距骨骨软骨损伤的诊断与治疗研究进展

距骨骨软骨损伤(osteochondral lesions of the talus,OLT)是指在创伤或非创伤性因素作用下,距骨滑车局限性关节软骨剥脱,通常累及深部软骨下骨损伤,并往往引发关节疼痛、积液肿胀等症状,严重者可致关节功能障碍的踝关节疾病。病变通常与踝关节扭伤及骨折等创伤性因素相关,因此大部分患者有踝关节扭伤或不稳定病史,而非创伤性因素也已被报道可导致该病变。X线、计算机断层扫描(computed tomography,CT)、磁共振成像(magnetic resonance imaging,MRI)、锝-99m骨扫描、单光子发射计算机断层成像术(single-photon emission computed tomography,SPECT)及关节镜均已被用于诊断该疾病。保守治疗多用于骨软骨块无移位的儿童患者,疗效尚可,对于成人效果多不佳。多种手术方式如关节镜下病灶清理、微骨折及钻孔术、骨软骨块复位内固定术、自体或异体骨软骨移植术、自体软骨细胞移植术、自体骨-骨膜移植术、关节腔内注射生物附加物技术、组织工程技术等均已被大量文献报道,并取得良好的临床疗效。     

关节软骨修复材料研究进展

软骨缺损修复特别是大面积软骨缺损修复目前仍然是骨关节外科医生及骨科研究学者的难题.本文针对目前软骨修复材料的基础科学作一个较系统的回顾及总结,并将软骨修复材料分为三大类:(1)自体软骨转移;(2)异体骨软骨移植;(3)组织工程材料.在此基础上对临床软骨缺损修复提供一种理论上的选择,提出针对临床应用的软骨缺损修复解决方案和未来软骨修复研究的发展方向.     

正常骨骺的动态钆增强MRI研究

目的 运用动态钆增强MRI技术,评价正常骨骺软骨、生长板软骨、海绵状骨松质、干骺端等不同解剖区域的血液供应特征.材料与方法 10只2周大的健康乳猪,共20个股骨远端.采用GE 1.5 T磁共振扫描仪,作钆增强动态MRI,即运用时间分辨率为3 s的扰相梯度回波(SPGR)技术,在静脉注射钆之前、注射过程之中及之后连续扫描,全部成像时间为4 min多钟.计算在动态钆增强MRI上骨骺及干骺端各个解剖区域在不同时间的增强率,并与相应组织学发现作对照研究.结果 生长板软骨的增强率比骨骺软骨的增强率有明显增高(P＜0.001);与各解剖区域的增强率相比,海绵状骨松质的增强率最高(P＜0.001);与生长板和海绵状骨松质相比,骨骺软骨的强化最慢(P＜0.001),而生长板与海绵状骨松质强化快慢之间差异无统计学意义(P＞0.1).组织学研究所显示的生长板软骨、骨骺软骨、干骺端等不同解剖区域的血管密度分布特征与相应部位的增强率及强化快慢所提示的血供状态基本相吻合.结论 动态钆增强MRI能够显示骨骺不同解剖区域的血液灌注特征.     

跟骨结节骨折的临床研究现状

跟骨结节是跟骨的重要组成部分,对维持后足的外形和下肢的功能具有重要意义.然而,由于单纯跟骨结节骨折较为少见,一些轻微的跟骨结节骨折在诊疗过程中容易被忽视.因此,笔者针对目前跟骨结节骨折的研究现状作一综述,旨在加深对该骨折的认识. 1 跟骨结节部的解剖特点 跟骨结节部是跟骨的重要组成部分,在维持足弓及缓冲负重上有重要意义.跟骨结节部的后方呈基底在下的三角,表面覆盖了一层纤维软骨,其厚度从顶端约200 μm逐渐向基底增厚至约500 μm,与结节后部中下1/3软骨下聚集增厚的骨皮质区相适应,为跟腱的附着提供了充足的骨床[1].Lohrer等[2]发现跟腱附着区在横断面上如新月形,并向跟骨结节部的后内侧和后外侧延伸约1.0 mm和 3.5 mm.     

距骨全脱位的治疗进展

距骨全脱位在全身、下肢及足部脱位中所占比例均较少,临床上并不常见,但其并发症的发生率较高.距骨坏死、创伤性关节炎、脱位时皮肤受压造成的皮瓣坏死和开放性脱位而导致的感染、慢性骨髓炎等,是距骨脱位后治疗较困难的常见并发症.目前临床上对距骨全脱位及其并发症的治疗仍存在较多争议甚至误区.本文拟对现有文献进行总结归纳,为距骨全脱位的治疗提供依据.     

