The October 2024 Shoulder & Elbow Roundup360 looks at: Proximal humeral fractures with vascular compromise; Outcomes and challenges of revision arthroscopic rotator cuff repair: a systematic review; Evaluating treatment effectiveness for lateral elbow tendinopathy: a systematic review and network meta-analysis; Tendon transfer techniques for irreparable subscapularis tears: a comparative review; Impact of subscapularis repair in reverse shoulder arthroplasty; Isolated subscapularis tears strongly linked to shoulder pseudoparesis; Nexel and Coonrad-Morrey total elbow arthroplasties show comparable revision rates in New Zealand study; 3D MRI matches 3D CT in assessing bone loss and shoulder morphology in dislocation cases

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A local injection may be used as an early option in the treatment of Morton’s neuroma, and can be performed using various medications. The aim of this study was to compare the effects of injections of hyaluronic acid compared with corticosteroid in the treatment of this condition.

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Rotator cuff disease (RCD) can considerably decrease quality of life. Here, we investigated whether health-related quality of life (HRQoL) influences the need for surgery in patients with RCD.

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Rotator cuff tear (RCT) is the leading cause of shoulder pain, primarily associated with age-related tendon degeneration. This study aimed to elucidate the potential differential gene expressions in tendons across different age groups, and to investigate their roles in tendon degeneration.

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Steroid injections are used for subacromial pain syndrome and can be administered via the anterolateral or posterior approach to the subacromial space. It is not currently known which approach is superior in terms of improving clinical symptoms and function. This is the protocol for a randomized controlled trial (RCT) to compare the clinical effectiveness of a steroid injection given via the anterolateral or the posterior approach to the subacromial space.

Rotator cuff pathology is the main cause of shoulder pain and dysfunction in older adults. When a rotator cuff tear involves the subscapularis tendon, the symptoms are usually more severe and the prognosis after surgery must be guarded. Isolated subscapularis tears represent 18% of all rotator cuff tears and arthroscopic repair is a good alternative primary treatment. However, when the tendon is deemed irreparable, tendon transfers are the only option for younger or high-functioning patients. The aim of this review is to describe the indications, biomechanical principles, and outcomes which have been reported for tendon transfers, which are available for the treatment of irreparable subscapularis tears.

The best tendon to be transferred remains controversial. Pectoralis major transfer was described more than 30 years ago to treat patients with failed surgery for instability of the shoulder. It has subsequently been used extensively to manage irreparable subscapularis tendon tears in many clinical settings. Although pectoralis major reproduces the position and orientation of the subscapularis in the coronal plane, its position in the axial plane – anterior to the rib cage – is clearly different and does not allow it to function as an ideal transfer. Consistent relief of pain and moderate recovery of strength and function have been reported following the use of this transfer. In an attempt to improve on these results, latissimus dorsi tendon transfer was proposed as an alternative and the technique has evolved from an open to an arthroscopic procedure. Satisfactory relief of pain and improvements in functional shoulder scores have recently been reported following its use. Both pectoralis minor and upper trapezius transfers have also been used in these patients, but the outcomes that have been reported do not support their widespread use.

Cite this article: Bone Joint J 2024;106-B(9):970–977.

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The antidiabetic agent metformin inhibits fibrosis in various organs. This study aims to elucidate the effects of hyperglycaemia and metformin on knee joint capsule fibrosis in mice.

Aims. Achilles tendon re-rupture (ATRR) poses a significant risk of postoperative complication, even after a successful initial surgical repair. This study aimed to identify risk factors associated with Achilles tendon re-rupture following operative fixation. Methods. This retrospective cohort study analyzed a total of 43,287 patients from national health claims data spanning 2008 to 2018, focusing on patients who underwent surgical treatment for primary Achilles tendon rupture. Short-term ATRR was defined as cases that required revision surgery occurring between six weeks and one year after the initial surgical repair, while omitting cases with simultaneous infection or skin necrosis. Variables such as age, sex, the presence of Achilles tendinopathy, and comorbidities were systematically collected for the analysis. We employed multivariate stepwise logistic regression to identify potential risk factors associated with short-term ATRR. Results. From 2009 to 2018, the short-term re-rupture rate for Achilles tendon surgeries was 2.14%. Risk factors included male sex, younger age, and the presence of Achilles tendinopathy. Conclusion. This large-scale, big-data study reaffirmed known risk factors for short-term Achilles tendon re-rupture, specifically identifying male sex and younger age. Moreover, this study discovered that a prior history of Achilles tendinopathy emerges as an independent risk factor for re-rupture, even following initial operative fixation. Cite this article: Bone Joint Res 2024;13(7):315–320

