Transcutaneous carbon dioxide improves joint inflammation and articular cartilage degeneration in rat osteoarthritis models.

AIMS: As global ageing and life expectancy increase, the prevalence and incidence of osteoarthritis (OA) are expected to rise. Transcutaneous carbon dioxide (CO(2)) therapy has been shown to promote muscle regeneration, fracture healing, strengthen athletic endurance, and aid recovery from peripheral nerve damage and cancer. However, its effect on symptom modification and inflammation in OA is largely unknown. This study aimed to examine whether CO(2) therapy could slow the progression of OA and relieve OA-related inflammation in a chemically or surgically induced model in rats. METHODS: OA model was induced in 32 nine-week-old male Wistar rats by intra-articular injection of monosodium iodoacetate (MIA) and surgically induced by destabilization of the medial meniscus (DMM) in the knee joint. The pathogenesis period of MIA was set at two weeks, and for DMM at four weeks. After the creation of the OA model, either CO(2) therapy or sham intervention was applied daily for 20 minutes, and treatment was applied at two weeks. Behavioural assessments were completed at the end of the intervention period, and then knee joints were harvested. Non-demineralized frozen sections were prepared, and samples were examined histologically. RESULTS: Assessments of knee joint diameter showed that knee swelling in the DMM model improved significantly after two weeks of CO(2) therapy compared to the control group. The histomorphometric evaluation showed a significant increase in chondrocyte density in the CO(2) group compared to the MIA and DMM groups. Furthermore, the number of matrix metalloproteinase 13 (MMP13), a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), and proinflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 positive cells decreased in the CO(2) group. In contrast, the number of aggrecan and type II collagen-positive cells increased. CONCLUSION: Our results demonstrate that transcutaneous CO(2) therapy improves OA-related inflammation and suppresses the degeneration of articular cartilage.