双层支架材料构建组织工程骨软骨修复关节软骨缺损

随着对关节软骨及软骨下骨修复机制的进一步认识,人们日益重视将软骨和软骨下骨作为一个整体(即骨软骨单位)来指导关节软骨缺损的修复方案,而不是把焦点只放在关节表面的软骨上.如果忽略了修复支撑软骨再生的软骨下骨,那么修复方案可能失败[1].软骨下骨不仅支撑着软骨再生与整合,而且在负重关节中提供了有利的力学环境,提升了软骨组织的再生性能[2].近年来,新兴的双层支架材料构建组织工程骨软骨这一理念正是立足于恢复骨软骨单位的生理学特性,顺应软骨和软骨下骨的不同生物或功能属性,同时又满足软骨和软骨下骨一体化的要求,以期达到新生组织更接近正常关节表面并保持其力学属性的目标.     

同种异体关节移植的现状

同种异体关节移植较广泛应用于修复各种原因造成的大段骨关节端缺损，同种异体骨关节移植中存在的免疫排斥反应及骨延迟愈合、不愈合、疲劳骨折、创伤性关节炎、感染等并发症是影响治疗效果的重要因素。本文综述了近几年国内外临床及实验研究文献中对以上问题的分析及新近提出的有效应对措施，如在移植骨上复合生长因子促进移植骨与宿主骨愈合，利用骨膜和软骨膜移植、修复软骨缺损，利用碱性成纤维细胞生长因子（bFGF)、肝细胞生长因子（HGF）、血小板诱导生长因子（PDGF）、转移因子β（TGF－β）等生长因子促进软骨修复等措施。此外，还简要引述了制备、贮存供体材料的新观点。     

基质金属蛋白酶-1在创伤性骨关节炎软骨及滑膜中的表达

目的　观察基质金属蛋白酶 - 1(MMP - 1)在兔前交叉韧带切断 (ACLT)创伤性骨关节炎 (OA)软骨及滑膜中的表达和分布 ,探讨MMP - 1表达与创伤性软骨退变之间的关系。　方法大耳白兔 2 0只行单侧ACLT术 ,术后 4周及 8周各处死 10只 ,另选 10只行单侧膝关节切开术作为假手术对照 ,于术后 8周处死。于解剖显微镜下行股骨关节面软骨退变大体评分 ,用免疫组化的方法检测MMP - 1在软骨及滑膜中的表达及分布。　结果　大体评分显示ACLT组软骨退变明显重于对照组 (P <0 .0 1) ,其中 8周组软骨退变程度又明显高于 4周组 (P <0 .0 5 )。MMP - 1主要在软骨表层及中上层、滑膜衬里层表达 ,其表达量随OA进展逐渐增高 (P <0 .0 5 )。OA早期 ,MMP - 1在滑膜中的增长滞后于它在软骨中的增长。　结论　MMP - 1与创伤性OA软骨退变关系密切 ,早期软骨退变主要源于软骨自身代谢改变 ,其后滑膜亦参与软骨退变。     

采用定量MRI反映距骨软骨修复组织的胶原蛋白成分特性:T_2值测量与扩散加权双回波稳态序列的对比

<正>目的研究使用定量T2和扩散加权成像反映自体基质诱导软骨形成(AMIC)后距骨修复组织(RT)的胶原成分特性。方法在横断面影像上比较25例创伤性骨软骨损伤后     

全膝关节置换术治疗创伤性关节炎的相关问题

创伤性关节炎(PTOA)是指关节及周围组织创伤后, 引起关节软骨破坏、变性, 软骨下骨、滑膜、关节囊及周围肌肉韧带损伤, 导致骨关节炎和关节功能障碍。膝关节PTOA主要表现为膝关节疼痛、僵硬及运动能力下降, 其治疗包括物理治疗、药物干预和手术。药物和物理疗法只能暂时缓解疼痛, 长期预后欠佳。对于中晚期患者首选手术治疗, 手术包括关节镜下清理术、软骨修复术、截骨术、关节融合术, 终末期患者必须行全膝关节置换术(TKA)。由于既往手术史、软组织条件差、力线异常、关节合并症多、个体差异大等原因, TKA治疗难度增加, 尤其是目前TKA治疗仍缺乏相关的规范和标准。为此, 笔者就膝关节PTOA患者行TKA治疗的相关问题进行探讨, 为临床管理提供参考。     