Aim. Our collaborative study aims to demonstrate that acute partial Achilles Tendon Tears (ATTs) are not separate diagnostic entities from full ATTs. and should be thought of as a continuum rather than binary partial or full. Methods. We pooled anonymised data from four hospitals, identifying patients with acute partial ATTs on USS reports from 2019–2021. Patients were only included if they had an acute injury and no previous background Achilles tendinopathy. Results. 91 patients had acute partial ATTs reported on USS. 74/91 (81%) of patients had clinical findings in keeping with a full ATT (positive Simmonds test, palpable gap). 88/91 (97%) of patients were managed according to local full ATT protocols. 2 patients had MRIs – one showed no tear, the other showed a full rupture. 2 patients underwent surgical repair and both intra-operatively were found to have full ATTs. Conclusion. Our regional data suggests that a significant proportion (81%) of USS diagnosed partial ATTs may in fact be misdiagnosed full ATTs. All injuries clinically suspicious for an ATT should be managed according to local Achilles Protocol. USS is useful to diagnose the presence or absence of a tear but is not good at differentiating partial vs full tear. There is significant tendon end fibrillation and overlap on USS of an acute full ATT, which can give the impression of a partial ATT. More research is needed into whether any threshold exists to support the current distinction of “partial” and “full” as relates to management and outcomes

Introduction. Achilles tendon rupture (ATR) account for 10.7% of all tendon and ligament injuries and causes lasting muscular deficits and have a profound impact on patients’ quality of life. 1,2. The incidence, characteristics and management of ATR in the United Kingdom is poorly understood. Method. Data was collected prospectively from University Hospitals of Leicester Emergency Department (ED) between January 2016 and December 2020 and analysed retrospectively. The medical records were reviewed to determine management protocols (surgical/non-surgical) and limited mobilisation (VACOped™ boot) duration. Leicestershire population data was taken from Leicestershire County Council demography report. Findings. 277 individuals were diagnosed with an ATR during the 4-year period. The mean (SD) annual incidence was 56 (±6) ATR. An incidence rate of 8.02 per 100,000 people per annum. The average characteristics of those experiencing an ATR is male (78.3%), 46.8yrs old (±14.4), body mass index 29.1 (±6.3). Median (IQR) number of comorbidities 1 (2) and duration to present to ED was 0 days (1). The main mechanism of rupture was sporting activity (62.1%). 97.4% were non-surgically managed using a limited mobilisation boot (VACOped). The boot was worn for an average of 62.6 days (±8.9). 94 participants provided pre-ATR Achilles symptoms data. 16% (n=15/94) of participants reported a previous contralateral ATR. 7.4% reported a re-rupture (n=7/94). 15.4% (n=14/91) reported an Achilles tendinopathy on the ipsilateral side prior to ATR. 7.7% (n=7/91) reported bilateral Achilles tendinopathy and 1.1% (n=1/91) reported contralateral Achilles tendinopathy prior to ATR. Conclusion. The incidence of ATR is 8.02 cases per 100,000 people per annum. This is the first UK data on ATR incidence. Most ATR were managed non-surgically in this cohort. The majority of ruptures occurred during sporting activity. Those that had previous Achilles symptoms (24.2%) indicate tendons are not always asymptomatic prior to ATR

The June 2024 Foot & Ankle Roundup. 360. looks at: First MTPJ fusion in young versus old patients; Minimally invasive calcaneum Zadek osteotomy and the effect of sequential burr passes; Comparison between Achilles tendon reinsertion and dorsal closing wedge calcaneal osteotomy for the treatment of insertional Achilles tendinopathy; Revision ankle arthroplasty – is it worthwhile?; Tibiotalocalcaneal arthrodesis or below-knee amputation – salvage or sacrifice?; Fusion or replacement for hallux rigidus?

