scholarly journals Effectiveness of Ozone Therapy on Tendon Healing: An Experimental Study in Generated Achilles Tendon Injury Model in Rats

2018 ◽  
Vol 27 (4) ◽  
pp. 309-314
Author(s):  
Volkan Kizilkaya ◽  
Vedat Uruc ◽  
Ali Levent ◽  
Ozgur Kanat ◽  
Mustafa Turgut Yildizgoren ◽  
...  
2016 ◽  
Vol 42 ◽  
pp. 136-146 ◽  
Author(s):  
Issei Komatsu ◽  
James H-C. Wang ◽  
Kiyotaka Iwasaki ◽  
Tatsuya Shimizu ◽  
Teruo Okano

2018 ◽  
Vol 42 (8) ◽  
pp. 1905-1910 ◽  
Author(s):  
Ali Güleç ◽  
Yılmaz Türk ◽  
Bahattin Kerem Aydin ◽  
Ömer Faruk Erkoçak ◽  
Selim Safalı ◽  
...  

2011 ◽  
Vol 27 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Jon Joensen ◽  
Nils Roar Gjerdet ◽  
Steinar Hummelsund ◽  
Vegard Iversen ◽  
Rodrigo Alvaro B. Lopes-Martins ◽  
...  

1994 ◽  
Vol 29 (1) ◽  
pp. 36
Author(s):  
Goo Hyun Baek ◽  
Han Koo Lee ◽  
Sang Hoon Lee ◽  
Bong Goo Yeo ◽  
Kyu Hyoung Cho

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Yonghui Hou ◽  
Bingyu Zhou ◽  
Ming Ni ◽  
Min Wang ◽  
Lingli Ding ◽  
...  

Abstract Background Tendon is a major component of musculoskeletal system connecting the muscles to the bone. Tendon injuries are very common orthopedics problems leading to impeded motion. Up to now, there still lacks effective treatments for tendon diseases. Methods Tendon stem/progenitor cells (TSPCs) were isolated from the patellar tendons of SD rats. The expression levels of genes were evaluated by quantitative RT-PCR. Immunohistochemistry staining was performed to confirm the presence of tendon markers in tendon tissues. Bioinformatics analysis of data acquired by RNA-seq was used to find out the differentially expressed genes. Rat patellar tendon injury model was used to evaluate the effect of U0126 on tendon injury healing. Biomechanical testing was applied to evaluate the mechanical properties of newly formed tendon tissues. Results In this study, we have shown that ERK inhibitor U0126 rather PD98059 could effectively increase the expression of tendon-related genes and promote the tenogenesis of TSPCs in vitro. To explore the underlying mechanisms, RNA sequencing was performed to identify the molecular difference between U0126-treated and control TSPCs. The result showed that GDF6 was significantly increased by U0126, which is an important factor of the TGFβ superfamily regulating tendon development and tenogenesis. In addition, NBM (nonwoven-based gelatin/polycaprolactone membrane) which mimics the native microenvironment of the tendon tissue was used as an acellular scaffold to carry U0126. The results demonstrated that when NBM was used in combination with U0126, tendon healing was significantly promoted with better histological staining outcomes and mechanical properties. Conclusion Taken together, we have found U0126 promoted tenogenesis in TSPCs through activating GDF6, and NBM loaded with U0126 significantly promoted tendon defect healing, which provides a new treatment for tendon injury.


2017 ◽  
Vol 36 (6) ◽  
pp. 1767-1776 ◽  
Author(s):  
Shin Hyuk Kang ◽  
Min Seok Choi ◽  
Han Koo Kim ◽  
Woo Seob Kim ◽  
Tae Hui Bae ◽  
...  

