BACKGROUND: Due to its ability to provide stable fixation and permit early mobilization, volar plating has become the recommended technique for the surgical stabilization of distal radius fractures. The extensor pollicis longus (EPL) tendon may be injured or ruptured as a result of undetected screw penetration or drill plunging. During surgery, it is critical to detect any potential screw penetration so that it can be corrected.
METHODS: A 32-year-old woman presented six weeks post-distal radius plating with an inability to extend her left thumb. Clinical examination revealed loss of extension at the interphalangeal joint, stiff wrist, tender point over the dorsal aspect of the wrist, and an intact sensory nerve function.
CONCLUSIONS: Dynamic ultrasound and magnetic resonance imaging (MRI) both revealed no evidence of tendon rupture or EPL tendon movement. X-rays revealed the distal epiphyseal screws penetrating the far cortex. Intraoperatively, the EPL tendon was found to be impinged by a screw. The tendon was released, tenolysis was performed, and the distal screws were shortened.
CONCLUSIONS: In order to assess screw penetration into the far cortex, volar plating for distal radius fractures should be performed using intraoperative imaging views such as lateral, 45-degree supination, 45-degree pronation, dorsal tangential, and skyline views. Timely interventions after distal radius fracture fixation preserve tendon function, and early detection of tendon compromise is essential to preventing additional damage.

Tendon injury is a prevalent orthopedic disease that currently lacks effective treatment. Galangin (GLN) is a vital flavonoid found abundantly in galangal and is known for its natural activity. This study aimed to investigate the GLN-mediated molecular mechanism of tendon-derived stem cells (TDSCs) in tendon repair. The TDSCs were characterized using alkaline phosphatase staining, alizarin red S staining, oil red O staining, and flow cytometry. The effect of GLN treatment on collagen deposition was evaluated using Sirius red staining and quantitative (q)PCR, while a Western bot was used to assess protein levels and analyze pathways. Results showed that GLN treatment not only increased the collagen deposition but also elevated the mRNA expression and protein levels of multiple tendon markers like collagen type I alpha 1 (COL1A1), decorin (DCN) and tenomodulin (TNMD) in TDSCs. Moreover, GLN was also found to upregulate the protein levels of transforming growth factor β1 (TGF-β1) and p-Smad3 to activate the TGF-β1/Smad3 signaling pathway, while GLN mediated collagen deposition in TDSCs was reversed by LY3200882, a TGF-β receptor inhibitor. The study concluded that GLN-mediated TDSCs enhanced tendon repair by activating the TGF-β1/Smad3 signaling pathway, suggesting a novel therapeutic option in treating tendon repair.

OBJECTIVE: To evaluate the current evidence and literature on treatment options for proximal hamstring injuries.
RESULTS: Patients with 3-tendon complete tears with greater than 2 cm of retraction have worse outcomes and higher complication rates compared to those with less severe injuries. Endoscopic and open proximal hamstring repair both have favorable patient reported outcomes at 5-year follow up. Proximal hamstring repair in patients who are male, with isolated semimembranosus injury, and have proximal hamstring free tendon rupture are more likely to have earlier return to sports. The Parisian Hamstring Avulsion Score (PHAS) is a validated patient-reported outcome measure to predict return to sports. Proximal hamstring injuries may occur in both elite and recreational athletes and may present with varying degrees of chronicity and severity. Injuries occur most commonly during forceful eccentric contraction of the hamstrings and often present with ischial tuberosity tenderness, ecchymosis, and hamstring weakness. Treatment decision-making is dictated by the tendons involved and chronicity. Many proximal hamstring injuries can be successfully treated with non-surgical measures. However, operative treatment of appropriately indicated proximal hamstring tendon injuries can result in significantly better functional outcomes and faster and more reliable return to sports compared to nonoperative treatment. Both endoscopic and open surgical repair techniques show high satisfaction levels and excellent patient-reported outcomes at short- and mid-term follow-up. Postoperative rehabilitation protocols vary across the literature and ongoing study is needed to clarify the optimal program, though emphasis on eccentric hamstring strengthening may be beneficial.

Both acute and chronic tendon injuries are the most frequently occurring musculoskeletal diseases in human and veterinary medicine, with a limited repertoire of successful and evidenced-based therapeutic strategies. Inflammation has been suggested as a key driver for the formation of scar and adhesion tissue following tendon acute injury, as well as pathological alternations of degenerative tendinopathy. However, prior efforts to completely block this inflammatory process have yet to be largely successful. Recent investigations have indicated that a more precise targeted approach for modulating inflammation is critical to improve outcomes. The nuclear factor-kappaB (NF-κB) is a typical proinflammatory signal transduction pathway identified as a key factor leading to tendon disorders. Therefore, a comprehensive understanding of the mechanism or regulation of NF-κB in tendon disorders will aid in developing targeted therapeutic strategies for human and veterinary tendon disorders. In this review, we discuss what is currently known about molecular components and structures of basal NF-κB proteins and two activation pathways: the canonical activation pathway and the non-canonical activation pathway. Furthermore, we summarize the underlying mechanisms of the NF-κB signaling pathway in fibrosis and adhesion after acute tendon injury, as well as pathological changes of degenerative tendinopathy in all species and highlight the effect of targeting this signaling pathway in tendon disorders. However, to gain a comprehensive understanding of its mechanisms underlying tendon disorders, further investigations are required. In the future, extensive scientific examinations are warranted to full characterize the NF-κB, the exact mechanisms of action, and translate findings into clinical human and veterinary practice.

