RESUMO
Tendon injuries are the most common soft tissue injuries, caused by tissue overuse and age-related degeneration. However, the tendon repair process is slow and inefficient due to the lack of cellular structure and blood vessels in the tendon. Low-intensity pulsed ultrasound (LIPUS) has received increasing attention as a non-invasive, simple, and safe way to promote tendon healing. This review summarizes the effects and underlying mechanisms of LIPUS on tendon injury by comprehensively examining the published literature, including in vitro, in vivo, and clinical studies. This review reviewed 24 studies, with 87.5% showing improvement. The application of LIPUS in tendon diseases is a promising field worthy of further study.
Assuntos
Traumatismos dos Tendões , Terapia por Ultrassom , Humanos , Traumatismos dos Tendões/diagnóstico por imagem , Traumatismos dos Tendões/terapia , Cicatrização , Tendões/diagnóstico por imagem , Ondas UltrassônicasRESUMO
Transforming growth factor-ß(TGF-ß) plays an important but diverse role in tendon injuries, such as collagen synthesis, cell proliferation, cell differentiation, and cell adhesion, leading to tendon healing and tendon fibrosis. In the well-known canonical TGF-ß signalling pathway, TGF-ß activates Smad signalling through its two cell surface receptors, which leads to Smad-mediated transcriptional regulation and is also regulated by inhibitory Smads, forming a negative feedback regulatory pathway. In the context of the canonical TGF-ß signalling mechanism mediated by Smad, the activated receptors also send signals through other signal transducers, which in the backdrop of TGF-ß signaling are collectively known as non-Smad signalling pathways. Activated TGF-ß binds to the receptor and acts through these signalling pathways. Understanding the mechanism of the TGF-ß signalling pathway and its role in tendon repair is of great significance for targeting the TGF-ß signalling pathway to accelerate tendon healing and reduce tendon fibrosis.
Assuntos
Transdução de Sinais , Fator de Crescimento Transformador beta , Fibrose , Humanos , Transdução de Sinais/fisiologia , Proteínas Smad/metabolismo , Tendões/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Fator de Crescimento Transformador beta1 , Fatores de Crescimento Transformadores/metabolismoRESUMO
Self-healing alginate hydrogels play important roles in the biological field due to their biocompatibility and ability to recover after cracking. One of the primary targets for researchers in this field is to increase the self-healing speed. Sodium alginate was oxidized, generating aldehyde groups on the chains, which were then crosslinked by poly(amino) amine (PAMAM) via Schiff base reaction. The dendritic structure was introduced to the alginate hydrogel in this work, which was supposed to promote intermolecular interactions and accelerate the self-healing process. Results showed that the hydrogel (ADA-PAMAM) formed a gel within 2.5 min with stable rheological properties. Within 25 min, the hydrogel recovered under room temperature. Furthermore, the aldehyde degree of alginate dialdehyde with a different oxidation degree was characterized through gel permeation chromatograph aligned with multi-angle laser light scattering and ultraviolet (UV) absorption. The chemical structure of the hydrogel was characterized through Fourier transform infrared spectroscopy and UV-vis spectra. The SEM and laser scanning confocal microscope (CLSM) presented the antibiotic ability of ADA-PAMAM against both S. aureus and E. coli when incubated with 10-7 CFU microorganism under room temperature for 2 h. This work presented a strategy to promote the self-healing of hydrogel through forming a dendritic dynamic crosslinking network.
