Abstract
For many decades, we have viewed osteoarthritis (OA) as a homogeneous disease characterised by “wear and tear”. However, this view has been challenged recently and it is now clear that OA is a heterogeneous and low-grade inflammatory disease with multiple aetiologies and phenotypes. Each of these different phenotypes may be identified and targeted differently, opening up multiple pathways for therapeutic intervention. Combining imaging and carefully selected panels of biochemical markers can achieve enhanced patient stratification and lead to better-designed clinical trials. Analyses of observational studies and clinical trial datasets are underway to understand better the phenotypes responsible for why people develop OA and why, prognostically, they have differences in terms of disease progression. The aim of this presentation is to discuss the underlying mechanisms involved in common OA phenotypes, with a particular focus on low-grade inflammation and metabolic alterations. Aberrant cellular metabolism has been implicated in the pathogenesis of OA and this talk will summarise the current state of knowledge on the role of impaired metabolism in the cells of the osteoarthritic joint and highlight areas for future research, such as the potential to target metabolic pathways and mediators therapeutically.
