Transplant of Autologous Mesenchymal Stem Cells Halts Fatty Atrophy of Detached Rotator Cuff Muscle After Tendon Repair: Molecular, Microscopic, and Macroscopic Results From an Ovine Model

Background: The injection of mesenchymal stem cells (MSCs) mitigates fat accumulation in released rotator cuff muscle after tendon repair in rodents. Purpose: To investigate whether the injection of autologous MSCs halts muscle-to-fat conversion after tendon repair in a large animal model for rotator cuff tendon release via regional effects on extracellular fat tissue and muscle fiber regeneration. Study Design: Controlled laboratory study. Methods: Infraspinatus (ISP) muscles of the right shoulder of Swiss Alpine sheep (n = 14) were released by osteotomy and reattached 16 weeks later without (group T; n = 6) or with (group T-MSC; n = 8) electropulse-assisted injection of 0.9 Mio fluorescently labeled MSCs as microtissues with media in demarcated regions; animals were allowed 6 weeks of recovery. ISP volume and composition were documented with computed tomography and magnetic resonance imaging. Area percentages of muscle fiber types, fat, extracellular ground substance, and fluorescence-positive tissue; mean cross-sectional area (MCSA) of muscle fibers; and expression of myogenic (myogenin), regeneration (tenascin-C), and adipogenic markers (peroxisome proliferator-activated receptor gamma [PPARG2]) were quantified in injected and noninjected regions after recovery. Results: At 16 weeks after tendon release, the ISP volume was reduced and the fat fraction of ISP muscle was increased in group T (137 vs 185 mL; 49% vs 7%) and group T-MSC (130 vs 166 mL; 53% vs 10%). In group T-MSC versus group T, changes during recovery after tendon reattachment were abrogated for fat-free mass (–5% vs –29%, respectively; P = .018) and fat fraction (+1% vs +24%, respectively; P = .009%). The area percentage of fat was lower (9% vs 20%; P = .018) and the percentage of the extracellular ground substance was higher (26% vs 20%; P = .007) in the noninjected ISP region for group T-MSC versus group T, respectively. Regionally, MCS injection increased tenascin-C levels (+59%) and the water fraction, maintaining the reduced PPARG2 levels but not the 29% increased fiber MCSA, with media injection. Conclusion: In a sheep model, injection of autologous MSCs in degenerated rotator cuff muscle halted muscle-to-fat conversion during recovery from tendon repair by preserving fat-free mass in association with extracellular reactions and stopping adjuvant-induced muscle fiber hypertrophy. Clinical Relevance: A relatively small dose of MSCs is therapeutically effective to halt fatty atrophy in a large animal model.

Recommendations for the Management of Incidental Pancreatic Findings in Adults by the Canadian Association of Radiologists Incidental Findings Working Group

The Canadian Association of Radiologists Incidental Findings Working Group consists of both academic subspecialty and general radiologists and is tasked with adapting and expanding upon the American College of Radiology incidental findings white papers to more closely apply to Canadian practice patterns, particularly more comprehensively dealing with the role of ultrasound and pursuing more cost-effective approaches to the workup of incidental findings without compromising patient care. Presented here are the 2021 Canadian guidelines for the management of pancreatic incidental findings. Topics covered include anatomic variants, fatty atrophy, pancreatic calcifications, ductal ectasia, and management of incidental pancreatic cysts.

Flexor hallucis longus augmentation for Achilles tendon – is pre-operative evaluation of flexor hallucis longus by MRI required?

Objectives: Flexor hallucis longus (FHL) tendon transfer is the method of choice in reconstructing chronic neglected Achilles tendon rupture. We performed a retrospective study to assess the incidence and degree of fatty degeneration of FHL. Material and Methods: Two hundred and twenty-five consecutive MR of ankles were reviewed retrospectively and assessed for fatty atrophy based on Goutallier classification. Results: About 42.7% had Grade 1, 8.4% had Grade 2, 3.1% had Grade 3, and 1.8% had Grade 4 fatty atrophy of FHL. Other lesions identified included posterior ankle impingement, tenosynovitis, loose bodies, and giant cell tumors of the tendon sheath. Conclusion: We suggest pre-operative radiological assessment of the FHL to establish that the FHL muscle and tendon are normal and intact and suitable for transfer surgery. We also discuss the spectrum of pathologies affecting FHL.

