骨溶解与人工关节后期松动

骨溶解与人工关节后期松动戴克戎我国人工关节的设计、制作和安装技术的总体水平虽然仍与国际水平存在差距，但其近、中期效果近年来已有较大提高。由于置换术后长期病例的增多，使我们也开始面临国外学者所面临的同样挑战：人工关节后期松动。目前，国内也已开始在临床和...     

人工关节置换术后磨损颗粒与假体周围骨溶解的研究进展

人工关节置换术后磨损颗粒的产生是导致假体周围骨溶解的重要影响因素。目前研究认为磨损颗粒导致假体周围骨溶解的主要原因与植入假体的材料以及其产生的磨损颗粒通过各种作用对相关细胞如巨噬细胞、成骨细胞、破骨细胞等的刺激有关,诱导产生多种炎性细胞因子,激活和开放细胞信号和通路,产生长期慢性的炎症,导致假体周围骨溶解。为此,本文主要研究不同类型的磨损颗粒对假体周围骨溶解的影响,以及磨损颗粒在假体周围骨溶解进展过程中的机制,并且由此探讨如何减少磨损颗粒的产生以及阻断其在骨溶解进程的作用,以此来达到预防和治疗假体周围骨溶解的目的。     

成纤维细胞成骨潜能的研究进展

在体内组织中，有两类生成骨细胞的前体细胞：成骨前体细胞(DOPC)和可诱导的成骨前体细胞(IOPC)。前者主要存在于骨髓的基质细胞中，具有干细胞的特点，能自身复制分化成一定类型的细胞，此种基质细胞可分化成为成骨细胞、成纤维细胞、网状细胞等，即基质细胞中只有一部分属于骨祖细胞，能自发地分化为成骨细胞，骨髓多能干细胞在     

皮肤成纤维细胞在体外培养中的成骨作用

本实验采用新西兰家兔背部中厚皮片，通过组织培养获得成纤维细胞。成纤维细胞经传代培养８天时，发现标本中有不透光的骨小结节形成。培养３７天时，发现一些小结节扩大、延伸，形成骨小梁样结构；也有骨小片状结构形成。经四环素活体标记后，这些结节在蓝紫光荧光显微镜下显示金黄色荧光，表明它们是新生骨组织。该结构的钙盐染色、胶原染色也都呈阳性，充分反映骨结构中的钙及胶原成分，以及皮肤成纤维细胞在体外培养中的成骨作用     

骨保护素系统与假体周围骨溶解机制研究

晚期关节疾病的患者在接受全髋关节置换手术治疗后，关节疼痛消失或明显减轻，关节功能获得改善，从而使生活质量得以提高。但由于假体使用寿命的限制，该治疗手段还主要局限于老年患者，一些中青年患者往往需要先进行其他过渡性的且效果又不令人满意的治疗，以等待人工关节置换的时机。目前多数学者认为假体周围骨溶解是导致假体松动、手术远期失败，最终影响假体使用寿命的主要原因。既往研究证实单核巨噬细胞、成纤维细胞、成骨细胞等在磨损颗粒刺激下产生大量肿瘤坏死因子、白细胞介素、前列腺素等骨吸收刺激因子，进而激活了破骨细胞，…     

成纤维细胞成骨潜能的体外培养研究

本研究采用新西兰种家兔皮肤的成纤维细胞进行体外培养，通过活体相关显微缩时录像，体视显微镜摄影，ＨＥ染色以及组织化学染色等技术做系列观察。发现成纤维细胞在体外培养条件下，不仅能产生粘多糖，胶原等基质成分，而且还能提供钙盐沉积。培养中期，成纤维细胞培养液显示Ａ１Ｐ阳性反应；培养后期，培养液与成纤维细胞都可显示Ａ１Ｐ阳性反应。     

人工关节假体周围炎性骨溶解的生物学机制

许多研究揭示了与假体周围磨损颗粒相关的炎症反应,且这种炎症反应最终能促使假体周围的骨组织以骨吸收为主,而非骨形成。事实上,当机体假体周围组织受到破坏时,机体组织也会通过保护及再生机制对炎症反应进行紧密调节,试图平衡组织的结构,减轻反应程度。因此,发生骨溶解的真正原因就是局部组织内平衡机制的失代偿。     

成纤维细胞生长因子对骨生长及骨修复的调节作用

成纤维细胞生长因子对骨生长及骨修复的调节作用李亚非，张晶，胡蕴玉成纤维细胞生长因子（ＦＧＦ）在体内生物学效应广泛，本文就近年来ＦＧＦ及某些骨生长因子对骨生长、修复调节作用的研究综述如下。ＦＧＦ以两种密切相关的形式存在，即碱性成纤维细胞生长因子（ｂＦＧ...     

