Musculoskeletal tissues in the body exhibit unique biomechanical properties which enable tasks including load carrying capacity and movement, which can deteriorate in degenerative disease states and result in structural failure and subsequently loss of function. The study of the biomechanical contributions in injury models and repair implants may elucidate failure mechanisms and predict repair success, respectively. We hypothesize that (1) mechanically-driven knee injury models can replicate in vivo disease patterns in post-traumatic osteoarthritis (PTOA) in the rabbit and (2) reparative spine fusion implants for degenerative disc disease can be modulated to exhibit mechanical properties consistent with mechanobiological bone healing. This dissertation aimed to develop experimental biomechanical approaches for (1) inducing rabbit knee articular cartilage degeneration through ex vivo mechanical loading, and (2) assessing and comparing mechanical behavior of spine fusion cage designs.

A novel ex vivo approach was developed for rabbit knee articulation to rapidly induce cartilage damage, extending past in vivo rabbit studies of PTOA after anterior cruciate ligament transection (ACLT). In this ex vivo ACLT mechanical loading model, cycle-dependent cartilage degeneration was higher compared with sham surgery and non-loading controls, as assessed by gross and histological degeneration. These gross degenerative changes resembled changes observed in vivo at 4 weeks post-ACLT. This new ex vivo rabbit knee loading approach provides a platform to study mechanisms of joint-scale cartilage damage as well as possible interventions.

A novel ex vivo biomechanical approach for assessing loaded spinal fusion cages was developed, enabling high spatial resolution strain measures throughout an implant volume. These experimental studies extend past in vivo and numerical modeling studies, which are inherently limited by resolution and complexity of loading conditions. Using 3-D imaging to track affixed fiducial markers throughout a trussed spine implant under varying loads, truss-specific strains were quantified, with amplitudes consistent with bone mechanobiological homeostasis. The effect of cage design on truss strains was further studied, which demonstrated that varying design can be used to modulate strain amplitudes. These findings suggest that spine implant designs can be targeted to mechanobiological strain regimes for improved implant bone ingrowth and subsequent fusion success.