CQD人工腱修复兔跟腱的组织学观察

目的应用CQD人工腱修复兔跟腱，以期研究其组织形态学的改变。方法随机选择实验兔一侧后肢作为实验侧，游离跟腱并切除中间束，CQD人工腱替代缺损部，编织缝合于正常肌腱的上下端，生物膜将CQD人工腱包好，全层缝合皮肤。另一侧后肢作为对照侧，除不用生物膜包裹人工腱体外，手术方法与实验组相同。随机分为2周、1、2、3、4个月组，每组4只，自身对照。观察指标有：一般情况、大体标本观察、组织学观察、超微结构观察。结果一般情况：术后动物活动不受限，无局部感染，10天后伤口愈合，缝线自然脱落。但从组织学、电镜的观察实验组的愈合均较对照组提前。结论CQD人工腱能够在动物体内腱化并替代肌腱，这将为临床应用提供新的人工腱采料。     

中长跑运动员急慢性跟腱腱围炎的治疗

中长跑运动员急慢性跟腱腱围炎的治疗国家体育总局训练局医务处（北京１０００６１）何国荣创伤性跟腱腱围炎是中长跑运动员多发病之一。这种疾病病期长，治疗见效慢，对训练影响很大。因此，早期采取正确治疗方法以及调整训练计划是治疗的关键。本文就作者在日本某公司中...     

定量超声弹性成像技术应用于兔跟腱离断模型力学及组织学肌腱愈合的量化评估

<正>摘要目的探讨跟腱离断兔模型跟腱撕裂愈合部位应变率(SR)的时间依从性变化,评估修复组织SR与力学、组织学特性的相关性。材料与方法本实验方法已通过实验动物使用和管理委员会批准。24只(48肢)新西兰白兔的跟腱经外科手术离断,分别在跟腱离断后2、4、8及12周应用基于加压的定量超声弹性成像技术计算得出跟腱的SR。通过在体的弹性成像,收集得到左侧跟腱极限负荷、极限应力、弹性系数和线性刚度的力学测试结果,以及右侧跟腱Bonar分     

以阿是穴为主,采用平刺与围刺法治疗跟腱慢性损伤126例临床分析

以阿是穴为主 ,采用平刺与围刺法治疗跟腱慢性损伤 (跟腱炎、跟腱腱围炎、跟腱止点末端病 ) 1 2 6例 ,临床治愈率为 72 . 8%,显效率为 1 0 0 %。根据多年临床观察 ,提出了跟腱炎、跟腱腱围炎与跟腱止点末端病三者在病理改变上可能存在着一定的内在联系 ,即病理变化的早、中、晚三期。在跟腱慢性损伤的早期 ,及时进行有效治疗 ,有利于保证系统训练。同时 ,为了巩固远期疗效与预防再伤 ,作者还提出了有针对性的运动处方———小腿三头肌与跟腱牵拉练习。     

微量元素锌对跟腱创伤后修复过程的影响

本文分两部分对微量元素锌在跟腱断裂后修复过程中的作用进行研究。动物实验采用80只大白鼠为对象,按食物配方造成低锌、低蛋白补锌及手术后补锌的条件,观察跟腱断裂后愈合的状况,人体观察采用我所跟腱断裂手术的病例,观察血清锌在手术前后的变化。本实验结果表明在组织受创伤时,机体有调整体内锌分布的能力以保证组织愈合的需要。缺锌对跟腱修复有不良影响。机体在低蛋白状况时,单纯补锌的作用是极其有限的。     

内皮型一氧化氮合酶在大鼠末端病中的表达

目的:观察末端病大鼠跟腱末端区内皮型一氧化氮合酶(eNOS)的分布,探讨eNOS与血管新生的关系及其在末端病中对机体的保护作用。方法:将8只Wistar大鼠随机分为对照组和造模组,采用电刺激跳跃法造模,4周后处死动物,取其双后足跟腱及部分跟骨,制成观察标本,采用ImageProPlus5.0图像分析系统测定标本镜下视野照片的阳性信号积分光密度值(IOD)。结果:对照组主要在腱围处有eNOS的大量表达;造模组大鼠跟腱、纤维软骨、钙化软骨、跟骨、骨髓腔、腱骨关节面及腱围等部位eNOS表达明显,腱围及骨髓腔处表达最多。两组间不同部位IOD值均有显著差异。结果提示:eNOS可能参与了末端病组织血管的新生,组织结构功能适应及抑制细胞凋亡等代偿性反应。     

