The current status of various preclinical therapeutic approaches for tendon repair.

Tendons are fibroblastic structures that link muscle and bone. There are two kinds of tendon injuries, including acute and chronic. Each form of injury or deterioration can result in significant pain and loss of tendon function. The recovery of tendon damage is a complex and time-consuming recovery process. Depending on the anatomical location of the tendon tissue, the clinical outcomes are not the same. The healing of the wound process is divided into three stages that overlap: inflammation, proliferation, and tissue remodeling. Furthermore, the curing tendon has a high re-tear rate. Faced with the challenges, tendon injury management is still a clinical issue that must be resolved as soon as possible. Several newer directions and breakthroughs in tendon recovery have emerged in recent years. This article describes tendon injury and summarizes recent advances in tendon recovery, along with stem cell therapy, gene therapy, Platelet-rich plasma remedy, growth factors, drug treatment, and tissue engineering. Despite the recent fast-growing research in tendon recovery treatment, still, none of them translated to the clinical setting. This review provides a detailed overview of tendon injuries and potential preclinical approaches for treating tendon injuries.

Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration.

Tendon adhesion is a common complication after tendon injury with the development of accumulated fibrotic tissues without effective anti-fibrotic therapies, resulting in severe disability. Macrophages are widely recognized as a fibrotic trigger during peritendinous adhesion formation. However, different clusters of macrophages have various functions and receive multiple regulation, which are both still unknown. In our current study, multi-omics analysis including single-cell RNA sequencing and proteomics was performed on both human and mouse tendon adhesion tissue at different stages after tendon injury. The transcriptomes of over 74 000 human single cells were profiled. As results, we found that SPP1+ macrophages, RGCC+ endothelial cells, ACKR1+ endothelial cells and ADAM12+ fibroblasts participated in tendon adhesion formation. Interestingly, despite specific fibrotic clusters in tendon adhesion, FOLR2+ macrophages were identified as an antifibrotic cluster by in vitro experiments using human cells. Furthermore, ACKR1 was verified to regulate FOLR2+ macrophages migration at the injured peritendinous site by transplantation of bone marrow from Lysm-Cre;R26RtdTomato mice to lethally irradiated Ackr1-/- mice (Ackr1-/- chimeras; deficient in ACKR1) and control mice (WT chimeras). Compared with WT chimeras, the decline of FOLR2+ macrophages was also observed, indicating that ACKR1 was specifically involved in FOLR2+ macrophages migration. Taken together, our study not only characterized the fibrosis microenvironment landscape of tendon adhesion by multi-omics analysis, but also uncovered a novel antifibrotic cluster of macrophages and their origin. These results provide potential therapeutic targets against human tendon adhesion.

The learning curve for minimally invasive Achilles repair using the "lumbar puncture needle and oval forceps" technique.

INTRODUCTION: An acute Achilles tendon rupture represents a common tendon injury, and its operative methods have been developed over the years. This study aimed to quantify the learning curve for the minimally invasive acute Achilles tendon rupture repair. METHODS: From May 2020 to June 2022, sixty-seven patient cases who received minimally invasive tendon repair were reviewed. Baseline data and operative details were collected. The cumulative summation (CUSUM) control chart was used for the learning curve analyses. Achilles tendon rupture score (ATRS), American Orthopedic Foot and Ankle Society (AOFAS) ankle/hindfoot score, and visual analog scale (VAS) at 3/6/9/12 months were calculated to assess the clinical outcomes. RESULTS: Thirty-six cases underwent at least a year of follow up and were enrolled in this study. The gender ratio and average age were 80.5% and 32.5 years. The linear equation fitted well (R2 = 0.95), and CUSUM for operative time peaked in the 12th case, which was divided into the learning phase (n = 12) and master phase (n = 24). No significant difference was detected between the two groups in clinical variables, except for the operative time (71.1 ± 13.2 min vs 45.8 ± 7.2 min, p = 0.004). Moreover, we detected one case with a suture reaction and treated it properly. CONCLUSION: Minimally invasive Achilles repair provides an opportunity for early rehabilitation. Notably, the learning curve showed that the "lumbar puncture needle and oval forceps" technique was accessible to surgeons.

[Effectiveness of Kirschner wire fixation for proximal phalangeal bone avulsion fracture caused by A2 circular trochlea injury of flexor digitorum tendon].

