Modified tendon stripper for obtaining palmaris longus tendon graft

Tendon graft harvesting is a challenging part of hand surgery. It is not only a time-consuming procedure but also carries the potential complications associated with it. Various alternatives for this procedure are presented in the literature to overcome these difficulties. In this paper, we are presenting a series of cases in which a newly modified tendon stripper was used for tendon graft harvesting.     

Effect of supraspinatus tendon repair technique on the infraspinatus tendon

Supraspinatus tendon tears are common and often propagate into larger tears that include the infraspinatus tendon, resulting in loss of function and increased pain. Previously, we showed that the supraspinatus and infraspinatus tendons mechanically interact through a range of rotation angles, potentially shielding the torn supraspinatus tendon from further injury while subjecting the infraspinatus tendon to increased risk of injury. Surgical repair of torn supraspinatus tendons is common, yet the effect of the repair on the infraspinatus tendon is unknown. Since we have established a relationship between strain in the supraspinatus and infraspinatus tendons the success of a supraspinatus tendon repair depends on its effect on the loading environment in the infraspinatus tendon. More specifically, the effect of transosseous supraspinatus tendon repair in comparison to one that utilizes suture anchors, as is commonly done with arthroscopic repairs, on this interaction through these joint positions will be evaluated. We hypothesize that at all joint positions evaluated, both repairs will restore the interaction between the two tendons. For both repairs, (1) increasing supraspinatus tendon load will increase infraspinatus tendon strain and (2) altering the rotation angle from internal to external will increase strain in the infraspinatus tendon. Strains were measured in the infraspinatus tendon insertion through a range of joint rotation angles and supraspinatus tendon loads, for the intact, transosseous, and suture anchor repaired supraspinatus tendons. Images corresponding to specific supraspinatus tendon loads were isolated for the infraspinatus tendon insertion for analysis. The effect of supraspinatus tendon repair on infraspinatus tendon strain differed with joint position. Altering the joint rotation did not change strain in the infraspinatus tendon for any supraspinatus tendon condition. Finally, increasing supraspinatus tendon load resulted in an increase in average maximum and decrease in average minimum principal strain in the infraspinatus tendon. There is a significant difference in infraspinatus tendon strain between the intact and arthroscopically (but not transosseous) repaired supraspinatus tendons that increases with greater loads. Results suggest that at low loads neither supraspinatus tendon repair technique subjects the infraspinatus tendon to potentially detrimental loads; however, at high loads, transosseous repairs may be more advantageous over arthroscopic repairs for the health of the infraspinatus tendon. Results emphasize the importance of limiting loading of the repaired supraspinatus tendon and that at low loads, both repair techniques restore the interaction to the intact supraspinatus tendon case.     

Mechanobiology of tendon

Tendons are able to respond to mechanical forces by altering their structure, composition, and mechanical properties--a process called tissue mechanical adaptation. The fact that mechanical adaptation is effected by cells in tendons is clearly understood; however, how cells sense mechanical forces and convert them into biochemical signals that ultimately lead to tendon adaptive physiological or pathological changes is not well understood. Mechanobiology is an interdisciplinary study that can enhance our understanding of mechanotransduction mechanisms at the tissue, cellular, and molecular levels. The purpose of this article is to provide an overview of tendon mechanobiology. The discussion begins with the mechanical forces acting on tendons in vivo, tendon structure and composition, and its mechanical properties. Then the tendon's response to exercise, disuse, and overuse are presented, followed by a discussion of tendon healing and the role of mechanical loading and fibroblast contraction in tissue healing. Next, mechanobiological responses of tendon fibroblasts to repetitive mechanical loading conditions are presented, and major cellular mechanotransduction mechanisms are briefly reviewed. Finally, future research directions in tendon mechanobiology research are discussed.     

A tendon approximator

A tendon approximator designed to hold tendon ends together for suturing is described. The method of use and the situations where it may be of value are described.     

Exosomes from tendon stem cells promote injury tendon healing through balancing synthesis and degradation of the tendon extracellular matrix

Tendon injuries are common musculoskeletal system disorders in clinical, but the regeneration ability of tendon is limited. Tendon stem cells (TSCs) have shown promising effect on tissue engineering and been used for the treatment of tendon injury. Exosomes that serve as genetic information carriers have been implicated in many diseases and physiological processes, but effect of exosomes from TSCs on tendon injury repair is unclear. The aim of this study is to make clear that the effect of exosomes from TSCs on tendon injury healing. Exosomes were harvested from conditioned culture media of TSCs by a sequential centrifugation process. Rat Achilles tendon tendinopathy model was established by collagenase‐I injection. This was followed by intra‐Achilles‐tendon injection with TSCs or exosomes. Tendon healing and matrix degradation were evaluated by histology analysis and biomechanical test at the post‐injury 5 weeks. In vitro, TSCs treated with interleukin 1 beta were added by conditioned medium including exosomes or not, or by exosomes or not. Tendon matrix related markers and tenogenesis related markers were measured by immunostaining and western blot. We found that TSCs injection and exosomes injection significantly decreased matrix metalloproteinases (MMP)‐3 expression, increased expression of tissue inhibitor of metalloproteinase‐3 (TIMP‐3) and Col‐1a1, and increased biomechanical properties of the ultimate stress and maximum loading. In vitro, conditioned medium with exosomes and exosomes also significantly decreased MMP‐3, and increased expression of tenomodulin, Col‐1a1 and TIMP‐3. Exosomes from TSCs could be an ideal therapeutic strategy in tendon injury healing for its balancing tendon extracellular matrix and promoting the tenogenesis of TSCs.     

