Abstract
A new mechanism of physiological lubrication is proposed to explain how low-viscosity synovial fluid prevents articular surfaces from contacting and wearing. The new mechanism is based on the hypothesis that the hyaluronic acid chains in synovial fluid bind to the cartilage surfaces through electrostatic charges, with the phospholipid layer on an articular surface supplying the necessary attractive charges. The stationary hyaluronic acid network causes a large hydrodynamic resistance to outward flow from the gap. To determine the effectiveness of the network in preventing contact, squeeze-film flow between two incompressible, permeable disks is analyzed when a constant load is suddenly applied, and the solvent--synovial fluid minus the hyaluronic acid--escapes through the network and through the permeable disks. The analysis yields the approximate time for the gap distance to decrease to asperity size. For realistic physiological parameters, the time for the surfaces to contact is a minimum of several minutes and likely much longer. The role of albumin in the synovial fluid is included because the large protein molecules are trapped by the small openings in the hyaluronic acid network, which increases the flow resistance of the network and thereby delays contact of the surfaces.
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