Comparison of knee injury threshold during tibial compression based on limb orientation in mice

Hsia, Allison W.; Tarke, Franklin D.; Shelton, Trevor J.; Tjandra, Priscilla M.; Christiansen, Blaine A.

doi:10.1016/j.jbiomech.2018.04.014

Cited by 9 publications

(4 citation statements)

References 29 publications

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“…Conversely, other reports showed that a force of 12 N was required for ACL rupture in C57BL/6 mice using a compression device 17, 18 . We obtained a lower force value than the previous study using a compression device, which may be attributed to differences in the knee flexion degree and contact of the joint surfaces 23 . No histological, macroscopic, or morphological differences were found between the INTACT and ACL-R groups.…”

Section: Discussioncontrasting

confidence: 88%

Joint Instability Causes Catabolic Enzyme Production in Chondrocytes prior to Synovial Cells in Novel Non-Invasive ACL ruptured Mouse Model

Takahata

Arakawa

Enomoto

et al. 2022

Preprint

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Objective: Mechanical stress is one of the most exacerbating factors on knee osteoarthritis (OA). We recently reported the effect of shear stress on OA progression in vivo using controlled abnormal tibial translation (CATT), which suppressed shear stress in vivo due to ACL transection (ACL-T). However, surgical ACL-T mice models were used, thus effect of shear stress cannot be clarified exactly. So, we aimed to establish a novel Non-Invasive ACL-T without intra-articular injuries and reveal the onset mechanism of knee OA induced by shear stress. Design: First, twelve-week-old C57BL/6 male mice were used to make a novel Non-Invasive ACL-T model. After creating the model, injuries of intra-articular tissues were observed histologically, macroscopically, and morphologically. Next, twelve-week-old C57BL/6 male mice were categorized into ACL-T, CATT, and Sham groups. After 2,4 and 8 weeks, we performed the anterior drawer test, safranin-O/fast green staining, and immunohistochemical staining for MMP-3 and TNF-α. Results: In a novel Non-Invasive ACL-T model, no injuries, including cartilage, meniscus, and bone were not observed except ACL rupture. Regarding OA progression, the anterior tibial translation in the ACL-T group was significantly higher than that of the other groups at all weeks, and cartilage degeneration in the ACL-T group increased significantly compared with the other groups at 8 weeks. Although synovitis score in the ACL-T and CATT groups was significantly higher than the Sham group at 2 and 8 weeks, there were no differences between the ACL-T and CATT groups. In addition, the MMP-3 positive cell rate in the cartilage of the ACL-T group was higher than the other groups at 4 and 8 weeks. However, that in the synovium of the ACL-T group was higher than the other groups at 8 weeks. TNF-α positive cell rates in both cartilage and synovium were not changed between the ACL-T and CATT groups. Conclusion: We have successfully established a new Non-Invasive ACL-T model without intra-articular tissue damage, which induces knee OA due to shear stress. In the OA progression caused by shear stress, chondrocytes first showed a molecular biological response, leading to a local increase in MMP-3. On the other hand, synovitis is not directly induced by mechanical stress but is indirectly caused by intra-articular degeneration associated with knee OA progression.

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Section: Discussioncontrasting

confidence: 88%

Joint Instability Causes Catabolic Enzyme Production in Chondrocytes prior to Synovial Cells in Novel Non-Invasive ACL ruptured Mouse Model

Takahata

Arakawa

Enomoto

et al. 2022

Preprint

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“…( 49,50 ) Previously we showed that the ACL was not directly damaged by a single bout of cyclic loading and no structural damage to cartilage, bone, ligaments, or other joint tissues was present at 1 h following loading. ( 37 ) Given the repeatable nature of the cyclic loading model and work examining ACL damage in various loading configurations, ( 51 ) we are confident that the ACL was not ruptured by loading in the present study. However, a single bout of loading could have induced a subcritical level of damage to the ACL and other tissues that initiated further joint degradation.…”

Section: Discussionmentioning

confidence: 66%

Early inhibition of subchondral bone remodeling slows load-induced posttraumatic osteoarthritis development in mice

