Obesity, Osteoarthritis and Aging: The Biomechanical Links

AbstractObesity increases osteoarthritis (OA) risk in both knee and hand joints, although the greatest impact is on the knee. The accelerated onset of OA that occurs with obesity has major health and financial consequences for individuals and society. Thus, it is critical to understand how obesity increases the risk of OA to develop effective strategies to prevent disease onset and/or slow disease progression. Obesity alters knee joint loading by increasing the knee adduction moment; however, it is difficult to predict how obesity affects the local cartilage mechanical environment because obesity alters joint loading frequency, magnitude, and duration both positively and negatively depending on the anatomical location and time-scale of analysis. In particular, obesity is associated with significant reductions in overall physical activity levels. Recent advances in the use of MRI to quantify in vivo diurnal strains provide a new approach for identifying the net effect of obesity on articular cartilage deformation. A growing number of clinical and animal studies indicate a role for systemic factors, such as high dietary fat and excess adiposity, in increasing OA risk. Adipose tissue secretes immunoregulatory molecules called adipokines, which are increasingly recognized for their ability to perturb joint tissue homeostasis. However, identifying a specific role for systemic inflammatory factors in knee OA pathogenesis is not well understood due to the challenge of isolating the biomechanical aspects of aging and obesity from the inflammatory changes. Identifying the role of adipokines in modifying OA risk is expected to require a better understanding of the connection between (1) systemic and local joint inflammation, and (2) the interaction of inflammatory and biomechanical signaling pathways. In this chapter, we review how changes in biomechanical stimulation associated with obesity and aging may increase OA risk by modifying cartilage susceptibility to inflammation and oxidative stress-mediated catabolic pathways.KeywordsMitochondrial Reactive Oxygen SpeciesJoint LoadingMitochondrial Reactive Oxygen Species ProductionKnee Adduction MomentJoint StressThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.