During the osteoarthritis (OA) process, activation of immune systems, whether innate or adaptive, is strongly associated with low-grade systemic inflammation. This process is initiated and driven in the synovial membrane, especially by synovium cells, themselves previously activated by damage-associated molecular patterns (DAMPs) released during cartilage degradation. These fragments exert their biological activities through pattern recognition receptors (PRRs) that, as a consequence, induce the activation of signaling pathways and beyond the release of inflammatory mediators, the latter contributing to the vicious cycle between cartilage and synovial membrane. The primary endpoint of this review is to provide the reader with an overview of these many molecules categorized as DAMPs and the contribution of the latter to the pathophysiology of OA. We will also discuss the different strategies to control their effects. We are convinced that a better understanding of DAMPs, their receptors, and associated pathological mechanisms represents a decisive issue for degenerative joint diseases such as OA.

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five were different at the time of ACL reconstruction surgery, six were different 6 months post-surgery, and eight were different 12 monthspost surgery. L-methionine, Glyoxylic acid, and Malonic acid concentrations were significantly lower across all time points in ACL injured cases compared to uninjured matched controls. L-Lysine concentrations were significantly higher in ACL injured cases across all time points. Succinic acid concentrations were significantly higher in ACL injured cases at the time of injury and at 6 months and 12 months post-surgery. Arachidonic acid concentrations were significantly higher in ACL injured cases at the time of injury, the time of surgery, and 12 months post-surgery. The total percentage of explained variance by the first two principal components was 55.0% at the time of ACL injury, 58.0% at the time of ACL reconstruction surgery, 59.8% at 6 months post-surgery, and 56.6% 12 months post-surgery. As demonstrated in the figure, modest separation was observed between ACL injured cases and uninjured matched controls at the first two time points (time of injury and surgery) and notable separation was observed at the latter two time points (6 months and 12 months post-surgery). The proportion of cumulative explained variance with the first four principal components improved to 78.2% to 84.5% across all time points. Conclusions: Plasma concentrations for several metabolites appear to differentiate between ACL injured cases and uninjured controls matched for sex, age, height, and weight. This differentiation between groups appears to improve at 6 and 12 months following ACL reconstruction. The metabolites identified may provide insight into the pathways associated with the initiation and progression of post-traumatic osteoarthritis following ACL injury; however, further research and longer term follow-up in this cohort is needed to confirm this. 412