Mechanical Stimulation as Both the Cause and the Cure of Tendon and Ligament Injuries

Paschall, Lauren; Pedaprolu, Krishna; Carrozzi, Sabrina; Dhawan, Aman; Szczesny, Spencer E.

doi:10.1007/978-3-030-95884-8_11

Cited by 3 publications

(4 citation statements)

References 196 publications

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“…This heightened rerupture rate in allografts is likely not due to differences in graft tissue properties since, prior to surgery, the mechanics of non-irradiated allografts and autografts are identical 14,15,16,17 . However, shortly after implantation, the mechanical properties of both graft types dramatically decreases as they undergo significant structural remodeling in a process termed "ligamentization" 18,19,20,21,22 . Over time, the grafts regain their mechanical properties, but this mechanical recovery is slower in allografts compared to autografts 23,24,25 .…”

Section: Introductionmentioning

confidence: 99%

Allograft and Autograft Anterior Cruciate Ligament Reconstructions Exhibit a Similar Biological Response to Cyclic Loading

Paschall,

Tsai,

Tabdanov

et al. 2024

Preprint

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ObjectiveAnterior cruciate ligament (ACL) reconstruction is one of the most commonly performed orthopaedic procedures. While outcomes are similar in the general patient population, the rerupture rate of non-irradiated allografts are 3-4 times higher than autografts in young active individuals. Previous studies suggest that the difference in clinical performance between graft types is due to impaired remodeling in allografts in response to loading. The objective of this study was to compare the remodeling response of autografts and allografts to cyclic loading. Furthermore, given that allografts are a foreign object and that immune cell signaling affects fibroblast mechanobiology, we compared markers of the immune cell composition between graft types.MethodsACL reconstructions were performed on New Zealand white rabbits, harvested 8 weeks post-surgery, and cyclically loaded to 2 MPa in a tensile bioreactor. Expression of markers for anabolic and catabolic tissue remodeling, as well as inflammatory cytokines and immune cells, were quantified using quantitative reverse transcription polymerase chain reaction.ResultsWe found that the expression of markers for tissue remodeling were not different between allografts and autografts. Similarly, we found that the expression of markers for immune cells were not different between allografts and autografts.ConclusionsThese data suggest that the poor clinical outcomes and impaired remodeling of allograft reconstructions compared to autografts is not due to a difference in graft mechanobiology.

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Section: Introductionmentioning

confidence: 99%

Allograft and Autograft Anterior Cruciate Ligament Reconstructions Exhibit a Similar Biological Response to Cyclic Loading

Paschall,

Tsai,

Tabdanov

et al. 2024

Preprint

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“…5,6 In addition to direct mechanical damage, data from tendons suggest that fatigue loading of ACLs may also induce tissue degeneration that further weakens the tissue and accelerates fatigue failure. 7 Previous literature studying tendons demonstrate that fatigue loading and microstructural damage is accompanied by a degenerative cell response characterized by an increase in expression of catabolic proteases (MMPs) and inflammatory cytokines. [8][9][10][11] Given the similarities between tendons and ligaments, it is possible that fatigue-induced degeneration also contributes to ACL rupture.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, repetitive subfailure loading has been shown to cause the accumulation of microstructural tissue damage that weakens the ACL 4 and ultimately predisposes the ACL to injury 5,6 . In addition to direct mechanical damage, data from tendons suggest that fatigue loading of ACLs may also induce tissue degeneration that further weakens the tissue and accelerates fatigue failure 7 . Previous literature studying tendons demonstrate that fatigue loading and microstructural damage is accompanied by a degenerative cell response characterized by an increase in expression of catabolic proteases (MMPs) and inflammatory cytokines 8–11 .…”

Section: Introductionmentioning

confidence: 99%

Cyclic loading induces anabolic gene expression in ACLs in a load‐dependent and sex‐specific manner