Disease-specific clinical problems associated with the subchondral bone

The subchondral bone is involved in a variety of diseases affecting both the articular cartilage and bone. Osteochondral defects in distinct locations and of variable sizes are the final results of different etiologies. These include traumatic osteochondral defects, osteochondritis dissecans, osteonecrosis, and osteoarthritis. Traumatic osteochondral defects are caused by osteochondral fractures, separating an osteochondral fragment that includes articular cartilage and both subchondral and trabecular bone from the joint surface. In osteochondritis dissecans, the disease originates in the subchondral bone and secondarily affects the articular cartilage. Location, stage, size, and depth of osteochondral lesions play a role in the treatment of traumatic osteochondral defects and osteochondritis dissecans. Surgical options include fragment refixation, transplantation of osteochondral autografts, or bone restoration by impacted cancellous bone grafts combined with autologous chondrocyte transplantation. An insufficiency fracture of the subchondral bone may be the initiating factor of what was formerly believed to be a spontaneous osteonecrosis of the knee (SPONK). Recent histopathological studies suggest that each stage of SPONK reflects different types of bone repair reactions following a fracture of the subchondral bone plate. Osteoarthritis is a disease that does affect not only the articular cartilage, but also the subchondral bone. Reconstructive surgical techniques aim at preserving joint function, inducing fibrocartilaginous repair, and at correcting malalignment. This review summarizes the current status of the clinical treatment of traumatic osteochondral defects, osteochondritis dissecans, osteonecrosis, and osteoarthritis as they affect the subchondral bone region and its adjacent structures.     

The basic science of the subchondral bone

In the past decades, considerable efforts have been made to propose experimental and clinical treatments for articular cartilage defects. Yet, the problem of cartilage defects extending deep in the underlying subchondral bone has not received adequate attention. A profound understanding of the basic anatomic aspects of this particular site, together with the pathophysiology of diseases affecting the subchondral bone is the key to develop targeted and effective therapeutic strategies to treat osteochondral defects. The subchondral bone consists of the subchondral bone plate and the subarticular spongiosa. It is separated by the cement line from the calcified zone of the articular cartilage. A variable anatomy is characteristic for the subchondral region, reflected in differences in thickness, density, and composition of the subchondral bone plate, contour of the tidemark and cement line, and the number and types of channels penetrating into the calcified cartilage. This review aims at providing insights into the anatomy, morphology, and pathology of the subchondral bone. Individual diseases affecting the subchondral bone, such as traumatic osteochondral defects, osteochondritis dissecans, osteonecrosis, and osteoarthritis are also discussed. A better knowledge of the basic science of the subchondral region, together with additional investigations in animal models and patients may translate into improved therapies for articular cartilage defects that arise from or extend into the subchondral bone.     

The subchondral bone in articular cartilage repair: current problems in the surgical management

As the understanding of interactions between articular cartilage and subchondral bone continues to evolve, increased attention is being directed at treatment options for the entire osteochondral unit, rather than focusing on the articular surface only. It is becoming apparent that without support from an intact subchondral bed, any treatment of the surface chondral lesion is likely to fail. This article reviews issues affecting the entire osteochondral unit, such as subchondral changes after marrow-stimulation techniques and meniscectomy or large osteochondral defects created by prosthetic resurfacing techniques. Also discussed are surgical techniques designed to address these issues, including the use of osteochondral allografts, autologous bone grafting, next generation cell-based implants, as well as strategies after failed subchondral repair and problems specific to the ankle joint. Lastly, since this area remains in constant evolution, the requirements for prospective studies needed to evaluate these emerging technologies will be reviewed.     

Aspects of Magnetic Resonance in the surgical treatment of osteochondral lesions of the knee

