胞内能量代谢重新引起人们的兴趣,因为这些过程有可能成为骨质疏松症治疗的靶点。成骨细胞是骨骼重塑单位的骨形成细胞,对骨骼的生长和稳定至关重要。本文拟探讨骨形成过程中骨髓间充质干细胞和成骨细胞等成骨相关细胞的生物能学,主要包含葡萄糖、脂肪酸、氨基酸在成骨过程中分解代谢并产生能量的特点。     

骨质疏松症相关细胞因子研究进展

骨质疏松症是一类多发于老年人的全身性骨病,是老年患者致残、致死的主要原因。骨质疏松症的发生、发展不仅与骨量减低、骨髓中脂肪含量增多有关,还与全身骨骼肌含量、强度等关系密切。鉴于骨骼、肌肉及脂肪组织的相关细胞因子在此过程中发挥的重要作用,本文针对近年来颇受关注的骨形态发生蛋白、转化生长因子beta、成纤维细胞生长因子等细胞因子作以下综述,以期为骨质疏松症的早期诊断、疗效观察及并发症治疗等提供新的视角。     

骨代谢标志物在骨质疏松症中医药诊疗中的应用研究进展

骨质疏松症是一种以骨代谢异常,骨微结构破坏,导致脆性骨折危险性增高为特征的慢性全身性骨病,对人体的健康有着重要的影响。传统中医学对骨质疏松症有着深刻的认识,骨质疏松属于中医"骨痿"、"骨痹"的范畴,其发病多以肾虚为本,血瘀为标,中医药在预防、治疗治骨质疏松症方面的的作用举足轻重。骨代谢生化标志物是从血液、尿液中可检测出的骨代谢生化产物或相关激素,可反映人体骨代谢状态,是协助代谢性骨病的诊断、鉴别诊断、治疗以及疗效评价的重要指标,目前已广泛应用于骨质疏松症的中医体质辨识、证候的诊断及药物疗效评价等方面。本文通过文献综述的方式,对近些年来骨代谢标志物在骨质疏松症中医诊疗中的应用研究进行归纳,以期为今后的研究提供参考。     

骨血管与运动改善骨质疏松的研究进展

骨质疏松症是一种严重危害健康的全身性骨病,近年来许多研究报道了骨质疏松症的发生与机体骨微环境血管生成能力的退化有关,认为骨形成与骨血管生成之间存在密切的时空关系,被称为“血管生成-成骨耦联”。除了将氧气和各种营养物质输送到骨中,血管内皮细胞自身还可分泌某些因子影响成骨、破骨细胞的活动,且成骨、破骨细胞分泌的某些因子也可以作用于内皮细胞,影响血管的生成。其中骨内的H亚型毛细血管与骨代谢的关系尤为密切,因此逐渐成为骨质疏松症治疗的新焦点。运动作为治疗骨质疏松症的手段之一,其疗效和可靠性已被广泛认可。运动时肌骨系统之间的对话增强,肌肉分泌的某些肌肉因子、代谢小分子和骨骼肌特异性miRNA可能会影响骨血管的生成,另外运动也可直接影响成骨、破骨细胞的活动,从而间接地调节骨血管的生成。本文将介绍骨内的血管系统、骨质疏松时骨血管的改变以及骨血管改善骨质疏松症的作用机制,并重点综述运动时骨血管的变化以及运动影响骨血管生成的机制,以求为运动促进骨健康寻找新的证据。     

原发性骨质疏松症的骨科临床诊治——骨科专家讨论会纪要

骨质疏松症（osteoporosis,OP）是一种以骨量低下,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（世界卫生组织,WHO）。2001年美国国立卫生研究院（NIH）提出骨质疏松症是以骨强度下降、骨折风险性增加为特征的骨骼系统疾病。骨质疏松症分为原发性和继发性二大类。     

运动影响骨生物力学的研究进展

骨的生物力学效应主要由松质骨和骨转化决定.骨的微结构及转化率是一个终生渐变的过程,骨生物力学也受其影响不断变换.现代生活方式导致人们体育活动强度极低,对骨骼健康和生物力学有负面影响.有规律的科学运动对骨骼健康有很好的作用,且年轻时的体育活动与老年后的骨密度及力学性能有很好的相关性.运动的力学刺激激活了骨重建机制,使骨骼...     

Physical activity and bone

It has been shown in many circumstances that immobilization can cause loss of bone mineral content. There is also evidence that athletes from various sports have higher bone mineral density than less active controls. In studies of non-athletic populations the relationship between exercise and bone has not been unambiguous. However, physically active life-style is recommended as an effective means of preventing bone loss with age. In addition, exercise maintains and improves muscle strength, coordination and balance and may thus reduce the risk of fractures.     

