Tendinopathy is accompanied by a cascade of inflammatory events promoting tendon degeneration. Among various cytokines, interleukin-1β plays a central role in driving catabolic processes, ultimately resulting in the activation of matrix metalloproteinases and a diminished collagen synthesis, both of which promote tendon extracellular matrix degradation. Pulsed electromagnetic field (PEMF) therapy is often used for pain management, osteoarthritis, and delayed wound healing. In vitro PEMF treatment of tendon-derived cells was shown to modulate pro-inflammatory cytokines, potentially limiting their catabolic effects. However, our understanding of the underlying cellular and molecular mechanisms remains limited. We therefore investigated the transcriptome-wide responses of Il-1β-primed rat Achilles tendon cell-derived 3D tendon-like constructs to high-energy PEMF treatment. RNASeq analysis and gene ontology assignment revealed various biological processes to be affected by PEMF, including extracellular matrix remodeling and negative regulation of apoptosis. Further, we show that members of the cytoprotective Il-6/gp130 family and the Il-1β decoy receptor Il1r2 are positively regulated upon PEMF exposure. In conclusion, our results provide fundamental mechanistic insight into the cellular and molecular mode of action of PEMF on tendon cells and can help to optimize treatment protocols for the non-invasive therapy of tendinopathies.

Vascular endothelial growth factor (VEGF) signaling is crucial for a large variety of cellular processes, not only related to angiogenesis but also in nonvascular cell types. We have previously shown that controlling angiogenesis by reducing VEGF‐A signaling positively affects tendon healing. We now hypothesize that VEGF signaling in non‐endothelial cells may contribute to tendon pathologies. By immunohistochemistry we show that VEGFR1, VEGFR2, and VEGFR3 are expressed in murine and human tendon cells in vivo. In a rat Achilles tendon defect model we show that VEGFR1, VEGFR3, and VEGF‐D expression are increased after injury. On cultured rat tendon cells we show that VEGF‐D stimulates cell proliferation in a dose‐dependent manner; the specific VEGFR3 inhibitor SAR131675 reduces cell proliferation and cell migration. Furthermore, activation of VEGFR2 and ‐3 in tendon‐derived cells affects the expression of mRNAs encoding extracellular matrix and matrix remodeling proteins. Using explant model systems, we provide evidence, that VEGFR3 inhibition prevents biomechanical deterioration in rat tail tendon fascicles cultured without load and attenuates matrix damage if exposed to dynamic overload in a bioreactor system. Together, these results suggest a strong role of tendon cell VEGF signaling in mediation of degenerative processes. These findings give novel insight into tendon cell biology and may pave the way for novel treatment options for degenerative tendon diseases.

Background: Understanding muscle and tendon anatomy is of tremendous importance to achieve optimal surgical execution and results in tendon transfers around the shoulder. The aim of this study was to introduce and describe an additional distal muscle slip of the teres major (TM).Methods: Sixteen fresh-frozen cadaver shoulders were dissected with the deltopectoral approach. The ventral latissimus dorsi (LD) tendon was harvested, and the shoulders were analyzed for the presence/absence of a distal teres major slip (dTMs) and its dimensions and relationship with the TM and LD tendons.Results: The dTMs was identified in 12 shoulders (75%). It was always distal to the TM tendon and visible during the deltopectoral approach. There was a clear separation between the TM proximally and dTMs tendon distally. At the humeral insertion, both tendons had a common epimyseal sheet around the teres major and inserted continuously at the humerus. The mean width of the dTMs tendon at the insertion was 13 ± 4 mm (range, 7–22 mm). The total lengths of the dTMs tendon and LD tendon were 40 ± 7 mm (range, 25–57 mm) and 69 ± 7 mm (range, 57–79 mm), respectively (p < 0.001). The dTMs muscle showed direct adhesions in ten shoulders (83%) with the LD muscle.Conclusions: This is the first macroscopic description of an additional distal slip of the teres major muscle. The dTMs has a separate (distal) but continuous (mediolateral) insertion at the humerus within a common epimyseal sheet around the TM. The dTMs tendon is visible during the deltopectoral approach and can therefore provide a lead structure, particularly in ventral LD transfers with the deltopectoral approach.

