Explore the vast range of titles available.

This study compared arthroscopic biceps tenodesis with biceps repair for isolated type II superior labrum anterior and posterior (SLAP) lesions in patients older than 35 years. The authors identified isolated type II SLAP lesions that were surgically managed over a 5-year period. Minimum 2-year follow-up data were available for 22 patients who underwent biceps repair (repair group) and for 15 patients who underwent a primary biceps tenodesis (tenodesis group). Mean age at surgery was 45.2±5.5 years in the repair group and 52.0±8.0 years in the tenodesis group. In the repair group, functional outcome improved from baseline to final follow-up using the American Shoulder and Elbow Surgeons (ASES) (47.5 to 87.4, respectively; P <.0001) and University of California, Los Angeles (UCLA) scores (18.5 to 31.2, respectively; P <.0001). In the tenodesis group, similar findings were observed for the ASES (43.4 to 89.9, respectively; P <.0001) and UCLA scores (19.0 to 32.7, respectively; P <.0001). No difference was found in functional outcome between the groups. Full range of motion recovery was delayed by approximately 3 months in the repair group compared with the tenodesis group ( P =.0631). Two patients in the repair group required a secondary capsular release. Seventy-seven percent of patients in the repair group and 100% of patients in the tenodesis group were satisfied and returned to normal activity ( P =.0673). In the current study, individuals older than 35 years with an isolated type II SLAP lesion had a shorter postoperative recovery, a more predictable functional outcome, and a higher rate of satisfaction and return to activity with a biceps tenodesis compared with a biceps repair. Based on these observations, biceps tenodesis is preferable to biceps repair for isolated type II SLAP lesions in nonoverhead athletes older than 35 years.

Categorical grading and other measurable MRI parameters are frequently utilised for predicting the outcome of hamstring injuries. However, the reliability and smallest detectable difference (SDD) have not been previously evaluated. It therefore remains unclear if the variability in previously reported results reflects reporting variation or actual injury status. 25 hamstring injuries were scored by two experienced radiologists using the Peetrons grading and specific prognostic MRI parameters: distance from ischial tuberosity (cm), extent (cranio to caudal, anterior to posterior, medial to lateral; (cm)), maximum cross-sectional area (%), volume (cm(3)) of the oedema. The interobserver and intraobserver reliability was calculated along with the SDDs for each scale variable. There were 3 Grade 0 (12%), 11 grade 1 (44%), 9 grade 2 (36%) and 2 grade 3 (8%) injuries. Cronbach's α values for grading were 1.00 (inter) and 0.96 (intra), respectively. The intraclass correlation coefficients for the prognostic MRI parameters were between 0.77 and 1.0. The SDDs varied between each parameter. Excellent interobserver and intraobserver reliability was found for grading and prognostic MRI parameters in acute hamstring injuries. In daily practice and research, we can be confident that scoring hamstring injuries by experienced radiologists is reproducible. The documented SDDs allow meaningful clinical inferences to be made when assessing observed and reported changes in MRI status.

Background Controversy exists regarding the optimal treatment for acute Achilles tendon ruptures. Conservative and surgical treatments have been reported with variable results and complications rates. The purpose of this study is to compare the postoperative clinical and functional results of percutaneous versus open repair of acute Achilles tendon ruptures. Materials and methods We present 34 patients with acute Achilles tendon ruptures treated with open and percutaneous surgical repair. There were 15 patients who had open surgical repair and 19 patients who had percutaneous repair. The mean follow-up was 22 months (range 10–24 months) for the open repair group and 20 months (range 9–24 months) for the percutaneous repair group; no patient was lost to follow-up. Postoperative rehabilitation was the same for both groups. Wound healing, complications, ankle range of motion, and patients’ return to work, activity level, weight-bearing, and subjective assessment of their treatment were recorded. Results No significant difference was observed with respect to any of the examined variables between the open and percutaneous repair groups. Tendon healing was observed in all patients of both groups by 7–9 weeks. The mean time of patients’ return to work was 7 weeks for the open repair group and 9 weeks for the percutaneous repair group. All patients were capable of full weight bearing by the 8th postoperative week time; the time to return to previous activities including non-contact sports was 5 months for both groups. All patients expressed satisfaction and graded their treatment as good. As expected, cosmetic appearance was significantly better in the percutaneous repair group. One patient who had open repair experienced skin incision pain and dysesthesia and graded his operation as fair. No patient experienced other complications such as re-rupture, infection, sural neuroma, or Achilles tendinitis within the period of this study. Conclusions The present study showed similarly successful clinical and functional results after both open and percutaneous repair of acute Achilles tendon ruptures are similar. Cosmetic appearance is superior in the group of patients who had a percutaneous treatment.

