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.
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 [
The clinical presentation of knee OA is characterized by pain, limitation of movement, tenderness, and local inflammation [
In this study, we will specifically investigate STS movement, which is characterized by the transition from a wide base of support (BoS), provided by the feet, thighs, and buttocks, to a small BoS, provided by the feet alone. Moreover, high knee and hip extensor moments are required to lift the centre of mass (CoM) against gravity [
From previous research it is known that knee OA patients show increased weight-bearing asymmetry [
Although there are quite some studies that have investigated the effects of knee OA on STS movements, most of those studies fail to distinguish between effects of OA itself and effects of high body mass index (BMI), which is closely associated with OA. As obesity itself may modulate movement patterns during STS, it should not be neglected in biomechanical analyses [
In this case-control study three groups were studied: healthy controls (BMI = 20-25 kg/m2), lean knee OA patients (BMI = 20-25 kg/m2), and obese knee OA patients (BMI = 30-40 kg/m2). Subjects having a Kellgren-Lawrence (KL) score between 1 and 3 at the medial tibiofemoral site were included in the OA groups [
Exclusion criteria were any inflammatory arthritis, trauma, OA at any other joint, and moderate to severe OA in the ipsilateral patellofemoral OA and/or lateral tibiofemoral OA, anterior cruciate ligament injury, medial and collateral ligament injury, and psychiatric illness according to the Diagnostic and Statistical Manual of Mental Disorders classification criteria for psychiatric illnesses (patients were excluded when diagnoses were present in their medical files). Healthy women were nonobese, did not meet the exclusion criteria, and did not have knee OA according to the American College of Rheumatology classification criteria [
All subjects were informed on the purpose of the study and gave informed consent before participating in this study. This study was ethically approved by the METC aZM/UM.
Radiographic imaging was used to evaluate knee cartilage health and knee OA status. Presence of knee OA was assessed from X-ray images by the KL knee score [
To more accurately assess cartilage health in all study groups, MRI was performed using a 3T Philips Intera Scanner
Movement analysis was performed with an eight-camera, three-dimensional (3D) motion capture system
Subjects were asked to rise from a chair on a self-selected, comfortable speed. The chair had no arm and backrests and height was adjusted to knee and hip angles of 90 degrees. Use of the arms was prohibited, which was ensured by positioning each hand on the contralateral shoulder. Further, trials were performed barefoot and feet were placed parallel and in line with the shoulders. The dominant (control group) or affected (knee OA groups) leg was placed on the force platform. Leg dominance was assessed by asking the subject which leg would be used to kick a ball. After completion of the STS transfer, subjects were asked to sit again from the obtained standing position. Two test trials were performed to get familiar with the movement. Measurements were repeated seven times with 10 seconds of resting intervals.
Data were processed via MATLAB to generate the variables of study. Parameters of interest were total time, subphase duration, ankle/knee/hip ROM in the sagittal plane, ankle/knee/hip extension moments, knee adduction moments, and the vectors of the ground reaction forces: anterior-posterior (GRFy), vertical (GRFz), and mediolateral (GRFx). Joint moments and GRFz were corrected for body weight (BW). Trials were normalized to 100% of the STS task with intervals of 0.5%. The start of the trial was defined by the first moment the GRFz exceeded 20% of the maximal GRFz, with a threshold of 40 N. End of the trial was defined by the moment when the GRFz was lower than 20% of the maximal GRFz. Trials were subdivided into three phases based on joint kinematic events. Those phases included the leaning phase (start, maximal hip flexion), momentum phase (maximal hip flexion, maximum ankle dorsiflexion), and extension phase (maximum ankle dorsiflexion, end of trial) [
Normality of data was tested with the Shapiro-Wilk test. Averages were calculated over the different trials for the following parameters: STS time, subphase duration, GRF (all vectors), ankle/knee/hip sagittal ROM, ankle/knee/hip sagittal moments, and frontal knee moments. Reliability of the kinetic data for the knee and hip was tested using the intraclass correlation (ICC) [
Fifty-five subjects were included in this study (Table
Patient characteristics of the three different study groups, presented as mean (± SD).
| | ||
---|---|---|---|
Control (n=22) | Lean knee OA (n=14) | Obese knee OA (n=19) | |
Age (years) | 58.7 (4.4) | 60.1 (3.5) | 59.0 (5.1) |
Height (m) | 1.66 (0.04) | 1.67 (0.05) | 1.62 (0.07)1,2 |
Weight (kg) | 62.9 (6.1) | 66.1 (7.3) | 86.4 (12.3)1,2 |
BMI (kg/m2) | 22.5 (2.0) | 23.7 (2.3) | 32.4 (3.4)1,2 |
KL-score | - | 2.21 (0.74) | 2.38 (0.70) |
MOAKS (score/items) | 0.50 (0.42) | 1.01 (0.69)1 | 1.22 (0.66)1 |
1 = significantly different from control.
2 = significantly different from lean knee OA.
