Biomechanical and biochemical degradation models were utilized to estimate fixed charge density (FCD) loss using a patient-specific finite element model of an anterior cruciate ligament reconstructed knee joint. Biomechanical degradation was based on the excessive maximum shear strains that may result in cell apoptosis, while biochemical degradation was driven by the diffusion of pro-inflammatory cytokines. The biomechanical model predicted substantial localized FCD loss near the lesion and on the medial areas of the lateral tibial cartilage. In turn, the biochemical model predicted FCD loss all around the lesion and also at intact areas.

Multibody dynamic simulation of knee function was used to evaluate groove-deepening trochleoplasty to treat patellar dislocations. Compared to the preoperative condition, trochleoplasty significantly decreased lateral patellar tracking from full extension to 60° of knee flexion. The average contact area decreased by approximately 10% in mid-flexion, with a corresponding increase in the maximum contact pressure of 13%–23%. Decreased lateral patellar maltracking reduces the risk of patellar dislocations, but elevated patellofemoral contact pressures could contribute to long-term cartilage degradation.

High fat (HF) diet led to obesity and inferior vertebral trabecular bone structure and function in mice of both sexes with greater effects in females. HF diet did not result in intervertebral disc degeneration in either sex but did cause inferior vertebral cortical bone structure in males. Systemic ablation of the receptor for advanced glycation endproducts (RAGE-KO) had few modifying effects. These early structural deficiencies may increase risk for spinal injury and degeneration with aging and additional stressors.