Tendinopathy can commonly occur around the foot and ankle resulting in isolated rupture, debilitating pain and degenerative foot deformity. The pathophysiology and key cells involved are not fully understood. This is partly because the dense collagen matrix that surrounds relatively few resident cells limits the ability of previous techniques to identify and target those cells of interest. In this study, we apply novel single cell RNA sequencing (CITE-Seq) techniques to healthy and tendinopathic foot/ankle tendons. For the first time we have identified multiple sub-populations of cells in human tendons. These findings challenge the view that there is a single principal tendon cell type and open new avenues for further study. Healthy tendon samples were obtained from patients undergoing tendon transfer procedures; including tibialis posterior and FHL. Diseased tendon samples were obtained during debridement of intractable Achilles and peroneal tendinopathy, and during fusion of degenerative joints. Single cell RNA sequencing with surface proteomic analysis identified 10 sub-populations of human tendon derived cells. These included groups expressing genes associated with fibro-adipogenic progenitors (FAPs) as well as ITGA7+VCAM1- recently described in mouse muscle but, as yet, not human tendon. In addition we have identified previously unrecognised sub-classes of collagen type 1 associated tendon cells. Each sub-class expresses a different set of extra-cellular matrix genes suggesting they each play a unique role in maintaining the structural integrity of normal tendon. Diseased tendon harboured a greater proportion of macrophages and cytotoxic lymphocytes than healthy tendon. This inflammatory response is potentially driven by resident tendon fibroblasts which show increased expression of pro-inflammatory cytokines. Finally, identification of a previously unknown sub-population of cells found predominantly in tendinopathic tissue offers new insight into the underlying pathophysiology. Further work aims to identify novel proteins targets for possible therapeutic pathways

Gluteal Tendinopathy is a poorly understood condition that predominantly affects post-menopausal women. It causes lateral hip pain, worse when lying on the affected side or when walking up a hill or stairs. It has been labelled ˜Greater Trochanteric Pain Syndrome” a name that recognises the lack of understanding of the condition. Surgical reconstruction of the gluteal cuff is well established and has been undertaken numerous times over the last 16 years by the senior author (AJL). However, the quality of collagen in the tendons can be very poor and this leads to compromised results. We present the results of gluteal cuff reconstruction combined with augmentation using a bioinductive implant. 14 patients (11 female, 3 male; mean age 74.2 ± 6.3 years) with significant symptoms secondary to gluteal tendinopathy that had failed conservative treatment (ultrasound guided injection and structured physiotherapy) underwent surgical reconstruction by the senior author using an open approach. In all cases the iliotibial band was lengthened and the trochanteric bursa excised. The gluteal cuff was reattached using Healicoil anchors (3–5×4.75mm anchors; single anchors but double row repair) and then augmented using a Regeneten patch. Patients were mobilised fully weight bearing post-operatively but were asked to use crutches until they were no longer limping. All had structured post-surgery rehabilitation courtesy of trained physiotherapists. There were no post-operative complications and all patients reported an improvement in pain levels (Visual Analogue Scale 7.8 pre-op; 2.6 post-op) and functional levels (UCLA Activity Score 3.5 pre-op; 7.1 post-op) at 6 months post surgery. Surgery for gluteal tendinopathy produces good outcomes and the use of Regeneten as an augment for poor quality collagen is seemingly a safe, helpful addition. Further comparative studies would help clarify this

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Mechanical impingement of the iliopsoas (IP) tendon accounts for 2% to 6% of persistent postoperative pain after total hip arthroplasty (THA). The most common initiator is anterior acetabular component protrusion, where the anterior margin is not covered by anterior acetabular wall. A CT scan can be used to identify and measure this overhang; however, no threshold exists for determining symptomatic anterior IP impingement due to overhang. A case-control study was conducted in which CT scan measurements were used to define a threshold that differentiates patients with IP impingement from asymptomatic patients after THA.

The February 2024 Shoulder & Elbow Roundup³⁶⁰ looks at: Does indomethacin prevent heterotopic ossification following elbow fracture fixation?; Arthroscopic capsular shift in atraumatic shoulder joint instability; Ultrasound-guided lavage with corticosteroid injection versus sham; Combined surgical and exercise-based interventions following primary traumatic anterior shoulder dislocation: a systematic review and meta-analysis; Are vascularized fibula autografts a long-lasting reconstruction after intercalary resection of the humerus for primary bone tumours?; Anatomical versus reverse total shoulder arthroplasty with limited forward elevation; Tension band or plate fixation for simple displaced olecranon fractures?; Is long-term follow-up and monitoring in shoulder and elbow arthroplasty needed?