Objective: To explore the mechanism, surgical method, and effectiveness of proximal phalangeal bone avulsion fracture caused by A2 circular trochlea injury of the flexor digitorum tendon. Methods: A retrospective analysis was conducted on the clinical data of 4 patients with proximal phalangeal bone avulsion fracture caused by A2 circular trochlea injury of flexor digitorum tendon admitted between May 2018 and September 2022. The patients were all male, the age ranged from 26 to 52 years, with an average of 33 years. The injured fingers included 1 case of middle finger and 3 cases of ring finger. The causes of injury were rock climbing of 2 cases and carrying heavy objects of 2 cases. Preoperative anteroposterior and lateral X-ray films and CT examination of the fingers showed a lateral avulsion fracture of the proximal phalanx, with a fracture block length of 15-22 mm and a width of 3-5 mm. The total active range of motion (TAM) of the injured finger before operation was (148.75±10.11)°. The grip strength of the middle and ring fingers was (15.50±2.88) kg, which was significantly lower than that of the healthy side (50.50±7.93) kg ( t=-8.280, P<0.001). The time from injury to operation was 2-7 days, with an average of 3.5 days. One Kirschner wire with a diameter of 1.0 mm was used for direct fixation through the fracture block, while two Kirschner wires with a diameter of 1.0 mm were used for compression fixation against the fracture block. The fracture healing was observed, and the TAM of the injured finger and the grip strength of the middle and ring fingers were measured. The finger function was evaluated according to the upper limb functional assessment trial standards of the Chinese Medical Association Hand Surgery Society. Results: The incisions all healed by first intention after operation. All patients were followed up 6-28 months, with an average of 19 months. X-ray films showed that all avulsion fractures of proximal phalanx reached bony union, and the healing time ranged from 4 to 8 weeks, with an average of 4.6 weeks. At last follow-up, the grip strength of the middle and ring fingers was (50.50±7.76) kg, which significantly improved when compared with preoperative one ( t=-8.440, P<0.001). The TAM of the injured finger reached (265.50±2.08)°, and there was a significant difference when compared with preoperative one ( t=-21.235, P<0.001). According to the upper limb functional assessment trial standards of the Chinese Medical Association Hand Surgery Society, the finger function was all evaluated as excellent in 4 cases. Conclusion: Using Kirschner wire fixation through bone blocks and external compression fixation of bone blocks for treating proximal phalangeal bone avulsion fracture caused by A2 circular trochlear injury of the flexor digitorum tendon can achieve good effectiveness.

Extensor tendon rupture and preoperative mri confirmations of suture anchor prolapse: a case report and literature review.

BACKGROUND: While suture anchors are widely used in medical procedures for their advantages, they can sometimes lead to complications, including anchor prolapse. This article presents a unique case of suture anchor prolapse at the base of the distal phalanx of the little finger after extensor tendon rupture reconstruction surgery. CASE PRESENTATION: A 35-year-old male, underwent extensor tendon rupture reconstruction using a non-absorbable suture anchor. After seven years the patient visited our outpatients complaining of stiffness, pain, and protrusion at the surgical site. Initial X-ray imaging suggested suggesting either a fracture of the distal phalanx or tendon adhesion but lacked a definitive diagnosis. Subsequent magnetic resonance imaging (MRI) revealed bone connectivity between the middle and distal phalanges with irregular signal shadow and unclear boundaries while maintaining a regular finger shape. MRI proved superior in diagnosing prolapsed suture anchors, marking the first reported case of its kind. Surgical intervention confirmed MRI findings. CONCLUSIONS: Suture anchor complications, such as prolapse, are a concern in medical practice. This case underscores the significance of MRI for accurate diagnosis and the importance of tailored surgical management in addressing this uncommon complication.

[Ultrasound in sports traumatology]. / Ultraschall in der Sporttraumatologie.

