Paul W Hodges1, Wolbert van den Hoorn2, Tim V Wrigley3, Rana S Hinman4, Kelly-Ann Bowles5, Flavia Cicuttini6, Yuanyuan Wang7, Kim Bennell8. 1. The University of Queensland, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, 4072 Queensland, Australia; The University of Melbourne, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne, Parkville, 3010 Victoria, Australia. Electronic address: p.hodges@uq.edu.au. 2. The University of Queensland, Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, 4072 Queensland, Australia. Electronic address: w.vandenhoorn@uq.edu.au. 3. The University of Melbourne, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne, Parkville, 3010 Victoria, Australia. Electronic address: timw@unimelb.edu.au. 4. The University of Melbourne, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne, Parkville, 3010 Victoria, Australia. Electronic address: ranash@unimelb.edu.au. 5. The University of Melbourne, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne, Parkville, 3010 Victoria, Australia. Electronic address: k.bowles.kab@gmail.com. 6. Department of Epidemiology and Preventive Medicine, Alfred Hospital, Monash University, Melbourne, Victoria, Australia. Electronic address: flavia.cicuttini@monash.edu. 7. Department of Epidemiology and Preventive Medicine, Alfred Hospital, Monash University, Melbourne, Victoria, Australia. Electronic address: yuanyuan.wang@monash.edu. 8. The University of Melbourne, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne, Parkville, 3010 Victoria, Australia. Electronic address: k.bennell@unimelb.edu.au.
Abstract
BACKGROUND: As knee osteoarthritis (OA) cannot be cured, treatments that slow structural disease progression are a priority. Knee muscle activation has a potential role in OA pathogenesis. Although enhanced knee muscle co-contraction augments joint stability; this may speed structural disease progression by increased joint load. OBJECTIVE: This study investigated the relationship between cartilage loss and duration of co-contraction of medial/lateral knee muscles in medial knee OA. DESIGN: Prospective cohort study. METHODS: Medial (vastus medialis; semimembranosus) and lateral (vastus lateralis; biceps femoris) knee muscle myoelectric activity was recorded in 50 people with medial knee OA during natural speed walking at baseline. Medial tibial cartilage volume was measured from MRI at baseline and 12 months. Relationships between percent volume loss and duration of co-contraction of medial/lateral muscles around stance phase and ratio of duration of medial to lateral muscle co-contraction were evaluated with multiple linear regression. RESULTS: Greater duration of medial muscle co-contraction and greater duration of medial relative to lateral co-contraction correlated positively with annual percent loss of medial tibial cartilage volume (P = 0.003). Estimated cartilage loss was 0.14 (95% confidence interval -0.23 to -0.05) greater for each increase in medial muscle co-contraction duration of 1% of the gait cycle. Lateral muscle co-contraction inversely correlated with cartilage loss. CONCLUSION: Data support the hypothesis that augmented medial knee muscle co-contraction underpins faster progression of medial knee OA. Increased duration of lateral muscle co-contraction protected against medial cartilage loss. Exercise and biomechanical interventions to change knee muscle activation patterns provide possible candidates to slow progression of knee OA.
BACKGROUND: As knee osteoarthritis (OA) cannot be cured, treatments that slow structural disease progression are a priority. Knee muscle activation has a potential role in OA pathogenesis. Although enhanced knee muscle co-contraction augments joint stability; this may speed structural disease progression by increased joint load. OBJECTIVE: This study investigated the relationship between cartilage loss and duration of co-contraction of medial/lateral knee muscles in medial knee OA. DESIGN: Prospective cohort study. METHODS: Medial (vastus medialis; semimembranosus) and lateral (vastus lateralis; biceps femoris) knee muscle myoelectric activity was recorded in 50 people with medial knee OA during natural speed walking at baseline. Medial tibial cartilage volume was measured from MRI at baseline and 12 months. Relationships between percent volume loss and duration of co-contraction of medial/lateral muscles around stance phase and ratio of duration of medial to lateral muscle co-contraction were evaluated with multiple linear regression. RESULTS: Greater duration of medial muscle co-contraction and greater duration of medial relative to lateral co-contraction correlated positively with annual percent loss of medial tibial cartilage volume (P = 0.003). Estimated cartilage loss was 0.14 (95% confidence interval -0.23 to -0.05) greater for each increase in medial muscle co-contraction duration of 1% of the gait cycle. Lateral muscle co-contraction inversely correlated with cartilage loss. CONCLUSION: Data support the hypothesis that augmented medial knee muscle co-contraction underpins faster progression of medial knee OA. Increased duration of lateral muscle co-contraction protected against medial cartilage loss. Exercise and biomechanical interventions to change knee muscle activation patterns provide possible candidates to slow progression of knee OA.
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