Growing evidence has revealed the pivotal role of inflammatory biomarkers in the pathogenesis of osteoarthritis. There is significant interest in the prognostic value of select biomarkers, given the potential for early identification and treatment of patients at risk of osteoarthritis prior to the development of irreversible clinical disease. Clinical trials of novel therapeutics that disrupt the inflammatory pathways of osteoarthritis are also ongoing. The purpose of this review is to summarize the current literature on key biomarkers within the context of osteoarthritis pathogenesis, clinical symptom development, and treatment capabilities. Multiple recent studies have established biomarkers that signal the existence of osteoarthritis pathology and the development of clinical symptomology. However, prior to implementation in clinical practice, additional research is required to precisely define the prognostic value for numerous biomarkers and standardize their measurement. Biomarker-driven investigations represent a promising avenue for the early diagnosis and treatment of osteoarthritis.

OBJECTIVES: Continuous, therapeutic anticoagulation is the standard of care for patients on extracorporeal membrane oxygenation (ECMO). The risks of hemorrhage exacerbated by anticoagulation must be weighed with the thrombotic risks associated with ECMO. We hypothesized increased thrombotic events in patients who had interrupted (vs. continuous) anticoagulation during venovenous ECMO. DESIGN: This is a retrospective, observational study. SETTING: Enrollment of individuals took place at three adult ECMO centers in Minnesota from 2013 to 2022. PATIENTS: This study consists of 346 patients supported with venovenous ECMO. INTERVENTIONS: Anticoagulation administration was collected from electronic health records, including frequency and duration of anticoagulation interruptions (IAs) and timing and type of thrombotic events, and data were analyzed using descriptive statistics. MEASUREMENTS AND MAIN RESULTS: A total of 156 patients had IA during their ECMO run and 190 had continuous anticoagulation. Risk adjusted logistic regression demonstrated that individuals in the IA group were not statistically more likely to experience a thrombotic complication (odds ratio [OR], 0.69; 95% CI, 0.27–1.70) or require ECMO circuit change (OR, 1.36; 95% CI, 0.52–3.49). Subgroup analysis demonstrated greater frequency of overall thrombotic events with increasing frequency and duration of anticoagulation being interrupted (p = 0.001). CONCLUSIONS: Our multicenter analysis found a similar frequency of thrombotic events in patients on ECMO when anticoagulation was interrupted vs. administered continuously. Further investigation into the impact of the frequency and duration of these interruptions is warranted.