Biomaterials employed in the articular joint cavity, such as polycarbonate urethane (PCU) for meniscus replacement, lack of lubrication ability, leading to pain and tissue degradation. We present a nanostructured adhesive coating based on dopaminemodified hyaluronan (HADN) and poly-lysine (PLL), which can reestablish boundary lubrication between the cartilage and biomaterial. Lubrication restoration takes place without the need of exogenous lubricious molecules but through a novel strategy of recruitment of native lubricious molecules present in the surrounding milieu. The biomimetic adhesive coating PLL− HADN (78 nm thickness) shows a high adhesive strength (0.51 MPa) to PCU and a high synovial fluid responsiveness. The quartz crystal microbalance with dissipation monitoring shows the formation of a thick and softer layer when these coatings are brought in contact with the synovial fluid. X-ray photoelectron spectroscopy and ConA-Alexa staining show clear signs of lubricious protein (PRG4) recruitment on the PLL−HADN surface. Effective recruitment of a lubricious protein by PLL−HADN caused it to dissipate only one-third of the frictional energy as compared to bare PCU when rubbed against the cartilage. Histology shows that this reduction makes the PLL−HADN highly chondroprotective, whereas PLL−HA coatings still show signs of cartilage wear. Shear forces in the range of 0.07−0.1 N were able to remove ∼80% of the PRG4 from the PCU−PLL−HA but only 27% from the PCU−PLL−HADN. Thus, in this study, we have shown that surface recruitment and strong adsorption of biomacromolecules from the surrounding milieu is an effective biomaterial lubrication strategy. This opens up new possibilities for lubrication system reconstruction for medical devices.

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Catheterization is a common medical operation to diagnose and treat cardiovascular diseases. The blood vessel lumen is coated with endothelial glycocalyx layer (EGL), which is important for the permeability and diffusion through the blood vessels wall, blood hemodynamics and mechanotransduction. However EGL's role in catheter-blood vessel friction is not explored. We use a porcine aorta to mimic the blood vessel and a catheter loop was made to rub in reciprocating sliding mode against it to understand the role of catheter loop curvature, stiffness, normal load, sliding speed and EGL on the friction properties. Trypsin treatment was used to cause a degradation of the EGL. Decrease in catheter loop stiffness and EGL degradation were the strongest factors which dramatically increased the coefficient of friction (COF) and frictional energy dissipation at the aortacatheter interface. Increasing sliding speed caused an increase but increase in normal load first caused a decrease and then an increase in the COF and frictional energy. These results provide the basic data for safety of operation and damage control during catheterization in patients with degraded EGL. Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels 1. Although the incidence and the mortality rate of CVDs has decreased 2-5 , they still remain a leading cause of death all over the world according to the world health organization. In 2016, 17.9 million people died due to CVDs which was 31% of all global deaths 6. The decline in CVD deaths is due to the health awareness and lifestyle changes but also due to the effective diagnosis and intervention. Minimally invasive transcatheter cardiovascular interventions are the most popular operations with about 200 million endovascular catheterizations taking place every year 7. Often radial (forehand) or femoral (thigh) artery is chosen for catheter insertion. For the catheter to reach the vicinity of the heart, it commonly requires a catheter of 100 cm in length. Depending on the pathogenesis, a catheter may spend a few seconds to few days in vivo for diagnosis and treatment 8,9. Both the insertion of catheter and intervention requires continuous sliding contact between the catheter and the lumen of the blood vessels. A thin (~ 500 nm), gel-like endothelial glycocalyx layer (EGL) is present on the luminal side of the blood vessel. The EGL on the luminal surface of the aorta mainly consists of mesh of membrane bound proteoglycans e.g. syndecan-1 and glypican containing chondroitin sulfate and heparin sulfate side chains and secreted glycosaminoglycans like hyaluronic acid and associated plasma proteins 10-12. The polyanionic nature of these molecules provides an overall negative charge to the EGL 11 which plays an important role in protection, regulation, diffusion and antiadhesion 13,14 on the luminal surface of blood vessel. The EGL is delicate and the degradation of glycocalyx structures was found to occur after provocation with inflammatory and atherogenic stimuli, such as TNF...