2017 ◽  
Vol 45 (6) ◽  
pp. 1429-1439 ◽  
Author(s):  
Sang Yoon Lee ◽  
Bomi Kwon ◽  
Kyoungbun Lee ◽  
Young Hoon Son ◽  
Sun G. Chung

Background: Although survival of transplanted stem cells in vivo and differentiation of stem cells into tenocytes in vitro have been reported, there have been no in vivo studies demonstrating that mesenchymal stem cells (MSCs) could secrete their own proteins as differentiated tenogenic cells. Purpose/Hypothesis: Using a xenogeneic MSC transplantation model, we aimed to investigate whether MSCs could differentiate into the tenogenic lineage and secrete their own proteins. The hypothesis was that human MSCs would differentiate into the human tenogenic lineage and the cells would be able to secrete human-specific proteins in a rat tendon injury model. Study Design: Controlled laboratory study. Methods: The Achilles tendons of 57 Sprague Dawley rats received full-thickness rectangular defects. After the modeling, the defective tendons were randomly assigned to 3 groups: (1) cell group, implantation with human adipose-derived mesenchymal stem cells (hASCs) and fibrin glue (106 cells in 60 μL); (2) fibrin group, implantation with fibrin glue and same volume of cell media; and (3) sham group, identical surgical procedure without any treatment. Gross observation and biomechanical, histopathological, immunohistochemistry, and Western blot analyses were performed at 2 and 4 weeks after modeling. Results: hASCs implanted into the defective rat tendons were viable for 4 weeks as detected by immunofluorescence staining. Tendons treated with hASCs showed better gross morphological and biomechanical recovery than those in the fibrin and sham groups. Furthermore, the expression of both human-specific collagen type I and tenascin-C was significantly higher in the cell group than in the other 2 groups. Conclusion: Transplantation of hASCs enhanced rat tendon healing biomechanically. hASCs implanted into the rat tendon defect model survived for at least 4 weeks and secreted human-specific collagen type I and tenascin-C. These findings suggest that transplanted MSCs may be able to differentiate into the tenogenic lineage and contribute their own proteins to tendon healing. Clinical Relevance: In tendon injury, MSCs can enhance tendon healing by secreting their own protein and have potential as a therapeutic option in human tendinopathy.


Author(s):  
Corinne N. Riggin ◽  
Joseph J. Sarver ◽  
Benjamin R. Freedman ◽  
Stephen J. Thomas ◽  
Louis J. Soslowsky

Achilles tendon ruptures are traumatic injuries that frequently occur in active individuals and result in significant medical expense. Common techniques for assessing outcomes of surgical repair and rehabilitation rely heavily on patient-based measures of pain and function. While these measures can provide evidence for recovery of functional performance, they do not directly assess tendon healing which, if insufficient, can lead to re-rupture. The clinical evaluation of collagen organization following Achilles tendon injury may provide a more accurate measure of healing than traditional, functional performance tests. It has been shown that changes in collagen organization precede and correlate with changes in mechanical properties in tendons [1–3] and that load and injury effect collagen organization [4–6]. Ultimately, if collagen organization could be quantified in vivo, it would represent a powerful, diagnostic tool to measure the progression of tendon healing, as well as to monitor damage accumulation due to injury.


2021 ◽  
Vol 22 (18) ◽  
pp. 9729
Author(s):  
Neil Marr ◽  
Richard Meeson ◽  
Elizabeth F. Kelly ◽  
Yongxiang Fang ◽  
Mandy J. Peffers ◽  
...  

The interfascicular matrix (IFM) binds tendon fascicles and contains a population of morphologically distinct cells. However, the role of IFM-localised cell populations in tendon repair remains to be determined. The basement membrane protein laminin-α4 also localises to the IFM. Laminin-α4 is a ligand for several cell surface receptors, including CD146, a marker of pericyte and progenitor cells. We used a needle injury model in the rat Achilles tendon to test the hypothesis that the IFM is a niche for CD146+ cells that are mobilised in response to tendon damage. We also aimed to establish how expression patterns of circulating non-coding RNAs alter with tendon injury and identify potential RNA-based markers of tendon disease. The results demonstrate the formation of a focal lesion at the injury site, which increased in size and cellularity for up to 21 days post injury. In healthy tendon, CD146+ cells localised to the IFM, compared with injury, where CD146+ cells migrated towards the lesion at days 4 and 7, and populated the lesion 21 days post injury. This was accompanied by increased laminin-α4, suggesting that laminin-α4 facilitates CD146+ cell recruitment at injury sites. We also identified a panel of circulating microRNAs that are dysregulated with tendon injury. We propose that the IFM cell niche mediates the intrinsic response to injury, whereby an injury stimulus induces CD146+ cell migration. Further work is required to fully characterise CD146+ subpopulations within the IFM and establish their precise roles during tendon healing.


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