Ultrasound (US) has numerous applications in sports traumatology. The technical progress of mobile US devices has led to increasing use of ultrasound as a primary diagnostic tool. New applications such as elastography and 3 D vascularization are used for special indications.The purpose of this review is to present the current status of ultrasound in the diagnosis of sports injuries and sport traumatology including established applications and new technical advances. US is presented both in its comparison to other imaging modalities and as a sole diagnostic tool.US can be used for initial diagnosis to improve the clinical examination and for intensive shortterm follow-up imaging. The main areas of application are currently the diagnosis of acute muscle and tendon injuries as well as overuse injuries. In particular, the exclusion of structural muscle injuries can be adequately ensured with US in the majority of anatomical regions. The recently published guideline on fracture ultrasound has strengthened the clinical evidence in this area, especially in comparison to conventional radiography and in the development of algorithms and standards. The increasing use of mobile ultrasound equipment with adequate image quality makes US a location-independent modality that can also be used at training sites or during road games.

Achilles Tendon Rupture.

There are many high-level studies comparing nonoperative treatment, open repair, and minimally invasive repair for Achilles tendon ruptures. This article summarizes the most up-to-date literature comparing these treatment options. The authors' preferred protocol for nonoperative treatment is discussed. Preferred techniques for open repair and chronic Achilles repair are discussed with reference to the literature.

In vivo study on the repair of rat Achilles tendon injury treated with non-thermal atmospheric-pressure helium microplasma jet.

Non-thermal atmospheric-pressure plasma (NTAPP) has been widely studied for clinical applications, e.g., disinfection, wound healing, cancer therapy, hemostasis, and bone regeneration. It is being revealed that the physical and chemical actions of plasma have enabled these clinical applications. Based on our previous report regarding plasma-stimulated bone regeneration, this study focused on Achilles tendon repair by NTAPP. This is the first study to reveal that exposure to NTAPP can accelerate Achilles tendon repair using a well-established Achilles tendon injury rat model. Histological evaluation using the Stoll's and histological scores showed a significant improvement at 2 and 4 weeks, with type I collagen content being substantial at the early time point of 2 weeks post-surgery. Notably, the replacement of type III collagen with type I collagen occurred more frequently in the plasma-treated groups at the early stage of repair. Tensile strength test results showed that the maximum breaking strength in the plasma-treated group at two weeks was significantly higher than that in the untreated group. Overall, our results indicate that a single event of NTAPP treatment during the surgery can contribute to an early recovery of an injured tendon.

The effect of papaverine on tendon healing and adhesion in rats following Achilles tendon repair.

OBJECTIVES: The study aimed to examine the histopathological and biomechanical effects of papaverine administered intraperitoneally and locally on Achilles tendon healing in a rat model. MATERIALS AND METHODS: Forty-eight adult male Sprague-Dawley rats (range, 300 to 400 g) were used in this study conducted between October and November 2022. The rats were divided into three groups, with each group further subdivided into two for sacrifice on either the 15th (early period) or 30th (late period) day after surgery. The first (control) group received no treatment following Achilles tendon repair, while papaverine was intraperitoneally administered every other day for 10 days in the second group and locally in the third group after surgery. On the 15th and 30th days, the rats were sacrificed, and their Achilles tendons were subjected to biomechanical testing and histopathological evaluation. RESULTS: Histopathologically, there were no significant differences among the groups on the 15th day. However, on the 30th day, the locally applied papaverine group exhibited superior histopathological outcomes compared to the control group (p<0.05). Concerning the highest tensile strength values before rupture, the biomechanical assessment showed that the group receiving local papaverine treatment in the early period and both the group with systemic papaverine treatment and the one with local papaverine treatment in the late period displayed a statistically significant advantage compared to the control group (p<0.05). CONCLUSION: Locally administered papaverine has positive biomechanical effects in the early period and exhibits a positive correlation both histopathologically and biomechanically in the late period. Novel therapeutic options may be provided for patients through these findings.

Biomechanical strength of triceps tendon repairs: systematic review and meta-regression analysis of human cadaveric studies.