Assuntos
Alginatos , Hidrogéis , Alginatos/química , Hidrogéis/química , Staphylococcus aureus , Escherichia coli , Materiais Biocompatíveis/química , AldeídosRESUMO
BACKGROUND: Syndesmosis injury is proposed to contribute to ankle stability and osteoarthritis (OA). However, whether distal tibiofibular syndesmosis structure is closely related to ankle OA is unclear. We hypothesized that different DTS morphology classifications would affect the biomechanics properties in ankle OA. The study aimed to determine the association between the distal tibiofibular syndesmosis (DTS) morphological classification and ankle OA. METHODS: This is a retrospective study examining imaging data of 147 patients (87 males and 60 females) with ankle OA. Magnetic resonance imaging was used to access the DTS morphological classification, according to measuring various parameters. Joint space narrowing and osteophytes were measured using ankle weight-bearing radiography. The classification and parameters were analyzed to determine the relationship between the syndesmosis classification and the abnormality of ankle OA. RESULTS: Five morphological classifications of the DTS, including Chevron (19.6%), Widow's peak (16.2%), Flat (22.3%), Trapezoid (32.0%), and Crescent (19.6%), were shown. There were statistical differences between DTS classification and tibial angle surface angle (TAS) (P = .009) and talar tilt angle (TTA) (P = .014). The TAS (degree) of the Crescent (86.47 ± 3.21) was less than Chevron (88.75 ± 2.72) (P = .006), Widow's peak (89.26 ± 3.15) (P = .001), Flat (88.83 ± 3.62) (P = .003) and Trapezoid (88.11 ± 2.62) (P = .041), respectively. The TTA (degree) of Crescent (86.83 ± 5.30) was less than Chevron (89.28 ± 2.46) and Widow's peak (89.82 ± 3.41). The men were greater than women for TAS (P = .008) and angle (P = .003), which are consistent with osteophyte (P = .019) and the modified Kellgren-Lawrence grades (P = .041) between gender. CONCLUSIONS: DTS morphological classification might affect the biomechanics properties in TAS and TTA in ankle OA. In clinical practice, surgeons should pay attention to the effects of DTS on ankle OA. LEVEL OF EVIDENCE: Level III, retrospective study.
Assuntos
Osteoartrite , Osteófito , Masculino , Humanos , Feminino , Estudos Retrospectivos , Articulação do Tornozelo/diagnóstico por imagem , Articulação do Tornozelo/cirurgia , Tornozelo , Osteoartrite/diagnóstico por imagem , Tíbia/anatomia & histologia , Osteófito/diagnóstico por imagemRESUMO
Around a quarter of annual worldwide silver consumption comes from recycling. It remains a primary target for researchers to increase the silver ion adsorption capacity of the chelate resin. Herein, a series of flower-like thiourea-formaldehyde microspheres (FTFM) possessing diameters of 15-20 µm were prepared via a one-step reaction under acidic conditions, and the effects of the monomer molar ratio and reaction time on the micro-flower morphology, specific surface area, and silver ion adsorption performance were explored. The nanoflower-like microstructure showed the maximum specific surface area 18.98 ± 0.949 m2/g, which was 55.8 times higher than that of the solid microsphere control. As a result, the maximum silver ion adsorption capacity was 7.95 ± 0.396 mmol/g, which was 10.9 times higher than that of the control. Kinetic studies showed that the equilibrium adsorption amount of FT1F4M was 12.61 ± 0.016 mmol/g, which was 11.6 times higher than that of the control. Additionally, the isotherm study of the adsorption process was performed, and the maximum adsorption capacity of FT1F4M was 18.17 ± 1.28 mmol/g, which was 13.8 times that of the control according to the Langmuir adsorption model. Its high absorption efficiency, convenient preparation strategy, and low cost recommend FTFM bright for further use in industrial applications.
RESUMO
The introduction of 'defects' to the thermoset crosslinking network is one of the most applicable strategies for improving the modulus and toughness simultaneously. However, the reinforcement effect disappears when the 'defects' proportion exceeds the threshold. The speculated mechanism was that the aggregation and entanglement of the 'defects' chains changed the matrix topology, making the stacking structure more compact. However, the 'defects' are hardly directly observed in the experiment. As the result, the relationship between the 'defects' proportion and the package state of the matrix, and the effect on the material's mechanical performance was not explored. Herein, the network of bisphenol-A diglycidyl (DGEBA) with diethyltoluenediamine (DETDA) as the hardener was constructed using MD simulation, and n-butylamine was decorated on the matrix by replacing a proportion of DETDA acting as the 'defects'. The results indicated that the aliphatic chains aggregated and entangled at a low concentration, occupying the voids in the rigid aromatic crosslinking structure, thus lowering the free volume. The strong non-bonding interactions drew the matrix segments close together, thus reinforcing the resin. However, the microphases formed by the aliphatic chains no longer filled the voids but created a new free volume and loosened the network when the content increased, which reduced the mechanical performance of the material. The experimental results were consistent with the findings in the simulations. The moduli of the resin increased with the increase in the n-butylamine content first and then declined. The maximum moduli of the thermosets was 3.4 GPa in S30, which was about 25% higher compared with the control; the corresponding elongation at break was 8.9%, which was about 46% improved compared with the control.
