Osteoarthritis-related biomarkers following anterior cruciate ligament injury and reconstruction: a systematic review

Harkey, Matthew S.; Bressollette, L; Golightly, Yvonne M.; Thomas, Abbey C.; Driban, Jeffrey B.; Hackney, Anthony C.; Pietrosimone, Brian

doi:10.1016/j.joca.2014.09.004

Cited by 110 publications

(93 citation statements)

References 44 publications

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“…This observation suggests that other factors such as altered biology 52; 53 , in addition to altered biomechanics, play a significant role in development of premature knee OA in the ACLR limb. It is also of interest to note that patient-reported outcome measures (Table 1) showed minimal changes from 2 to 8 years prospectively while gait demonstrated significant changes.…”

Section: Discussionmentioning

confidence: 97%

Longitudinal changes in knee gait mechanics between 2 and 8 years after anterior cruciate ligament reconstruction

Erhart‐Hledik

Chu

Asay

et al. 2017

Journal Orthopaedic Research

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The purpose of this study was to longitudinally investigate changes in knee joint kinematics and kinetics from 2 to 8 years post-ACLR. Seventeen subjects with primary unilateral transtibial ACLR performed bilateral gait analysis approximately 2 years and 8 years post-ACLR. Seventeen matched healthy control subjects were also analyzed. Kinematic and kinetic comparisons between the ACLR and contralateral limbs over time were completed using a 2 × 2 (time, limb) repeated-measures ANOVA. Unpaired Student's t-tests were used to compare the ACLR and contralateral kinematics and kinetics to the control group. The ACLR and contralateral limbs had similar gait changes over time. Kinetic changes over time included a reduction in first (p = 0.048) and second (p < 0.001) peak extension moments, internal rotation moment (p < 0.001), adduction moment (first peak: p = 0.002, second peak: p = 0.009, impulse: p = 0.004) and an increase in peak knee flexion moment (p = 0.002). Kinematic changes over time included increases in peak knee flexion angle in the first half of stance (p = 0.026), minimum knee flexion angle in the second half of stance (p < 0.001), and average external rotation angle during stance (p = 0.007), and a reduction in average anterior femoral displacement during stance (p = 0.006). Comparison to healthy controls demonstrated improvement in some gait metrics over time. The results demonstrated longitudinal changes from 2 to 8 years after ACLR in knee joint kinetics and kinematics that have been related to clinical outcome after ACLR and the progression of knee OA, and support future larger and comprehensive investigations into long-term changes in joint mechanics in the ACLR population. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1478-1486, 2018.

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Section: Discussionmentioning

confidence: 97%

Longitudinal changes in knee gait mechanics between 2 and 8 years after anterior cruciate ligament reconstruction

Erhart‐Hledik

Chu

Asay

et al. 2017

Journal Orthopaedic Research

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“…None of these studies employ longitudinal sampling of SF from the same patients. A recent review of cross-sectional studies from ACL-injured patients [20] concluded that in the first week post-injury, [20] levels of IL-6, IL-8, and IL-1Ra were consistently elevated, while there was more variability in reported levels of IL-1α and β. In the subacute period (1 week to 2 months), IL-6 levels remain elevated across studies, and other cytokines and chemokines such as MCP-1, MIP-1β, and IFNγ have been reported.…”

Section: Methodsmentioning

confidence: 99%

Inflammation in joint injury and post-traumatic osteoarthritis

Lieberthal

Sambamurthy

Scanzello

2015

Osteoarthritis and Cartilage

380

350

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Inflammation is a variable feature of osteoarthritis (OA), associated with joint symptoms and progression of disease. Signs of inflammation can be observed in joint fluids and tissues from patients with joint injuries at risk for development of post-traumatic osteoarthritis (PTOA). Furthermore, inflammatory mechanisms are hypothesized to contribute to the risk of OA development and progression after injury. Animal models of PTOA have been instrumental in understanding factors and mechanisms involved in chronic progressive cartilage degradation observed after a predisposing injury. Specific aspects of inflammation observed in humans, including cytokine and chemokine production, synovial reaction, cellular infiltration and inflammatory pathway activation, are also observed in models of PTOA. Many of these models are now being utilized to understand the impact of post-injury inflammatory response on PTOA development and progression, including risk of progressive cartilage degeneration and development of chronic symptoms post-injury. As evidenced from these models, a vigorous inflammatory response occurs very early after joint injury but is then sustained at a lower level at the later phases. This early inflammatory response contributes to the development of PTOA features including cartilage erosion and is potentially modifiable, but specific mediators may also play a role in tissue repair. Although the optimal approach and timing of anti-inflammatory interventions after joint injury are yet to be determined, this body of work should provide hope for the future of disease modification tin PTOA.

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“…49 In fact, up to 90% of ACL injuries are accompanied by osteochondral lesions, suggesting that trauma to the articular cartilage occurs with ACL rupture. 4 Increased presence of inflammatory markers and biomarkers of cartilage degradation have also been reported after ACL injury and reconstruction 50 and meniscal injury. 51 However, the prognostic importance of these biomarkers is presently unknown, as it is unclear if the elevated concentrations of these markers are a healthy or pathologic adaptation to injury.…”

Section: Risk Factors For Ptoa Joint Injurymentioning

confidence: 98%

“…51 However, the prognostic importance of these biomarkers is presently unknown, as it is unclear if the elevated concentrations of these markers are a healthy or pathologic adaptation to injury. 50 Altered loading about the injured joint has also been suggested to contribute to PTOA development. Biomechanical changes in ACL-deficient and -reconstructed individuals may change the regions where tibiofemoral joint contact occurs, thereby loading areas of cartilage that were previously unloaded and decreasing loads to areas of cartilage normally experiencing higher loads during weight bearing.…”

Section: Risk Factors For Ptoa Joint Injurymentioning

confidence: 99%

Epidemiology of Posttraumatic Osteoarthritis

Thomas

Hubbard-Turner

Wikstrom

et al. 2017

Journal of Athletic Training

280

199

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Osteoarthritis is a leading cause of disability whose prevalence and incidence continue to increase. History of joint injury represents an important risk factor for posttraumatic osteoarthritis and is a significant contributor to the rapidly growing percentage of the population with osteoarthritis. This review will present the epidemiology associated with posttraumatic osteoarthritis, with particular emphasis on the knee and ankle joints. It is important to understand the effect of posttraumatic osteoarthritis on the population so that sufficient resources can be devoted to countering the disease and promoting optimal long-term health for patients after joint injury.

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Osteoarthritis-related biomarkers following anterior cruciate ligament injury and reconstruction: a systematic review

Abstract: Patients with ACL-D or ACL-R have altered biomarkers indicative of OA. More research with standardized reporting is needed to effectively determine which biomarkers are the most indicative for OA development and progression following ACL injury.

Cited by 110 publications

References 44 publications

Longitudinal changes in knee gait mechanics between 2 and 8 years after anterior cruciate ligament reconstruction

Longitudinal changes in knee gait mechanics between 2 and 8 years after anterior cruciate ligament reconstruction

Inflammation in joint injury and post-traumatic osteoarthritis

Epidemiology of Posttraumatic Osteoarthritis

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