PURPOSE: It is unclear which triceps tendon repair constructs and techniques produce the strongest biomechanical performance while minimizing the risk of gap formation and repair failure. We aimed to determine associations of construct and technique variables with the biomechanical strength of triceps tendon repairs. PubMed, Embase, Cochrane Library, Web of Science, Scopus, and ClinicalTrials.gov were systematically searched for peer-reviewed studies on biomechanical strength of triceps tendon repairs in human cadavers. 6 articles met the search criteria. Meta-regression was performed on the pooled dataset (123 specimens). Outcomes of interest included gap formation, failure mode, and ultimate failure load. Covariates were fixation type; number of implants; and number of sutures. Stratification by covariates was performed. We found no association between fixation type and ultimate failure load; however, suture anchor fixation was associated with less gap formation compared with transosseous direct repair (ß = - 1.1; 95% confidence interval [CI]:- 2.2, - 0.04). A greater number of implants was associated with smaller gap formation (ß = - 0.77; 95% CI: - 1.3, - 0.28) while a greater number of sutures was associated with higher ultimate failure load ( ß= 3; 95% CI: 21, 125). In human cadaveric models, the number of sutures used in triceps tendon repairs may be more important than the fixation type or number of implants for overall strength. If using a transosseous direct repair approach to repair triceps tendon tears, surgeons may choose to use more sutures in their repair in order to balance the risk of larger gap formation when compared to indirect repair techniques. LEVEL OF EVIDENCE: Level III.

Effect of cilostazol on healing of achilles tendon ruptures: an experimental study on rats.

PURPOSE: This study aimed to evaluate whether cilostazol (phosphodiesterase III inhibitor) could enhance the healing of Achilles tendon ruptures in rats. MATERIALS AND METHODS: The Achilles tendons of 24 healthy male adult rats were incised and repaired. The rats were randomly allocated to cilostazol and control groups. The cilostazol group received daily intragastric administration of 50 mg/kg cilostazol for 28 days, while the control group did not receive any medication. The rats were sacrificed on the 30th day, and the Achilles tendon was evaluated for biomechanical properties, histopathological characteristics, and immunohistochemical analysis. RESULTS: All rats completed the experiment. The Movin sum score of the control group was significantly higher (p = 0.008) than that of the cilostazol group, with means of 11 ± 0.63 and 7.50 ± 1.15, respectively. Similarly, the mean Bonar score was significantly higher (p = 0.026) in the control group compared to the cilostazol group (8.33 ± 1.50 vs. 5.5 ± 0.54, respectively). Moreover, the Type I/Type III Collagen ratio was notably higher (p = 0.016) in the cilostazol group (52.2 ± 8.4) than in the control group (34.6 ± 10.2). The load to failure was substantially higher in the cilostazol group than in the control group (p = 0.034), suggesting that the tendons in the cilostazol group were stronger and exhibited greater resistance to failure. CONCLUSIONS: The results of this study suggest that cilostazol treatment significantly improves the biomechanical and histopathological parameters of the healing Achilles tendon in rats. Cilostazol might be a valuable supplementary therapy in treating Achilles tendon ruptures in humans. Additional clinical studies are, however, required to verify these outcomes.

Aged Tendons Exhibit Altered Mechanisms of Strain-Dependent Extracellular Matrix Remodeling.

Aging is a primary risk factor for degenerative tendon injuries, yet the etiology and progression of this degeneration are poorly understood. While aged tendons have innate cellular differences that support a reduced ability to maintain mechanical tissue homeostasis, the response of aged tendons to altered levels of mechanical loading has not yet been studied. To address this question, we subjected young and aged murine flexor tendon explants to various levels of in vitro tensile strain. We first compared the effect of static and cyclic strain on matrix remodeling in young tendons, finding that cyclic strain is optimal for studying remodeling in vitro. We then investigated the remodeling response of young and aged tendon explants after 7 days of varied mechanical stimulus (stress deprivation, 1%, 3%, 5%, or 7% cyclic strain) via assessment of tissue composition, biosynthetic capacity, and degradation profiles. We hypothesized that aged tendons would show muted adaptive responses to changes in tensile strain and exhibit a shifted mechanical setpoint, at which the remodeling balance is optimal. Interestingly, we found that 1% cyclic strain best maintains native physiology while promoting extracellular matrix (ECM) turnover for both age groups. However, aged tendons display fewer strain-dependent changes, suggesting a reduced ability to adapt to altered levels of mechanical loading. This work has a significant impact on understanding the regulation of tissue homeostasis in aged tendons, which can inform clinical rehabilitation strategies for treating elderly patients.

Malvidin attenuates trauma-induced heterotopic ossification of tendon in rats by targeting Rheb for degradation via the ubiquitin-proteasome pathway.