RESUMO
Intervertebral disc degeneration (IDD) disease has been considered as the main cause of low back pain (LBP), which is a very common symptom and the leading cause of disability worldwide today. The pathological mechanism of IDD remains quite complicated, and genetic, developmental, biochemical, and biomechanical factors all contribute to the development of the disease. There exists no effective, non-surgical treatment for IDD nowadays, which is largely related to the lack of knowledge of the specific mechanisms of IDD, and the lack of effective specific targets. Recently, non-coding RNA, including miRNA, has been recognized as an important regulator of gene expression. Current studies on the effects of miRNA in IDD have confirmed that a variety of miRNAs play a crucial role in the process of IDD via nucleus pulposus cells (NPC) apoptosis, abnormal proliferation, inflammatory factors, the extracellular matrix (ECM) degradation, and annulus fibrosus (AF) degeneration. In the past 10 years, research on miRNA has been quite active in IDD. This review summarizes the current research progression of miRNA in the IDD and puts forward some prospects and challenges on non-surgical treatment for IDD.
Assuntos
Degeneração do Disco Intervertebral , Disco Intervertebral , Dor Lombar , MicroRNAs , Núcleo Pulposo , Apoptose , Humanos , Disco Intervertebral/fisiopatologia , Degeneração do Disco Intervertebral/genética , Degeneração do Disco Intervertebral/terapia , MicroRNAs/genética , Núcleo Pulposo/fisiopatologiaRESUMO
Tendon injury is a common disease of the musculoskeletal system, accounting for roughly 30%-40% of sports system disorder injuries. In recent years, its incidence is increasing. Many studies have shown that low-level laser therapy (LLLT) has a significant effect on tendon repair by firstly activating cytochrome C oxidase and thus carrying out the photon absorption process, secondly acting in all the three phases of tendon repair, and finally improving tendon recovery. The repair mechanisms of LLLT are different in the three phases of tendon repair. In the inflammatory phase, LLLT mainly activates a large number of VEGF and promotes angiogenesis under hypoxia. During the proliferation phase, LLLT increases the amount of collagen type III by promoting the proliferation of fibroblasts. Throughout the remodeling phase, LLLT mainly activates M2 macrophages and downregulates inflammatory factors, thus reducing inflammatory responses. However, it should also be noted that in the final phase of tendon repair, the use of LLLT causes excessive upregulation of some growth factors, which will lead to tendon fibrosis. In summary, we need to further investigate the functions and mechanisms of LLLT in the treatment of tendon injury and to clarify the nature of LLLT for the treatment of diverse tendon injury diseases.
RESUMO
Tendinopathy is a degenerative disease of the tendons caused by prolonged overstretching or overuse of the tendons. It accounts for a large proportion of musculoskeletal disorders which can occur in all age groups. The management of tendinopathy is typically conservative. In clinical practice, when other conservative treatments fail, extracorporeal shock wave therapy (ESWT) is normally used as an efficient alternative to surgical management. Several basic studies have shown that ESWT with lower energy flux densities can produce some biological responses in vivo to tendinopathy and may accelerate the initiation of the healing process in injured tendons. ESWT has a positive impact on the interactive chain of biological response, enhancing the signaling pathways of angiogenesis through mechanical conduction, and promoting cell proliferation and collagen formation. Finally, it helps tissue regeneration by controlling inflammation. The purpose of this review is to summarize the biological responses generated by ESWT in tendinopathy through a comprehensive review of the published literature. Although ESWT has been used clinically for the treatment of tendinopathies for nearly decades, less is known about the experimental studies of its biological effects on tendon tissue. Further studies on the biological response of ESWT for tendon injuries in vivo are needed in the future in order to provide better management to patients.