丹参及其活性单体成分调控骨质疏松症相关信号通路的研究进展

骨质疏松症是目前临床上常见的一种骨科疾病，其特征是每单位体积的骨量减少，使得骨强度受损，从而导致患骨发生骨折。而现阶段治疗骨质疏松症多以西药为主，但存在如费用高、有不良反应等缺点。近年来，随着中药药理学研究的不断深入，相关人员发现，丹参及其活性单体可调节相关骨性细胞增殖、凋亡以及分化，从而促进骨骼的生长和愈合。然而目前该领域的相关研究较为零散，多数仅仅局限于某个活性单体在某种骨性细胞上的作用，而中医治疗具有多靶点、多途径的特点，因此笔者通过总结近年来丹参及其活性单体在防治骨质疏松方面的相关研究，从整体方面来对丹参的抗骨质疏松机制进行探讨，并总结目前相关研究所存在的一些问题，从而为中医药防治骨质疏松研究提供一些帮助。     

生物玻璃结合自体红骨髓复合移植的实验研究

目的　研究生物玻璃结合自体红骨髓复合移植在骨缺损修复过程中对于成骨细胞活性的影响情况。方法　应用影像学观察、病理切片组织学观察、多媒体彩色病理分析系统监测成骨细胞活性水平的表达情况。结果　在影像学方面 ,自体红骨髓结合人工骨组术后 3周即可见可能的骨连接迹象 ,术后 1 5个月可见植入物与骨的确实性结合迹象。在组织学方面 ,自体红骨髓结合人工骨组可明显促进成软骨细胞和骨祖细胞向成骨细胞的分化 ,在骨小梁的重建及钙质沉积方面明显优于单独自体红骨髓或人工骨移植。多媒体彩色病理分析活动性成骨细胞表面长 (AOS)亦可得出相同结果。结论　生物玻璃结合自体红骨髓复合移植结合了无机材料和有机材料的共同优点 ,对于骨缺损的修复有明显的作用 ,在骨延迟愈合、骨肿瘤缺损充填及人工假体固定等临床应用方面有广阔的前景     

"The chemistry of bone mineral".

In this treatise there has been a general introduction to the nature of bone mineral. Without the studies on the chemistry and structure of hydroxyapatites precipitated under physiological conditions it would have been difficult to interpret the data from bone mineral. Earlier studies on well-crystallized apatite systems helped to delineate the nature of the smaller bone crystals which are so difficult to study by standard crystallographic methods. It was shown that bone mineral is submicroscopic in crystal size and thus, has a high surface area which is highly reactive to specific chemical species. Bone mineral apatite is not an equilibrium phase and is slowly perfecting chemically and in crystal size. It is this lack of perfection resulting from crystalline imperfections due to (a) the presence of carbonate, sodium and other ions, and, (b) the deficiency in Ca and OH, which combine to make bone mineral metabolically active. In closing, it is necessary to point out that this is just a brief introduction to the subject of bone mineral. The interested reader is encouraged to seek more details in the bone text books of Vaughan (1975), Bourne (1972) and Zipkin (1973) and the various review articles noted in the body of this exposition.     

In vitro transformation of osteoblasts: putative formation of osteosarcoma in vitro

The study of bone cancer has been difficult in part due to a lack of appropriate in vitro osteosarcoma model systems. The development of such systems is essential if a clearer understanding of the biology of and mechanisms behind the formation and progression of bone cancers is to be obtained. We report here the development of an in vitro model system which demonstrates important characteristics generally associated with osteosarcoma. The chick periosteal osteogenesis model was infected with the Fujinami Sarcoma Virus (FSV) containing the v-fps oncogene which encodes for a P140gag-fps protein-tyrosine kinase. Under the appropriate conditions FSV infected cultures developed bone and cartilaginous tissues which showed histopathological findings consistent with osteosarcoma. Biochemical data indicating massive increases in alkaline phosphatase activity, protein content, 3H-Thymidine incorporation as well as expression of active P140gag-fps confirm that transformation has occurred in FSV infected cultures. This novel in vitro model system should prove most useful in the study of bone cancer.     

