The Proximal Tibia Loses Bone Mineral Density After Anterior Cruciate Ligament Injury: Measurement Technique and Validation of a Quantitative Computed Tomography Method

Marigi, Erick M.; Holmes, David R.; Murthy, Naveen S.; Levy, Bruce A.; Stuart, Michael J.; Dahm, Diane L.; Rhee, Peter C.; Krych, Aaron J.

doi:10.1016/j.asmr.2021.09.010

Cited by 1 publication

(4 citation statements)

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“…Overall, this study demonstrated that patient findings of significant osteoclast activity 33,41 are reproduced in our in vivo rodent model, despite a locomotive difference between the 2 species and that the majority of ACL injuries in our model were partial in nature. Although we did not confirm our hypothesis, we demonstrated that the presence of osteoclast activity within the mineralized matrices in response to injury was associated with a significant reduction in bone volume by 28 days in both condylar and entheseal regions.…”

Section: Discussionmentioning

confidence: 52%

“…Analyses of their ACL entheseal tissue, removed during ACLR bone tunneling, found significant catabolic activity in patients ~4 to 7 weeks after injury, compared with age-matched cadaveric controls. Recently, a complementary study conducted by Marigi et al 33 found a similar phenomenon within the tibial tunnel of patients with an ACL injury compared with a comparable tunnel region analyzed in their contralateral knee and a cohort of healthy individuals. However, neither study investigated the bone outside of the tunnel region, so it remains unknown if ACL entheseal bone loss is different from global loss bone that occurs across the injured joint.…”

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confidence: 70%

“…The findings of Patton et al 41 and Marigi et al 33 led us to hypothesize that bone loss in the mineralized matrices comprising the femoral and tibial ACL entheses results from localized disuse osteopenia after a loss of ACL tensile load and/or chronic inflammation. Further, we postulated that this bone loss is distinct from that typically observed across the condylar regions via bone mineral density assessments after injury.…”

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confidence: 99%

“…17 Although this type of biologic failure is more prevalent when soft tissue allografts devoid of bone are used with suspensory fixation (eg, hamstring tendon), this phenomenon is also a significant factor for failed bone-patellar tendon-bone autografts and allografts. 44 The findings of Patton et al 41 and Marigi et al 33 led us to hypothesize that bone loss in the mineralized matrices comprising the femoral and tibial ACL entheses results from localized disuse osteopenia after a loss of ACL tensile load and/or chronic inflammation. Further, we postulated that this bone loss is distinct from that typically observed across the condylar regions via bone mineral density assessments after injury.…”

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confidence: 99%

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Acute Bone Loss and Infrapatellar Fat Pad Fibrosis in the Knee After an In Vivo ACL Injury in Adolescent Mice

et al. 2023

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Background: Young patients are 6 times more likely than adults to have a primary anterior cruciate ligament (ACL) graft failure. Biological factors (ie, tunnel osteolysis) may account for up to a third of these failures. Previous evaluations of patient ACL explants indicated significant bone loss within the entheseal regions. However, it remains unknown if the degree of bone loss within the ACL insertion regions, wherein ACL grafts are fixated, exceeds that of the femoral and tibial condylar bone. Hypothesis: Bone loss in the mineralized matrices of the femoral and tibial ACL entheses is distinct from that clinically reported across the whole knee after injury. Study Design: Controlled laboratory study. Methods: We developed a clinically relevant in vivo mouse ACL injury model to cross-sectionally track the morphological and physiological postinjury changes within the ACL, femoral and tibial entheses, synovial joint space, and load-bearing epiphyseal cortical and trabecular bone components of the knee joint. Right ACLs of 10-week-old C57BL/6J female mice (N = 75) were injured in vivo with the contralateral ACLs serving as controls. Mice were euthanized at 1, 3, 7, 14, or 28 days after injury (n = 12/cohort). Downstream analyses included volumetric cortical and trabecular bone analyses and histopathologic assessments of the knee joint after injury. Gait analyses across all time points were also performed (n = 15 mice). Results: The majority of the ACL injuries in mice were partial tears. The femoral and tibial cortical bone volumes were 39% and 32% lower, respectively, at 28 days after injury than those of the uninjured contralateral knees ( P < .01). Trabecular bone measures demonstrated little difference between injured and control knees after injury. Across all bone measures, bone loss was similar between the injured knee condyles and ACL entheses. There was also significant inflammatory activity within the knee after injury. By 7 days after injury, synovitis and fibrosis were sigificantly elevated in the injured knee compared with the controls ( P < .01), which corresponded with significantly higher osteoclast activity in bone at this time point compared with the controls. This inflammatory response signficantly persisted throughout the duration of the study ( P < .01). The hindlimb gait after injury deviated from normal, but mice habitually loaded their injured knee throughout the study. Conclusion: Bone loss was acute and persisted for 4 weeks after injury in mice. However, the authors’ hypothesis was not confirmed, as bone quality was not significantly lower in the entheses compared with the condylar bone regions after injury. With relatively normal hindlimb loading but a significant physiological response after injury, bone loss in this model may be driven by inflammation. Clinical Relevance: There is persistent bone resorption and fibrotic tissue development after injury that is not resolved. Inflammatory and catabolic activity may have a significant role in the postinjury decline of bone quality in the knee.

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Section: Discussionmentioning

confidence: 52%

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confidence: 70%

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confidence: 99%

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confidence: 99%

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