LRSAM1 and the RING domain: Charcot–Marie–Tooth disease and beyond

In the past decade, mutations in LRSAM1 were identified as the genetic cause of both dominant and recessive forms of axonal CMT type 2P (CMT2P). Despite demonstrating different inheritance patterns, dominant CMT2P is usually characterized by relatively mild, slowly progressive axonal neuropathy, mainly involving lower limbs, with age of onset between the second and fifth decades of life. Asymptomatic individuals were identified in several pedigrees exemplifying the strong phenotypic variability of these patients requiring serial clinical evaluation to establish correct diagnosis; in this respect, magnetic resonance imaging of lower-limb musculature showing fatty atrophy might be helpful in detecting subclinical gene mutation carriers. LRSAM1 is a universally expressed RING-type E3 ubiquitin protein ligase catalysing the final step in the ubiquitination cascade. Strikingly, TSG101 remains the only known ubiquitination target hampering our mechanistic understanding of the role of LRSAM1 in the cell. The recessive CMT mutations lead to complete loss of LRSAM1, contrary to the heterozygous dominant variants. These tightly cluster in the C-terminal RING domain highlighting its importance in governing the CMT disease. The domain is crucial for the ubiquitination function of LRSAM1 and CMT mutations disrupt its function, however it remains unknown how this leads to the peripheral neuropathy. Additionally, recent studies have linked LRSAM1 with other neurodegenerative diseases of peripheral and central nervous systems. In this review we share our experience with the challenging clinical diagnosis of CMT2P and summarize the mechanistic insights about the LRSAM1 dysfunction that might be helpful for the neurodegenerative field at large.

Two different types of postoperative sagittal imbalance after long instrumented fusion to the sacrum for degenerative sagittal imbalance

OBJECTIVEFew studies have addressed that dynamic sagittal imbalance can develop distal to the spinal fusion and cause sagittal malalignment, unlike proximal junctional kyphosis (PJK) in the proximal portion. The purpose of this study was to investigate risk factors between the 2 different types of postoperative sagittal imbalance after long fusion to the sacrum for the treatment of degenerative sagittal imbalance (DSI).METHODSEighty patients who had undergone surgical correction for DSI were included. Radiographic measurements included spinopelvic parameters on whole-spine plain radiographs and degeneration of paravertebral muscles on MRI. Univariate and multivariate analyses for clinical and radiological factors were conducted for respective risk factors. In subgroup analyses, the 2 different types of postoperative sagittal imbalance were directly compared.RESULTSForty patients (50%) developed postoperative sagittal imbalance; of these patients, 22 (55.0%) developed static proximal kyphosis from PJK, and 18 patients (45.0%) developed dynamic sagittal imbalance without PJK. The independent risk factors in proximal kyphosis were greater postoperative pelvic tilt (HR 1.11) and less change in sacral slope (SS) (HR 1.09), whereas there were more fusion levels (HR 3.11), less change in SS (HR 1.28), and less change in thoracic kyphosis (HR 1.26) in dynamic sagittal imbalance. Directly compared with the proximal kyphosis group, dynamic sagittal imbalance was more commonly found in patients who had less correction of sagittal parameters as well as fatty atrophy of the paravertebral muscles. Clinical outcomes in the dynamic sagittal imbalance group were superior to those in the proximal kyphosis group.CONCLUSIONSOptimal correction of sagittal alignment should be considered in long instrumented fusion for DSI, because insufficient correction might cause one of 2 different types of postoperative sagittal imbalance at different sites of decompression. Dynamic sagittal imbalance compared with proximal kyphosis was significantly associated with less correction of sagittal alignment, in conjunction with more fusion levels and degeneration of the paravertebral muscles.

Greater Trochanteric Pain Syndrome: Abductors, External Rotators

Chronic pain and tenderness at the greater trochanter characterizes trochanteric pain syndrome. For a long time, trochanteric bursitis was thought to be the only underlying pathology; however, investigations have shown that tendinopathy of the abductors is the main cause, followed by iliotibial band thickening and, to a lesser extent, abductor tendon tears. Trochanteric bursitis can be associated with it. On magnetic resonance imaging (MRI), peritrochanteric T2 abnormalities are evident in greater trochanteric pain syndrome. However, this is also frequently encountered in asymptomatic patients. In the postoperative setting, patients with total hip arthroplasties and transtendinous lateral or posterior surgical access are prone to tendon injury. Symptomatic patients typically present with tendon tears, whereas peritrochanteric fluid, thickening, and signal alterations of the abductors and fatty atrophy of the gluteus minimus muscle are often encountered in asymptomatic postoperative hips. MRI and ultrasound are proven and reliable imaging modalities in patients with greater trochanteric pain syndrome. Awareness of typical imaging findings, in particular in postoperative patients, are helpful in the evaluation of patients.