Rotator cuff (RC) tears have a high prevalence, and RC repair surgery is frequently performed. Evaluation of deltoid activation has been reported as an easy to measure proxy for RC functionality. Our goal was to test the success of RC repair in restoring muscle function, by assessing deltoid activation with varying arm abduction moment loading tasks in controls and in RC tear patients before and 1 year after RC repair. Averaged rectified electromyography recordings (rEMG) of the deltoid during 2-s isometric arm abduction tasks were assessed in 22 controls and 33 patients before and after RC repair. Changes in deltoid activation as a response to increased arm abduction moment loading (large vs. small moment), without changing task force magnitude, were expressed as: R  = (rEMG Large  − rEMG Small )/(rEMG Large  + rEMG Small ), where R  > 0 indicates an increase in muscle activation with larger moment loading. In controls, a significant increase in deltoid activation was observed with large abduction moment loading: R  = 0.11 (95 % CI 0.06–0.16). In patients, R was larger: 0.20 (95 % CI 0.13–0.27) preoperatively and 0.16 (95 % CI 0.09–0.22) postoperatively. Increased compensatory deltoid activation was found in pre-operative RC tear patients. The post-operative decrease in compensatory deltoid activation, although not significant, could indicate (partially) restored RC function in at least some patients.

Achilles tendon rupture (ATR) alters stiffness of the tendon and other structures within the triceps surae muscle–tendon unit. Although stiffness of the tendon has been studied after rupture, regional adaptations of the medial gastrocnemius (MG) muscle and aponeurosis mechanical properties are unknown. Therefore, we assessed changes in MG muscle and aponeurosis shear wave (SW) velocity and morphology during a 1-year follow-up after unilateral ATR. Twenty-three (17 males, 6 females) participants were assessed for SW velocity of MG muscle and aponeurosis and morphological properties at 2, 6 and 12 months at rest. Linear mixed models were used to investigate the differences between limbs at different time points, and partial correlations controlled for age to explore associations between SW velocity and morphological properties. Regional SW stiffness of the injured MG muscle and aponeurosis were lower at 2 months but recovered by 6 months after ATR. When comparing limbs, MG muscle and aponeurosis SW velocity were lower in the injured limb at 2 months with a mean difference of −0.34 m/s (−0.48 to −0.21 m/s, t = -5.10), and −1.6 m/s (−2.39 to 0.89 m/s, t = 4.38). SW velocity did not differ at the muscle or aponeurosis between limbs at 6 or 12 months. Fascicle length of the MG muscle was negatively correlated with SW velocity of the MG muscle (r = -0.25, p = 0.041) and positively correlated with aponeurosis SW velocity (r = 0.29, p = 0.018). The remodelling of the MG muscle to shorter fascicles might help to enhance stiffness and maintain tension at the muscle.

Background Peritendinous adhesion is among the common complications after tendon injury. Numerous studies have been carried out to prevent its formation, including modifications of surgical procedures, postoperative cares, application of medicines, etc. This study dynamically monitored fluctuations of inflammation, state of oxidative stress, and histopathologic changes around injured tendon to provide theoretical basis for further exploration in mechanisms of peritendinous adhesion formation. Methods Eighteen mature Sprague-Dawley male rats were randomly allocated into 6 equal groups. Compared with control and sham group, every rat’s right hind Achilles tendon in experimental groups was cut and repaired by the modified Kessler technique. Besides control and sham group, samples of tendon margin and serum were collected at different time points after the surgery. Content of TNF-α, IL-1β, and TGF-β were assayed in harvested serum. Reactive oxygen species (ROS) were detected, expression levels of related genes (IL-1β, IL-6, SOD1, SOD2, COL1, HIF1A) were quantified by qPCR, and various histopathological evaluations were performed. Results Indicators (TNF-α, IL-1β, TGF-β1, ROS) were noticed to have a similar trend of significant rising 24 h after the surgery except TGF-β which was rising 72 h later. So were the expression trends of IL-1β, IL-6, SOD1, SOD2, and COL1. HIF1A, inversely correlated with SOD2, showed the progressive relief of regional tissue hypoxia. Histological evaluation showed the same tendency that fibrosis and inflammation were getting serious 48 h later after the surgery. Conclusions Inflammation, oxidative stress in injured tendon resulted from acute trauma, would be getting intense in 24 h. Peritendinous adhesion emerges and aggravates after 48 h. Thus, prompt efficient measures are advised to be taken after the injury as soon as possible.

