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Tendinopathies negatively affect the life quality of millions of people in occupational and athletic settings, as well as the general population. Tendon healing is a slow process, often with insufficient results to restore complete endurance and functionality of the tissue. Tissue engineering, using tendon progenitors, artificial matrices and bioreactors for mechanical stimulation, could be an important approach for treating rips, fraying and tissue rupture. In our work, C3H10T1/2 murine fibroblast cell line was exposed to a combination of stimuli: a biochemical stimulus provided by Transforming Growth Factor Beta (TGF‐β) and Ascorbic Acid (AA); a three‐dimensional environment represented by PEGylated‐Fibrinogen (PEG‐Fibrinogen) biomimetic matrix; and a mechanical induction exploiting a custom bioreactor applying uniaxial stretching. In vitro analyses by immunofluorescence and mechanical testing revealed that the proposed combined approach favours the organization of a three‐dimensional tissue‐like structure promoting a remarkable arrangement of the cells and the neo‐extracellular matrix, reflecting into enhanced mechanical strength. The proposed method represents a novel approach for tendon tissue engineering, demonstrating how the combined effect of biochemical and mechanical stimuli ameliorates biological and mechanical properties of the artificial tissue compared to those obtained with single inducement.

This paper presents the development and application of an optical fiber-embedded tendon based on biomimetic multifunctional structures. The tendon was fabricated using a thermocure resin (polyurethane) and the three optical fibers with one fiber Bragg grating (FBG) inscribed in each fiber. The first step in the FBG-integrated artificial tendon analysis is the mechanical properties assessment through stress–strain curves, which indicated the customization of the proposed device, since it is possible to tailor the Young’s modulus and strain limit of the tendon as a function of the integrated optical fibers, where the coated and uncoated fibers lead to differences in both parameters, i.e., strain limits and Young’s modulus. Then, the artificial tendon integrated with FBG sensors undergoes three types of characterization, which assesses the influence of temperature, single-axis strain, and curvature. Results show similarities in the temperature responses in all analyzed FBGs, where the variations are related to the heterogeneity on the polyurethane matrix distribution. In contrast, the FBGs embedded in the tendon presented a reduction in the strain sensitivity when compared with the bare FBGs (i.e., without the integration in the artificial tendon). Such results demonstrated a reduction in the sensitivity as high as 77% when compared with the bare FBGs, which is related to strain field distributions in the FBGs when embedded in the tendon. In addition, the curvature tests indicated variations in both optical power and wavelength shift, where both parameters are used on the angle estimation using the proposed multifunctional artificial tendon. To that extent, root mean squared error of around 3.25° is obtained when both spectral features are considered. Therefore, the proposed approach indicates a suitable method for the development of smart structures in which the multifunctional capability of the device leads to the possibility of using not only as a structural element in tendon-driven actuators and devices, but also as a sensor element for the different structures.

The control of tendon-driven actuators is mainly affected by the tendon behavior under stress or strain. The measurement of these parameters on artificial tendons brings benefits on the control and novel approaches for soft robotics actuators. This paper presents the development of polymer optical fiber sensors fabricated through the light spinning polymerization process (LPS-POF) in artificial tendons. This fiber has exceptionally low Young’s modulus and high strain limits, suitable for sensing applications in soft structures. Two different configurations are tested, indicating the possibility of measuring strain and stress applied in the tendon with determination coefficients of 0.996 and 0.994, respectively.

Textile materials are soft, flexible, and strong, and thus resemble the physical and mechanical properties of many biological structures within the human body. By careful control of the polymer and fiber structures and also by appropriate surface treatment, textile-based materials can be engineered into two- or three-dimensional structures that can be used as artificial ligaments, hernia meshes, vascular prostheses, and many other novel implants. This chapter introduces the characteristics of textile-based implant materials and describes the clinical applications of artificial ligaments and tendons, surgical meshes, and vascular prostheses. In addition, the emerging field of textiles for regenerative medicine is described.