骨折二期愈合过程中的纤维细胞成骨作用

家兔桡骨骨折二期愈合过程中，骨折血肿经机化而形成大量纤维骨痂。通过透射电镜，对纤维骨痂进行超微结构水平的观察。发现：由于成纤维细胞具有成骨细胞的表型，具备成骨所必需的条件，以及其自身独特演变的能力，使纤维痂逐步演变成为骨性骨痂。     

人工关节假体植入后骨溶解的研究进展

假体植入后松动是许多行关节置换术病人面临的严重问题,解决这一问题对于提高人工关节置换的疗效有重要意义.目前认为导致假体植入后松动的主要原因是关节活动使得假体表面之间长期摩擦,因此产生大量磨损微粒,微粒在骨-假体界面之间迁移,诱发局部环境中细胞分泌各种细胞因子导致假体周围的骨溶解.为此,本文主要研究磨损微粒的产生过程以及微粒的产生对关节假体使用寿命的重要影响,在此基础上探讨如何减少微粒的产生以及限制其在假体周围的迁移,以此来预防骨溶解发生.……     

Osteocytic osteolysis

A dorsal and ventral gland composed of large, flask-shaped cells located in the margin of the mantle ofLittorina give rise to the inner and outer layers of the periostracum respectively. The material comprising the periostracum is derived from secretory granules elaborated by the Golgi apparatus. When the Golgi granules of the ventral gland which consist of a substance exhibiting a definite periodicity, are discharged at the surface in contact with sea water, they are widely dispersed and consist of particles embedded in a substrate. Formation of the outer periostracum involves the re-aggregation of the Golgi secretory particles into a dense sheet which exhibits a periodicity of 300 . Viewed in transverse section the periostracum exhibits a lattice pattern suggestive of a crystalline substance. The outer layer eventually reaches a thickness of 4–5 . The inner layer is derived from the secretory granules of the dorsal gland. The formation of the inner layer occurs in a manner similar to that of the outer layer. It does not, however, exhibit a periodicity. In the mature state it attains a thickness of 0.4–0.5 . In addition to a protective function the periostracum provides a barrier between the sea water and the pallial space and also regulates the site and arrangement of mineral crystal formation at the growing margin of the shell.This investigation was aided (in part) by Grant DE-01825, N.I.D.R., U.S.P.H. Service.     

Wear particulate and osteolysis

Total joint replacements of the hip and knee are generally highly successful, with satisfactory longevity and clinical results. Using modern biocompatible materials, optimal component design, and meticulous surgical technique, survivorship of cemented or cementless joint replacements is approximately 15 years with more than a 90% probability. The host's biologic response is critical to implant longevity. Particulate disease refers to the host's adverse biologic response to wear debris and byproducts generated from the prosthesis. Initially, emphasis was placed on particulate polymethylmethacrylate (cement disease), but more recently polyethylene wear debris has been underscored. Debris from several materials in sufficient quantities and physicochemical forms, however, can generate an inflammatory cascade resulting in periprosthetic bone destruction (osteolysis), jeopardizing long-term success of the implant.     

Reversible osteolysis

This is a case report of a 44-year-old patient in whom osteolytic changes that developed around the distal end of the femoral prosthesis appeared to reverse with the use of antiinflammatory medication and pulsed electromagnetic field stimulation. Most reported cases of osteolysis have been described as showing progressive change at a variable rate. There has not been any previously documented case in which there has been reversal of osteolytic change.     

Familial expansile osteolysis

Familial expansile osteolysis (FEO) is a unique bone dysplasia, which has, over five generations, affected 42 members of a Northern Ireland family. The disease follows a classic autosomal dominant pattern of inheritance. The condition is distinct enough in its clinical features and natural history to be recognized as a new and unique disease. There are both general and focal skeletal changes, the latter having a predominantly peripheral distribution and an onset from the second decade. Progressive osteoclastic resorption accompanied by medullary expansion leads to severe and painful disabling deformities with a tendency to pathologic fracture. Most affected members of the family have an associated early-onset deafness and loss of dentition as a result of unique middle ear and dental abnormalities. The serum alkaline phosphatase and urinary hydroxyproline are elevated to a variable degree, whereas other biochemical indices are normal. The response of the disease to a therapeutic trial using parenteral dichloro-methylene-diphosphonate (dichloro-MDP) produced an initial rapid biochemical response, which was not sustained.     

Particle bioreactivity and wear-mediated osteolysis

This review focuses on wear debris-mediated osteolysis, a major factor compromising the long-term success of total joint arthroplasty. Studies on retrieved implants and animal models, as well as in vitro studies on particle bioreactivity, suggest that wear-mediated periprosthetic osteolysis is unlikely to be caused solely by 1 particular cell type or particulate species, but is rather the cumulative consequence of a number of biological reactions. Our recent findings suggest 3 novel mechanisms of particle bioreactivity that may contribute to osteolysis: 1) exacerbated inflammation caused by elevated reactive oxygen species production by activated macrophages and osteoclasts, (2) impaired periprosthetic bone formation secondary to disrupted osteogenesis, and (3) compromised bone regeneration resulting from increased cytotoxic response of mesenchymal osteoprogenitor cells. Understanding the pathogenesis of wear-mediated osteolysis is needed to improve orthopedic implant biocompatibility and wear reduction, and to develop effective pharmacotherapies.