综合疗法治疗20例运动员创伤性跟腱腱围炎

运动员创伤性跟腱腱围炎多见于跑跳项目,是运动创伤中病期较长、治疗难度较大的创伤之一,严重影响运动员的训练和比赛。近两年,笔者在国家田径队采用快罐、红外线照射及冷疗等综合疗法治疗运动员创伤性跟腱腱围炎20例,现报告如下。     

肌肉包埋法旷置大段裸露跟腱的初步报告

目的 探讨肌肉包埋法旷置大段裸露跟腱的手术方法和疗效.方法 本组21例跟腱断裂合并跟区皮肤缺损,16例合并胫腓骨粉碎骨折及动脉、神经损伤,13例合并休克,6例合并骨盆骨折,2例合并同侧开放性股骨骨折,3例合并肝脾破裂.急诊手术固定骨折,修复动脉、神经损伤,修复肝脾破裂;清创后小腿三头肌包埋、旷置跟腱.二次手术修复跟腱和跟区皮肤缺损.结果 跟腱与肌肉组织紧密粘连,外膜新鲜有光泽,腱性组织坚韧有力,无变黑、坏死、液化和感染.二次手术后随访15～27个月,平均18个月.疗效评定为优15例,良4例,差2例,优良率为90%.皮瓣均成活,伤口Ⅰ期愈合,跟腱无再次断裂.结论 肌肉包埋法可以有效避免跟腱暴露所致的缺血坏死和感染,为Ⅱ期手术提供条件.     

预防肌腱粘连的研究进展

肌腱手术后粘连仍是难题之一。随着肌腱愈合理论的不断发展，对肌腱粘连预防的研究也在不断深入，现就这方面的研究进展综述如下。肌腱粘连与肌腱愈合的关系肌腱愈合过程中是否一定会形成粘连，一直存在着争议。持外源性愈合观点者认为，肌腱愈合过程是腱周组织来源的粘连带入血运和修复细胞来完成的，粘连不可避免。持内源性愈合观点者则认为，肌腱细胞本身具有修复损伤的能力，肌腱愈合并不是必须靠腱周组织增生来完成，粘连是可以避免的。最近的研究表明，肌腱愈合过程中内、外源愈合是同时存在的，哪种方式占主导地位，取决于肌腱内外的…     

电场促进兔肌腱愈合实验研究

电刺激已被证实有增强各种组织再生作用。本实验应用方形波耦合电场刺激一侧损伤的兔屈趾深肌腱,并与未受电刺激的对侧进行比较。于损伤后不同时期分别测定腱内羟脯氨酸含量、光学显微镜下组织学检查及测试腱修复处愈合强度。统计学处理后证实经该电场刺激后在第14、21和42天可提高腱内羟脯氨酸含量,第42天时腱愈合强度明显高于非刺激侧,组织学检查表明该电场刺激可增强损伤肌腱的早期愈合反应及加快恢复腱内胶原定向排列结构。     

Muscle transplant in the rabbit's Achilles tendon

Achilles tendinopathy (AT) is a degenerative disorder resulting from functional overload, especially during running and jumping, with some inflammatory features at the insertions, bursae, and paratenon. The Achilles tendon is poorly vascularized, especially in the middle third, and the consequent slow metabolic rate allows it to work at very low oxygen tensions but prevents on the other hand a rapid healing. PURPOSE: To create an animal model to study a novel surgical technique employed in AT: transplanting some fibers of the soleus muscle into the tendon in order to improve its vascularization and healing and to study the histological appearance of the soleus graft incorporated in the tendon. METHODS: We operated on 10 white New Zealand rabbits (eight rabbits underwent the procedure, two rabbits the sham operation with incision of the tendon without graft). Two animals were euthanized at 1 wk, 1, 2, and 3 months. RESULTS: Histology showed that after 3 months the muscle fibers were still viable within the tendons, interspersed within connective tissue fibers. Tendon and muscle tissues were intimately fused. CONCLUSIONS: The persistence of the soleus muscle pedicle graft within the Achilles tendon tissue is an index of sound blood supply. This surgical model is suitable for application in further studies on tendon healing.     