Paschall,

Carrozzi,

Tabdanov

et al. 2023

Journal Orthopaedic Research

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Anterior cruciate ligament (ACL) injuries are historically thought to be a result of a single acute overload or traumatic event. However, recent studies suggest that ACL failure may be a consequence of fatigue damage. Additionally, the remodeling response of ACLs to fatigue loading is unknown. Therefore, the objective of this study was to investigate the remodeling response of ACLs to cyclic loading. Furthermore, given that women have an increased rate of ACL rupture, we investigated whether this remodeling response is sex specific. ACLs were harvested from male and female New Zealand white rabbits and cyclically loaded in a tensile bioreactor mimicking the full range of physiological loading (2, 4, and 8 MPa). Expression of markers for anabolic and catabolic tissue remodeling, as well as inflammatory cytokines, was quantified using RT‐qPCR. We found that the expression of markers for tissue remodeling of the ACL is dependent on the magnitude of loading and is sex specific. Male ACLs activated an anabolic response to cyclic loading at 4 MPa but turned off remodeling at 8 MPa. These data support the hypothesis that noncontact ACL injury may be a consequence of failed tissue remodeling and inadequate repair of microtrauma resulting from elevated loading. Compared to males, female ACLs failed to increase anabolic gene expression with loading and exhibited higher expression of catabolic genes at all loading levels, which may explain the increased rate of ACL tears in women. Together, these data provide insight into load‐induced ACL remodeling and potential causes of tissue rupture.This article is protected by copyright. All rights reserved.

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“…However, recent studies have provided evidence to suggest that ACLs are susceptible to fatigue failure, where repetitive subfailure loading induces the accumulation of microstructural tissue damage that predisposes the ACL to injury 4,5 . In addition to direct mechanical damage, data from tendon suggest that fatigue loading of ACLs may also induce tissue degeneration that further weakens the tissue and accelerates fatigue failure 6 . Previous literature studying tendons demonstrate that fatigue loading and microstructural damage is accompanied by a degenerative cell response characterized by an increase in expression of catabolic proteases (MMPs) and inflammatory cytokines [7][8][9][10] .…”

Section: Introductionmentioning

confidence: 99%

Cyclic Loading Induces Anabolic and Catabolic Gene Expression in ACLs in a Load-Dependent and Sex-Specific Manner

Paschall

Carrozzi

Tabdanov

et al. 2022

Preprint

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Anterior cruciate ligament (ACL) injuries are historically thought to be a result of a single acute overload or traumatic event. However, recent studies suggest that ACL failure may be a consequence of fatigue damage. Additionally, the remodeling response of ACLs to fatigue loading is unknown. Therefore, the objective of this study was to investigate the remodeling response of ACLs to cyclic loading. Furthermore, given that women have an increased rate of ACL rupture, we investigated whether this remodeling response is sex specific. ACLs were harvested from male and female New Zealand white rabbits and cyclically loaded in a tensile bioreactor mimicking the full range of physiological loading (2, 4, and 8 MPa). Expression of markers for anabolic and catabolic tissue remodeling, as well as inflammatory cytokines, was quantified using RT-qPCR. We found that the expression of markers for tissue remodeling of the ACL is dependent on the magnitude of loading and is sex specific. Male ACLs activated a tissue remodeling response to cyclic loading below 4 MPa loads but turned off remodeling at 8 MPa. These data support the hypothesis that noncontact ACL injury is a consequence of failed tissue remodeling and inadequate repair of microtrauma resulting from fatigue loading. Conversely, female ACLs downregulate genes responsible for tissue remodeling in response to cyclic loading at all magnitudes, which may explain the increased rate of ACL tears in women. Together, these data provide insight into the remodeling response of ACLs in vivo and potentially offer novel approaches for preventing ACL rupture.

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Mechanical Stimulation as Both the Cause and the Cure of Tendon and Ligament Injuries

Cited by 3 publications

References 196 publications

Allograft and Autograft Anterior Cruciate Ligament Reconstructions Exhibit a Similar Biological Response to Cyclic Loading

Allograft and Autograft Anterior Cruciate Ligament Reconstructions Exhibit a Similar Biological Response to Cyclic Loading

Cyclic loading induces anabolic gene expression in ACLs in a load‐dependent and sex‐specific manner

Cyclic Loading Induces Anabolic and Catabolic Gene Expression in ACLs in a Load-Dependent and Sex-Specific Manner

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