Mechanisms underpinning the peak knee flexion moment increase over 2-years following arthroscopic partial meniscectomy☆
Introduction
People following Arthroscopic partial meniscectomy (APM) are at increased risk of developing knee osteoarthritis in both the tibiofemoral and patellofemoral compartments (Englund and Lohmander, 2005, Wang et al., 2012). Although knee osteoarthritis is considered in part a mechanical disease (Felson, 2013), the pathogenesis of this debilitating condition is not well understood in patients following APM. Higher joint loading inferred through external knee joint moments during gait has been associated with compromised cartilage health following APM (Hall et al., 2015) as well as in those with established osteoarthritis (OA) (Bennell et al., 2011, Chang et al., 2015, Chehab et al., 2014, Miyazaki et al., 2002). Although most literature highlights the role of the external knee adduction moment in structural change (Bennell et al., 2011, Chehab et al., 2014, Miyazaki et al., 2002), the external knee flexion moment (KFM) is increasingly being implicated as a factor in the pathogenesis of knee osteoarthritis (Chehab et al., 2014, Creaby, 2015, Hall et al., 2015, Teng et al., 2015).
Indeed, the peak KFM may be clinically relevant in people following APM. Three months following APM, we observed that a higher peak KFM during normal pace gait was associated with reduced patellar cartilage volume, over the subsequent 2 years (Hall et al., 2015). The peak KFM increased by approximately 13% over time, such that the peak KFM was 6–11% higher during walking in APM patients compared to healthy controls 2 years later (Hall et al., 2013). Furthermore, a higher KFM during gait has also recently been associated with medial tibial cartilage (Chehab et al., 2014) and patellofemoral joint (Teng et al., 2015) deterioration. Therefore, considering both an increase in KFM over time following APM and a potential link between higher KFM and subsequent adverse cartilage changes, the KFM may constitute a potential target for interventions aiming to preserve knee joint cartilage integrity. However, designing interventions to target the KFM requires an understanding of mechanisms responsible for the increase in peak KFM over time in individuals following APM.
The KFM during gait is predominately a product of the magnitude of the sagittal plane ground reaction force (GRF), which can be increased by a faster walking speed and greater body mass, and the sagittal plane moment arm (i.e. the perpendicular distance of the GRF vector to the knee joint centre). We have previously found a significant increase in peak vertical GRF (vGRF) over 2 years in the affected leg of patients who have undergone an APM compared to healthy controls (Hall et al., 2015). Knee flexion kinematics have not been longitudinally described in patients following APM. This is important to consider as an increase in knee flexion angle may partly explain the change in peak KFM by increasing the sagittal plane GRF moment arm (Creaby et al., 2013).
The KFM moment is supported predominantly by the quadriceps (Winter, 1984), and an increase in the KFM moment is likely to place a greater demand on quadriceps function. Indeed, a lower peak KFM moment is associated with reduced knee extension strength in patients with knee osteoarthritis (Farrokhi et al., 2015) and in those following anterior cruciate ligament reconstruction (Lewek et al., 2002). We have previously reported that the quadriceps were weaker in the APM leg compared to healthy controls at 3 months following surgery (Sturnieks et al., 2008) and that quadriceps strength significantly increased in these patients over 2 years (Hall et al., 2013), As such, an increase in peak KFM over time may reflect the improvement in quadriceps strength in these patients. Although improving quadriceps strength is typically encouraged following knee arthroscopy (Panisset and Prudhon, 2012), it has not been shown that an increase in quadriceps strength is indeed associated with the peak KFM increase in these patients.
The purpose of this study in people assessed 3 months following APM (baseline) and 2-years later (follow-up) was to explore potentially modifiable biomechanical characteristics that explain the change in peak KFM over time. We hypothesized that an increase in walking speed, greater knee flexion angle during stance, an increase in vertical GRF magnitude and increase in quadriceps strength would partially explain the 2-year increase in peak KFM observed in people following APM.
Section snippets
Participants
This is a further analysis of a 2-year prospective study (Hall et al., 2013). We recruited 82 participants aged between 30 and 50 years who had undergone an isolated medial APM 3 months prior. People were excluded if they had: evidence of lateral meniscal resection; greater than one third of medial meniscus resected; > 2 tibiofemoral cartilage lesions; a single tibiofemoral cartilage lesion > approximately 10 mm in diameter as assessed at arthroscopy; previous knee or lower limb surgery (other than
Results
Eighty percent of participants returned at follow-up assessment (n = 66). For normal pace walking, one participant had incomplete data and two different participants had incomplete data for fast pace walking. In total, all 66 participants were included in the analyses, with 65 included in normal pace analyses and 64 participants included in fast pace analyses. Participants evaluated were largely male (n = 56; 86%) and middle-aged (mean 41.3 years, SD 5.4 years), 1.75 m (SD 0.1) tall, and overweight
Discussion
Understanding factors related to the increase in peak KFM during gait is potentially meaningful given that a higher peak KFM during gait at 3-months post-APM is related to the subsequent 2-year patellar cartilage volume loss (Hall et al., 2015). The main finding of this study is that an increase in the peak vGRF and change in knee flexion angle explain up to 75% of the change in peak KFM. The increase in the peak vGRF is primarily related to increase in walking speed. Our observations may
Acknowledgements
This study was funded by an Australian National Health and Medical Research Council project grant (#NHMRC 334151) and the Western Australian Health and Medical Research Infrastructure Fund. Professor KLB is supported by a NHMRC Principal Research Fellowship (#1058440) and A/Professor RSH is supported by an Australian Research Council Research Future Fellowship (#FT 130100175). The study sponsors did not play any role in the study design, collection, analysis or interpretation of data; nor in
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Conflict of interest: No authors have a conflict of interest.