Bridging tendon defects using autologous tenocyte engineered tendon in a hen model

Tendon defects remain a major concern in plastic surgery because of the limited availability of tendon autografts. Whereas immune rejection prohibits the use of tendon allografts, most prosthetic replacements also fail to achieve a satisfactory long-term result of tendon repair. The tissue engineering technique, however, can generate different tissues using autologous cells and thus may provide an optimal approach to address this concern. The purpose of this study was to test the feasibility of engineering tendon tissues with autologous tenocytes to bridge a tendon defect in either a tendon sheath open model or a partial open model in the hen. In a total of 40 Leghorn hens, flexor tendons were harvested from the left feet and were digested with 0.25% type II collagenase. The isolated tenocytes were expanded in vitro and mixed with unwoven polyglycolic acid fibers to form a cell-scaffold construct in the shape of a tendon. The constructs were wrapped with intestinal submucosa and then cultured in Dulbecco's Modified Eagle Medium plus 10% fetal bovine serum for 1 week before in vivo transplantation. On the feet, a defect of 3 to 4 cm was created at the second flexor digitorum profundus tendon by resecting a tendon fragment. The defects were bridged either with a cell-scaffold construct in the experimental group ( n= 20) or with scaffold material alone in the control group ( n= 20). Specimens were harvested at 8, 12, and 14 weeks postrepair for gross and histologic examination and for biomechanical analysis. In the experimental group, a cordlike tissue bridging the tendon defect was formed at 8 weeks postrepair. At 14 weeks, the engineered tendons resembled the natural tendons grossly in both color and texture. Histologic examination at 8 weeks showed that the neo-tendon contained abundant tenocytes and collagen; most collagen bundles were randomly arranged. The undegraded polyglycolic acid fibers surrounded by inflammatory cells were also observed. At 12 weeks, tenocytes and collagen fibers became longitudinally aligned, with good interface healing to normal tendon. At 14 weeks, the engineered tendons displayed a typical tendon structure hardly distinguishable from that of normal tendons. Biomechanical analysis demonstrated increased breaking strength of the engineered tendons with time, which reached 83 percent of normal tendon strength at 14 weeks. In the control group, polyglycolic acid constructs were mostly degraded at 8 weeks and disappeared at 14 weeks. However, the breaking strength of the scaffold materials accounted for only 9 percent of normal tendon strength. The results of this study indicated that tendon tissue could be engineered in vivo to bridge a tendon defect. The engineered tendons resembled natural tendons not only in gross appearance and histologic structure but also in biomechanical properties.     

Achilles tendon rupture: avoiding tendon lengthening during surgical repair and rehabilitation

Achilles tendon rupture is a serious injury for which the best treatment is still controversial. Its primary goal should be to restore normal length and tension, thus obtaining an optimal function. Tendon elongation correlates significantly with clinical outcome; lengthening is an important cause of morbidity and may produce permanent functional impairment. In this article, we review all factors that may influence the repair, including the type of surgical technique, suture material, and rehabilitation program, among many others.     

Chiropteran tendon locking mechanism

Rather than the usual mammalian scheme in which tendon and sheath surfaces provide as little friction as possible, the tendons and sheaths of many bats have a locking segment on the manual and pedal flexor tendon complex. This tendon locking mechanism (TLM) exists opposite the proximal phalanges of each toe and pollex of many bats. Its structure, similar to a ratchet mechanism, assists bats in hanging with little muscular effort. The third digit of the pelvic limb and the pollex of species representing 15 chiropteran families were studied to determine the presence or absence, morphology, and function of the TLM. Most of the species studied have a TLM consisting of a patch of tubercles on the ventral surface of the flexor tendon associated with the proximal phalanx of each pollex or toe. The sheath adjacent to this portion of the flexor tendon has a series of transverse folds or ridges, which, when engaged with the tubercles on the tendon, lock the tendon in place. The TLM is similar in megachiropterans and microchiropterans possessing it. The TLM is absent, however, in some of the microchiropterans studied, most notably in the phyllostomids. Since many birds have a TLM similar to that of bats, it is an excellent example of the convergent evolution of a feature brought about by similar functional pressures on birds and bats. © 1993 Wiley-Liss, Inc.     

