Background: Rotator cuff tears are common, affecting more than 60% of individuals older than 80 years, and they have been implicated in 70% of patients with shoulder pain. M1 polarization-related inflammation has been reported to be associated with poor healing outcomes of rotator cuff injury, and leptin, an adipokine, has been reported to be a potential activator of inflammation. However, whether leptin affects rotator cuff repair remains unknown. Questions/purposes: Using in vitro cell experiments and an in vivo rat rotator cuff tear model, we therefore asked: (1) Does leptin promote the M1 polarization of macrophages in vitro and in vivo? (2) Does leptin impair biomechanical strength, the histologic structure of the tendon-bone interface, bone mineral density (BMD), or gait in the rotator cuff tear scenario? (3) Does leptin promote M1 polarization by upregulating the tumor necrosis factor (TNF) pathway? Methods: The impact of leptin on M1 macrophage polarization in vitro was determined by reverse transcription–polymerase chain reaction (RT-PCR), the Western blot test, and immunofluorescence staining. The effect of leptin on tendon-bone healing was assessed in an in vivo rat rotator cuff tear model by comparing a leptin group with a suture group in terms of gait, biomechanical tensile strength, the histologic structure of the tendon-bone interface, and BMD. In the in vivo experiments, 8-week-old male Sprague Dawley rats were used, adapting a previously developed rat rotator cuff tear model. The supraspinatus tendon was resected from the greater tuberosity bilaterally, and then the tendon was secured to its anatomical footprint using the transosseous single-row technique. In total, 30 rats were randomized into two groups (suture, leptin) by drawing lots (15 rats in each group). They were assessed at 2, 4, and 8 weeks after the surgery. In the suture group, 100 µL of normal saline was injected into the subacromial space after the deltoid muscle was restitched to the original position. In the leptin group, 100 µL of leptin solution (200 ng/mL) was injected into the subacromial space after the deltoid muscle was restitched to the original position. Biomechanical properties including maximal failure load, stiffness, and tensile failure stress were determined to assess the biomechanical strength at 4 and 8 weeks after the surgery. Histologic staining was conducted to compare the structure of the tendon-bone interface between treatment groups. Micro-MRI and micro-CT assessments were conducted to compare the overall healing outcome and BMD between treatment groups. Gait analysis was conducted to compare the stride length and strength between treatment groups. M1 macrophage polarization in vivo at the tendon-bone interface was assessed by immunofluorescence staining. Finally, to explore the underlying mechanism of the effects of leptin, Necrostatin-1 (Nec-1) was used to block the TNF signaling pathway in the in vitro macrophage study, and RT-PCR and Western blot were used to explore the underlying mechanism. Results: Leptin enhanced LPS-induced M1 polarization of macrophages in vitro, showing increased gene expression of CD86, Nos2, and TNF-α as well as increased protein expression of CD86, TNF-α, interleukin-6 (IL-6), and inducible NO synthase (iNOS). The in vivo polarization showed that the M1 polarization of macrophages at the tendon-bone interface was promoted. At 2 weeks postoperatively, there were more M1 cells in the leptin group (53 ± 5 versus 77 ± 8, mean difference 24 [95% confidence interval (CI) 11 to 37]; p = 0.002), although the proportion of M1 cells (ratio of the number of M1 cells to the total number of macrophages) was not higher (18.6% ± 2.9% versus 21.5% ± 1.7%, mean difference 2.9% [95% CI -2.8% to 8.7%]; p = 0.36). At 4 weeks postoperatively, the leptin group exhibited more M1 cells (31 ± 4 versus 50 ± 6, mean difference 19 [95% CI 6 to 32]; p = 0.008) and at a higher proportion (16.4% ± 2.6% versus 23.0% ± 3.0%, mean difference 6.6% [95% CI 0.8% to 12.4%]; p = 0.03). The in vivo experiments showed that leptin impaired tendon-bone healing. At 4 weeks postoperatively, the biomechanical properties of both groups were not different in terms of maximal failure load (12.7 ± 1.6 N versus 12.4 ± 1.8 N, mean difference -0.3 N [95% CI -2.6 to 1.8]; p = 0.91), stiffness (5.1 ± 0.7 N/mm versus 4.6 ± 0.8 N/mm, mean difference -0.5 N/mm [95% CI -1.3 to 0.5]; p = 0.44), and tensile failure stress (2.0 ± 0.3 N/mm² versus 2.0 ± 0.3 N/mm², mean difference 0.0 N/mm² [95% CI -0.4 to 0.4]; p = 0.99). At 8 weeks postoperatively, the leptin group showed worse maximal failure load (17.6 ± 1.4 N versus 14.1 ± 1.4 N, mean difference -3.5 N [95% CI -5.7 to -1.3]; p = 0.002), stiffness (7.0 ± 0.6 N/mm versus 5.2 ± 0.6 N/mm, mean difference -1.8 N/mm [95% CI -2.7 to -0.9]; p < 0.001), and tensile failure stress (3.4 ± 0.3 N/mm² versus 2.8 ± 0.4 N/mm², mean difference -0.6 N/mm² [95% CI -1.0 to -0.2]; p = 0.007). Results of histologic staining, image assessments, and gait analysis also demonstrated that leptin impaired the healing process. In vitro experiments showed that leptin upregulated the gene expression of molecules in the TNF pathway, including CCL2 and receptor-interacting protein kinase 1 (RIPK1), and M1 markers, such as TNF-α, CD86, and Nos2; the addition of Nec-1 neutralized the effect of leptin on macrophage polarization, reducing the expression of M1 markers, including TNF-α, CD86, and Nos2, and blocking the TNF signaling pathway, including CCL2 and RIPK. The protein expression exhibited similar trends. Conclusion: Based on the results of this study, leptin appears to impair tendon-bone healing in a rat model of rotator cuff tear, promote M1 macrophage polarization at the tendon-bone interface, and upregulate the TNF signaling pathway in macrophages to promote M1 polarization. Clinical Relevance: Obesity and fatty infiltration of the rotator cuff muscle are associated with poor healing of rotator cuff tears. In this study, the effect of leptin, an adipose factor, on tendon-bone healing and the underlying mechanism were explored. Future studies might focus on developing novel approaches to improve the tendon-bone healing in patients with obesity by targeting leptin or the TNF signaling pathway with the aid of biomaterials.

