Aims

To explore key stakeholder views around feasibility and acceptability of trials seeking to prevent post-traumatic osteoarthritis (PTOA) following knee injury, and provide guidance for next steps in PTOA trial design.

Introduction Late degeneration of the ACL injured knee may be in part due to repeat injury, but also due to aberrant kinematics altering the wear pattern at the chondral surface. The aim of this study was to use tibio-femoral contact mapping by MRI to examine kinematic changes due to chronic ACL deficiency. Methods Twenty-three subjects with a history of chronic ACL deficiency (mean 18 years since injury) performed a closed chain leg press, relaxed and against a 15 kilogram weight. MRI recorded the tibio-femoral contact position at 15° intervals from 0° to 90° of knee flexion. Intra-articular pathology was assessed for all subjects by MRI, and at arthroscopy for 10 subjects. Results The tibio-femoral contact pattern of the ACL injured knee differed from the healthy contralateral knee (p=0.003). This difference was greatest in the medial compartment, particularly at 0° and 15° of knee flexion (p< 0.01), with the femur two millimetres (mean, SD 3.2 mm) posterior on the tibial plateau. Damage to the chondral surface was seen in the medial compartment in 16 subjects and lateral compartment in 12; medial meniscus damage was present in 16 subjects and lateral meniscus in 15. Chondral surface damage correlated with the difference in the tibio-femoral contact pattern between the healthy and injured knee in the medial compartment of the knee. Joint damage was not related significantly to time since injury, or Cincinnati knee score. Joint damage was related to level of sports participation, but probably indicates that as the joint failed, subjects curtailed their activity. Conclusions The kinematic consequences of chronic ACL injury may in part be responsible for the pattern of degenerative change, especially in the medial compartment of the knee. In relation to the conduct of this study, one or more of the authors is in receipt of a research grant from a non-commercial source

Summary Statement. Using a weight-bearing force control task, age-related changes in muscle action were observed in osteoarthritic subjects, however, greater activation of rectus femoris and medial hamstring muscles in the OA group compared to control indicates greater cocontraction and varied stabilisation strategies. Introduction. Osteoarthritis (OA) is the most debilitating condition among older adults. OA is thought to be mechanically driven by altering the stabilising integrity of the joint. The main contributor to knee joint stability is that of muscular contraction. In cases where the history of a traumatic knee joint injury is not a causal factor, a change in muscle function, resulting in reduced strength and force control in believed to induce OA development and progression. Since age is also a determining factor of OA, the purpose of this study was to investigate the muscle activation patterns of young healthy adults (YC), older healthy adults (OC), and adults with OA during a standing isometric force control task. Patients & Methods. A force matching protocol was used to evaluate muscle activation patterns of 41 YC (23.1±1.9 years of age) 18 OC (59.7±5.14 years), and 19 OA (63.5±8.1 years). Subjects stood with their leg of interest fixed to a force platform and modulated ground reaction forces while exposing equal body weight to each leg. Surface electromyography (EMG) of 8 muscles that cross the knee joint, kinetics and kinematics were recorded while subjects generated 30% of their maximal force in 12 different directions, corresponding to various combinations of medial-lateral-anterior-posterior ground reaction forces. Processed EMG was normalised to previously recorded maximum voluntary isometric contraction (MVIC) and ensemble averaged into group means for each loading direction. Muscle activation patterns were displayed in EMG polar plots and were quantified with symmetry analyses, mean activation levels (X. EMG. ), directions (Φ), and specificity indices (SI). Group differences were tested with independent T-tests at the p<0.05 level. Results. Muscle activation patterns were similar between groups (i.e. symmetry and Φ). However, X. EMG. of 7 muscles was significantly greater in both the OA and OC groups compared to YC. OA group also demonstrated significantly greater X. EMG. in the rectus femoris and tensor fascia lata as well as lower SI in semitendinosus hamstrings compared to OC. Discussion/Conclusion. Our results indicate that regardless of loading direction, both OC and OA groups have greater levels of muscle co-contraction than YC. This is suggested to be an adaptive response to age-related changes in muscle strength and force control. Since individuals with OA have reduced muscle strength and force control compared to age-matched controls, our results suggest that the OA group's greater, less specific activation of knee joint muscles relative to the OC is this “stiffening” response adapted by the OA group, however, to an extent that may expose the joint to detrimental loading conditions, contributing to the progression of OA. Further investigation regarding age-related neuromuscular changes and their influence on joint loading conditions and development of OA is warranted

Aims

Interleukin (IL)-1β is one of the major pathogenic regulators during the pathological development of intervertebral disc degeneration (IDD). However, effective treatment options for IDD are limited. Suramin is used to treat African sleeping sickness. This study aimed to investigate the pharmacological effects of suramin on mitigating IDD and to characterize the underlying mechanism.

Objectives

Metabolic syndrome and low-grade systemic inflammation are associated with knee osteoarthritis (OA), but the relationships between these factors and OA in other synovial joints are unclear. The aim of this study was to determine if a high-fat/high-sucrose (HFS) diet results in OA-like joint damage in the shoulders, knees, and hips of rats after induction of obesity, and to identify potential joint-specific risks for OA-like changes.