Abstract

Osteoarthritis is one of the major causes of immobility and its current prevalence in elderly (>60 years) is 18% in women and 9.6% in men. Patients with osteoarthritis display altered movement patterns to avoid pain and overcome movement limitations in activities of daily life, such as sit-to-stand transfers. Currently, there is a lack of evidence that distinguishes effects of knee osteoarthritis on sit-to-stand performance in patients with and without obesity. The purpose of this study was therefore to investigate differences in knee and hip kinetics during sit-to-stand movement between healthy controls and lean and obese knee osteoarthritis patients. Fifty-five subjects were included in this study, distributed over three groups: healthy controls (n=22), lean knee osteoarthritis (n=14), and obese knee OA patients (n=19). All subjects were instructed to perform sit-to-stand transfers at self-selected, comfortable speed. A three-dimensional movement analysis was performed to investigate compensatory mechanisms and knee and hip kinetics during sit-to-stand movement. No difference in sit-to-stand speed was found between lean knee OA patients and healthy controls. Obese knee osteoarthritis patients, however, have reduced hip and knee range of motion, which is associated with reduced peak hip and knee moments. Reduced vertical ground reaction force in terms of body weight and increased medial ground reaction forces indicates use of compensatory mechanisms to unload the affected knee in the obese knee osteoarthritis patients. We believe that an interplay between obesity and knee osteoarthritis leads to altered biomechanics during sit-to-stand movement, rather than knee osteoarthritis alone. From this perspective, obesity might be an important target to restore healthy sit-to-stand biomechanics in obese knee OA patients.

Highlights

  • Osteoarthritis (OA) is one of the world’s leading causes of immobility and is defined by degeneration of subchondral bone and articular cartilage in joint spaces [1]

  • Radiographic analysis indicated that both knee OA groups show average KL scores between two and three, confirming the presence of knee

  • GRFz corrected for bodyweight was lower in the obese knee OA group compared to the control group

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Summary

Introduction

Osteoarthritis (OA) is one of the world’s leading causes of immobility and is defined by degeneration of subchondral bone and articular cartilage in joint spaces [1]. OA affects weight-bearing joints such as the knee, which leads to severe alterations in biomechanics during activities of daily life [2]. Following the current rise in obesity and concomitant increase in life expectancy, prevalence of OA is expected to increase [4]. This poses OA as an increasing future health problem. While the exact pathophysiology of OA remains to be elucidated, it is currently believed that altered joint loading and cartilage metabolism are both key factors in cartilage degradation and subsequent OA development [7]

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