Ziemian

Witkowski

Wright

et al. 2020

Journal of Bone and Mineral Research

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Posttraumatic osteoarthritis (PTOA) is associated with abnormal and increased subchondral bone remodeling. Inhibiting altered remodeling immediately following joint damage can slow PTOA progression. Clinically, however, inhibiting remodeling when significant joint damage is already present has minimal effects in slowing further disease progression. We sought to determine the treatment window following PTOA initiation in which inhibiting remodeling can attenuate progression of joint damage. We hypothesized that the most effective treatment would be to inhibit remodeling immediately after PTOA initiation. We used an animal model in which a single bout of mechanical loading was applied to the left tibia of 26‐week‐old male C57Bl/6 mice at a peak load of 9 N to initiate load‐induced PTOA development. Following loading, we inhibited bone remodeling using daily alendronate (ALN) treatment administered either immediately or with 1 or 2 weeks' delay up to 3 or 6 weeks post‐loading. A vehicle (VEH) treatment group controlled for daily injections. Cartilage and subchondral bone morphology and osteophyte development were analyzed and compared among treatment groups. Inhibiting remodeling using ALN immediately after load‐induced PTOA initiation reduced cartilage degeneration, slowed osteophyte formation, and preserved subchondral bone volume compared to VEH treatment. Delaying the inhibition of bone remodeling at 1 or 2 weeks similarly attenuated cartilage degeneration at 6 weeks, but did not slow the development of osteoarthritis (OA)‐related changes in the subchondral bone, including osteophyte formation and subchondral bone erosions. Immediate inhibition of subchondral bone remodeling was most effective in slowing PTOA progression across the entire joint, indicating that abnormal bone remodeling within the first week following PTOA initiation played a critical role in subsequent cartilage damage, subchondral bone changes, and overall joint degeneration. These results highlight the potential of anti‐resorptive drugs as preemptive therapies for limiting PTOA development after joint injury, rather than as disease‐modifying therapies after joint damage is established. © 2021 American Society for Bone and Mineral Research (ASBMR).

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“…S1). Another possible fixturing approach is to make custom‐molded pads from hardened modeling clay or PMMA . This approach would allow a snug fit for the foot and knee but would require different sets of molds for mice of different age, sex, or genotype.…”

Section: Implementing the Mouse Axial Compression Tibial Loading Modelmentioning

confidence: 99%

Murine Axial Compression Tibial Loading Model to Study Bone Mechanobiology: Implementing the Model and Reporting Results

Main

Shefelbine

Meakin

et al. 2019

Journal Orthopaedic Research

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In vivo, tibial loading in mice is increasingly used to study bone adaptation and mechanotransduction. To achieve standardized and defined experimental conditions, loading parameters and animal-related factors must be considered when performing in vivo loading studies. In this review, we discuss these loading and animal-related experimental conditions, present methods to assess bone adaptation, and suggest reporting guidelines. This review originated from presentations by each of the authors at the workshop "Developing Best Practices for Mouse Models of In Vivo Loading" during the Preclinical Models Section at the Orthopaedic Research Society Annual Meeting, San Diego, CA, March 2017. Following the meeting, the authors engaged in detailed discussions with consideration of relevant literature. The guidelines and recommendations in this review are provided to help researchers perform in vivo loading experiments in mice, and thus further our knowledge of bone adaptation and the mechanisms involved in mechanotransduction.

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Comparison of knee injury threshold during tibial compression based on limb orientation in mice

Cited by 9 publications

References 29 publications

Joint Instability Causes Catabolic Enzyme Production in Chondrocytes prior to Synovial Cells in Novel Non-Invasive ACL ruptured Mouse Model

Joint Instability Causes Catabolic Enzyme Production in Chondrocytes prior to Synovial Cells in Novel Non-Invasive ACL ruptured Mouse Model

Early inhibition of subchondral bone remodeling slows load-induced posttraumatic osteoarthritis development in mice

Murine Axial Compression Tibial Loading Model to Study Bone Mechanobiology: Implementing the Model and Reporting Results

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