The pathogenesis of trauma-induced heterotopic ossification (HO) in the tendon remains unclear, posing a challenging hurdle in treatment. Recognizing inflammation as the root cause of HO, anti-inflammatory agents hold promise for its management. Malvidin (MA), possessing anti-inflammatory properties, emerges as a potential agent to impede HO progression. This study aimed to investigate the effect of MA in treating trauma-induced HO and unravel its underlying mechanisms. Herein, the effectiveness of MA in preventing HO formation was assessed through local injection in a rat model. The potential mechanism underlying MA's treatment was investigated in the tendon-resident progenitor cells of tendon-derived stem cells (TDSCs), exploring its pathway in HO formation. The findings demonstrated that MA effectively hindered the osteogenic differentiation of TDSCs by inhibiting the mTORC1 signalling pathway, consequently impeding the progression of trauma-induced HO of Achilles tendon in rats. Specifically, MA facilitated the degradation of Rheb through the K48-linked ubiquitination-proteasome pathway by modulating USP4 and intercepted the interaction between Rheb and the mTORC1 complex, thus inhibiting the mTORC1 signalling pathway. Hence, MA presents itself as a promising candidate for treating trauma-induced HO in the Achilles tendon, acting by targeting Rheb for degradation through the ubiquitin-proteasome pathway.

Effect of platelet-rich plasma in Achilles tendon allograft in rabbits.

BACKGROUND: Achilles tendon is composed of dense connective tissue and is one of the largest tendons in the body. In veterinary medicine, acute ruptures are associated with impact injury or sharp trauma. Healing of the ruptured tendon is challenging because of poor blood and nerve supply as well as the residual cell population. Platelet-rich plasma (PRP) contains numerous bioactive agents and growth factors and has been utilized to promote healing in bone, soft tissue, and tendons. OBJECTIVE: The purpose of this study was to evaluate the healing effect of PRP injected into the surrounding fascia of the Achilles tendon after allograft in rabbits. METHODS: Donor rabbits (n = 8) were anesthetized and 16 lateral gastrocnemius tendons were fully transected bilaterally. Transected tendons were decellularized and stored at -80°C prior to allograft. The allograft was placed on the partially transected medial gastrocnemius tendon in the left hindlimb of 16 rabbits. The allograft PRP group (n = 8) had 0.3 mL of PRP administered in the tendon and the allograft control group (n = 8) did not receive any treatment. After 8 weeks, rabbits were euthanatized and allograft tendons were transected for macroscopic, biomechanical, and histological assessment. RESULTS: The allograft PRP group exhibited superior macroscopic assessment scores, greater tensile strength, and a histologically enhanced healing process compared to those in the allograft control group. CONCLUSIONS: Our results suggest administration of PRP on an allograft tendon has a positive effect on the healing process in a ruptured Achilles tendon.

Acute Patellar Tendon Ruptures: An Update on Management.

Patellar tendon ruptures can be debilitating injuries. When incomplete, partial tears can be managed nonsurgically with immobilization and progressive rehabilitation. Although complete ruptures remain a relatively uncommon injury, they portend a high level of morbidity. Ruptures typically result from an acute mechanical overload to the extensor mechanism, such as with forced quadriceps contraction and knee flexion. However, chronically degenerated tendons are also predisposed to failure from low-energy injuries. Diagnosis can often be made clinically with recognition of a palpable defect to the tendon, localized patellar tendon tenderness, and inability to actively extend the knee. Diagnosis and surgical planning can be established with radiograph, ultrasonography, or magnetic resonance imaging. Surgical repair is the mainstay of treatment, and there have been many recent advances in repair technique, optimal reconstruction strategies, and supplemental fixation. Time to surgery for complete tears remains the most important prognosticator for success. Direct primary repair can be completed with transosseous tunnels, suture anchor repair, or end-to-end repair. Tendon reconstruction can be achieved with or without mechanical or biologic augments. Rehabilitation programs vary in specifics, but return to sport can be expected by 6 months postoperatively.

Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair.