AIM: To assess the magnetic resonance (MR) appearance of knee cartilage chondroplasty procedures and their evolution in order to evaluate the usefulness of the method in monitoring postoperative rehabilitation. MATERIALS AND METHODS: Sixty-two patients treated with knee chondroplasty for high-grade cartilage injuries (Noyes' stages II and III) were examined with MR. Forty patients were treated with abrasion chondroplasty, fifteen with osteochondral graft in the injury site and seven with the matrix-induced autologous chondrocyte transplant technique. All patients were operated on by the same orthopaedic team and examined with the same MR protocol. The MR follow-up was performed six months and one year after surgery in the patients treated with abrasion chondroplasty and osteochondral graft, and one week, three months and one year after surgery in the patients treated with cartilage transplant. In the patients treated with abrasion chondroplasty we assessed the fibrocartilage repair and the subchondral bone features, in the patients treated with osteochondral graft we examined the cartilage, the subchondral bone and the graft borders, while in the patients treated with cartilage transplant we evaluated the features and the evolution of the transplant and the subchondral bone. Arthrosynovitis was assessed in all patients. In seven patients a cartilage repair biopsy was performed in arthroscopy. RESULTS: In all the patients MR imaging proved useful in monitoring the chondroplasty. In the patients treated with abrasion chondroplasty the cartilage repair appeared as a hypointense non-homogeneous irregular strip of tissue that replaced the articular surface. The subchondral bone was sclerotic with some geodes. In the later examination the repair was unchanged. In the patients treated with osteochondral graft the articular cartilage was similar to the adjacent hyaline cartilage, although more non-homogeneous. The subchondral bone was sclerotic and in three cases oedematous. In four cases the graft extended beyond the articular border. In the cartilage transplant the matrix appeared as a hypointense stripe after a week due to hydration and it had thinned with signal reduction in the later follow-ups. In the cases with unfavourable clinical evolution the subchondral bone was oedematous and sclerotic in the later examinations. In the cases with unfavourable clinical evolution there was moderate arthrosynovitis, regardless of the chondroplasty technique performed. CONCLUSIONS: MR imaging is useful for monitoring the maturation and the integration of knee chondroplasty and can be proposed as a replacement of arthroscopy for the assessment of postoperative rehabilitation.     

Weightbearing ovine osteochondral defects heal with inadequate subchondral bone plate restoration: implications regarding osteochondral autograft harvesting

Purpose

It is unknown what causes donor site morbidity following the osteochondral autograft transfer procedure or how donor sites heal. Contact pressure and edge loading at donor sites may play a role in the healing process. It was hypothesized that an artificially created osteochondral defect in a weightbearing area of an ovine femoral condyle will cause osseous bridging of the defect from the upper edges, resulting in incomplete and irregular repair of the subchondral bone plate.

Methods

To simulate edge loading, large osteochondral defects were created in the most unfavourable weightbearing area of 24 ovine femoral condyles. After killing at 3 and 6?months, osteochondral defects were histologically and histomorphometrically evaluated with specific attention to subchondral bone healing and subchondral bone plate restoration.

Results

Osteochondral defect healing showed progressive osseous defect bridging by sclerotic circumferential bone apposition. Unfilled area decreased significantly from 3 to 6 months (P?=?0.004), whereas bone content increased (n.s.). Complete but irregular subchondral bone plate restoration occurred in ten animals. In fourteen animals, an incomplete subchondral bone plate was found. Further common findings included cavitary lesion formation, degenerative cartilage changes and cartilage and subchondral bone collapse.

Conclusions

Osteochondral defect healing starts with subchondral bone plate restoration. However, after 6 months, incomplete or irregular subchondral bone plate restoration and subsequent failure of osteochondral defect closure is common. Graft harvesting in the osteochondral autograft transfer procedure must be viewed critically, as similar changes are also present in humans.

Level of evidence

Prognostic study, Level III.     

Osteochondral tissue engineering approaches for articular cartilage and subchondral bone regeneration

Purpose

Osteochondral defects (i.e., defects which affect both the articular cartilage and underlying subchondral bone) are often associated with mechanical instability of the joint and therefore with the risk of inducing osteoarthritic degenerative changes. This review addresses the current surgical treatments and most promising tissue engineering approaches for articular cartilage and subchondral bone regeneration.

Methods

The capability to repair osteochondral or bone defects remains a challenging goal for surgeons and researchers. So far, most clinical approaches have been shown to have limited capacity to treat severe lesions. Current surgical repair strategies vary according to the nature and size of the lesion and the preference of the operating surgeon. Tissue engineering has emerged as a promising alternative strategy that essentially develops viable substitutes capable of repairing or regenerating the functions of damaged tissue.

Results

An overview of novel and most promising osteochondroconductive scaffolds, osteochondroinductive signals, osteochondrogenic precursor cells, and scaffold fixation approaches are presented addressing advantages, drawbacks, and future prospectives for osteochondral regenerative medicine.

Conclusion

Tissue engineering has emerged as an excellent approach for the repair and regeneration of damaged tissue, with the potential to circumvent all the limitations of autologous and allogeneic tissue repair.

Level of evidence

Systematic review, Level III.     