The effect of ciprofloxacin on tendon, paratenon, and capsular fibroblast metabolism

The pathologic mechanisms underlying fluoroquinolone-induced tendinopathy are poorly understood. The observed incidence of tendinitis and tendon rupture in patients treated with ciprofloxacin hydrochloride suggests that the fluoroquinolone antibiotics alter tendon fibroblast metabolism. The purpose of this study was to examine the effect of ciprofloxacin on fibroblast metabolism in vitro. Canine Achilles tendon, paratenon, and shoulder capsule specimens were maintained in culture with ciprofloxacin (5, 10, or 50 microg/ml). Fibroblast proliferation, collagen synthesis, proteoglycan synthesis, and matrix-degrading activity were analyzed. Incubation of Achilles tendon, Achilles paratenon, and shoulder capsule fibroblasts with ciprofloxacin resulted in a statistically significant 66% to 68% decrease in cell proliferation compared with control cells at day 3 in culture. Ciprofloxacin caused a statistically significant 36% to 48% decrease in collagen synthesis compared with controls in all fibroblast cultures. Ciprofloxacin caused a statistically significant 14% to 60% decrease in proteoglycan synthesis in all fibroblast cell lines. Compared with unstimulated control fibroblasts, culture media from Achilles tendon, paratenon, and shoulder capsule cells that were exposed to ciprofloxacin demonstrated statistically significant increases in matrix-degrading proteolytic activity after 72 hours in culture. This study demonstrates that ciprofloxacin stimulates matrix-degrading protease activity from fibroblasts and that it exerts an inhibitory effect on fibroblast metabolism. The increase in protease activity and the inhibition of both cell proliferation and the synthesis of matrix ground substance may contribute to the clinically described tendinopathies associated with ciprofloxacin therapy.     

Mid-portion Achilles tendinopathy: why painful? An evidence-based philosophy

Chronic mid-portion Achilles tendinopathy is generally difficult to treat as the background to the pain mechanisms has not yet been clarified. A wide range of conservative and surgical treatment options are available. Most address intratendinous degenerative changes when present, as it is believed that these changes are responsible for the symptoms. Since up to 34% of asymptomatic tendons show histopathological changes, we believe that the tendon proper is not the cause of pain in the majority of patients. Chronic painful tendons show the ingrowth of sensory and sympathetic nerves from the paratenon with release of nociceptive substances. Denervating the Achilles tendon by release of the paratenon is sufficient to cause pain relief in the majority of patients. This type of treatment has the additional advantage that it is associated with a shorter recovery time when compared with treatment options that address the tendon itself. An evidence-based philosophy on the cause of pain in chronic mid-portion Achilles tendinopathy is presented.     

Achilles tendon rupture: experimental results on spontaneous repair in a sheep-model

We studied the course of spontaneous healing of Achilles tendons in a sheep model after transection and partial resection of the tendon by means of histological and biomechanical analyses. In 18 sheep used for another animal study the operated knee had to be excluded from weight-bearing; therefore the Achilles tendons were transected and for 1.5 cm partially resected in the middle substance of the tendon. For evaluation these spontaneously healed tendons (n = 18) were compared with the contralateral noninvolved tendons (n = 18). Specimens were analyzed 3, 6, and 12 months postoperatively by means of histology, polarized light, angiography, and mechanically analyzing the specific tensile strength and absolute tensile strength. We found that in all animals the resected tendon healed spontaneously. All animals exhibited a normal gait pattern at least 6 weeks postoperatively. Histologically, the tendinous area of healing demonstrated after 3 months a fibrous collagenous tissue with a loose fiber orientation. The cross-sectional area had at 3 months increased to maximum but decreased later. Concomitantly the fiber orientation improved with time and 12 months after transection the specimens showed a nearly normal histological structure of the healed tendon. Biomechanically the specimens exhibited a rather low specific rupture force after 3 months (28.8% of normal tendons) and 6 months (30.2%) but increased after 12 months (56.7%). In regard to the resulting total rupture force the decrease in the spontaneously healed tendons was less (75.6% after 3 months, 56.1% after 6 months, 81.18% after 12 months), because the cross-sectional area of the healing tendon had significantly (P < 0.05) increased to maximum after 3 and 6 months. Sheep Achilles tendons thus healed spontaneously without any immobilization. The initial healing mechanism is thickening of the scar tissue with improvement of the fiber orientation towards a tendonlike structure within 1 year. Parallel to this, the specific rupture force increased and the thickness of the newly tendonlike area decreased.     

