While functional reconstruction of massive irreparable rotator cuff tears remains a challenge, current techniques aimed at recentering and preventing superior migration of the humeral head allow for clinical and biomechanical improvements in shoulder pain and function. Recentering of the glenohumeral joint reduces the moment arm and helps the deltoid to recruit more fibers, which compensates for insufficient rotator cuff function and reduces joint pressure. In the past, the concept of a superior capsular reconstruction with a patch secured by suture anchors has been used. However, several innovative arthroscopic treatment options have also been developed. The purpose of this article is to present an overview of new strategies and surgical techniques and if existing present initial clinical results. Techniques that will be covered include rerouting the long head of the biceps tendon, utilization of the biceps tendon as an autograft to reconstruct the superior capsule, utilization of a semitendinosus tendon allograft to reconstruct the superior capsule, superior capsular reconstruction with dermal allografts, and subacromial spacers.

Most shoulder rotator cuff tears (RCTs) are caused by non-traumatic age-related rotator cuff degeneration, of which hyperglycemia is a risk factor due to its glycation reaction and oxidative stress. We aimed to identify the influence of diabetes-induced glycation and oxidative stress in patients with non-traumatic shoulder RCTs. Twenty patients, aged over 50 years, with non-traumatic shoulder RCTs participated in this study. Patients with a history of diabetes mellitus or preoperative HbA1c ≥ 6.5% were assigned to the diabetic group (n = 10), and the rest to the non-diabetic group (n = 10). Cell proliferation; expression of genes related to oxidative stress, glycation reaction, inflammation, and collagen; intracellular reactive oxygen species (ROS) levels; and apoptosis rates were analyzed. The diabetic group had significantly lower cell proliferation than the non-diabetic group. In the diabetic group, the mRNA expression levels of NOX1, NOX4, IL6, RAGE, type III collagen, MMP2, TIMP1, and TIMP2 were significantly higher; type I collagen expression was significantly lower; and the rate of ROS-positive cells and apoptotic cells, as well as the expression of advanced glycation end-products (AGEs) and the receptor for AGEs (RAGE), was significantly higher. In conclusion, hyperglycemia caused by diabetes mellitus increased AGE and RAGE expression, and led to increased NOX expression, ROS production, and apoptosis in the human rotator cuff. This provides scope to find a preventive treatment for non-traumatic RCTs by inhibiting glycation and oxidative stress.

Although electromyography is the routine diagnostic method for cubital tunnel syndrome (CuTS), imaging diagnosis by measuring cross-sectional area (CSA) with ultrasonography (US) has also been attempted in recent years. In this study, deep learning (DL), an artificial intelligence (AI) method, was used on US images, and its diagnostic performance for detecting CuTS was investigated. Elbow images of 30 healthy volunteers and 30 patients diagnosed with CuTS were used. Three thousand US images were prepared per each group to visualize the short axis of the ulnar nerve. Transfer learning was performed on 5000 randomly selected training images using three pre-trained models, and the remaining images were used for testing. The model was evaluated by analyzing a confusion matrix and the area under the receiver operating characteristic curve. Occlusion sensitivity and locally interpretable model-agnostic explanations were used to visualize the features deemed important by the AI. The highest score had an accuracy of 0.90, a precision of 0.86, a recall of 1.00, and an F-measure of 0.92. Visualization results show that the DL models focused on the epineurium of the ulnar nerve and the surrounding soft tissue. The proposed technique enables the accurate prediction of CuTS without the need to measure CSA.

Aging impairs tendon healing and is a potential risk factor for chronic tendinitis. During normal aging, tendons undergo structural and biomechanical degenerative changes, accompanied by a reduction in the number of tenocytes and changes to their properties. However, molecular changes in aged tendons under inflammatory conditions are not well understood. The present study analyzed the molecular changes in collagenase induced acute tendon injury using a senescence-accelerated mouse (SAM) model. SAMP6 mice were used as an aging animal model and SAMR1 mice were used as a control to represent a senescence-resistant inbred strain. All the mice used in the study were 40 weeks old. Collagenase I from Clostridium histolyticum (20 μL) was injected percutaneously to the tendon-bone junction of the Achilles tendon. Two weeks after treatment, the Achilles tendons were harvested and stained using Picrosirius Red to determine collagen expression. Real-time PCR was performed to analyze gene expression of IL-6, tenomodulin, type I and type II collagen, MMP-9, TIMP-1, and TIMP-2. Collagenase injection resulted in significantly higher gene expression of IL-6 but significantly lower tenomodulin expression compared with the control in SAMP6 and SAMR1 mice. In SAMP6 mice, gene expression of type III collagen and MMP-9 was significantly higher in the collagenase-injected group compared with the control group. SAMP6 mice also showed lower expression of type I collagen, TIMP-1, and TIMP-2 in the collagenase-injected group compared with the control group. Picrosirius Red staining showed the highest expression of type III collagen in the collagenase-injected SAMP6 group compared with the other groups. The collagenase-injected SAMP6 group showed higher expression of IL-6, MMP-9, and type III collagen and lower expression of type I collagen, TIMP-1, and TIMP-2, which are known to suppress metalloproteinases. The results indicate that aging may lead to dysfunction of the tendon healing process after acute tendon injury.

Pain is one of the primary indicators of a bone fracture and serves both a functional and practical role in guiding recovery. However, fracture pain can persist long after the fracture itself has clinically healed. The neural and molecular mechanisms that drive acute pain postfracture, and how these mechanisms are pathologically usurped to trap patients into persistent, debilitating, and often difficult to treat, chronic pain, are not well understood. The aim of this review is to provide insight into the risk factors for pain persistence after fracture, review the physiological and pathophysiological mechanisms of fracture pain, and critically evaluate the literature around fracture pain assessment techniques/models. Taken together, the concepts covered herein will provide a strong foundation to support the development of more effective treatments to better alleviate postfracture pain.