Flexor tendon injuries are common and heal poorly owing to both the deposition of function-limiting peritendinous scar tissue and insufficient healing of the tendon itself. Therapeutic options are limited due to a lack of understanding of the cell populations that contribute to these processes. Here, we identified the epitenon as a major source of cells that contribute to both peritendinous fibrosis and regenerative tendon healing following acute tendon injury. Using a combination of genetic lineage tracing and single cell RNA-sequencing (scRNA-seq), we profiled the behavior and contributions of each cell fate to the healing process in a spatio-temporal manner. Integrated scRNA-seq analysis of mouse healing with human peritendinous scar tissue revealed remarkable transcriptional similarity between mouse epitenon-derived cells and fibroblasts present in human peritendinous scar tissue, which was further validated by immunofluorescent staining for conserved markers. Finally, ablation of pro-fibrotic epitenon-derived cells post-tendon injury significantly improved functional recovery. Combined, these results clearly identify the epitenon as the cellular origin of an important progenitor cell population that could be leveraged to improve tendon healing. The cell populations that contribute to healing and scar tissue formation following tendon injury are poorly defined. Here the authors show that cells originating from the tendon epitenon give rise to both tenogenic and fibrotic populations and that ablation of pro-fibrotic epitenon-derived cells improves recovery.

Both acute and chronic tendon injuries are disabling sports medicine problems with no effective treatment at present. Sustained oxidative stress has been suggested as the major factor contributing to fibrosis and adhesion after acute tendon injury as well as pathological changes of degenerative tendinopathy. Numerous in vitro and in vivo studies have shown that the inhibition of oxidative stress can promote the tenogenic differentiation of tendon stem/progenitor cells, reduce tissue fibrosis and augment tendon repair. This review aims to systematically review the literature and summarize the clinical and pre-clinical evidence about the potential relationship of oxidative stress and tendon disorders. The literature in PubMed was searched using appropriate keywords. A total of 81 original pre-clinical and clinical articles directly related to the effects of oxidative stress and the activators or inhibitors of oxidative stress on the tendon were reviewed and included in this review article. The potential sources and mechanisms of oxidative stress in these debilitating tendon disorders is summarized. The anti-oxidative therapies that have been examined in the clinical and pre-clinical settings to reduce tendon fibrosis and adhesion or promote healing in tendinopathy are reviewed. The future research direction is also discussed.

Current stem cell-based strategies for tissue regeneration involve ex vivo manipulation of these cells to confer features of the desired progenitor population. Recently, the concept that endogenous stem/progenitor cells could be used for regenerating tissues has emerged as a promising approach that potentially overcomes the obstacles related to cell transplantation. Here we applied this strategy for the regeneration of injured tendons in a rat model. First, we identified a rare fraction of tendon cells that was positive for the known tendon stem cell marker CD146 and exhibited clonogenic capacity, as well as multilineage differentiation ability. These tendon-resident CD146+ stem/progenitor cells were selectively enriched by connective tissue growth factor delivery (CTGF delivery) in the early phase of tendon healing, followed by tenogenic differentiation in the later phase. The time-controlled proliferation and differentiation of CD146+ stem/progenitor cells by CTGF delivery successfully led to tendon regeneration with densely aligned collagen fibers, normal level of cellularity, and functional restoration. Using siRNA knockdown to evaluate factors involved in tendon generation, we demonstrated that the FAK/ERK1/2 signaling pathway regulates CTGF-induced proliferation and differentiation of CD146+ stem/progenitor cells. Together, our findings support the use of endogenous stem/progenitor cells as a strategy for tendon regeneration without cell transplantation and suggest this approach warrants exploration in other tissues.

Mechanical injury to connective tissue causes changes in collagen structure and material behaviour, but the role and mechanisms of molecular damage have not been established. In the case of mechanical subfailure damage, no apparent macroscale damage can be detected, yet this damage initiates and potentiates in pathological processes. Here, we utilize collagen hybridizing peptide (CHP), which binds unfolded collagen by triple helix formation, to detect molecular level subfailure damage to collagen in mechanically stretched rat tail tendon fascicle. Our results directly reveal that collagen triple helix unfolding occurs during tensile loading of collagenous tissues and thus is an important damage mechanism. Steered molecular dynamics simulations suggest that a likely mechanism for triple helix unfolding is intermolecular shearing of collagen α-chains. Our results elucidate a probable molecular failure mechanism associated with subfailure injuries, and demonstrate the potential of CHP targeting for diagnosis, treatment and monitoring of tissue disease and injury. Collagen denaturation is thought to occur during tissue mechanical damage, but its role in damage initiation is still unclear. Here, the authors use a collagen hybridizing peptide to provide insights into the molecular mechanisms leading to collagen unfolding during tendon mechanical stretch.