Background and Objectives: Achilles tendon ruptures in middle-aged individuals with systemic comorbidities represent a growing clinical challenge. Revision surgery, indicated in cases of tendon re-rupture, remains technically demanding and lacks standardized treatment protocols. This comprehensive review aimed to summarize current evidence regarding indications, outcomes, and complications associated with the most commonly employed revision techniques and explores the potential of artificial intelligence (AI) in improving management and outcomes. Materials and Methods: A literature review was performed in accordance with PRISMA guidelines. The PubMed, MEDLINE, and Cochrane Central databases were used to search keywords. We included articles (1) reporting indications, outcomes, and/or complications of revision surgery for Achilles tendon rupture; (2) reporting a minimum mean follow-up of >12 months; and (3) written in English. Six studies met the inclusion criteria, with a total of 3250 patients analyzed. A methodological quality assessment using the Modified Newcastle–Ottawa Quality Assessment Scale was performed, and all articles were found to be of high quality. Results: Surgical strategies were stratified based on defect size: <2 cm: end-to-end anastomosis; 2–5 cm: V-Y myotendinous lengthening, often combined with tendon transfer; and >5 cm: fascial turndown flaps, autografts (e.g., semitendinosus), or allografts. Tendon transfers showed satisfactory functional outcomes but varied in complication rates. Allografts offered reduced donor site morbidity. The use of AI and wearable sensors has demonstrated potential in preoperative planning, complication prediction, and real-time rehabilitation monitoring. Conclusions: Achilles tendon revision surgery requires a patient-specific, defect-oriented approach. Combined surgical techniques are often necessary for large or non-viable lesions. The integration of AI represents a promising advancement in enhancing surgical decision-making, optimizing rehabilitation, and improving long-term clinical outcomes.

Exercise increases muscle and bone strength and mass, but effects on tendons are less documented. We investigated the impact of voluntary exercise (wheel running) during early‐life exercise (weanling; 3 weeks old) compared to post‐skeletal maturity (young adult; 9 weeks old) on tendon morphology and material properties. We utilized a selectively bred High Runner (HR, N = 40) mouse line and a control line (N = 40). Mice underwent 8 weeks in cages either with or without wheels. HR mice ran ~3‐fold more and were smaller than controls, but exercise reduced body mass in both lines. Tendon cross‐sectional area was unaffected, but tendon length showed a line*exercise interaction (p = 0.0410) and a near‐significant line*age interaction (p = 0.0866). HR mice broadly had greater yield stress (p = 0.0262) and tended toward higher failure stress (p = 0.0676) than controls. Work to failure was greater in younger cohort mice (p = 0.0435), and marginal age‐related interactions were observed for modulus (line*exercise, p = 0.0632) and yield strain (line*age, p = 0.0535). HR mice were more responsive to exercise; older exercised HR mice had shorter tendons (p = 0.0282), and younger exercised HR mice showed lower yield and failure strains than sedentary counterparts (p = 0.0445, 0.0246). Exercise and its relative timing produced slight but complex effects on tendon properties, with HR mice showing the strongest structural and mechanical responses.

Mechanical forces between cells and extracellular matrix (ECM) influence cell shape and function. Tendons are ECM-rich tissues connecting muscles with bones that bear extreme tensional force. Analysis of transgenic zebrafish expressing mCherry driven by the tendon determinant scleraxis reveals that tendon fibroblasts (tenocytes) extend arrays of microtubule-rich projections at the onset of muscle contraction. In the trunk, these form a dense curtain along the myotendinous junctions at somite boundaries, perpendicular to myofibers, suggesting a role as force sensors to control ECM production and tendon strength. Paralysis or destabilization of microtubules reduces projection length and surrounding ECM, both of which are rescued by muscle stimulation. Paralysis also reduces SMAD3 phosphorylation in tenocytes and chemical inhibition of TGFβ signaling shortens tenocyte projections. These results suggest that TGFβ, released in response to force, acts on tenocytes to alter their morphology and ECM production, revealing a feedback mechanism by which tendons adapt to tension. Tendons – the fibrous structures that attach muscles to bones – must withstand some of the strongest forces in the body. Little is known about how tendons develop or adapt to withstand these forces. Studies have shown that muscles respond actively to force, as seen during exercise. Do tendons respond in similar ways? Tendons consist of collagen fibers surrounded by a ‘matrix’ of proteins. Also embedded in the matrix are specialized cells called tenocytes, which regulate the production of the different components of the tendon. A genetic modification allows tenocytes to be tracked using a fluorescent gene product that can be viewed using a microscope. Subramanian et al. have now used this technique in zebrafish to watch how the behaviors of the tenocytes change in response to forces applied to the tendon. Subramanian et al. show that at the start of muscle contraction, tenocytes put forth long projections from their cell bodies that extend perpendicular to the muscle fibers. This suggests that the projections act as force sensors. Consistent with this idea, paralyzing the muscle causes the projections to shrink. This shrinkage correlates with changes in how the tendon matrix proteins are organized. Further investigation reveals a force-responsive signaling pathway in the tenocytes that controls how these cells grow and produce key tendon matrix proteins. Subramanian et al. believe this pathway is central to how tendons adapt to the forces applied during muscle contraction. A better knowledge of how force affects tendon structure could ultimately help to improve treatments for tendon injuries and tendon atrophy. In particular, understanding how force affects how tenocytes develop could help researchers to develop new ways to regenerate and repair tendons.