Marked pathological changes proximal and distal to the site of rupture in acute Achilles tendon ruptures

A laboratory study was performed to evaluate the histopathological features of the macroscopically intact portion of the Achilles tendon in patients undergoing surgery for an acute rupture of the Achilles tendon. Tendon samples were harvested from 29 individuals (21 men, 8 women; mean age: 46 ± 12) who underwent repair of an Achilles tendon tear tear, and from 11 male patients who died of cardiovascular events (mean age: 61). Three pieces of tendon were harvested: at the rupture site, 4 cm proximal to the site of rupture, 1 cm proximal to the insertion of the Achilles tendon on the calcaneum. Slides were assessed using a semiquantitative grading scale assessing fiber structure and arrangement, rounding of the nuclei, regional variations in cellularity, increased vascularity, decreased collagen stainability, and hyalinization. Intra-observer reliability of the subscore readings was calculated. The pathological features were significantly more pronounced in the samples taken from the site of rupture than in the samples taken proximally and distal to it (0.008 < P < 0.01). There were no significant differences in the mean pathologic sum-scores in the samples taken proximally and distal to the site of rupture. Unruptured Achilles tendons, even at an advanced age, and ruptured Achilles tendons are clearly part of two distinct populations, with the latter demonstrating histopathological evidence of failed healing response even in areas macroscopically normal.     

Tenocytes from ruptured and tendinopathic achilles tendons produce greater quantities of type III collagen than tenocytes from normal achilles tendons. An in vitro model of human tendon healing

Type I collagen is the main collagen in tendons; type III collagen is present in small amounts. Ruptured Achilles tendons contain a significantly greater proportion of type Ill collagen, which predisposes them to rupture. We used an in vitro model to determine whether tenocytes from Achilles tendons that were ruptured (N = 22), nonruptured (N = 7), tendinopathic (N = 12), and fetal (N = 8) show different behavior. Samples of Achilles tendon were digested with collagenase and the released tenocytes were collected. Primary tenocyte cultures were established and subsequently cultured onto glass coverslips. Once a confluent monolayer was obtained, the cell populations were "wounded" by scraping a pipette tip along the surface. The cultures were further incubated for either 1, 4, 8, 12, 16, or 24 hours, and production of types I and II collagen was assessed by immunostaining. In cultures from ruptured and tendinopathic tendons, there was increased production of type Ill collagen. Athletic participation places excess stress on the Achilles tendon, which could potentially lead to areas of microtrauma within the tendon. These areas may heal by the production of type III collagen, which is an abnormal healing response. Accumulation of such episodes of microtrauma could resuit in a critical point where the resistance of the tissue to tensile forces is compromised and tendon rupture occurs.     

Functional anatomy of the Achilles tendon

The Achilles tendon is the strongest and thickest tendon in the human body. It is also the commonest tendon to rupture. It begins near the middle of the calf and is the conjoint tendon of the gastrocnemius and soleus muscles. The relative contribution of the two muscles to the tendon varies. Spiralisation of the fibres of the tendon produces an area of concentrated stress and confers a mechanical advantage. The calcaneal insertion is specialised and designed to aid the dissipation of stress from the tendon to the calcaneum. The insertion is crescent shaped and has significant medial and lateral projections. The blood supply of the tendon is from the musculotendinous junction, vessels in surrounding connective tissue and the osteotendinous junction. The vascular territories can be classified simply in three, with the midsection supplied by the peroneal artery, and the proximal and distal sections supplied by the posterior tibial artery. This leaves a relatively hypovascular area in the mid-portion of the tendon where most problems occur. The Achilles tendon derives its innervation from the sural nerve with a smaller supply from the tibial nerve. Tenocytes produce type I collagen and form 90% of the cellular component of the normal tendon. Evidence suggests ruptured or pathological tendon produce more type III collagen, which may affect the tensile strength of the tendon. Direct measurements of forces reveal loading in the Achilles tendon as high as 9 KN during running, which is up to 12.5 times body weight.     