RESUMO
Tendon injury is a disorder of the musculoskeletal system caused by overuse or trauma, which is characterized by pain and limitations in joint function. Since tendon healing is slowly and various treatments are generally ineffective, it remains a clinically challenging problem. Recent evidences suggest that basic fibroblast growth factor (bFGF) not only plays an important role in tendon healing, but also shows a positive effect in laboratory experimentations. The purpose of this review is to summarize the effects of bFGF in the tendon healing. Firstly, during the inflammatory phase, bFGF stimulates the proliferation and differentiation of vascular endothelial cells to foster neovascularization. Furthermore, bFGF enhances the production of pro-inflammatory factors during the early phase of tendon healing, thereby accelerating the inflammatory response. Secondly, the cell proliferation phase is accompanied by the synthesis of a large number of extracellular matrix components. bFGF speeds up tendon healing by stimulating fibroblasts to secrete type III collagen. Lastly, the remodeling phase is characterized by the transition from type III collagen to type I collagen, which can be promoted by bFGF. However, excessive injection of bFGF can cause tendon adhesions as well as scar tissue formation. In future studies, we need to explore further applications of bFGF in the tendon healing process.
RESUMO
Angiogenesis is crucial to facilitate tendon healing, such as delivering oxygen and nutrients, removing waste products, and controlling immune responses. Vascular endothelial growth factor (VEGF) is one of the most vital angiogenic factors that regulate blood vessel formation in tendon healing. Recently, biological therapies, including the application of exogenous VEGF, have been attracting increasing attention. However, at present, the effect of the application of exogenous VEGF in tendon healing is controversial, as the role of endogenous VEGF in tendons has also not been fully elucidated. This article will summarize the role of both endogenous and exogenous VEGF in tendon healing and discuss possible reasons for the controversy. The present review shows that tendon repair is facilitated only by proper angiogenesis and VEGF at the early stage, whereas the persistent high VEGF expression and prolonged presence of blood vessels may impair tendon repair at a later stage.
RESUMO
Tendon-related disorders are common musculoskeletal system disorders in clinical practice, accounting for 30-50% of all sports-related injuries, and they are difficult to treat due to the hypovascular structure of the tendons. Platelet-rich plasma (PRP), including pure PRP and leukocyte- and platelet-rich plasma (L-PRP), has been attracting increasing attention, as it may stimulate tissue regeneration through the release of growth factors and cytokines. The aim of the present review was to provide a summary of the effects of L-PRP on tendon disorders and the underlying mechanisms through a comprehensive examination of the published literature, including in vitro, animal and clinical studies. It has been demonstrated that L-PRP results in comparatively greater pain relief and improved function in patients suffering from tendon disorders. Furthermore, L-PRP may exert its effects through a diverse range of mechanisms, such as neovascularization, cell proliferation and differentiation of tendon/progenitor stem cells into tenocytes, as well as extracellular matrix reorganization by transforming type III to type I collagen fibers. It has also been indicated that the effects of leukocytes in L-PRP depend on the biological state of the injured tissue and its surrounding microenvironment. L-PRP is beneficial and promotes tendon healing at the early stage, whereas it is likely detrimental to the repair of tendon at a later stage because of the risk of excessive catabolic and inflammatory responses. Overall, the application of L-PRP in tendon disorders appears to be a promising field that is worthy of further research.
RESUMO
Intervertebral disc degeneration (IDD) is widely recognized as the main cause of low back pain, which leads to disability in aging populations and induces great losses both socially and economically worldwide. Unfortunately, current treatments for IDD are aimed at relieving symptoms instead of preserving disc structure and function. Researchers are forged to find new promising biological therapeutics to stop, and even reverse, IVD degeneration. Recently, the injection of growth factors has been shown to be a promising biological therapy for IDD. A number of growth factors have been investigated to modulate the synthesis of the extracellular matrix (ECM) through a variety of pathogenetic biological mechanisms, including suppressing inflammatory process and down-regulating degrading enzymes. However, growth factors, including Transforming Growth Factor-ß (TGF-ß), Fibroblast Growth Factor (FGF), and Insulin-like Growth Factor-1 (IGF-1), may induce unwanted blood vessel in-growth, which accelerates the process of IDD. On the contrary, studies have demonstrated that injection of GDF-5 into the intervertebral disc of mice can effectively alleviate the degeneration of the intervertebral disc, which elicits their response via BMPRII and will not induce blood vessel in-growth. This finding suggests that GDF-5 is more suitable for use in IDD treatment compared with the three other growth factors. Substantial evidence has suggested that GDF-5 may maintain the structure and function of the intervertebral disc (IVD). GDF-5 plays an important role in IDD and is a very promising therapeutic agent for IDD. This review is focused on the mechanisms and functions of GDF-5 in IDD.