Background: Carpal tunnel syndrome (CTS) is the most common entrapment syndrome, primarily affecting women between the ages of 40 and 70, and conservative treatments are the first option for mild-to-moderate CTS. However, the comparisons between extracorporeal shock wave therapy (ESWT) and other non-surgical methods in the treatment of mild-to-moderate CTS remain controversial, and an updated systematic review is needed. Methods: An electronic search was performed, and all available articles until August 2023 were included in the analysis. The overall quality of evidence was assessed by the GRADE approach. Meta-analyses were conducted using Manager V.5.3.3. Pooled effect sizes were expressed as the weighted mean difference (WMD) with 95% confidence intervals (CIs). Results: A total of 19 RCTs were included. Low-level quality evidence showed that ESWT outperformed the control intervention in terms of functional improvements, pain relief, electrodiagnostic parameters, and cross-sectional area of the median nerve at any time point of follow-up. Compared to local corticosteroid injection (LCI), there were statistically better improvements in functional improvements, pain relief, and electrodiagnostic parameters at 3 and 6 months of follow-up. Conclusions: There is low-level quality evidence to show that both fESWT and rESWT are more clinically effective than controls in symptom relief, functional enhancement, and electrophysiologic parameters’ improvement for patients with mild-to-moderate CTS at any time point of follow-up. Compared with LCI, ESWT yielded similar short-term (6 months) improvements in pain relief and functional recovery with fewer potential complications.

Purpose: Surgical options for long head of the biceps tendon (LHBT) lesions include tenotomy and tenodesis. This study aims to determine the optimal surgical strategy for LHBT lesions with updated evidence from randomised controlled trials (RCTs). Methods: Literature was retrieved from PubMed, Cochrane Library, Embase and Web of Science on 12 January 2022. Randomised controlled trials (RCTs) comparing the clinical outcomes of tenotomy and tenodesis were pooled in the meta-analyses. Results: Ten RCTs with 787 cases met the inclusion criteria, and were included in the meta-analysis. Constant scores (MD, −1.24; p = 0.001), improvement of Constant scores (MD, −1.54; p = 0.04), Simple Shoulder Test (SST) scores (MD, −0.73; p = 0.03) and improvement of SST (p < 0.05) were significantly better in patients with tenodesis. Tenotomy was associated with higher rates of Popeye deformity (OR, 3.34; p < 0.001) and cramping pain (OR, 3.36; p = 0.008]. No significant differences were noticed between tenotomy and tenodesis regarding pain (p = 0.59), American Shoulder and Elbow Surgeons (ASES) score (p = 0.42) and its improvement (p = 0.91), elbow flexion strength (p = 0.38), forearm supination strength (p = 0.68) and range of motion of shoulder external rotation (p = 0.62). Subgroup analyses showed higher Constant scores in all tenodesis types and significantly larger improvement of Constant scores regarding intracuff tenodesis (MD, −5.87; p = 0.001). Conclusions: According to the analyses of RCTs, tenodesis better improves shoulder function in terms of Constant scores and SST scores, and reduces the risk of Popeye deformity and cramping bicipital pain. Intracuff tenodesis might offer the best shoulder function as measured with Constant scores. However, tenotomy and tenodesis provide similar satisfactory results for pain relief, ASES score, biceps strength and shoulder range of motion.

Massive irreparable rotator cuff tears (MIRCTs) present a particularly complex and difficult challenge for the orthopedic surgeon. Fatty infiltration of muscles, chronic excessive retraction of tendons, and overall tissue degeneration predispose these cases to high failure rates following surgical treatment. Several approaches have been introduced for transferring the long head of the biceps tendon (LHBT) to help stabilize the humeral head and reestablish shoulder muscle strength. This article proposes a technical modification of capsular reconstruction using arthroscopic LHBT rerouting and fixation, which can enhance the repair of MIRCTs. The essential steps of this procedure involve exposing the native bicipital groove following full release of the rotator cuff, forming a new groove in the greater tuberosity, redirecting the LHBT into this newly created channel with secure fixation, and completing a side-to-side rotator cuff repair over the tendon, making the method suitable for most patients. Our clinical experience suggests this technique can be safely implemented following specific guidelines. We believe that the introduction of this technique offers new insights into reducing sharp graft angulation ("killer turn"), such as the sharp angulation seen in modified "Chinese Way" techniques, where the graft is positioned in the bicipital groove, thereby reducing graft wear caused by this acute angulation. This modification reduces graft wear caused by this acute angulation and provides better humeral head-depression effects. Additionally, the newly created groove facilitates healing between the LHBT and the greater tuberosity, lowering the risk of retear after rotator cuff repair.