Hyperbaric Oxygen Therapy Improves Subchondral Perfusion and Cartilage Integrity in Established Osteoarthritis: A Pharmacokinetic DCE-MRI and T2* Quantification Study

Objective This study investigated whether hyperbaric oxygen (HBO) therapy, initiated after disease establishment, exerts disease-modifying effects in a rat model of anterior cruciate ligament transection (ACLT)-induced post-traumatic osteoarthritis (PTOA). Design Thirty-six Sprague-Dawley rats underwent ACLT surgery. HBO therapy commenced at Week 11 (established OA phase) and continued for 6 weeks. Outcomes were assessed using Von Frey testing, multimodal 7T MRI (T2* quantification and pharmacokinetic DCE-MRI), and histopathology. Results By Week 10, ACLT induced significant mechanical allodynia, T2* prolongation, and SCB perfusion abnormalities ( A increase; k ep , k el decrease). Following HBO intervention, the ACLT+HBO group exhibited a marked recovery in mechanical withdrawal threshold and significantly lower T2* values compared to the ACLT-only group ( p < 0.01). DCE-MRI demonstrated that HBO restored clearance kinetics ( k el , k ep ) and suppressed pathological blood volume ( A ), effectively remediating subchondral venous congestion. Histologically, HBO reduced OARSI scores and suppressed α-SMA-positive vascular invasion across the tidemark. These findings suggest that HBO therapy may alleviate PTOA by suppressing catabolic activity and normalizing pathological subchondral angiogenesis. Conclusions HBO therapy, initiated post-pathogenesis, effectively attenuates nociception and preserves cartilage integrity by restoring subchondral microcirculatory homeostasis. These findings establish HBO as a potent, non-invasive disease-modifying strategy for PTOA.