Perbandingan Kadar Superoxide Dismutase (SOD), Malondialdehyde (MDA), dan Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) pada Kartilago Sehat dan Kartilago Osteoarthritis Sendi Lutut Manusia

Oleh :
David Hermawan Tedja - S932008002 - Fak. Kedokteran

Background: Oxidative stress is increasingly recognized as a key contributor to cartilage degeneration in osteoarthritis; however, direct evidence from human articular cartilage remains limited. Understanding redox imbalance in native human tissue is essential for advancing translational strategies in cartilage preservation and biomaterials research.Method: This observational case–control study analyzed human knee articular cartilage obtained from patients with end-stage osteoarthritis undergoing total knee arthroplasty and from non-osteoarthritic controls undergoing anterior cruciate ligament reconstruction. Levels of superoxide dismutase (SOD), malondialdehyde (MDA), and nuclear factor erythroid 2–related factor 2 (NRF2) were quantified using enzyme-linked immunosorbent assay. Between-group comparisons were performed using appropriate statistical tests, with results expressed as mean ± standard deviation and 95% confidence intervals.Results: Osteoarthritic cartilage demonstrated significantly reduced SOD levels compared with controls, indicating impaired antioxidant capacity. In contrast, MDA levels were markedly increased, reflecting enhanced lipid peroxidation and oxidative membrane damage. NRF2 expression was also significantly elevated in osteoarthritic cartilage, suggesting activation of compensatory redox-responsive signaling pathways. All between-group differences were statistically significant and demonstrated large effect sizes, indicating biologically meaningful separation between osteoarthritic and control cartilage samples.Conclusion: Human osteoarthritic knee cartilage exhibits a profound imbalance in redox homeostasis characterized by antioxidant failure, increased lipid peroxidation, and insufficient compensatory NRF2 activation. These findings provide direct human tissue–based evidence supporting oxidative stress as a central mechanism in osteoarthritis pathophysiology and offer a translational molecular framework relevant to the rational design of redox-responsive biomaterials and targeted antioxidant strategies for cartilage preservation.