Is resection of the tendon edge necessary to enhance the healing process? An evaluation of the expression of collagen type I, IL-1β, IFN-γ, IL-4, and IL-13 in the distal 1 cm of a torn supraspinatus tendon: part II

Fabiś, Jarosław; Szemraj, Janusz; Strek, Malgorzata; Fabiś, Anna; Dutkiewicz, Zbigniew; Zwierzchowski, Tomasz Jacek

doi:10.1016/j.jse.2014.08.023

Cited by 6 publications

(7 citation statements)

References 49 publications

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“…Furthermore, high levels of pro‐inflammatory cytokines (interleukin‐1 [IL‐1], interleukin‐6 [IL‐6], and tumor necrosis factor‐α [TNF‐α]) have been measured in human and animal models of acute tendon injury as well as in tendon disease. Concentrations have been reported as much as a 4,000‐fold increase compared with uninjured controls, with levels measured between 1 and 20 ng/ml depending on the cytokine . The presence of these cytokines has been shown to induce matrix degeneration through increased expression of matrix metalloproteinases, to promote non‐tenogenic morphology and signaling, and to induce apoptosis .…”

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confidence: 99%

Lose‐Dose Administration of Dexamethasone Is Beneficial in Preventing Secondary Tendon Damage in a Stress‐Deprived Joint Injury Explant Model

Connizzo

Grodzinsky

2019

Journal Orthopaedic Research

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Secondary joint damage is the process by which a single injury can lead to detrimental changes in adjacent tissue structures, typically through the spread of inflammatory responses. We recently developed an in vitro model of secondary joint damage using a murine rotator cuff explant system, in which injuries to muscle and bone cause massive cell death in otherwise uninjured tendon. The purpose of the present study was to test the ability cytokine‐targeted and broad‐spectrum therapeutics to prevent cell death and tissue degeneration associated with secondary joint damage. We treated injured bone‐tendon‐muscle explants with either interleukin‐1 receptor antagonist, etanercept, or dexamethasone (DEX) for up to 7 days in culture. Only the low‐dose DEX treatment was able to prevent cell death and tissue degeneration. We then identified a critical window between 24 and 72 h following injury for maximal benefit of DEX treatment through timed administration experiments. Finally, we performed two tendon‐only explant studies to identify mechanistic effects on tendon health. Interestingly, DEX did not prevent cell death and degeneration in a model of cytokine‐induced damage, suggesting other targets of DEX activity. Future studies will aim to identify factors in joint inflammation that may be targeted by DEX treatment, as well as to investigate novel delivery strategies. Statement of clinical significance: Overall, this work demonstrates beneficial effects of DEX administration on preventing tenocyte death and extracellular matrix degeneration in an explant model of secondary joint damage, supporting the clinical use of low‐dose glucocorticoids for short‐term treatment of joint inflammation. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:139–149, 2020

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confidence: 99%

Lose‐Dose Administration of Dexamethasone Is Beneficial in Preventing Secondary Tendon Damage in a Stress‐Deprived Joint Injury Explant Model

Connizzo

Grodzinsky

2019

Journal Orthopaedic Research

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“…These inconsistencies may be due to differences in mechanism of injury, tendon origin (Achilles vs. rotator cuff), or expression level (protein vs. gene expression). Moreover, a study comparing gene expression of cytokines across the proximal, middle, and distal torn edge of the supraspinatus tendon found significant differences in IL1β, IFNγ, IL4, and IL13 with corresponding changes in collagen I expression ( Fabiś et al, 2014 ). Interestingly, IFNγ (type I cytokine) expression was greatest at the distal edge, and lowest at the proximal edge, while IL4 (type II cytokine) had an inverse expression profile.…”

Section: Cytokinesmentioning

confidence: 99%

“…Given the broad role of IL13 in tissue repair, it is unsurprising that several studies also implicate IL13 in tendon repair. Histological assessment and gene expression of IL13 in human tendinopathy samples demonstrated robust presence of IL13 indicating clinical relevance ( Fabiś et al, 2014 ; Akbar, 2018 ). In vitro stimulation of human tenocytes with IL13 demonstrated a twofold increase in proliferation, in a dose-responsive fashion ( Courneya et al, 2010 ; Akbar, 2018 ).…”

Section: Cytokinesmentioning

confidence: 99%

Reparative and Maladaptive Inflammation in Tendon Healing

Arvind

Huang

2021

Front. Bioeng. Biotechnol.