Response to continuous and pulsatile PTH dosing: a mathematical model for parathyroid hormone receptor kinetics

In this paper, we propose a mathematical model for parathyroid hormone receptor (PTH1R) kinetics, focusing on the receptor's response to PTH dosing to discern bone formation responses from bone resorption. The PTH1R is a major target for new osteoporosis treatments, as pulsatile PTH dosing has been shown to induce net bone formation in both animals and humans, and PTH(1-34) was recently FDA approved for the treatment of post-menopausal osteoporosis. PTH has also been shown to cause net bone loss when given continuously, so that the net action of PTH on bone is dependent on the dosing pattern. We have developed a simplified two-state receptor kinetics model for the PTH1R, based on the concepts of Segel et al., to distinguish the activity of active and inactive receptor and receptor-ligand complexes. The goal is to develop a plausible model of the minimal essential biological relationships necessary for understanding the responses to PTH dosing. A two-state model is able to effectively discriminate between continuous and pulsatile PTH dosing using the active species as surrogates for the downstream anabolic response. For continuous PTH dosing, the model predicts a desensitized system dominated by the inactive receptor and complex, consistent with downstream net bone loss that has been demonstrated experimentally. Using pulsatile PTH dosing, the model system predicts a highly sensitized state dominated by the active receptor and complex, corresponding to net bone formation. These results are consistent with the hypothesis that the kinetics of the receptor plays a critical role in the downstream effects of PTH dosing. Moreover, these results indicate that within a range of biologically relevant PTH doses, the two-state model is able to capture the differential behavior of the system for both continuous and pulsatile PTH dosing. The development of such a model provides a rational basis for developing more biologically extensive models that may support the design of optimal dosing strategies for PTH-based anti-osteoporosis treatments. Moreover, this model provides a unique starting point from which to design experiments investigating PTH receptor biology.     

Ultrastructural localization of a tartrate-resistant acid ATPase in bone

Osteoclasts are effector cells in bone breakdown, and the active bone resorption is confined to the ruffled border zone of these cells. An acid milieu is maintained in this zone which is probably a prerequisite for bone resorption. Tartrate-resistant acid phosphatase (TRAP) activity has been recognized as a characteristic property of osteoclasts and in several studies proposed as a cytochemical marker of osteoclasts. We have previously isolated and characterized a tartrate-resistant and iron-activated acid ATPase (TrATPase) from rat bone, the enzyme being a member of the TRAP family. In the present study the ultrastructural localization of this enzyme was delineated by employing immunogold technique on low temperature-embedded maxillar rat bone. Intensive immunolabeling was seen on the bone surfaces facing the ruffled border zone while lower amounts of marker were seen in adjacent bone areas, that is, on the bone surfaces facing the clear zone and deeper-into the bone. Within the osteoclasts gold markers were observed mainly in vesicular structures interpreted as lysosomes. Immunolabeling was also observed in the recently described endocytic cells located near osteoblasts and osteoclasts. Also in these cells, the marker was confined to lysosomelike structures. The amount of label in bone facing osteoblasts was low, as was the amount within osteoblasts. Our observation of extracellular localization, in particular accumulation of TrATPase in bone matrix facing the ruffled border area of the osteoclasts, favors the view that the enzyme is exported to areas of active bone resorption, thereby indicating a potential role for the enzyme in this process.     

Morphologic features of bone in human osteopetrosis

Trabecular bone biopsies obtained from six patients with malignant osteopetrosis, one patient with benign osteopetrosis, and two controls were examined by light and electron microscopy. Osteopetrotic osteoclasts showed little to no signs of active involvement in bone resorption. Ruffled borders and clear zones were absent in most cells. In all patients there were large numbers of osteoclasts. Numbers of osteoblasts, bone lining cells, and bone marrow stromal cells were extremely low in all patients with malignant osteopetrosis. In six of the patients a mineralized layer of amorphous organic material lacking collagen fibrils was seen covering large areas of the bone or cartilage matrix. We suggest that this layer represents a pathological calcification on which subsequently organic material has accumulated. The abnormalities in osteopetrotic bone are discussed in the light of the pathogenesis of this disease.     

Histomorphometric study of trabecular channels in normal iliac bone

Summary Cancellous bone channels in the normal iliac crest have been studied histologically and by histomorphometry, and their biological role has been considered. Eighty percent of trabecular channels were typical osteons with the same structural and remodeling features as cortical osteons. The similarity of osteons in these two locations was corroborated by the comparability of morphometric features. The points of difference between osteons in the two types of bone were irregular configurations of trabecular osteons and marrow cells in the central canal in some. Since the number of trabecular osteons decreases with age, and since active trabecular resorption cavities were few in number, it is unlikely that additional osteons are formed in normal bone after the active modeling phase of bone growth. It is improbable that they make a significant contribution to bone remodeling since their number decreases with age, and since the available surface of trabecular channels for remodeling is extremely small. However, it is probable that they aid the intraosseous microcirculation and mineral exchange in thick trabecula and bifurcations, where they are mainly located. The demarcation curves at the 95% confidence interval, which suggest the normal range for numbers of channels, was calculated from the scatter diagram against bone area.