JOINT STIFFNESS AND ARTICULAR GELLING - INHIBITION OF THE FUSION OF ARTICULAR SURFACES BY SURFACTANT

It was proposed some years ago that, in osteoarthritis, one source of joint stiffness arises from 'articular gelling', but, if so, why does this not occur in the normal joint? In a preliminary experiment using agar gels, it is shown how such fusion of gel surfaces can be inhibite d by surface-active phospholipid (SAPL)-both synthetic and human-as qu antified by the shear stress needed to cause cleavage between samples after prolonged contact. On the other hand, normal bovine articular ca rtilage (BAC) does not fuse to itself, but can be made to do so if rin sed with a powerful lipid solvent known to remove the outermost layer of adsorbed SAPL along with the hydrophobicity so characteristic of th e normal 'waxy' surface it imparts. It is then shown how the inhibitio n of gel fusion can be restored by treating both bovine and human arti cular surfaces with exogenous SAPL derived from human AC and with synt hetic SAPL. Samples of human articular cartilage excised from osteoart hritic hips and knees during total joint replacement showed a 55% grea ter tendency to fuse together than normal BBC. This was exacerbated by solvent rinsing and can be attributed to a deficiency in the outermos t lining of SAPL previously studied as a load-bearing boundary lubrica nt capable of reducing friction and wear to the remarkably low levels observed physiologically. Hence, joint stiffness can be attributed, in part, to a deficiency in the lubricating layer of SAPL lining the nor mal articular surface where it can inhibit articular gelling/gel fusio n, possibly imparting other desirable physiological functions. The pos sibility of clinical replenishment of SAPL in the osteoarthritic joint is discussed.