Biomechanics of tendon healing

The biomechanics of tendon healing was investigated with unsutured rat achilles tendons. After two, three, and four weeks of healing tensile parameters were assayed with a bone-muscle-tendon-bone preparation elongated to failure at a controlled physiological strain rate.

In the third week of healing, stiffness, strength, and energy absorbing capacity all increased approximately 50%. These changes correlated with early fibroplasia.

In the fourth week of healing, strength, energy absorbing capacity and elongation to failure all increased relatively more than stiffness. Histologically, larger fibers with better longitudinal alignment developed during this period.

At the end of four weeks the tendon's strength was approximately 25% of normal.

To summarize, the return of stiffness in a healing tendon preparation correlated with the presence of fibroplasia and the return of other tensile parameters was a function of the amount and organization of the fibroplasia.     

Autophagy guards tendon homeostasis

Tendons are vital collagen-dense specialized connective tissues transducing the force from skeletal muscle to the bone, thus enabling movement of the human body. Tendon cells adjust matrix turnover in response to physiological tissue loading and pathological overloading (tendinopathy). Nevertheless, the regulation of tendon matrix quality control is still poorly understood and the pathogenesis of tendinopathy is presently unsolved. Autophagy, the major mechanism of degradation and recycling of cellular components, plays a fundamental role in the homeostasis of several tissues. Here, we investigate the contribution of autophagy to human tendons’ physiology, and we provide in vivo evidence that it is an active process in human tendon tissue. We show that selective autophagy of the endoplasmic reticulum (ER-phagy), regulates the secretion of type I procollagen (PC1), the major component of tendon extracellular matrix. Pharmacological activation of autophagy by inhibition of mTOR pathway alters the ultrastructural morphology of three-dimensional tissue-engineered tendons, shifting collagen fibrils size distribution. Moreover, autophagy induction negatively affects the biomechanical properties of the tissue-engineered tendons, causing a reduction in mechanical strength under tensile force. Overall, our results provide the first evidence that autophagy regulates tendon homeostasis by controlling PC1 quality control, thus potentially playing a role in the development of injured tendons.Subject terms: Physiology, Cell biology     

Inflammation and tendon healing

Tendons are extracellular matrix rich structures allowing the transmission of forces generated by skeletal muscles to bones in order to produce movements. Some intrinsic characteristics of tendons, namely hypovascularity and hypocellularity, may explain their slow rate of healing. A growing body of evidence suggests that the inflammatory process, essential for pathogen clearance and injury scavenging, may play opposite functions in tendon healing. For instance, inflammation can lead to degradation of intact collagen and to viable cell death, thereby increasing the functional deficit and recovery period. Paradoxically, many cellular and subcellular events occurring during the inflammatory response lead to the release of a plethora of growth factors that trigger the healing phase. Prostaglandins are implicated in the inflammatory process and may also contribute to the primary steps of tendon healing. Prolonged administration of non steroidal anti-inflammatory drugs (NSAIDs) is a common practice following musculoskeletal injuries. However, there is no clear consensus on the effect of NSAIDs on tendon healing. This review presents a contemporary vision of the inflammatory process following tendon injury and examines the roles of the constitutive and inducible COX-derived prostaglandins. The effect of COX inhibitors will be addressed and special attention will be taken to describe COX-independent effects of these pharmacological inhibitors. Together, this review is an attempt to guide readers toward a more conscientious use of NSAIDs following tendon injuries.     

Mechanical properties of human patellar tendon at the hierarchical levels of tendon and fibril

Tendons are strong hierarchical structures, but how tensile forces are transmitted between different levels remains incompletely understood. Collagen fibrils are thought to be primary determinants of whole tendon properties, and therefore we hypothesized that the whole human patellar tendon and its distinct collagen fibrils would display similar mechanical properties. Human patellar tendons (n = 5) were mechanically tested in vivo by ultrasonography. Biopsies were obtained from each tendon, and individual collagen fibrils were dissected and tested mechanically by atomic force microscopy. The Young's modulus was 2.0 ± 0.5 GPa, and the toe region reached 3.3 ± 1.9% strain in whole patellar tendons. Based on dry cross-sectional area, the Young's modulus of isolated collagen fibrils was 2.8 ± 0.3 GPa, and the toe region reached 0.86 ± 0.08% strain. The measured fibril modulus was insufficient to account for the modulus of the tendon in vivo when fibril content in the tendon was accounted for. Thus, our original hypothesis was not supported, although the in vitro fibril modulus corresponded well with reported in vitro tendon values. This correspondence together with the fibril modulus not being greater than that of tendon supports that fibrillar rather than interfibrillar properties govern the subfailure tendon response, making the fibrillar level a meaningful target of intervention. The lower modulus found in vitro suggests a possible adverse effect of removing the tissue from its natural environment. In addition to the primary work comparing the two hierarchical levels, we also verified the existence of viscoelastic behavior in isolated human collagen fibrils.