Emerging advances in immersive virtual reality incorporating optical hand-tracking present promising potential for application in orthopedic hand therapy. The system is designed to analyze hand movements, enabling users to \"use\" their hands virtually in any fabricated setting. This article, supplemented with videos, examines practical applications of immersive virtual reality in routine hand therapy and provides a scientific presentation of the interaction of immersive virtual reality with our physiological and neurological systems. Indications for immersive virtual reality use, critical evaluations and recommendations are comprehensively discussed. Immersive virtual reality has the potential to evolve into a standard treatment modality in orthopedic hand therapy.

The biomechanical properties of the tendon are affected due to the changes in composition of the tendon extracellular matrix (ECM). Age, overuse, trauma and metabolic disorders are a few associated conditions that contribute to tendon abnormalities. Hyperlipidemia is one of the leading factors that contribute to the compromised biomechanical. Injury was made on infraspinatus tendon of hyperlipidemic swines. After 8 weeks (i) infraspinatus tendon from the injury site, (ii) infraspinatus tendon from the contralateral side and (iii) Achilles tendon, were collected and analyzed for ECM components that form the major part in biomechanical properties. Immunostaining of infraspinatus tendon on the injury site had higher staining collagen type-1 (COL1A1), biglycan, prolyl 4-hydroxylase and mohawk but lower staining for decorin than the control group. The Achilles tendon of the swines that had injury on infraspinatus tendon showed a chronic adaptation towards load which was evident from a more organized ECM with increased decorin, mohawk and decreased biglycan, scleraxis. The mechanism behind the collagen turnover and chronic adaptation to load need to be studied in detail with the biomechanical properties.

Beyond the sensation of pain, peripheral nerves have been shown to play crucial roles in tissue regeneration and repair. As a highly innervated organ, bone can recover from injury without scar formation, making it an interesting model in which to study the role of nerves in tissue regeneration. As a comparison, tendon is a musculoskeletal tissue that is hypo-innervated, with repair often resulting in scar formation. Here, we reviewed the significance of innervation in three stages of injury repair (inflammatory, reparative, and remodeling) in two commonly injured musculoskeletal tissues: bone and tendon. Based on this focused review, we conclude that peripheral innervation is essential for phases of proper bone and tendon repair, and that nerves may dynamically regulate the repair process through interactions with the injury microenvironment via a variety of neuropeptides or neurotransmitters. A deeper understanding of neuronal regulation of musculoskeletal repair, and the crosstalk between nerves and the musculoskeletal system, will enable the development of future therapies for tissue healing.
Accumulating evidence has shown that, across organs systems, peripheral nerves regulate the process of tissue repair and regeneration. This is particularly relevant in the context of musculoskeletal injuries such as those affecting the bone and tendon. The question then arises: what is the function of peripheral innervation in the repair of bone and tendon injuries? This review offers an in-depth look at the ways in which nerves regulate the healing of bone and tendon injuries at various stages of recovery. A deeper comprehension of the influence of nerves on the repair of these tissues could pave the way for the development of future therapeutic strategies for tissue healing.

Tendons are vital components of the musculoskeletal system, facilitating movement and supporting mechanical loads. Emerging evidence suggests that vitamin D, beyond its well-established role in bone health, exerts significant effects on tendon physiology. The aim of this manuscript is to review the impact of vitamin D on tendons, focusing on its mechanisms of action, clinical implications, and therapeutic applications. A comprehensive search of scientific electronic databases was conducted to identify articles on the effects of vitamin D on tendon health. Fourteen studies were included in this review. Five studies were performed in vitro, and nine studies were conducted in vivo. Despite some conflicting results, the included studies showed that vitamin D regulates collagen synthesis, inflammation, and mineralization within tendons through its interaction with vitamin D receptors. Epidemiological studies link vitamin D deficiency with tendon disorders, including tendinopathy and impaired healing. Supplementation with vitamin D shows promise in improving tendon strength and function, particularly in at-risk populations such as athletes and the elderly. Future research should address optimal supplementation strategies and explore the interplay between vitamin D and other factors influencing tendon health. Integrating vitamin D optimization into clinical practice could enhance tendon integrity and reduce the burden of tendon-related pathologies.

Heterotopic ossification (HO), the pathological formation of bone within soft tissues such as tendon and muscle, is a notable complication resulting from severe injury. While soft tissue injury is necessary for HO development, the specific molecular pathology responsible for trauma-induced HO remains a mystery. The previous study detected abnormal autophagy function in the early stages of tendon HO. Nevertheless, it remains to be determined whether autophagy governs the process of HO generation. Here, trauma-induced tendon HO model is used to investigate the relationship between autophagy and tendon calcification. In the early stages of tenotomy, it is observed that autophagic flux is significantly impaired and that blocking autophagic flux promoted the development of more rampant calcification. Moreover, Gt(ROSA)26sor transgenic mouse model experiments disclosed lysosomal acid dysfunction as chief reason behind impaired autophagic flux. Stimulating V-ATPase activity reinstated both lysosomal acid functioning and autophagic flux, thereby reversing tendon HO. This present study demonstrates that autophagy-lysosomal dysfunction triggers HO in the stages of tendon injury, with potential therapeutic targeting implications for HO.

Tendon injuries often lead to joint dysfunction due to the limited self-regeneration capacity of tendons. Repairing tendons is a major challenge for surgeons and imposes a significant financial burden on society. Therefore, there is an urgent need to develop effective strategies for repairing injured tendons. Tendon tissue engineering using hydrogels has emerged as a promising approach that has attracted considerable interest. Hydrogels possess excellent biocompatibility and biodegradability, enabling them to create an extracellular matrix-like growth environment for cells. They can also serve as a carrier for cells or other substances to accelerate tendon repair. In the past decade, numerous studies have made significant progress in the preparation of hydrogel scaffolds for tendon healing. This review aims to provide an overview of recent research on the materials of hydrogel-based scaffolds used for tendon tissue engineering and discusses the delivery systems based on them.