Although angiogenesis following tendon injury was expected to provide nutrients for regeneration and repair, excessive angiogenesis may be associated with poor long-term outcomes in tendinopathy. Here we aim to explore the pathological role of angiogenesis in the progression of tendinopathy. Patients with tendinopathy were categorized into a hypervascularization group (HyperV) and a hypovascularization group (HypoV), and postarthroscopic outcome and histopathology were compared. In addiiton, tendon injury models and tenocyte stress models were employed to investigate the temporal–spatial vascular pattern characteristics and mechanisms involved in the progression of tendinopathy. This study finds that the HyperV group exhibited worse postoperative pain and functional outcomes and higher Bonar’s pathological scores and vascular density. Bulk RNA sequencing and pathological staining revealed that decreased FHL2 and increased YAP1/sFRP2 expression in tenocytes were strongly associated with disorganized tissue pathology, aggravated inflammation and increased vascular abundance in the HyperV group and tendon injury models (Td-Inj and Td-Sut groups). Three-dimensional vascular imaging demonstrated the formation of morphologically complex and abnormally distributed blood vessels in the Td-Inj and Td-Sut groups, which was significantly alleviated by YAP1 knockdown. In activated tenocytes, FHL2 deficiency-mediated YAP1 overexpression led to the overexpression and extracellular secretion of sFRP2, thereby enhancing endothelial angiogenesis. FHL2 overexpression partly mitigated vascular remodeling and improved tendon blood perfusion in rats. In summary, FHL2/YAP1/sFRP2-mediated pathological vascular remodeling disrupts the homeostasis of tendon repair and regeneration. This study underscores the importance of a systematic vascular assessment, incorporating abundance, morphology, and spatial distribution, in tendinopathy.

ObjectivesThe objective was to describe the typical duration of absence following the most common injury diagnoses in professional football.MethodsInjuries were registered by medical staff members of football clubs participating in the Union of European Football Association Elite Club Injury Study. Duration of absence due to an injury was defined by the number of days that passed between the date of the injury occurrence and the date when the medical team allowed the player to return to full participation. In total, 22 942 injuries registered during 494 team-seasons were included in the study.ResultsThe 31 most common injury diagnoses constituted a total of 78 % of all reported injuries. Most of these injuries were either mild (leading to a median absence of 7 days or less, 6440 cases = 42%) or moderate (median absence: 7–28 days, 56% = 8518 cases) while only few (2% = 311 cases) were severe (median absence of >28 days). The mean duration of absence from training and competition was significantly different (p < 0.05) between index injuries and re-injuries for six diagnoses (Achilles tendon pain, calf muscle injury, groin adductor pain, hamstring muscle injuries and quadriceps muscle injury) with longer absence following re-injuries for all six diagnosesConclusionsThe majority of all time loss due to injuries in professional football stems from injuries with an individual absence of up to 4 weeks. This article can provide guidelines for expected time away from training and competition for the most common injury types as well as for its realistic range.

Building upon the integrative framework of tendinopathy proposed by Gehwolf et al.—which elegantly connects mechanical stress, inflammation, and vascularity—this commentary extends the discussion by introducing novel mechanistic insights and future research directions that move beyond the established triad. A paradigm shift is proposed toward spatiotemporal multi‐omics deconstruction of tendon pathology, emphasizing the role of epigenetically driven cellular re‐programming in tendon stem/progenitor cells and the emergence of neuro‐immune‐vascular niches as functional units sustaining chronicity. Furthermore, redox‐mechanobiological integration through sensors such as TNIK and the potential of 4D‐bioprinted smart biomaterials for chrono‐specific therapeutic delivery are explored. By incorporating advanced computational approaches, including AI‐powered digital tendon twins, a transformative roadmap is outlined for translating the homeostatic failure model into precisely targeted, mechanism‐based diagnostics and therapies. This perspective aims to stimulate interdisciplinary innovation and position tendinopathy research at the forefront of musculoskeletal science.