The rotator cuff tendinopathy is one of the most common shoulder problems leading to full-thickness rotator cuff tendon tear and, eventually, to degenerative arthritis. Recent research on rotator cuff tendon degeneration has focused on its relationship to cell death. The types of cell death known to be associated with rotator cuff tendon degeneration are apoptosis, necrosis, and autophagic cell death. The increased incidence of cell death in degenerative tendon tissue may affect the rates of collagen synthesis and repair, possibly weakening tendon tissue and increasing the risk of tendon rupture. The biomolecular mechanisms of the degenerative changes leading to apoptotic cell death in rotator cuff tenofibroblasts have been identified as oxidative-stress-related cascade mechanisms. Furthermore, apoptosis, necrosis, and autophagic cell death are all known to be mediated by oxidative stress, a condition in which ROS (reactive oxygen species) are overproduced. Lower levels of oxidative stress trigger apoptosis; higher levels mediate necrosis. Although the signaltransduction pathway leading to autophagy has not yet been fully established, ROS are known to be essential to autophagy. A neuronal theory regarding rotator cuff degeneration has been developed from the findings that glutamate, a neural transmitter, is present in increased concentrations in tendon tissues with tendinopathy and that it induces rat supraspinatus tendon cell death. Recent studies have reported that hypoxia involved in rotator cuff tendon degeneration. Because antioxidants are known to scavenge for intracellular ROS, some studies have been conducted to determine whether antioxidants can reduce cell death in rotator cuff tendon-origin fibroblasts. The first study reported that an antioxidant has the ability to reduce apoptosis in oxidative-stressed rotator cuff tenofibroblasts. The second study reported that antioxidants have both antiapoptotic effects and antinecrotic effects on rotator cuff tendon-origin fibroblasts exposed to an oxidative stimulus. The third study reported that an antioxidant has antiautophagic-cell-death effects on rotator cuff tendon-origin fibroblasts exposed to an oxidative stimulus. The fourth study reported that glutamate markedly increases cell death in rotator cuff tendonorigin fibroblasts. The glutamate-induced cytotoxic effects were reduced by an antioxidant, demonstrating its cytoprotective effects against glutamate-induced tenofibroblast cell death. The fifth study reported that hypoxia significantly increases intracellular ROS and apoptosis. The hypoxia-induced cytotoxic effects were markedly attenuated by antioxidants, demonstrating their cytoprotective effects against hypoxia-induced tenofibroblast cell death. In conclusion, antioxidants have cytoprotective effects on tenofibroblasts exposed in vitro to an oxidative stressor, a neurotransmitter, or hypoxia. These cytoprotective effects result from antiapoptotic, antinecrotic, and antiautophagic actions involving the inhibition of ROS formation. These findings suggest that antioxidants may have therapeutic potential for rotator cuff tendinopathy. Further studies must be conducted in order to apply these in vitro findings to clinical situations

Stem cells represent an exciting biological therapy for the management of many musculoskeletal tissues that suffer degenerative disease and/or where the reparative process results in non-functional tissue (‘failed healing’). The original hypothesis was that implanted cells would differentiate into the target tissue cell type and synthesise new matrix. However, this has been little evidence that this happens in live animals compared to the laboratory, and more recent theories have focussed on the immunomodulatory effects via the release of paracrine factors that can still improve the outcome, especially since inflammation is now considered one of the central processes that drive poor tendon healing. Because of the initial ‘soft’ regulatory environment for the use of stem cells in domestic mammals, bone and fat-derived stem cells quickly established themselves as a useful treatment for naturally occurring musculoskeletal diseases in the horse more than 20 years ago (Smith, Korda et al. 2003). Since the tendinopathy in the horse has many similarities to human tendinopathy, we propose that the following challenges and, the lessons learnt, in this journey are highly relevant to the development of stem cells therapies for human tendinopathy:. Source – while MSCs can be recovered from many tissues, the predominant sources for autologous MSCs have been bone and fat. Other sources, including blood, amnion, synovium, and dental pulp have also been commercialised for allogenic treatments. Preparation – ex vivo culture requires transport from a licensed laboratory while ‘minimally manipulated’ preparations can be prepared patient-side. Cells also need a vehicle for transport and implantation. Delivery – transport of cells from the laboratory to the clinic for autologous ex vivo culture techniques; implantation technique (usually by ultrasound-guided injection to minimise damage to the cells (or, more rarely, incorporated into a scaffold). They can also be delivered by regional perfusion via venous or arterial routes. Retention – relatively poor although small numbers of cells do survive for at least 5 months. Immediate loss to the lungs if the cells are administered via vascular routes. Synovially administered cells do not engraft into tendon. Adverse effects – very safe although needle tracts often visible (but do not seen to adversely affect the outcome). Allogenic cells require careful characterisation for MHC Class II antigens to avoid anaphylaxis or reduced efficacy. Appropriate injuries to treat – requires a contained lesion when administered via intra-lesional injection. Intrasynovial tendon lesions are more often associated with surface defects and are therefore less appropriate for treatment. Earlier treatment appears to be more effective than delayed, when implantation by injection is more challenging. Efficacy - beneficial effects shown at both tissue and whole animal (clinical outcome) level in naturally-occurring equine tendinopathy using bone marrow-derived autologous MSCs Recent (licenced) allogenic MSC treatment has shown equivalent efficacy while intra-synovial administration of MSCs is ineffective for open intra-synovial tendon lesions. Regulatory hurdles – these have been lighter for veterinary treatments which has facilitated their development. There has been greater regulation of commercial allogenic MSC preparations which have required EMA marketing authorisation