The COL12A1 and COL14A1 genes and Achilles tendon injuries

Genes encoding for tenascin C and a subunit of type V collagen have previously been reported to be associated with Achilles tendon injuries. Types XII and XIV collagen may be involved in similar biological processes as these proteins in tendons. The aim of this study was therefore to test the association between polymorphisms within COL12A1 and COL14A1 and Achilles tendon injuries. Restriction fragment length polymorphism (RFLP) analysis was used to identify the relative frequencies of two polymorphisms within each of the COL12A1 and COL14A1 genes within 137 subjects with clinical symptoms of Achilles tendon injuries, consisting of 93 with Achilles tendinopathy and 44 with Achilles tendon rupture, and 131 asymptomatic control subjects. No statistically significant differences were identified in the genotype, allele or haplotype distributions between the affected and control subjects. The findings from this study suggest that although COL12A1 and COL14A1 are involved in similar biological processes as TNC and COL5A1, the polymorphisms tested are not associated with clinical symptoms of Achilles tendon injury within the investigated population.     

Surgical treatment of Achilles tendinitis by decompression of the retrocalcaneal bursa and the superior calcaneal tuberosity

BACKGROUND: Initial nonoperative treatment of pain at the Achilles tendon, often referred to as "tendinitis," is not always successful. HYPOTHESIS: Surgical treatment is effective for patients with insertional tendinitis unrelieved by nonoperative measures. STUDY DESIGN: Retrospective cohort study. METHODS: Thirty-five patients (41 feet) who had painful Achilles tendon syndrome unrelieved by 6 months of nonoperative measures were treated surgically. The technique consisted of a single incision along the lateral border of the Achilles tendon. The dissection exposed the retrocalcaneal bursa and fat pad, which were completely excised along with any scarred and thickened paratenon. A partial calcaneal exostectomy of the tubercle was performed. RESULTS: At a minimum follow-up of 20 months (average, 39), the patients' pain scores (rated from 0 to 6) improved from 4.7 (SD, 1.1) preoperatively to 1.5 (SD, 1.3); 90% had complete or significant relief of symptoms, 10% felt improved, and none felt unchanged or worse. CONCLUSIONS: Surgical treatment of chronic Achilles tendon pain with resection of the prominent tuberosity, complete debridement of the bursa, excision of thickened, scarred paratenon, and removal of accessible calcific deposits within the tendon is an effective treatment.     

Calcific insertional Achilles tendinopathy: reattachment with bone anchors

BACKGROUND: Recalcitrant calcific insertional Achilles tendinopathy is difficult to treat. HYPOTHESIS: Bursectomy, excision of the distal paratenon, disinsertion of the tendon, removal of the calcific deposit, and reinsertion of the Achilles tendon with bone anchors is safe and effective. STUDY DESIGN: Longitudinal study. METHODS: Twenty-one patients (six women) (21 feet) (average age 46.9 +/- 6.4 years) with recalcitrant calcific insertional Achilles tendinopathy were treated surgically with removal of the calcific deposit; the Achilles tendon was reinserted with bone anchors. RESULTS: At an average follow-up of 48.4 months, one patient necessitated a further operation. Eleven patients reported an excellent result, and five a good result. The remaining five patients could not return to their normal levels of sporting activity and kept fit by alternative means. The results of the VISA-A questionnaire were markedly improved in all patients, from an average of 62.4% to 88.1%. CONCLUSIONS: We recommend disinsertion of the Achilles tendon to excise the calcific deposit fully and reinsertion of the Achilles tendon in the calcaneus with suture anchors. No patient experienced a traumatic disinsertion of the reattached tendon. However, five patients were not able to return to their original level of physical activity.