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Tendon injuries are common and debilitating, with non-regenerative healing often resulting in chronic disease. While there has been considerable progress in identifying the cellular and molecular regulators of tendon healing, the role of inflammation in tendon healing is less well understood. While inflammation underlies chronic tendinopathy, it also aids debris clearance and signals tissue repair. Here, we highlight recent findings in this area, focusing on the cells and cytokines involved in reparative inflammation. We also discuss findings from other model systems when research in tendon is minimal, and explore recent studies in the treatment of human tendinopathy to glean further insights into the immunobiology of tendon healing.

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“…63 Similarly, cell apoptosis is seen throughout degenerated tendon, 64,65 with concurrent elevations in inflammatory and catabolic mediators. 66,67 These degenerative changes not only weaken the suture retention strength, thereby predisposing to surgical failure, 18 but also impair healing. Namely, it was recently reported that the severity of tendinosis, rather than tear size or fatty infiltration, was the greatest predictor of repair integrity at least 6 months after surgery.…”

Section: Mechanical Augmentation Of the Surgical Repairmentioning

confidence: 99%

The Rotator Cuff Organ: Integrating Developmental Biology, Tissue Engineering, and Surgical Considerations to Treat Chronic Massive Rotator Cuff Tears

Rothrauff

Pauyo

Debski

et al. 2017

Tissue Engineering Part B: Reviews

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The torn rotator cuff remains a persistent orthopedic challenge, with poor outcomes disproportionately associated with chronic, massive tears. Degenerative changes in the tissues that comprise the rotator cuff organ, including muscle, tendon, and bone, contribute to the poor healing capacity of chronic tears, resulting in poor function and an increased risk for repair failure. Tissue engineering strategies to augment rotator cuff repair have been developed in an effort to improve rotator cuff healing and have focused on three principal aims: (1) immediate mechanical augmentation of the surgical repair, (2) restoration of muscle quality and contractility, and (3) regeneration of native enthesis structure. Work in these areas will be reviewed in sequence, highlighting the relevant pathophysiology, developmental biology, and biomechanics, which must be considered when designing therapeutic applications. While the independent use of these strategies has shown promise, synergistic benefits may emerge from their combined application given the interdependence of the tissues that constitute the rotator cuff organ. Furthermore, controlled mobilization of augmented rotator cuff repairs during postoperative rehabilitation may provide mechanotransductive cues capable of guiding tissue regeneration and restoration of rotator cuff function. Present challenges and future possibilities will be identified, which if realized, may provide solutions to the vexing condition of chronic massive rotator cuff tears.

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Is resection of the tendon edge necessary to enhance the healing process? An evaluation of the expression of collagen type I, IL-1β, IFN-γ, IL-4, and IL-13 in the distal 1 cm of a torn supraspinatus tendon: part II

Cited by 6 publications

References 49 publications

Lose‐Dose Administration of Dexamethasone Is Beneficial in Preventing Secondary Tendon Damage in a Stress‐Deprived Joint Injury Explant Model

Lose‐Dose Administration of Dexamethasone Is Beneficial in Preventing Secondary Tendon Damage in a Stress‐Deprived Joint Injury Explant Model

Reparative and Maladaptive Inflammation in Tendon Healing

The Rotator Cuff Organ: Integrating Developmental Biology, Tissue Engineering, and Surgical Considerations to Treat Chronic Massive Rotator Cuff Tears

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