Rationale: To our knowledge, no study has investigated concomitant injuries of the sternoclavicular joint (SCJ) in acute clavicle fractures. The purpose of this study was to determine the effect of an ipsilateral clavicle fracture on the SCJ in a systematic computer tomography (CT) morphologic evaluation. Methods: CT scans in the axial and coronal plane of 45 consecutive patients with clavicle fractures were retrospectively analyzed. The scans were assessed regarding anatomic congruence of bilateral SCJs—joint space width (JSW); the position of bilateral medial clavicles (PC); and the non-fusion of epiphyses, arthritis, calcifications, and intra-articular gas. Results: The mean SCJ JSW was significantly different in the coronal (cJSW; 8.70 mm ± 2.61 mm in affected vs. 7.63 mm ± 2.58 mm in non-affected side; p = 0.001) and axial plane (aJSW; 9.40 mm ± 2.76 mm in affected vs. 9.02 ± 2.99 in non-affected SCJs; p = 0.044). The position of the medial clavicle showed a significant difference in the coronal plane (cPC; 14.31 mm ± 3.66 mm in the affected vs. 13.49 ± 3.34 in the non-affected side; p = 0.011), indicating a superior shift. Conclusion: Acute clavicle fractures may be associated with an enlargement of the ipsilateral SCJ space width and a superior shift of the proximal clavicle. Both morphologic alterations could indicate concomitant injuries of the SCJ as well as a potential increase in the risk of SCJ instability.

Posterior shoulder dislocation (PSD) is less common than anterior dislocation (ASD) but is increasingly recognized. Understanding the osseous characteristics of PSD is essential for guiding management. However, direct comparative radiographic analyses between PSD and ASD remain limited. The purpose of this study was to perform a matched-pair radiographic comparison of acromial, glenoidal, and (reverse) Hill-Sachs lesion morphology between patients with first-time traumatic PSD and ASD, and to identify osseous features that may predispose to posterior shoulder instability. In this retrospective single-center study, 24 patients (24 shoulders) with cross-sectional imaging (computed tomography [CT] or magnetic resonance imaging [MRI]) following first-time traumatic PSD between 2011 and 2020 were included and matched 1:1 by sex, age, and laterality to 24 patients with first-time traumatic anterior shoulder dislocation. Two independent raters performed standardized radiological measurements on CT/MRI, assessing the following parameters: posterior acromial height (PAH), posterior acromial coverage (PAC), anterior acromial coverage (AAC), and total acromial coverage (TAC), acromial tilt (AT), glenoid bone loss (GBL, glenoid offset, glenoid retroversion, glenoid depth, scapular neck angle, defect size, width and depth of Hill-Sachs lesion (HSL)/reverse Hill-Sachs lesion (rHSL). PAH was greater in PSD than ASD (22.5 mm vs. 15.9 mm, p < 0.001). The PAC was lower in PSD (58.7° vs. 68.0°, p < 0.001), while AAC was higher (4.9° vs. -3.0°, p = 0.0015). No statistically significant difference was found for TAC. The AT was greater in PSD (65.5° vs. 55.2°, p < 0.001). The GBL was smaller in PSD than ASD (8.1% vs. 12.2%, p = 0.0073). Glenoid offset and neck angle showed no statistically significant differences. Retroversion was higher in PSD (8.0° vs. 3.3°, p < 0.001), and glenoid depth was greater (2.0 mm vs. 1.2 mm, p = 0.0053). The rHSL width was smaller in PSD than HSL width in ASD (13.0 mm vs. 17.0 mm, p = 0.037), while lesion depth and surface area did not differ. PSD is associated with distinct alterations in bony shoulder anatomy including a higher, flatter acromion resulting in reduced posterior containment of the humeral head, increased glenoid retroversion, less GBL, and deeper glenoid concavity compared with ASD. Retrospective matched-pair cohort study, 3.

Heterotopic ossifications (HO) in the shoulder are rare. The effectiveness of conservative treatment is limited, and therefore, symptomatic cases are usually treated surgically. However, there are no guidelines for the surgical treatment of HO. Herein, we report the case of a 45-year-old man with severe HO and proximal entrapment of the ulnar nerve following primary anterior shoulder dislocation without concomitant injuries (e.g., fracture and rotator cuff tears). Surgical intervention was indicated, including resection of HO and neurolysis of the brachial plexus. Nine months after surgery, the patient presented with restored shoulder function, pain relief, and good patient satisfaction. The case shows that the ulnar nerve can also be impaired due to HO following shoulder dislocation.