OA developed in the contralateral intact knee with the progress of OA in the immobilized knee in a rabbit model of immobilization-induced OA.
We hypothesized that OA also developed in the contralateral mobile knee with the progress of OA in the immobilized knee in the rabbit model of immobilization-induced OA.
The present study demonstrated that OA developed in the contralateral mobile knees in association with the progression of OA in immobilized knees in a rabbit model of immobilization-induced OA.
In a rat model of immobilization-induced knee flexion contracture, the capsular contribution was demonstrated by sectioning the posterior knee joint muscles and failure to restore the full ROM thereby attributing the limitation to the capsule [ 35].
Our model of immobilization-induced knee flexion contractures and sham operated controls was designed to isolate the joint response to immobilization and previously published results indicate a detrimental role of immobilization on mechanical function, cartilage structure and capsule elasticity.
In a well-established rat model of immobilization-induced knee flexion contractures that do not directly injure the joint [ 35], changes in gene expression in the chondrocytes of articular cartilage have been identified.
More specifically, using a new mouse model of hindlimb immobilization, we attempted to: (1) characterize immobilization-induced changes in mTOR signaling, protein synthesis and muscle mass, (2) define the role of mTOR in these changes, and (3) determine whether forced activation of mTOR signaling can rescue the decline in protein synthesis and fiber size that is observed in immobilized muscles.
GLPG0492, a non-steroidal SARM, was evaluated and compared to TP in a mouse model of hindlimb immobilization.
To accomplish this, the authors first characterized key features of disuse atrophy by employing a new mouse model of hindlimb immobilization.
The anabolic properties of the recently identified SARM, GLPG0492, were evaluated in the adapted mouse model of hindlimb immobilization as described by Okamato and coworkers [ 28].
In order to define the role of mTOR signaling, we employed a mouse model of hindlimb immobilization along with pharmacological, mechanical and genetic means to modulate mTOR signaling.