MicroRNA (miR) delivery to regulate chronic inflammation hold extraordinary promise, with new therapeutic possibilities emanating from their ability to fine-tune multiple target gene regulation pathways which is an important factor in controlling aberrant inflammatory reactions in complex multifactorial disease. However, several hurdles have prevented advancements in miR-based therapies. These include off-target effects of miRs, limited trafficking, and inefficient delivery. We propose a magnetically guided nanocarrier to transport therapeutically relevant miRs to assist self- resolving inflammation processes at injury sites and reduce the impact of chronic inflammation- related diseases such as tendinopathies. The high prevalence, significant socio-economic burden and increasing recognition of dysregulated immune mediated pathways in tendon disease provide a compelling rationale for exploring inflammation-targeting strategies as novel treatments in this condition. By combining cationic polymers, miR species (e.g., miR 29a, miR155 antagonist), and magnetic nanoparticles in the form of magnetoplexes with highly efficient magnetofection procedures, we developed inexpensive, easy-to-fabricate, and biocompatible systems with competent miR-binding and fast cellular uptake into different types of human cells, namely macrophages and tendon-derived cells. The system was shown to be cell-compatible and to successfully modulate the expression and production of inflammatory markers in tendon cells, with evidence of functional pro-healing changes in immune cell phenotypes. Hence, magnetoplexes represent a simple, safe, and non-viral nanoplatform that enables contactless miR delivery and high- precision control to reprogram cell profiles toward improved pro-regenerative environments. Acknowledgements: ERC CoG MagTendon No.772817; FCT Doctoral Grant SFRD/BD/144816/2019, and TERM. RES Hub (Norte-01-0145-FEDER-022190)

Tendinopathy is the most common form of chronic tendon disorders, accounting for up 30% of all musculoskeletal clinic visits [1]. In tendon disease, the largely avascular tendon tissue often becomes hypervascularized and fibrotic [2]. As blood vessel growth and angiogenic signaling molecules are often induced by the lack of adequate nutrients and oxygen, hypoxic signaling is speculated to be a root cause of tendon neovascularization and tendinopathy [3,4,5]. However, how the vascular switch is initiated in tendons, and how vascularization contributes to tendon pathology remains unknown. In this talk, we provide evidence that HIF-1α is implicated in tendon disease and HIF-1α stabilization in human tendon cells induces vascular recruitment of endothelial cells via VEGFa secretion. More interesting, HIF-1α stabilization in tendon cells in vivo, seems to recapitulate all main features of fibrotic human tendon disease, including vascular ingrowth, matrix disorganization, changes in tissue mechanics, cell proliferation and innervation. Surprisingly, in vivo knock-out of VEGFa rescued angiogenesis in the tendon core but it did not affect tendon mechanical properties and tissue pathophysiological changes, suggesting that blood vessels ingrowth might not be a primary cause but a consequence of HIF-1α activation

Tendons are characterised by an inferior healing capacity when compared to other tissues, ultimately resulting in the formation of a pathologically altered extracellular matrix structure. Although our understanding of the underlying causes for the development and progression of tendinopathies remains incomplete, mounting evidence indicates a coordinated interplay between tendon-resident cells and the ECM is critical. Our recent results demonstrate that the matricellular protein SPARC (Secreted protein acidic and rich in cysteine) is essential for regulating tendon tissue homeostasis and maturation by modulating the tissue mechanical properties and aiding in collagen fibrillogenesis [1,2]. Consequently, we speculate that SPARC may also be relevant for tendon healing. In a rat patellar tendon window defect model, we investigated whether the administration of recombinant SPARC protein can modulate tendon healing. Besides the increased mRNA expression of collagen type 1 and the downregulation of collagen type 3, a robust increase in the expression of pro-regenerative fibroblast markers in the repair tissue after a single treatment with rSPARC protein was observed. Additionally, pro-fibrotic markers were significantly decreased by the administration of rSPARC. Determination of structural characteristics was also assessed, indicating that the ECM structure can be improved by the application of rSPARC protein. Therefore, we believe that SPARC plays an important role for tendon healing and the application of recombinant SPARC to tendon defects has great potential to improve functional tendon repair