Epidemiology and imaging of the subchondral bone in articular cartilage repair

Articular cartilage and the subchondral bone act as a functional unit. Following trauma, osteochondritis dissecans, osteonecrosis or osteoarthritis, this intimate connection may become disrupted. Osteochondral defects—the type of defects that extend into the subchondral bone—account for about 5% of all articular cartilage lesions. They are very often caused by trauma, in about one-third of the cases by osteoarthritis and rarely by osteochondritis dissecans. Osteochondral defects are predominantly located on the medial femoral condyle and also on the patella. Frequently, they are associated with lesions of the menisci or the anterior cruciate ligament. Because of the close relationship between the articular cartilage and the subchondral bone, imaging of cartilage defects or cartilage repair should also focus on the subchondral bone. Magnetic resonance imaging is currently considered to be the key modality for the evaluation of cartilage and underlying subchondral bone. However, the choice of imaging technique also depends on the nature of the disease that caused the subchondral bone lesion. For example, radiography is still the golden standard for imaging features of osteoarthritis. Bone scintigraphy is one of the most valuable techniques for early diagnosis of spontaneous osteonecrosis about the knee. A CT scan is a useful technique to rule out a possible depression of the subchondral bone plate, whereas a CT arthrography is highly accurate to evaluate the stability of the osteochondral fragment in osteochondritis dissecans. Particularly for the problem of subchondral bone lesions, image evaluation methods need to be refined for adequate and reproducible analysis. This article highlights recent studies on the epidemiology and imaging of the subchondral bone, with an emphasis on magnetic resonance imaging.     

Articular cartilage: injury pathways and treatment options

Articular cartilage injury and degeneration is a frequent occurrence in synovial joints. Treatment of these articular cartilage lesions are a challenge because this tissue is incapable of quality repair and/or regeneration to its native state. Nonoperative treatments endeavor to control symptoms, and include anti-inflammatory medication, viscosupplementation, bracing, orthotics, and activity modification. Techniques to stimulate the intrinsic repair (fibrocartilage) process include drilling, abrasion, and microfracture of the subchondral bone. Currently, the clinical biologic approaches to treat cartilage defects include autologous chondrocyte implantation, periosteal transfer, and osteochondral autograft or allograft transplantation. Newer strategies employing tissue engineering being studied involve the use of combinations of progenitor cells, bioactive factors, and matrices, and the use of focal synthetic devices. Many new and innovative treatments are being explored in this exciting field. However, there is a paucity of prospective, randomized controlled clinical trials that have compared the various techniques, treatment options, indications and efficacy.     

Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures)

Fractures involving the articulating surfaces of bone are a common cause of chronic disability after joint injury. Acute fractures of the articular surface typically run parallel to the surface and are confined to the cartilage and/or the immediate subchondral cancellous bone. They should be distinguished from vertical or oblique bone fractures with intra-articular extension. This article reviews the mechanism of acute articular surface injuries, as well as their incidence, clinical presentation, radiologic appearance and treatment. A classification is presented based on direct inspection (arthroscopy) and imaging (especially MRI), emphasizing the distinction between lesions with intact (subchondral impaction and subchondral bone bruises) and disrupted (chondral, osteochondral lesions) cartilage. Hyaline cartilage, subchondral bone plate and subchondral cancellous bone are to be considered an anatomic unit. Subchondral articular surface lesions, osteochondral fractures and solely chondral fractures are different manifestations of impaction injuries that affect the articulating surface. Of the noninvasive imaging modalities, conventional radiography and MRI provide the most relevant information. The appropriate use of short tau inversion recovery, T1-weighted and T2-weighted (turbo) spin-echo as well as gradient-echo sequences, enables MRI to classify the various acute articular surface lesions with great accuracy and provides therapeutic guidance. Received: 5 April 1999 Revision requested: 6 May 1999 Revision received: 21 June 1999 Accepted: 12 July 1999     

Osteochondral defects in the ankle: why painful?

Osteochondral defects of the ankle can either heal and remain asymptomatic or progress to deep ankle pain on weight bearing and formation of subchondral bone cysts. The development of a symptomatic OD depends on various factors, including the damage and insufficient repair of the subchondral bone plate. The ankle joint has a high congruency. During loading, compressed cartilage forces its water into the microfractured subchondral bone, leading to a localized high increased flow and pressure of fluid in the subchondral bone. This will result in local osteolysis and can explain the slow development of a subchondral cyst. The pain does not arise from the cartilage lesion, but is most probably caused by repetitive high fluid pressure during walking, which results in stimulation of the highly innervated subchondral bone underneath the cartilage defect. Understanding the natural history of osteochondral defects could lead to the development of strategies for preventing progressive joint damage.