Tendons enable locomotion by transferring muscle forces to bones. They rely on a tough tendon core comprising collagen fibers and stromal cell populations. This load-bearing core is encompassed, nourished, and repaired by a synovial-like tissue layer comprising the extrinsic tendon compartment. Despite this sophisticated design, tendon injuries are common, and clinical treatment still relies on physiotherapy and surgery. The limitations of available experimental model systems have slowed the development of novel disease-modifying treatments and relapse-preventing clinical regimes. In vivo human studies are limited to comparing healthy tendons to end-stage diseased or ruptured tissues sampled during repair surgery and do not allow the longitudinal study of the underlying tendon disease. In vivo animal models also present important limits regarding opaque physiological complexity, the ethical burden on the animals, and large economic costs associated with their use. Further, in vivo animal models are poorly suited to systematic probing of drugs and multicellular, multi-tissue interaction pathways. Simpler in vitro model systems have also fallen short. One major reason is a failure to adequately replicate the three-dimensional mechanical loading necessary to meaningfully study tendon cells and their function. The new 3D model system presented here alleviates some of these issues by exploiting murine tail tendon core explants. Importantly, these explants are easily accessible in large numbers from a single mouse, retain 3D in situ loading patterns at the cellular level, and feature an in vivo-like extracellular matrix. In this protocol, step-by-step instructions are given on how to augment tendon core explants with collagen hydrogels laden with muscle-derived endothelial cells, tendon-derived fibroblasts, and bone marrow-derived macrophages to substitute disease- and injury-activated cell populations within the extrinsic tendon compartment. It is demonstrated how the resulting tendon assembloids can be challenged mechanically or through defined microenvironmental stimuli to investigate emerging multicellular crosstalk during disease and injury.

Establishment of a Mouse Degenerative Model of Patellar Tendinopathy with Upregulation of Inflammation.

There is no mouse model of patellar tendinopathy. This study aimed to establish a mouse inflammatory and degenerative patellar tendon injury model, which will facilitate research on patellar tendinopathy using advanced molecular tools including transgenic models. Collagenase at different doses (low dose (LD), medium dose (MD), high dose (HD)) or saline was injected over the mouse patellar tendon. At weeks 1, 2, 4, and 8 post-injection, the tendons were harvested for histology and further examined by micro-computed tomography (microCT) imaging at week 8. The optimal dose group and the saline group were further evaluated by immunohistochemical staining, gait pattern, and biomechanical properties. The histopathological score increased dose-dependently post-collagenase injection. Ectopic mineralization was observed and increased with collagenase dose. The LD group was selected for further analysis. The expression of IL-10, TNF-α, and MMP-1 significantly increased post-injection. The changes of limb idleness index (ΔLII) compared to preinjury state were significantly higher, while the ultimate load, stiffness, ultimate stress, and maximum Young's modulus were significantly lower in the LD group compared to the saline group. A mouse inflammatory degenerative model of patellar tendon injury resembling tendinopathy was established as indicated by the dose-dependent increase in tendon histopathology, ectopic calcification, decrease in biomechanical properties, and pain-associated gait changes.

Surgical treatment of patellar tendon rupture after total knee arthroplasty with a double-row repair method using the hamstring tendons: A novel technique with functional results.

BACKGROUND: Patellar tendon rupture (PTR) is extremely rare but serious complication after primary or revision total knee arthroplasty. Due to the serious failure rates of end-to-end repair techniques, various augmentation techniques have been described. In this study, the results of patients with PTR after reconstruction using our own technique with semitendinosus (ST) and gracilis tendons taken from the affected side were evaluated retrospectively. METHODS: A total of 14 patients, whose diagnosis was made based on physical examination and clinical findings, and supported radiologically (ultrasonography), were included in the study. In these patients, reconstruction was performed using double-row repair technique with the ST and gracilis tendons. Active-passive knee joint range of motion, active knee extension loss, and the Caton-Deschamps index at preoperative and final follow-up visits were compared. Tegner-Lysholm knee score and Kujala score were used to evaluate functional results. RESULTS: In 14 patients (8 women and 6 men) with a mean age of 68.1 years, the median time between injury and surgery was 6.6 weeks. In all patients, the rupture was in the distal part of the patellar tendon. While the median preoperative Caton-Deschamps index was 1.8, the postoperative median value was found to be 1.25 after an average follow-up of 3.8 years (P = .014). The median preoperative knee extension loss decreased from 25° to 5° postoperatively. Tegner-Lysholm knee score and Kujala score of the patients at their last follow-up were significantly increased (P < .01). CONCLUSION: For PTR developing after total knee arthroplasty, the double-row reconstruction technique with ST and gracilis tendons is effective.