No significant differences between groups were observed in the duration of the STS task. (Table
STS-parameters for all different groups. Data are presented as mean (±SD).
| | ||
---|---|---|---|
Control (n=22) | Lean knee OA (n=14) | Obese knee OA (n=19) | |
| |||
Total | 0.99 (0.21) | 1.11 (0.28) | 1.17 (0.43) |
| |||
Leaning phase | 17.8 (6.1) | 19.2 (6.2) | 21.2 (9.6) |
Momentum phase | 16.0 (6.0) | 12.1 (4.7) | 14.7 (5.1) |
Extension phase | 66.2 (7.0) | 68.7 (5.1) | 64.1 (7.8) |
| |||
Ankle (sagittal) | 18.8 (6.6) | 18.9 (6.1) | 14.2 (6.5) |
Knee (sagittal) | 85.5 (11.4) | 85.8 (8.2) | 75.9 (10.3)1,2 |
Hip (sagittal) | 79.7 (7.4) | 81.7 (5.4) | 73.1 (12.3)1,2 |
| |||
Ankle (sagittal) | 0.32 (0.12) | 0.32 (0.09) | 0.29 (0.08) |
Knee (sagittal) | 0.89 (0.20) | 0.83 (0.16) | 0.70 (0.18)1 |
Knee (frontal) | 0.30 (0.22) | 0.26 (0.21) | 0.27 (0.18) |
Hip (sagittal) | 0.87 (0.19) | 0.79 (0.15) | 0.67 (0.16)1 |
| |||
GRFz max | 0.62 (0.06) | 0.58 (0.05) | 0.54 (0.08)1 |
| |||
GRFz max | 374.6 (48.8) | 376.2 (52.9) | 459.0 (89.4)1,2 |
GRFx max | 33.9 (8.22) | 37.1 (10.2) | 45.9 (16.5)1,2 |
GRFy max | 37.4 (12.2) | 34.9 (12.4) | 47.7 (12.6)1,2 |
1 = significantly different from control.
2 = significantly different from lean knee OA.
Kinetic data for the knee and hip in the sagittal plane showed high repeatability with an ICC of 0.970 and 0.917, respectively. Knee ROM in the sagittal plane was significantly lower in the obese knee OA group compared to both healthy controls (p=0.007) and lean knee OA patients (p=0.009). Similarly, hip ROM was significantly lower in the obese knee OA group, compared to healthy controls (p=0.023) and lean knee OA patients (p=0.009). The reductions in knee and hip ROM corresponded with lower maximal knee (p=0.002) and hip extension moments (p=0.001) in the obese knee OA group compared to the control group (Figure
Sagittal joint moment during STS transfer for the three different groups for knee (a) and hip (b). The horizontal lines indicate the mean group values.
The maximum of GRFz, after correction for bodyweight, was lower in the obese knee OA group, when compared to healthy controls (p=0.001). No differences in GRFz were found between the lean knee OA group and the controls. GRFx was higher in the obese knee OA group compared to both lean knee OA (p=0.045) and controls (p=0.003). Similarly, GRFy was higher in the obese knee OA group compared to both the lean knee OA patients (p=0.005) and healthy controls (p=0.01).
A significant correlation between knee OA severity, defined by the sum of the MOAKS score divided by the number of items scored, and time to perform the STS transfer was found (r=0.338; p=0.02).
The aim of the current study was to investigate differences in knee and hip kinetics during STS movement between healthy controls and lean and obese knee OA patients. Second, use of compensatory strategies was investigated in the different study groups. We were able to show reduced knee and hip ROM, accompanied by reduced peak hip and knee moments in the obese knee OA group. In addition, GRFz corrected for bodyweight was lower in the obese knee OA group compared to the control group. Obese subjects also showed a greater GRFx than both other groups, indicating the use of compensatory mechanisms to unload the affected knee. Total time to perform STS was not different between groups. Furthermore, none of the investigated STS parameters was different between the lean knee OA group and controls.
In previous research it has been shown that knee OA patients show alterations in STS movement [
Adequate hip and knee extension forces are also essential for efficient STS performance [
Generally, STS performance is quantified by the total time to perform the task. Although we did expect to find differences in STS duration, total time was not significantly different between groups, which is in contrast with studies of Su et al. and Turcot et al. [
In short, alterations in lower limb biomechanics seem to be only apparent in presence of both obesity and knee OA during STS movement. Within this group, compensatory mechanisms might be necessary to avoid pain and to preserve the ability to perform the task. Although our current study design allowed distinguishing between effects of knee OA and obesity, there were some limitations. We could not explain the occurrence of compensatory mechanisms by pain avoidance, as pain was not measured in this study. Besides, no markers were placed on the trunk to investigate its role in movement adaptations. Furthermore, muscle activity was not measured. Future studies on STS movement should be performed with a similar study design that includes electromyographic data, trunk biomechanics, and pain measurements. Finally to investigate the exact influence of BMI, our suggestion would be to include a second control non-OA obese group.
Our study shows that the biomechanical alterations during sit-to-stand movement are the result of an interplay between high body mass and knee OA, rather than knee OA alone. The combination of obesity and knee OA leads to reduced ROM in the knee and hip of the affected leg. Similarly, peak extension moments are decreased in both joints. This might be explained by asymmetrical loading, characterized by a lower GRFz, corrected for bodyweight, and higher GRFx of the affected leg. Since only obese knee OA patients show movement alterations, losing weight could restore sit-to-stand biomechanics to a healthy pattern. Future studies should examine the differences in muscle activity and trunk biomechanics between the different study groups for more insight in employed compensatory strategies.
The data used to support the findings of this study are included within the article.
The authors declare that there are no conflicts of interest regarding the publication of this paper.
We want to thank Wouter Bijnens for his support in data analysis.