SYNOVIAL FLUID ALTERATIONS CONTRIBUTE TO TRIBOLOGICAL IMBALANCES IN OSTEOARTHRITIC CARTILAGE

Low friction in the knee joint arises from an interplay between articular cartilage (AC) and synovial fluid (SF). In osteoarthritis (OA), AC degradation and changes in SF composition alter this tribological interface. However, the specific impact of OA-related SF changes on AC friction under physiological loading is not fully understood. Therefore, the aim of this study was to investigate patient-specific correlations between SF composition, viscosity, and cartilage friction coefficients to identify key SF alterations contributing to increased friction as a potential risk factor for OA progression. Following IRB approval, SF samples and tibial plateaus were collected from 12 patients undergoing knee arthroplasty (age 75 ± 8 years; KL score: 3–4). SF samples were centrifuged and analyzed for biochemical properties and viscosity. Cylindrical cartilage samples (Ø 5mm) were extracted for friction tests in a cartilage-against-glass configuration using 0.1 ml patient-specific SF as lubricant. Simulated gait loading was applied, and friction coefficients (µ) were calculated at different gait phases and time points. Cartilage structure was assessed via thickness (h 0 ) and ICRS score. Hyaluronic acid (HAC), lubricin (PRG4), and total protein concentration (TPC) were analyzed biochemically. SF viscosity was measured using a rheometer. Spearman correlation coefficients (ρ) were calculated to evaluate relationships among variables, with p < 0.05 considered significant. Strong negative correlations were observed between PRG4 concentration and µ endGait , µ endStance , and µ endSwing Moderate correlations showed that µ 0Stance was negatively associated with HAC, but positively associated with µ endGait and µ endStance . TPC showed moderate negative correlations with µ0 values. SF viscosity correlated negatively with µ0, except for η0.01 at 25°C. HAC strongly correlated with ICRS score and h 0 . Moderate negative correlations were found between SF viscosity and cartilage structure. The results confirm PRG4 as a critical boundary lubricant, with lower concentrations associated with higher friction, particularly after prolonged testing]. Reduced PRG4 and low SF viscosity impair lubrication, leading to higher friction which might promote OA progression. High TPC may disrupt lubrication layer formation by competing with other molecules. SF changes contribute to altered cartilage friction and may be risk factors for OA progression. These findings highlight the need for injectable tribo-supplements to restore SF composition and reduce joint friction, thereby advancing OA treatment.